tag:blogger.com,1999:blog-36812181155016987812024-03-15T04:52:58.273+00:00Critical PediatricsAjay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.comBlogger14125tag:blogger.com,1999:blog-3681218115501698781.post-30358729721277434622018-08-12T20:10:00.121+01:002024-02-28T16:11:41.249+00:00Comprehensive Guide to Pediatric NIV Mask Selection, Types, Troubleshooting and more<img loading="lazy" alt="" border="0" data-original-height="355" height="355" data-original-width="640" width="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi8yBDMe5vilqaeXY89NjNQkGke2BFQ656Jf3oyzAKtVC16PszymjguoJ63GlAwaHDWe2yRxA7rM_b_1VbvQX6FUZN3IUK2Ou9upXFZkB8QtyWTFJXpD0mV9dEVVB5a26vHGsyPnM7eGcsJ9NvAshXw3lGRpft9oiMdPpQZwjRXEhz_Y3zATRac9b-MXuE/s1600/NIV%20in%20children.jpeg"/>
<p>In the realm of Pediatric Intensive Care, achieving optimal patient safety is a pursuit that demands meticulous attention, particularly when delving into the intricate world of Non-Invasive Ventilation (NIV). Thinking NIV as just a mask that delivers pressure is non-sensical, it is a subject as complex as mechanical ventilation if not more. The consequences of overlooking the nuances of the NIV setup can reverberate through the Pediatric Intensive Care Unit (PICU), impacting the delicate balance of patient care.</p>
<p>The correct setup of <strong>NIV masks, their accompanying circuits,</strong> and essential accessories emerge as a cornerstone in this endeavor. The meticulous assembly and seamless interface of these components become not just procedural nuances but rather <strong>pivotal elements,</strong> where precision is paramount to avoid or reduce the NIV failure rates.</p>
<a name='more'></a>
<p>In the first segment, we delve into the <strong>science of various masks</strong> that are used in non-invasive ventilation setups. This discussion is not only valuable for understanding the components but can prove beneficial when procuring NIV masks, circuits, and essential accessories for PICUs, <strong>especially in India</strong>.</p>
<p>Disclaimer: While I've mentioned specific company names and masks here, it's important to note that I derive no financial benefits from these mentions. The inclusion is solely to ensure the availability of these crucial resources in the PICU.</p>
<h2>Structure of NIV setup</h2>
<p>The basic NIV setup for both intensive care NIV or home ventilation NIV includes the following 3 components</p>
<ol>
<li>A machine that delivers flow, pressure, and volume</li>
<li>The circuit that connects the NIV machine to the mask</li>
<li>NIV Mask</li>
</ol>
<p>In this post, we will discuss the intricacies of NIV masks, including their types based on their operation principles, structure, problems with mask fit, and how to troubleshoot them. Let's begin...</p>
<h2>Types of NIV Mask - Based on ventilation physiology</h2>
<p>The NIV masks can be grouped into two different categories: <strong>vented and non-vented. </strong>They operate on different physical principles for CO2 clearance. As the name suggests, a vented mask assists in ventilation (CO2 clearance) on its own. On the other side, a non-vented mask will not support CO2 clearance by itself but will require an additional mechanism for the process, such as an <strong>active circuit with an exhalation valve</strong> or a <strong>leak port</strong> in a passive circuit. We will discuss these in the second part of NIV.</p>
<img class="lazy" alt="vented vs non-vented NIV mask" border="0" data-original-height="450" data-original-width="726" height="450" width="726" src="data:image/png;base64,R0lGODlhAQABAAD/ACwAAAAAAQABAAACADs=" data-src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjTzMABdM746LoQaESPRLvBwwsDg2mlIxQECizNY8LRy0ZuqMMhNjR7Krjz03XLy6X1h3UidLx-lHfzJdNEftZpKsCY3RBB9FvSruWaBmcmYxqzT-FEmcJVy2tPzEFvwIiunvAQTa35YFkI8TQOX-RokKfWkMb0fmVVmAiHH7vauiGAbmFfLjKH5ncHHdc/s1600/Vented%20mask.jpg"/>
<p>Now, let's delve into the detailed comparison of vented vs. non-vented masks.</p>
<h3><strong>Vented NIV mask</strong></h3>
<p>Vented masks feature small <strong>perforations</strong> or leak ports designed to facilitate the clearance of CO2 when a patient exhales.</p>
<p>These vents are typically situated on the <strong>body of the mask</strong>, or in some cases, an <strong>adapter or elbow</strong> is fitted to create a gap at the joint, allowing expired gases to escape. Notably, in some brands these elbows or adapters can be replaced, <strong>converting a vented mask into a non-vented</strong> one, providing greater flexibility without the need to change the entire mask (e.g., Hamilton BiTrac), See image below.</p>
<img class="lazy" alt="types of vented NIV mask" border="0" data-original-height="450" data-original-width="726" height="450" width="726" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjGs_gMoAe-vysOkPJ4LN2KPWxx-MUTTjlThqnoDtGxM1mn9r5Z4Nk5Z97qB0DP7TdNf3PuYdAI0XO4yAHMV0_X0IVuFKdcTL_1nGWv4hn2mQwnkYmHlhoPhxslzQijpXrwOHwyyMQY4apRjnDFnVzZPl9KDVMW_4zfREHB7p9trDiHFyVugWWlGvoOgZo/s1600/Types%20of%20NIV%20mask%20-%20Vented%20mask%20%281%29%20%281%29.png"/>
<p class="listen">In younger children, it is advisable to opt for a vented mask with perforations positioned close to the nose. This is particularly beneficial due to the limited tidal volume displacement in this age group, and having perforations nearer to the nose enhances CO2 clearance more effectively.</p>
<p>Vented masks are commonly connected to <strong>single-limb</strong> non-invasive ventilation (NIV) circuits and are compatible with standalone conventional NIV machines or BiPAP machines. However, it's important to note that they <strong>cannot be used with mechanical ventilators</strong> due to the risk of ineffective mean airway pressures. Additionally, the presence of a <strong>dedicated expiration limb in double-limb circuits</strong> eliminates the need for exhalation vents. Consequently, these masks can be used without anti-asphyxiation valves, which are necessary for non-vented masks in case of equipment failure and inadequate flow</p>
<p>The standard elbow that comes with non-vented masks is usually <strong>white / transparent</strong> in color for ease of identification.</p>
<h3><strong>Non-vented mask</strong></h3>
<p>There are no perforations or leak ports, CO2 clearance relies on <strong>either a leak valve</strong> in a single-limb circuit or an <strong>exhalation valve</strong> in a double-limb circuit. These masks are typically employed with double-limb circuits and mechanical ventilators equipped with a dedicated expiration valve. Refer to post on NIV curcuits for detail discussion in elbows and different types of NIV curcuits.</p>
<p>The <strong>mask elbow</strong> is usually <strong>colored blue</strong> to “warn” the user that it does not have an exhalation port. In some brands, you can change the elbow which fits in such as way that a gap is produced to leak air converting it into a vented mask.</p>
<p>Refer to post on type of mask elbows here.</p>
<h2>Types of Mask - Based on Anatomy</h2>
<p>There are several types of Pediatric NIV masks, ranging from full facial masks to more delicate<strong> nasal pillows</strong>.</p>
<ol>
<li>Full face mask (Never used it, I think adult ICUs might be using those)</li>
<li>Partial face masks or oronasal masks</li>
<li>Nasal mask</li>
<li>Nasal pillow / Nasal prongs</li>
</ol>
<img alt="types of Pediatric NIV mask" border="0" class="lazy" height="450" width="726" data-original-height="450" data-original-width="726" src="data:image/png;base64,R0lGODlhAQABAAD/ACwAAAAAAQABAAACADs=" data-src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjIZSoCrSthQpMyd8UNbxjLsdat870G10rvCOfYytgiivnJgMXRCTCx7Ey0EQEqSmGT3p5D1MIN38Ge7KYsBF-hcoOpf0Qc-z3PhJsvYDH65KSp8k8ze5gdzjeXskpMgqcOI3Qnl6tDQeMAPLCes1ArTNhVty-5gYHr1NlUOJcagSjB4Zan8ICeODEtupc/s1600/Type%20of%20NIV%20mask%20based%20on%20Anatomy.png"/>
<figure class="wp-block-table"><table><tbody><tr><td><strong>Nasal Mask and Pillows</strong></td><td><strong>Face mask/Oronasal mask</strong></td></tr><tr><td><strong>Advantages</strong><br>Less dead space<br>Less claustrophobia<br>Freedom for expectoration, vomiting, oral intake, vocalization<br>Lightweight interface<br>Easy for any sleeping position</td><td><strong>Advantages</strong><br>Fever air leaks<br>More stable Mean Airway pressure</td></tr><tr><td><strong>Disadvantages</strong><br>More air leaks<br>Less stable Mean Airway pressure<br></td><td><strong>Disadvantages</strong><br>More dead space<br>Less freedom for expectoration, vomiting, oral intake, vocalization<br>Heavier interface<br>Difficult for some sleeping positions</td></tr></tbody></table></figure>
<h3>Face Masks/Oronasal mask</h3>
<p>Face masks are the most commonly used interface. Face masks can be full face masks covering the entire face including eyes, I have never used one as such. A partial face mask also referred to as an oronasal mask covers just the mouth and nose. </p>
<p>These are especially important for children with respiratory failure or NIV-dependent neuromuscular cases. face masks are designed to cover both the mouth and nose, ensure a snug and comfortable fit, and also mitigate pressure loss by preventing air leakage around the mask's edges. Many kids with advanced respiratory morbidity resort to mouth breathing to overcome nasal flow resistance where these masks can be extremely effective.</p>
<h3>Nasal Masks</h3>
<p>Nasal CPAP masks are made to snugly fit over the nose, providing a comfortable interface for delivering airflow. Due to their minimalist design, these masks often offer a less claustrophobic experience compared to their full-face counterparts and also look less scary to children and parents. </p>
<p>These masks find primary use in situations where a reasonable leak is permissible, such as in the application of CPAP for conditions like Obstructive Sleep Apnea (OSA) or other forms of sleep-disordered breathing, as well as in airway stenting.</p>
<h3>Nasal Pillows</h3>
<p>These options are even more minimalistic. The nasal pillow fits directly into the nostrils, creating a perfect seal through a cushioned surface, in contrast to nasal prongs used for HFNC. </p>
<p>The airflow is directed straight into the nostrils, which might be uncomfortable for some children. Similar to nasal masks, these are typically employed for CPAP rather than BIPAP. Personally, I have primarily used them in older children and only on rare occasions.</p>
<p>I have used nasal pillow during my PICU training occasionaly for older children. For this article, I've scoured the internet for nasal pillows designed for young children but haven't come across suitable options. The majority of these products are tailored for adolescents and adults. </p>
<p>Nasal pillows are exceptionally lightweight, providing greater flexibility in and around the interface. Thus far, I've identified the Philips Respironics DreamWear Nasal Cushion, ResMed Nasal Pillows like AirFit P30i and AirFit P10, and the Philips 3100SP Therapy Nasal Pillow Mask. If you're aware of more options, feel free to share them in the comments.</p>
<p>I am sharing a compiled list of masks I have created for easy reference at the bottom of this post. It's important to note that I derive no financial benefits from disclosing the names of the available brands.</p>
<h2>Optimal Tips for Selecting the Right NIV Mask – A Comprehensive Guide</h2>
<h3>Why it is difficult to find correct NIV masks in children?</h3>
<p>In my perspective, the most challenging aspect in the entire initiation process of Non-Invasive Ventilation (NIV) is securing a suitable fit for the NIV mask, particularly in children. </p>
<p>Children present with diverse shapes and sizes, whereas NIV masks, unfortunately, lack corresponding variations, compounded by the limited availability of such options. This scarcity is attributed partly to logistical constraints and partly to a lack of awareness within our community.</p>
<h3>Mask Fitting - how important it is?</h3>
<p>Selecting the correct mask size is crucial for more than just leak prevention. Consider following things.</p>
<ul>
<li>It ensures stable mean airway pressure, appropriate tidal volume</li>
<li>Enhances patient comfort by minimizing space, allowing clear vision, facilitating daily care, and reducing eye irritation. </li>
<li>Larger masks, despite minimal leakage, may have increased dead space and are unsuitable for smaller children.</li>
</ul>
<p>The success or failure of Non-Invasive Ventilation (NIV) is, in part, determined by the <strong>adequacy of the mask fit</strong>, and entirely so if the patient <strong>selection was appropriate before</strong> initiation.</p>
<h3>There is no perfect NIV mask! </h3>
<p>There is no perfect mask, but there are solutions. Work on knowledge, logistics, and past experiences to make choices while selecting NIV masks.</p>
<h3>Logistic factors </h3>
<p>An important issue lies in the companies producing NIV masks, where it seems that ethnic variations, shapes, and sizes are not adequately considered in the manufacturing process. Many of these providers are based outside of Asia, and as a result, the masks may not cater well to the relatively smaller face sizes of Asian children. Consequently, even the very small masks tend to be relatively larger. As a compromise, many of us resort to using nasal masks as oronasal masks in numerous children, a situation that is indeed outrageous</p>
<p>The lack of uniformity in the supply chain poses a challenge as the masks we require are frequently unavailable through local vendors. I've encountered instances where vendors claim, '<strong>Oh, this mask isn't available in India</strong>,' which may not be accurate. I've observed that the same mask is often accessible through other vendors. It's essential for us to <strong>conduct our own research and not solely rely on vendor statements</strong>.</p>
<h4>Logistics - Troubleshooting</h4>
<p>While we may not have the ability to alter the manufacturing process, we can make an <strong>effort to convey these concerns to manufacturers in any possible manner</strong>, aiming to assist them in making improvements</p>
<p>Few tips</p>
<ul>
<li>Gather the list of Pediatric masks from the <strong>manufacturers' websites</strong>. ( Find my list at the bottom of this page).</li>
<li>Gather the list of <strong>available masks</strong> from multiple vendors in your area.</li>
<li>Check whether they are willing to ensure an uninterrupted supply of these interfaces and provide support. It's essential to have multiple options for providers</li>
</ul>
<h3>Compatibility</h3>
<p>Brands often have a tendency to design masks in a way that aligns with their specific NIV machines or ventilators, potentially prioritizing their supply chain over broader compatibility.</p>
<h4>Compatibility - troubleshooting</h4>
<p>Verify the compatibility of the masks with your NIV machines or ventilators. For example, many of us use F&P ventilator tubings, so it's crucial to ensure that NIV masks from other brands can be seamlessly fitted to these tubings or opt for the same brand.</p>
<h3>Clinical factors</h3>
<p>The judicious selection of masks based on clinical situations is paramount, as using an inappropriate mask can result in NIV failure. </p>
<h4>Troubleshooting</h4>
<p>Know which mask in general is <strong>appropriate for the given clinical situation</strong>. For instance, when aiming to maintain a stable mean airway pressure, especially in cases of post-extubation failure or children with restrictive lung disease, a non-vented orofacial mask should be the preferred choice. Conversely, in situations where airway stenting is necessary, such as in laryngomalacia, a nasal NIV mask can be employed.</p>
<p>Take into account the <strong>patient's age and tolerance</strong> when utilizing high-flow devices. In scenarios where an oro-facial mask might be suitable but patient tolerance is low, opting for a nasal mask initially may be preferable. Once patients become accustomed to the high flows, <strong>transitioning from nasal to oro-nasal masks</strong> can be more easily accomplished</p>
<p>Exploring different interfaces to determine the most suitable mask is, in fact, a viable strategy. <strong>Suitability </strong>can be defined by achieving <strong>improved clinical parameter</strong>s, enhanced patient <strong>tolerance</strong>, or a combination of both.</p>
<h4>The initial measurement for NIV mask fit</h4>
<p>In addition to selecting sizes based on age or experience, consider adopting a formal approach. Utilize sterilized older masks for fit assessments, or alternatively, maintain at least one of each type in the ICU specifically for <strong>fit assessment</strong> purposes</p>
<p>While reusing NIV masks is unadvisable, maintaining sterilized masks solely for fit checks before NIV initiation appears to be a <strong>reasonable option</strong>. Opening a brand new mask and subsequently being unable to use it due to misfit not only compromises economic considerations but also underscores the importance of <strong>pre-assessment</strong></p>
<p>Many brands have a scale given in a top compartment in the pack which can be used to measure the appropriate mask size without needing to open the compartment that stores the mask. This can be pretty useful, see the image below.</p>
<img alt="NIV mask fit testing" border="0" class="lazy" height="450" width="726" data-original-height="450" data-original-width="726" src="data:image/png;base64,R0lGODlhAQABAAD/ACwAAAAAAQABAAACADs=" data-src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg4XgnmkbfGo0mRpHvkeYqAeDEjeRxsT-B40To4_iCt8xoBpiwDuqs6JF10iwx_Gj9s5w7nfHAlWXPK4YLk2zOsIF6BPVHl-Y5KzGZYJmAyv4BqmJVqhk9B3IMCrdkfKy_4keymUTE4bXlRzHgJLs3cNCUvzcKy1_JADRQJxnw9zBOGymJFTAdFBNiS1bE/s1600/NIV%20Mask%20with%20scale%20for%20measurements.png"/>
<h2>Face mask Brand That can be used in a Hospital setting</h2>
<h3>F&P Nivairo Full Face Mask</h3>
<p>Although labeled as full face masks, I refer to them as oronasal masks for clarity, as they do not cover the eyes and the entire rim of the face. The F & P masks are available in four sizes: extra small, small, medium, and large. In my experience with ICU patients, I predominantly used extra small and small sizes, with medium being a rare choice. I've observed that the ergonomics are more fitting for non-Asian individuals, as they tend to be relatively larger for Indian faces</p>
<p>F & P Nivairo is available in both vented and non-vented variations. The non-vented mask is further divided into two categories: one without an <strong>anti-asphyxiation valve</strong> (as explained here) and the other with it. The elbows are fixed, preventing the ability to modify non-vented masks by adding a leak port or changing the standard elbow to the one with an anti-asphyxiation valve. This lack of mix-and-match options simplifies the configuration, which may be beneficial for new users by avoiding confusion. Further details about various types of elbows, circuits, and anti-asphyxiation valves will be discussed in the next post.</p>
<h4>The mask and sizes available </h4>
<ol>
<li>Vented mask - <strong>RT047</strong> (Xs, S, M, and L sizes, just add the letters after the product code to order size, like so, RT047XS )</li>
<li>Non-vented without anti-asphyxiation valve - <strong>RT046</strong>. This can be used with dual limb circuits only like in conventional mechanical ventilators with NIV mode. Sizes same as above.</li>
<li>Non-vented with anti-asphyxiation valve - <strong>RT045</strong>. This can be used in single-limb circuits like in-home ventilators or standalone NIV machines after connecting it to the leak port ( Learn here). Sizes same as above.</li>
</ol>
<p>All of these masks are designated as non-reusable. In my personal opinion, F & P employs the simplest nomenclature, making it easy to distinguish between their various masks</p>
<h4>Visairo Face Mask</h4>
<p>I have never seen these in any units where I worked so far, but they look very minimalistic, leaving the nose bridge off the pressure grid and not obstructing vision.</p>
<p>Product codes given on the website are - RT075, 76, and 77, classified just as above. There are some more fancy masks called Nivairo+ mentioned on their website. There are several other masks for home ventilation use given on their website which are quite confusing, <a href="https://www.fphcare.com/en-ca/products/homecare-products/masks/" target="_blank" rel="noreferrer noopener">take a look if you want to.</a></p>
<h3>Resmed</h3>
<p>ResMed mentions the <strong>hospital-grade full face mask</strong> by the same name, It is available in 3 sizes small (60703), medium (60704), and Large (60705), </p>
<p><strong>AcuCare F1-0</strong> is a non-vented, disposable face mask available in small (60768), medium (60769) and large (60770). I am surprised that even though these masks are seen on the Indian website of Resmed while trying to download the size and fit documents, it says it is a restricted download here. Hmmm.</p>
<p><strong>AcuCare F1-1 </strong>is again non-vented but with anti-asphyxiation valve. <strong>AcuCare F1-4</strong> is a vented, disposable mask for hospital use, with similar size options. There is no extra small size that we can use for younger children, so the target is adult patients but again I guess may be useful for older children and adolescents. <strong>Honestly, why do any of these companies provide these many options for pediatric agegroup?</strong></p>
<p>During my search, I found a very useful compatibility <a href="https://document.resmed.com/documents/products/serviceandsupport/maskdevicecompatibility/mask-device-compatibility-list_row_eng.pdf" data-type="link" data-id="https://document.resmed.com/documents/products/serviceandsupport/maskdevicecompatibility/mask-device-compatibility-list_row_eng.pdf" target="_blank" rel="noreferrer noopener">list of various masks and NIV machines on ResMed's website</a>.</p>
<h3>MiniMe 2 NIV pediatric nasal mask by Dragger</h3>
<p>This is primarily a nasal mask but if the facial profile is very small, I think it might be suitable as an orofacial mask. The official document recommended an age group of 2-12 years.</p>
<p>This comes both as <strong>vented small </strong>(MP01553), <strong>vented large </strong>(MP01554), and <strong>non-vented small</strong> (MP01555) and <strong>non-vented large </strong>(MP01556) masks. The vented one comes with a leak port.</p>
<h3>MiniMe 2 pediatric nasal NIV mask by Intersurgical</h3>
<p>I don't know why both Dragger and intersurgical nasal masks have the same name but more importantly, these mask comes in 4 sizes, Xs (part no 2570000), S (part no 2370000), M (part no 2371000), and L (part no 2571000). These sizes are available as both vented and non-vented categories giving more options to choose from.</p>
<p>Again these are <strong>nasal masks but can be used as orofacial masks</strong>, and it is <strong>purely my opinion</strong>.</p>
<h2>Nasal NIV masks</h2>
<p>Already mentioned the nasal mask by Dragger and Intersurgical above for older kids, for very small kids, the following two options are more suitable.</p>
<h3>Pixie mask by Resmed</h3>
<p>The official documents recommend ages <strong>2 to 7 years</strong> but we have used for little younger children with post-extubation stridor. It is a <strong>vented mask</strong>, I have seen young children comfortably tolerating it, it has a very minimalistic design, and a <strong>circuit can be attached to either side</strong>. It comes in a single size but with different cushion sizes in the pack.</p>
<h3>Wisp pediatric Nasal mask by Philips Respironics</h3>
<p>Aesthetically good mask, mostly seen during my training in resipirology in the UK for home CPAP use. As per documentation suitable for children above 10kg. Wisp pediatric nasal mask part numbers Fit pack with 3 cushion sizes, 1104953, Headgear 1104973, Elbow/tube with cover 1104977, Small cushions (SCS) 1104969, Medium cushions (SCM) 1104970, Large cushions (SCL) 1104971</p>
<h3><strong>Mirage Kidsta pediatric nasal CPAP mask by Resmed</strong></h3>
<p>Nasal mask for older children that can be used on Multiple patients of age <strong>above 7 years</strong> or above 40lb. It is a <strong>vented </strong>mask. The item code is 61011. I was not able to download any documentation since it is restricted in India, so I assume this is not available here.</p>
<h2>Nasal Pillows</h2>
<h3>ResMed AirFit P30i Nasal Pillow Mask and AirFit P10 Nasal Pillow Mask</h3>
<p>Mostly for adolescent and older children, have used them occasionally during training in PICU.</p>
<h3>F&P Evora </h3>
<p>It is basically a nasal pillow, never used it. Looks very large, and may be suitable for older kids with large facial profiles.</p>
<div class="related-box">
<h2>References / Further reading</h2>
<ol>
<li>Interfaces and humidification for noninvasive mechanical ventilation. Nava S1, Navalesi P, Gregoretti C. Respir Care. 2009 Jan;54(1):71-84.</li>
<li>Trilogy accessory guide</li>
<li>Ventilator modes and settings during non-invasive ventilation: effects on respiratory events and implications for their identification. Thorax. 2011 Feb;66(2):170-8. doi: 10.1136/thx.2010.142661. Epub 2010 Oct 14.</li>
<li>Non-invasive Ventilation – A century of experience, Frank van Rooyen, Krisztina Soltész</li>
<li>Patel, BK, Wolfe, KS, Pohlman, AS, et al. 2016. Effect of noninvasive ventilation delivered by helmet vs face mask on the rate of endotracheal intubation in patients with acute respiratory distress syndrome: a randomized clinical trial. JAMA. 315: 2435–2441. <a href="https://pubmed.ncbi.nlm.nih.gov/26614241/" target="_blank" rel="noreferrer noopener">PMID: 27179847</a></li>
<li>Allison, MG and Winters, ME. 2016. Noninvasive ventilation for the emergency physician. <em>Emerg Med Clin North Am</em>. <strong>34</strong>: 51–62. <a href="https://pubmed.ncbi.nlm.nih.gov/26614241/" target="_blank" rel="noreferrer noopener">PMID: 26614241</a></li>
<li>Antonelli, M, Pennisi, MA, and Conti, G. 2003. New advances in the use of noninvasive ventilation for acute hypoxaemic respiratory failure. <em>Eur Respir J Suppl</em>. <strong>42</strong>: 65s–71s. <a href="https://pubmed.ncbi.nlm.nih.gov/12946003/" target="_blank" rel="noreferrer noopener">PMID: 12946003</a></li>
<li>Meyer, TJ and Hill, NS. 1994. Noninvasive positive pressure ventilation to treat respiratory failure. <em>Ann Intern Med</em>. <strong>120</strong>: 760–770. <a href="https://pubmed.ncbi.nlm.nih.gov/8147550/" target="_blank" rel="noreferrer noopener">PMID: 8147550</a></li>
</ol></div>
<section class="profile"><div class="details-2"><h2 class="name bichme">Author</h2><img alt="about authors" class="photo lazy" data-src="https://1.bp.blogspot.com/-YBnfRvlorB8/X9-B39s1MmI/AAAAAAAAF18/SpYb28pe-lEdFodTxH-1VgQekQMSKdO_gCNcBGAsYHQ/s100/sharp%2Bcircle%2Bbw%2B125.jpg" src="data:image/png;base64,R0lGODlhAQABAAD/ACwAAAAAAQABAAACADs=" /><ul class="socialLink"><li><a aria-label="LinkedIn" class="link" href="https://www.linkedin.com/in/ajay-agade-intensivist/"><svg class="c-1" viewbox="0 0 32 32"><path d="M24,3H8A5,5,0,0,0,3,8V24a5,5,0,0,0,5,5H24a5,5,0,0,0,5-5V8A5,5,0,0,0,24,3Zm3,21a3,3,0,0,1-3,3H8a3,3,0,0,1-3-3V8A3,3,0,0,1,8,5H24a3,3,0,0,1,3,3Z"></path><path d="M11,14a1,1,0,0,0-1,1v6a1,1,0,0,0,2,0V15A1,1,0,0,0,11,14Z"></path><path d="M19,13a4,4,0,0,0-4,4v4a1,1,0,0,0,2,0V17a2,2,0,0,1,4,0v4a1,1,0,0,0,2,0V17A4,4,0,0,0,19,13Z"></path><circle cx="11" cy="11" r="1"></circle></svg></a></li><li><a aria-label="Twitter" class="link" href="https://twitter.com/CriticalPeds"><svg class="c-1" viewbox="0 0 32 32"><path d="M13.35,28A13.66,13.66,0,0,1,2.18,22.16a1,1,0,0,1,.69-1.56l2.84-.39A12,12,0,0,1,5.44,4.35a1,1,0,0,1,1.7.31,9.87,9.87,0,0,0,5.33,5.68,7.39,7.39,0,0,1,7.24-6.15,7.29,7.29,0,0,1,5.88,3H29a1,1,0,0,1,.9.56,1,1,0,0,1-.11,1.06L27,12.27c0,.14,0,.28-.05.41a12.46,12.46,0,0,1,.09,1.43A13.82,13.82,0,0,1,13.35,28ZM4.9,22.34A11.63,11.63,0,0,0,13.35,26,11.82,11.82,0,0,0,25.07,14.11,11.42,11.42,0,0,0,25,12.77a1.11,1.11,0,0,1,0-.26c0-.22.05-.43.06-.65a1,1,0,0,1,.22-.58l1.67-2.11H25.06a1,1,0,0,1-.85-.47,5.3,5.3,0,0,0-4.5-2.51,5.41,5.41,0,0,0-5.36,5.45,1.07,1.07,0,0,1-.4.83,1,1,0,0,1-.87.2A11.83,11.83,0,0,1,6,7,10,10,0,0,0,8.57,20.12a1,1,0,0,1,.37,1.05,1,1,0,0,1-.83.74Z"></path></svg></a></li></ul></div><div class="details"><p class="name">Ajay Agade | DNB(Pediatrics), FNB(Pediatric Intensive Care), Fellowship in Pediatric pulmonology and LTV</p><p class="about">Ajay is a Paediatric Intensivist, currently working in Pediatric Pulmonology & LTV at Great Ormond Street Hospital NHS, London</p></div></section>
Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-5555145513768001322018-08-03T10:59:00.017+01:002024-02-29T10:26:00.604+00:00Nutrition in Critically ill Children<div class="separator" style="clear: both;"><img alt="" border="0" data-original-height="350" data-original-width="725" loading="lazy" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiKS4XA3t7H4l2AkVpolJARddPP58VCi_nop-UlldqATRrMABrbvPtXLbAv1TpkHi-t-OqRUSLgAPa8io-vM5nc-qeaEMUDfcN23xnUIdUHgli-k-yc8V58uMOiGm8BlVWcpH3gSbzGQj0/s0/Nutrition+in+critically+ill+children+%25281%2529.png" /></div>
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<p><br>The collaborative effort between the American Society of Parenteral and Enteral Nutrition (ESPEN) and the Society of Critical Care Medicine (SCCM) in formulating the ESPEN/SCCM guidelines in 2016 marked a pivotal advancement in critical care nutrition for adults. These guidelines served as a robust foundation for in-depth analyses, particularly in the domain of dogmalysis.</p>
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<p><code>Subsequent to this significant milestone, the focus extended to the pediatric population, leading to the unveiling of the "Best Practices for Nutrition in Critically Ill Children 2017." This release, tailored for children aged over 1 month and under 18 years, reflects a nuanced approach in addressing the distinctive nutritional challenges faced by critically ill pediatric patients.</code></p>
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<p>I have tried to summarise the salient points and common questions that arise in day-to-day rounds in the PICU, and dogma lysis of some of the concepts that are still prevalent among many of us in the Pediatric ICU.</p>
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<h2 class="wp-block-heading">Literature review</h2>
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<p>The guidelines were formulated after reviewing the following literature.</p>
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<li>16 randomized controlled trials</li>
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<li>37 cohort studies</li>
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<li>The above studies were used to answer eight preidentified questions for eight practice areas. I like these guidelines since they have more practical approach and based on day to day questions and dicsussion.</li>
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<p class="note gg">Tip-These can be used to stop the argument occasionally with surgeon. (But use the tip with caution)</p>
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<h2 class="wp-block-heading">Guidelines Limitations</h2>
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<p>The following limitation can be noted.</p>
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<li>The guideline is based on general consensus among a group of professionals.</li>
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<li>The literature used has variations in study design, small sample size, and patient heterogeneity, There is a variability in disease severity amongst the sample. </li>
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<li>There is a lack of information on baseline nutritional status.</li>
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<li>There is no high-quality statistical data available for analysis.</li>
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<p>These are some of the questions that the guideline answers or points that are recommended.</p>
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<h2 class="wp-block-heading">1 A. What is the Impact of nutritional status on outcomes in critically ill children </h2>
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<p><strong>Quality of evidence:</strong> very low</p>
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<p><strong>Grade of recommendatio</strong>n: strong</p>
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<h3 class="wp-block-heading"><strong>Answer:</strong></h3>
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<p>Malnutrition, including obesity, is associated with following adverse clinical outcomes.</p>
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<li>longer periods of ventilation,</li>
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<li>higher risk of hospital-acquired infection,</li>
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<li>longer PICU and hospital stay, and</li>
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<li>increased mortality.</li>
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<p><strong>Do this for all PICU admissions</strong></p>
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<li>Detailed nutritional assessment within 48 hr of admission.</li>
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<li>Re-evaluate at least weekly throughout hospitalization.</li>
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<h2 class="wp-block-heading">1 B. What are the best practices for screening and identifying patients with malnutrition or at risk of malnutrition in the PICU?</h2>
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<p><strong>Quality of evidence:</strong> very low<br><strong>Grade of recommendation:</strong> strong</p>
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<h3 class="wp-block-heading"><strong>Answer:</strong></h3>
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<ul><!-- wp:list-item -->
<li><strong>Weight and height/length</strong> to be measured on admission to the PICU,</li>
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<li>Z scores for BMI for age and weight-for-length should be recorded for ages < 2 yr</li>
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<li>Weight-for-age, in case accurate height is not available, should be used to screen for nutrition status.</li>
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<li>In children under the age of 36 months, head circumference must be documented.</li>
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<h3 class="wp-block-heading"><strong>Additional Points</strong></h3>
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<p>BMI z scores may additionally be useful to screen for patients at risk of poor outcomes in the PICU</p>
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<h2 class="wp-block-heading">2 A. What is the recommended energy requirement for critically ill children?</h2>
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<p>Predicting calorie assessment in critically ill pediatric patients has been a perplexing journey, marked by varying numbers and explanations. The gold standard, indirect calorimetry (IC), remains out of reach in many units, mirroring my own experience in training and subsequent work settings where its provision was absent. </p>
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<p><strong>Quality of evidence</strong>: low<br><strong>Grade of recommendation:</strong> weak</p>
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<p>Indirect calorimetry (IC) to be used to determine energy expenditure (REE) and guide prescription of the daily energy requirements</p>
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<h2 class="wp-block-heading">2 B. How to determine energy requirement in the absence of indirect calorimetry?</h2>
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<p>The guidelines, however, outline steps to take when IC is not available. This disjunction between the ideal and the practical underscores the ongoing challenge of ensuring precise nutritional management for critically ill individuals. Both IC and optional steps have a low quality of evidence.</p>
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<p><strong>Quality of evidence: </strong>very low<br><strong>Grade of recommendation:</strong> weak</p>
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<h3 class="wp-block-heading"><strong>If IC measurement is not available</strong></h3>
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<p>Use the <a href="https://en.wikipedia.org/wiki/Schofield_equation" data-type="link" data-id="https://en.wikipedia.org/wiki/Schofield_equation" target="_blank" rel="noreferrer noopener">Schofield</a> or <a href="https://www.fao.org/3/y5686e/y5686e06.htm#TopOfPage" data-type="link" data-id="https://www.fao.org/3/y5686e/y5686e06.htm#TopOfPage" target="_blank" rel="noreferrer noopener">Food Agriculture Organization/World Health Organization/United Nations University equations</a> <strong>“without” the addition of stress factors</strong> to estimate energy<br>expenditure in PICU.</p>
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<p><strong>Note</strong></p>
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<p>Many of us have been using the Harris benedicts equation to estimate calorie requirement. The guideline recommends <strong>against the use of the Harris-Benedict equations and the RDAs </strong>to determine energy requirements in critically ill children. </p>
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<h2 class="wp-block-heading">What is the Harris-Benedict equation?</h2>
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<p>The body's<strong> basal metabolic rate </strong>(BMR) represents the energy needed for essential metabolic functions like respiration, thermogenesis for maintaining body temperature, and digestion. This energy expenditure occurs at rest, devoid of any additional activity. </p>
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<p>It exclusively sustains vital organ functions, encompassing the heart, lungs, nervous system, kidneys, liver, intestine,, muscles, and skin. So, Basal metabolic rate (<strong>BMR) is the amount of calories burnt during an </strong>inactive period such as sleep. It can be calculated from height, weight, age, and gender.</p>
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<p>Harris-Benedict equation estimates the BMR in step 1 and then in step 2, it estimates the total energy expenditure for a particular activity level, and the calorie requirement for that individual for that activity level.</p>
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<h4 class="wp-block-heading">BMR calculation for men</h4>
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<p>BMR = 66.47 + ( 13.75 x weight in kg ) + ( 5.003 x height in cm ) - ( 6.755 x age in years )</p>
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<h4 class="wp-block-heading">BMR calculation for women </h4>
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<p>BMR = 655.1 + ( 9.563 x weight in kg ) + ( 1.850 x height in cm ) - ( 4.676 x age in years )</p>
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<p>The Harris-Benedict Equation uses BMI and calculates the total energy expenditure (TEE) for the given activity by using the activity factor as follows.</p>
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<figure class="wp-block-table"><table><tbody><tr><td>Activity level</td><td>Total energy expenditure (TEE)</td></tr><tr><td>Sedentary or light activity TEE</td><td>BMR x 1.53</td></tr><tr><td>Active or moderately active TEE</td><td>BMR x 1.76</td></tr><tr><td>Vigorously active</td><td>BMR x 2.25</td></tr></tbody></table></figure>
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<h3 class="wp-block-heading">2C. What should be the target energy intake in critically ill children</h3>
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<p><strong>Quality of evidence:</strong> low</p>
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<p>The recommendation emphasizes the aim of delivering a <strong>minimum of two-thirds</strong> of the prescribed daily energy requirement <strong>by the close of the first week</strong> in the Pediatric Intensive Care Unit (PICU). </p>
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<p>Recognizing and managing<strong> energy deficits within this initial critical week </strong>may correlate with <strong>favorable clinical and nutrition outcomes</strong>.</p>
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<p>The guidance underscores a focus on <strong>individualized </strong>energy requirements, prompt <strong>initiation</strong>, and successful <strong>achievement </strong>of energy targets. This multifaceted approach seeks to avert <strong>unintended cumulative caloric deficits or excesses</strong>, fostering optimal nutritional support in the PICU setting.</p>
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<h2 class="wp-block-heading">3A. What should be the minimum recommended protein requirement for critically ill children?</h2>
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<p><strong>Quality of evidence:</strong> moderate<br><strong>Grade of recommendation: s</strong>trong</p>
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<p><strong>Minimum </strong>recommended protein intake is 1.5 g/kg/d.</p>
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<p>Higher than this threshold is shown to <strong>prevent cumulative negative protein balance</strong> in RCTs. The optimal protein intake required to attain a positive protein balance <strong>may be higher than this</strong> minimum threshold in sick children.</p>
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<p>Negative protein balance may result in loss of lean muscle mass, which has been associated with <strong>poor outcomes </strong>in critically ill patients.</p>
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<p>Higher protein intake may be associated with lower 60-day mortality in mechanically ventilated children. (Observational study )</p>
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<h2 class="wp-block-heading">3B. What is the optimal strategy to deliver protein in the PICU?</h2>
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<p><strong>Quality of evidence:</strong> moderate<br><strong>Grade of recommendation: </strong>weak</p>
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<p>Based on the findings from randomized trials, the suggestion is to <strong>initiate protein provision early</strong> in the trajectory of critical illness, aiming to meet protein delivery goals and foster a positive nitrogen balance. </p>
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<p>Notably, observational studies have indicated that achieving a higher proportion of the protein goal correlates with positive clinical outcomes. This recommendation underscores the significance of early and effective protein delivery in optimizing patient responses during critical illness.</p>
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<h2 class="wp-block-heading">3C. How to set protein delivery goals in PICU?</h2>
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<p><strong>Quality of evidence: </strong>moderate<br><strong>Grade of recommendation:</strong> strong</p>
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<p><strong>Nothing is clarified </strong>here, unfortunately. What is the optimal protein dose that will improve clinical outcomes is<strong> not known</strong>. <strong>RDA values </strong>were developed for healthy children and often <strong>underestimate </strong>the protein needs during critical illness.</p>
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<p>The optimal protein dose associated with improved clinical outcomes is not known. We do not recommend the use of RDA values to guide protein prescription in critically ill children. These values were developed for healthy children and often underestimate the protein needs during critical illness.</p>
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<h2 class="wp-block-heading">4A. Should we start enteral nutrition in critically ill children?</h2>
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<p><strong>Quality of evidence: </strong>low<br><strong>Grade of recommendation:</strong> strong</p>
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<p>Yes, as per guidelines, enteral nutrition is the preferred mode in critically ill children over any other route.</p>
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<h3 class="wp-block-heading">Who can receive it?</h3>
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<ol><!-- wp:list-item -->
<li>Kids with medical diagnoses</li>
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<li>Kids with surgical diagnoses</li>
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<li>Those receiving vasoactive medications for shock.</li>
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<h3 class="wp-block-heading">What are common barriers to EN in the PICU?</h3>
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<p>I can not agree to this more than anything. The common interruptions are</p>
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<ul><!-- wp:list-item -->
<li> Delayed initiation, </li>
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<li>Interruptions due to perceived intolerance</li>
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<li>Prolonged fasting around procedures.</li>
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<p>Identifying these Interruptions to EN and minimizing them to achieve nutrient delivery goals is the key.</p>
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<h2 class="wp-block-heading">4B. What are the benefits of enteral nutrition in sick children?</h2>
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<p><strong>Quality of evidence:</strong> low<br><strong>Grade of recommendation: </strong>weak</p>
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<p>The administration of nutrients via Enteral Nutrition (EN) has proven advantageous for maintaining gastrointestinal <strong>mucosal integrity and promoting motility</strong>. </p>
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<p>Notably, early commencement of EN within the<strong> initial 24-48 hours</strong> of Pediatric Intensive Care Unit (PICU) admission, coupled with <strong>achieving up to two-thirds</strong> of the nutrient goal within the first week of critical illness, has demonstrated a <strong>positive correlation</strong> with enhanced clinical outcomes, as evidenced by large cohort studies. </p>
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<p>This highlights the significance of<strong> timely initiation and effective nutrient</strong> delivery through EN in contributing to improved patient responses during critical illness.</p>
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<h2 class="wp-block-heading">5A. What is the best method for advancing EN in the PICU population?</h2>
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<p><strong>Quality of evidence:</strong> low<br><strong>Grade of recommendation: </strong>weak</p>
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<p>Straightforward guidance is not provided here. Again the circus of words "Use of a stepwise algorithmic approach to advance EN in children admitted to the PICU". The stepwise algorithm must include <strong>bedside support to guide</strong> the detection and management of EN <strong>intolerance </strong>and the <strong>optimal rate of increase</strong> in EN delivery. It means get your stuff right your way.</p>
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<h2 class="wp-block-heading">5B. What is the role of a nutrition support team or a dedicated dietitian in optimizing nutrition?</h2>
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<p><strong>Quality of evidence:</strong> low<br><strong>Grade of recommendation: </strong>weak</p>
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<p>The nutrition support team, including a <strong>dedicated dietitian,</strong> should be included in the PICU team, to facilitate timely nutritional assessment and optimal nutrient delivery.</p>
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<h2 class="wp-block-heading">6A. What is the best site for enteral nutrition delivery - gastric or small bowel?</h2>
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<p><strong>Quality of evidence:</strong> low<br><strong>Grade of recommendation:</strong> weak</p>
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<p>The preferred route is gastric, however, in select patients, the <strong>postpyloric route</strong> may be used in those who are unable to tolerate gastric feeding or those at high risk for aspiration.</p>
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<p>Their data is <strong>Insufficient </strong>to make recommendations regarding the use of <strong>continuous vs intermittent</strong> gastric feeding.</p>
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<h2 class="wp-block-heading">6B. When to initiate enteral nutrition?</h2>
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<p><strong>Quality of evidence:</strong> low<br><strong>Grade of recommendation</strong>: weak</p>
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<ul><!-- wp:list-item -->
<li>Enteral nutrition should be initiated in all critically ill children unless contraindicated.</li>
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<li>Consider early initiation, within the first 24–48 hr after admission to the PICU, if not contraindicated.</li>
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<h2 class="wp-block-heading">7A. What is the indication for and optimal timing of PN in critically ill children?</h2>
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<p><strong>Quality of evidence: </strong>moderate<br><strong>Grade of recommendation: </strong>strong</p>
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<p>There are 3 main questions we all face in PICU. 7A and 7B try to answer those questions.</p>
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<ul><!-- wp:list-item -->
<li>Whether to use of PN as a supplement to EN in case we cannot increment it further?</li>
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<li>When should we start PN?</li>
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<li>What is the targeted for macronutrient goal'</li>
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<p>There is no data to answer any of these firstly in these guidelines. However, they have quoted the following study.</p>
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<h3 class="wp-block-heading">3-center RCT, PEPaNIC trial - Early versus Late Parenteral Nutrition in the Pediatric Intensive Care Unit. </h3>
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<li>The trial addresses the timing of supplemental PN in critically ill children, the group with late initiation of PN on day 8, demonstrated better outcomes in terms of fewer new infections and shorter length of PICU stay when compared with the early initiation group receiving PN within 24 hours of admission. </li>
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<li>Also, the late PN group was likely to have an earlier live discharge from the PICU, shorter duration of mechanical ventilation, and lower odds of renal replacement therapy.</li>
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<p>based on this, my take-home message is PN should be considered when EN is not feasible or is contraindicated but don't be in a hurry to start it.</p>
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<h2 class="wp-block-heading">7B. Is there a role of parenteral nutrition as a supplement to inadequate EN?</h2>
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<p><strong>Quality of evidence: </strong>low<br><strong>Grade of recommendation:</strong> weak</p>
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<h3 class="wp-block-heading">No PN in the first week</h3>
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<p>Stepwise advancement of nutrient delivery via the enteral route and delaying commencement of PN. The role of supplemental PN to reach a specific goal for energy delivery is not known.</p>
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<p>The time when PN should be initiated to supplement insufficient enteral nutrition is unknown. Based on the above RCT, supplemental PN should be delayed until 1 week after PICU admission in patients with normal baseline nutritional state and low risk of nutritional deterioration.</p>
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<h3 class="wp-block-heading">PN in the first week</h3>
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<p>Children who are unable to receive any EN during the first week in the PICU can be started on PN. In patients who are severely malnourished or at risk of nutritional deterioration, PN may be supplemented in the first week if they are unable to advance volumes of EN.</p>
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<h2 class="wp-block-heading">8. Is there any role of immunonutrition in critically ill children?</h2>
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<p><strong>Quality of evidence:</strong> moderate<br><strong>Grade of recommendation recommendation: </strong>strong</p>
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<p>None.</p>
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<h3 class="wp-block-heading">Summary</h3>
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<ol><!-- wp:list-item -->
<li>Nutritional assessment within 48 hours of admission, re-evaluate weekly.</li>
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<li>Use z scores for BMI, weight-for-length, weight-for-age, and HC for assessment.</li>
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<li>Use Indirect calorimetry if available. Don't use Harris-Benedict equations, or RDAs as guides to requirements.</li>
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<li>Initiate enteral nutrition within 24 to 48 hours unless contraindicated. Achieve at least 2/3rd of calories by the end of 1st week unless contraindicated. The <strong>minimum </strong>protein intake should be 1.5 g/kg/d. </li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li>Prefer enteral nutrition over parenteral, there is no data on which is better - gastric or post-pyloric.</li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li>Don't give immuno-nutrition, it doesn't help.</li>
<!-- /wp:list-item --></ol>
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<h2 class="wp-block-heading"><br>Myths in ICU nutrition </h2>
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<p>In my exploration of guidelines, I stumbled upon <a href="https://crashingpatient.com/wp-content/uploads/2011/07/Myths_2013.pdf">Paul E. Marik's enlightening post dissecting <strong>prevalent myths</strong> surrounding ICU nutrition.</a> As an advocate of dogma lysis, I feel compelled to share these insights, recognizing their relevance not only in the adult sphere but equally so in the pediatric population. </p>
<!-- /wp:paragraph -->
<!-- wp:paragraph -->
<p>The critical examination of established beliefs in nutrition aligns seamlessly with my experiences and practices in pediatric critical care settings.</p>
<!-- /wp:paragraph -->
<!-- wp:paragraph -->
<p></p>
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<ul><!-- wp:list-item -->
<li><code>Myth no. 1: Starvation or undernutrition is “okay” -wrong </code></li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li><code>Myth no. 2: Parenteral nutrition is safe -wrong </code></li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li><code>Myth no. 3: En contraindicated with vasopressors -wrong </code></li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li><code>Myth no. 4: Early enteral nutrition is not important in patients receiving mechanical ventilation</code> - wrong</li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li><code>Myth no. 5: En is contraindicated with high gastric residual volume</code> -wrong</li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li><code>Myth no. 6: Postpyloric feeding reduces the risk of aspiration</code> -wrong</li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li><code>Myth no. 7: En is contraindicated in patients without bowel sound and/or a postoperative ileus - wrong </code></li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li><code>Myth no. 8: En is contraindicated following gi surgery - wrong </code></li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li><code>Myth no. 9: En is contraindicated in patients with an open abdomen - wrong </code></li>
<!-- /wp:list-item -->
<!-- wp:list-item -->
<li><code>Myth no. 10: En is contraindicated in patients with pancreatitis</code> - Wrong</li>
<!-- /wp:list-item --></ul>
<!-- /wp:list -->Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-45504719160034475542015-05-27T21:37:00.052+01:002024-02-29T06:05:03.365+00:00Pediatric liver function test: smarter interpretation<div class="separator hideapic" style="clear: both;"><img alt="" border="0" data-original-height="450" data-original-width="725" loading="lazy" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiHJaSM6gi9WuIXWlRC9GvejjCF6HswHz1OGKygWeyr3O9iX5Pla43kgD-fmGTlZ4Sp1DwwRBnC6ioxKqST3lO4ssVpM6DQGuNMkYLqCJN1HdWF2PeEYYXWLbsAaPq1bTlZ9vYchyphenhyphen4eQaABBnbo_5jBhN8uSRR0w-EIacXNlGKf-_-RYLIW0uARaEaZL44/s726/Liver%20function%20tests%20in%20Children%20%281%29.png" /></div>
<p>Navigating through Liver Function Tests (LFTs) has been a perpetual puzzle for me! This post serves as my endeavor to unravel the complexities surrounding LFTs, aiming not only to clear my own confusion but also to offer clarity to anyone who stumbles upon it. Join me on this journey of understanding liver function, and let's demystify these intricate tests together. Your insights and feedback are not only welcome but crucial in making this exploration beneficial for all.</p><a name='more'></a>
<p>Part One: Tests that detect injury to hepatocytes (serum enzyme tests)</p>
<h2>1. ALT/SGPT</h2>
<p>ALT or SGPT (always confuses me so I prefer to call ALT always) is a <strong>primary marker</strong> of liver cell injury (I remember L for Liver) and is <strong>more sensitive and specific </strong>than AST. When liver cells die, they leak into the blood, but there is <strong>no correlation with the extent of the damage</strong>.</p>
<h3>A) High ALT (>15-20 times)</h3>
<ol>
<li>Ischaemia (Much Higher) (Shock, hypotension, CCF, comes down rapidly)</li>
<li>Viral hepatitis, Autoimmune</li>
<li>Drug toxicity (PCM), Severe toxic hepatitis</li>
<li>Acute Budd Chiari syndrome</li>
</ol>
<h3>B) Moderate ALT (5-15 times)</h3>
<ol>
<li>Liver – Chronic Liver disease (eg Chronic hepatitis)</li>
<li>Cholestasis (with ALP, GGT)</li>
<li>Cardiac –Severe hepatic congestion in cardiac failure</li>
<li>Other: Muscle injury, Kidney injury</li>
</ol>
<h3>C) Slight increase in ALT (<5 times)</h3>
<ol>
<li>Liver: Neonatal hepatitis</li>
<li>Hemochromatosis</li>
<li>Autoimmune hepatitis</li>
<li>NASH, EHBA</li>
<li>Alpha1-antitrypsin deficiency, Wilson’s disease</li>
<li>Infection: Infectious mononucleosis</li>
<li>Drugs: Almost any drug. (ATT, AED, Antibiotics, NASAIDS), PCM therapeutic doses.</li>
</ol>
<div class='listen'>
<h4>False low ALT</h4>
<p class='energy'>Patient on dialysis, Pyridoxine deficiency can show relatively lower values of ALT. Also, drugs are more likely to cause an asymptomatic abnormality in liver function.</p></div>
<h2>2) AST/SGOT</h2>
<p>AST is less sensitive marker for liver injury and can be elevated in other organ dysfunction as well.</p>
<div class="table"><table style='white-space: nowrap;'><tbody><tr><td>Origin</td><td>Liver, cardiac, skeletal muscle, kidney, brain, pancreas.</td></tr><tr><td>Reflects </td><td>Reflects damage to the hepatic cell, but less specific for liver disease than ALT (l for liver).</td></tr><tr><td>Normal Value</td><td></td></tr></tbody></table></div>
<h3>A) High rise in AST (>20 times)</h3>
<ol>
<li>Ischaemic liver injury(Shock, hypoperfusion)</li>
<li>Acute viral hepatitis</li>
<li>Drug-induced hepatic injury</li>
</ol>
<h3>B) Moderate rise in AST (15-20 times)</h3>
<ol>
<li><strong>Cardiovascular system</strong>: Congestive cardiac failure</li>
<li><strong>Infection</strong>: Infectious mononucleosis</li>
<li><strong>Liver</strong>: Alcoholic cirrhosis</li>
</ol>
<h3>C) Mild rise in AST (5-10 times)</h3>
<ol>
<li><strong>Liver</strong>: Chronic hepatitis Especially alcoholic</li>
<li><strong>Skeletal muscle</strong>: DMD, Dermatomyositis, Infl. B calf muscle myositis</li>
</ol>
<h3>D) Even milder rise in AST (<5 times)</h3>
<ol>
<li><strong>Blood</strong>: Haemolytic anemia, hemolysis</li>
<li><strong>Liver</strong>: Fatty liver, Metastatic hepatic tumor</li>
<li><strong>Drugs</strong>: Almost any drug</li>
</ol>
<h2>Asymptomatic Transaminitis</h2>
<p>Slight elevations of AST or ALT levels, within 1.5 times the normal range, <strong>should not immediately be interpreted as signs of liver disease</strong>. It's important to consider other factors and further examinations before jumping to conclusions about the presence of liver-related injury.</p>
<p>Often, <strong>in the early course of the disease</strong>, only a slight elevation may be observed in the patient. It is not until a follow-up test that a significant rise becomes apparent.</p>
<div class="note gg">
<p><strong>WHY?</strong><br>Unlike the values in many other biochemical tests, AST and ALT levels do not follow a normal bellshaped distribution in the population.</p><p>They have a skewed distribution characterized by a <strong>long tail</strong> at the high end of the scale.</p>
</div>
<h2>Ratios between AST and ALT </h2>
<p>AST/ALT ratio can be a very useful tool to in differentiating primary pathologies.</p>
<h3>AST: ALT =1 (Equal rise)</h3>
<p>Similar and simultaneous rise in AST and ALT can be seen in</p>
<ol>
<li>Ischaemia</li>
<li>Shock and hypo-perfusion </li>
<li>Hypoxic injury</li>
</ol>
<h3>AST: ALT <1 </h3>
<p>When comparing ALT and AST levels, <strong>a notable increase in ALT in comparison to AST is </strong>commonly observed in pathologies primarily associated with Hepatocellular damage, particularly in acute conditions.</p>
<ol>
<li>PCM poisoning with hepatocellular necrosis.</li>
<li> Viral hepatitis</li>
<li>Toxic hepatitis</li>
<li>Cholestatic hepatitis</li>
<li>Chronic active hepatitis, NASH, etc</li>
</ol>
<h3>AST: ALT >2.5</h3>
<p>The <strong>AST levels increase more significantly compared to ALT </strong>in the following pathologies.</p>
<ol>
<li>CLD, cirrhosis</li>
<li>Wilsons disease, cirrhosis</li>
<li>Bile duct obstruction, Tumours</li>
<li>Alcoholic liver disease</li>
</ol>
<div class="listen">
<p><strong>WHY</strong>?</p>
<p class="spark">Depletion of vitamin B6 in chronic alcoholics. ALT and AST both use B6 as a coenzyme, but the synthesis of ALT is more strongly inhibited by pyridoxine deficiency than is the synthesis of AST. Alcohol also causes mitochondrial injury, which releases the mitochondrial isoenzyme of AST.</p>
</div>
<h3>3. ALKALINE PHOSPHATASE (ALP)</h3>
<div class="table"><table style='white-space: nowrap;'><tbody><tr><td>Source </td><td>Liver, bone, placenta and intestine</td></tr><tr><td>Reason for rise</td><td>Result of increased synthesis of the enzymes by cells lining the bile canaliculi, in response to cholestasis that may be intra or extra-hepatic.</td></tr><tr><td>Primary value</td><td>To identify cholestatic disorders, can rise even before the rise in bilirubin.</td></tr></tbody></table></div>
<h3>Increased ALP</h3>
<p>The normal value of alkaline phosphatase is between 30 and 120 IU/L, this may vary a bit from lab to lab.</p>
<ol>
<li><strong>Liver</strong>
<ul>
<li>Sensitive for biliary obstruction,</li>
<li>Intrahepatic/Extrahepatic cholestasis. (Highest levels)</li>
<li>EHBA (Marked rise)</li>
<li>Viral hepatitis</li>
</ul>
</li>
<li><strong>Renal</strong>
<ul>
<li>Renal failure</li>
</ul>
</li>
<li><strong>Infiltration</strong>
<ul>
<li>Hepatic metastasis, </li>
<li>amyloidosis, </li>
<li>granulomatous diseases</li>
</ul>
</li>
<li><strong>Cardiovascular</strong>
<ul>
<li>Heart failure (Milder)</li>
</ul>
</li>
<li><strong>Infections</strong>
<ul>
<li>Inf mononucleosis, </li>
<li>Fungal infection (Marked rise)</li>
</ul>
</li>
<li><strong>Bone</strong>
<ul>
<li>Usually non-pathological in growing children</li>
<li>Osteomalacia, Bone metastasis, Paget's disease (very very high)</li>
<li>Deficiency-induced rise in rickets, Rapid bone growth</li>
<li>Hyperparathyroidism</li>
</ul>
</li>
<li><strong>Physiological</strong>
<ul>
<li>Released in excess from the placenta in late pregnancy.</li>
<li>Blood type O and B: Released from the small intestine after a fatty meal.</li>
</ul>
</li>
</ol>
<ol></ol>
<h3>Isolated rise in ALP</h3>
<p>The significance of ALP elevation with otherwise normal transaminase and bilirubin values remains unclear, however, isolated elevation of ALP can be seen in</p>
<ol>
<li>Use of drugs such as Cimetidine, furosemide, phenobarb (Enzyme induction)</li>
<li>CCF but Often associated with AST and ALT rise.</li>
<li>Diabetes</li>
<li>Hyperthyroidism</li>
</ol>
<h2>Low ALP</h2>
<p>Lower levels of alkaline phosphatase can give clues toward following pathologies.</p>
<ol>
<li>Malnutrition</li>
<li>Zn deficiency</li>
<li>Vit c Deficiency</li>
<li>Hypothyroidism</li>
<li>Pernicious anemia</li>
<li>Congenital Hypophosphatasia</li>
</ol>
<h2>How to confirm the Liver Origin of alkaline phosphatase?</h2>
<p>There are two ways to differentiate whether or not the origin of rise in ALP if from liver or non-liver origin.</p>
<h3>Isoenzyme assays</h3>
<p>There are 60 types of Isoenzymes of ALP, that can be separated by electrophoresis to identify the liver and other organ-specific isoenzymes. This is expensive and mostly for research purposes. (Expensive)</p>
<h3>Raised GGT and 5′-nucleotidase</h3>
<p>GGT and 5′-nucleotidase are often raised in primary liver pathologies. An elevated serum alkaline phosphatase with a normal GGT or 5'-nucleotidase should always warrant prompt evaluation for bone diseases.</p>
<div class="note yellow">
<p>Normal agewise Variation in ALP</p>
<p>ALP levels vary with age. ALP levels are generally <strong>higher in children and adolescents </strong>because of physiological osteoblastic activity.</p>
<p>Levels may be up to <strong>3 times higher than in healthy adults</strong>, coinciding with periods of maximum bone growth velocity</p>
</div>
<br>
<div class="table"><table style='white-space: nowrap;'><tbody><tr><td><strong>Test</strong></td><td><strong>Cholestatic</strong></td><td><strong>Infiltrative</strong></td><td><strong>Hepatocellular</strong></td></tr><tr><td>AST, ALT > ALP</td><td> Typical</td><td></td><td></td></tr><tr><td>ALP > AST, ALT</td><td></td><td>Typical</td><td></td></tr><tr><td>Elevation ALP but<br>normal AST, ALT levels </td><td></td><td>Typical</td><td>Typical</td></tr></tbody></table></div>
<h3>Low ALP/ bilirubin ratio: Role in prognosis</h3>
<p>A low ALP/ bilirubin ratio can be seen in fulminant Wilson disease.<br>Regardless of the cause of acute hepatic failure, a <strong>low ALP/bilirubin ratio is associated with a poor prognosis</strong>.</p>
<h3>4. GAMMA-GLUTAMYL TRANSPEPTIDASE (GGT) </h3>
<div class="table"><table style='white-space: nowrap;'><tbody><tr><td><strong>Source</strong></td><td>Liver (Biliary tract), Renal tubules, Brain, pancreas, intestinal cells and prostrate glands</td></tr><tr><td><strong>Normal levels</strong></td><td>10 - 30 IU/L</td></tr><tr><td><strong>Use</strong></td><td>To detect hepatobiliary damage</td></tr></tbody></table></div>
<h3>Note: Normal agewise Variation in GGT</h3>
<p>In normal <strong>full-term neonates,</strong> serum GGT activity is <strong>six to seven times</strong> the upper limit of the adult reference range; levels decline and<strong> reach adult levels by 5 to 7 months </strong>of age</p>
<p>GGT is the most sensitive (More than ALT) investigation for detecting hepatobiliary disease, but its use is limited by lack of specificity. It is particularly sensitive to alcoholic liver disease.</p>
<h3>Increased levels of serum GGT</h3>
<p>High levels of GGT are seen in </p>
<ol>
<li><strong> Liver diseases with Hepatobilliary insult</strong>
<ul>
<li>EHBA - Marked elevation, </li>
<li>Any obstructive jaundice</li>
<li>Acute viral hepatitis, peaks in 2nd or 3rd week, and may remain elevated for 6 weeks.</li>
</ul>
</li>
<li><strong>Other</strong>
<ul>
<li>GBS, </li>
<li>Dystrophica myotonia, </li>
<li>Pancreatitis, </li>
<li>Brain tumours, </li>
<li>Renal failure, </li>
<li>Diabetes Mellitus, </li>
<li>Prostatic disease, </li>
<li>Cardiac disease.</li>
</ul>
</li>
</ol>
<h3>Isolated elevation of GGT level </h3>
<p>Isolated levels of GGT can be seen in the following, <strong>without any evidence of liver injury.</strong></p>
<ol>
<li>Drugs such as Phenobarbitone, phenytoin, paracetamol, tricyclics</li>
<li>Alcohol-induced liver disease</li>
</ol>
<h2>Uses of GAMMA-GLUTAMYL TRANSPEPTIDASE (GGT) </h2>
<ol>
<li>It confers <strong>liver specificity to an elevated alkaline phosphatase</strong> level.</li>
<li>It is more specific for <strong>cholestatic liver disease</strong> except in some PFIC. </li>
<li>In cases of transaminitis with <strong>AST/ALT >2</strong>, the elevation of GGTP further supports the diagnosis of <strong>alcoholic liver disease.</strong></li>
</ol>
<div class="listen">
<p>Note: </p>
<ol>
<li>An<strong> isolated elevation of the GGTP </strong>level does not need to be further evaluated unless there are additional clinical risk factors for liver disease.</li>
<li>Common bile duct stone Condition <strong>can simulate acute hepatitis</strong>, although AST and ALT elevation can be seen immediately, the elevation of <strong>ALP and GGT can take some time.</strong></li>
</ol></div>
<h2>ALP and γ-glutamyltransferase (GGT) in the diagnosis of cholestasis</h2>
<ol>
<li>ALP and γ-glutamyltransferase (GGT) levels <strong>typically rise to several times after several days of bile duct obstruction</strong> or intrahepatic cholestasis.</li>
<li><strong>Diagnostic confusion </strong>can occur when a patient presents within a few hours after acute bile duct obstruction from a gallstone. In this situation, AST and ALT levels often reach 500 u/L or more in the first hours and then decline, <strong>whereas ALP and GGT levels can take several days to rise.</strong></li>
</ol>
<h3>5. Lactate Dehydrogenase (LDH)</h3>
<div class="table"><table><tbody><tr><td>Source</td><td>Heart, red blood cells (e.g., hemolysis)</td></tr><tr><td>How it is produced?</td><td>Non-specific rise in liver diseases needs to be interpreted with other tests.</td></tr><tr><td>Use</td><td>Non-specific rise in liver diseases, needs to be interpreted with other tests.</td></tr></tbody></table></div>
<h3>Organ-specific Isoenzymes</h3>
<p>There are 5 isoenzymes of LDH, the identification of isoenzymes for specific organ involvement is not possible in routine clinical practice.</p>
<div class="table"><table style='white-space: nowrap;'><tbody><tr><td>LD1 and LD2 </td><td>Heart, RBC, kidneys</td></tr><tr><td>LD3</td><td>Lungs</td></tr><tr><td>LD4 and LD5</td><td>Liver and skeletal muscle</td></tr></tbody></table></div>
<h2>Raised LDH</h2>
<ol>
<li><strong>CVS</strong>
<ul>
<li>Hepatic congestion (ccf), </li>
<li>Rheumatic HD, </li>
<li>Myocarditis, </li>
<li>Shock</li>
</ul>
</li>
<li><strong>RS</strong>
<ul>
<li>Pulmonary embolus</li>
<li>Infarction</li>
</ul>
</li>
<li><strong>Haematological</strong>
<ul>
<li>Pernicious anaemia</li>
<li>Haemolytic anaemia</li>
<li>Sickle cell anaemia</li>
</ul>
</li>
<li><strong>Hepatobiliary</strong>
<ul>
<li>Hepatitis, </li>
<li>Active cirrhosis</li>
<li>Hepatic congestion due to any cause</li>
</ul>
</li>
</ol>
<p><strong>Part 2: Shortly</strong><br>Tests of the Liver’s biosynthetic capacity.<br>Tests of the liver’s capacity to transport organic anions and to metabolize drugs.</p>
<div class="related-box">
<h2>References</h2>
<ol>
<li>Liver Function Tests and their Interpretation B.R. Thapa and Anuj Walia Indian Journal of Pediatrics, Volume 74—July, 2007.</li>
<li>AGA Technical Review on the Evaluation of Liver Chemistry Tests. Gastroenterology 2002;123:1367–1384.</li>
<li>David e. Johnston, MD. Special Considerations in Interpreting Liver Function Tests. Am Fam Physician. 1999 Apr 15;59(8):22232230.</li>
<li>Jose C Cabrera-Abreu and Anne Green. Gamma-Glutamyltransferase: value of its measurement in paediatrics. Ann Clin Biochem 2002; 39: 22- 25.</li>
<li>"Isolated" elevation of alkaline phosphatase: significance in hospitalized patients. J Clin Gastroenterol. 1990 Aug;12(4):415-9.</li>
<li>William D. Carey, MD. Approach to the Patient with Liver Disease: <a href="https://my.clevelandclinic.org/departments/digestive/medical-professionals/hepatology/liver-tests" target="_blank">A Guide to Commonly Used Liver Tests</a></li>
<li>Mildly Elevated Liver Transaminase Levels: Causes and Evaluation. OBERT C. OH, MD, MPH, THOMAS R. HUSTEAD, MD, SYED M. ALI, MD, AND MATTHEW W. PANTSARI, MD. Am Fam Physician. 2017;96(11):709-715</li>
</ol></div>
<section><div class="profile"><div class="details-2"><h2 class="name bichme">Author</h2><img alt="about authors" class="photo lazy" data-src="https://1.bp.blogspot.com/-YBnfRvlorB8/X9-B39s1MmI/AAAAAAAAF18/SpYb28pe-lEdFodTxH-1VgQekQMSKdO_gCNcBGAsYHQ/s100/sharp%2Bcircle%2Bbw%2B125.jpg" src="data:image/png;base64,R0lGODlhAQABAAD/ACwAAAAAAQABAAACADs=" /><ul class="socialLink"><li><a aria-label="LinkedIn" class="link" href="https://www.linkedin.com/in/ajay-agade-intensivist/"><svg class="c-1" viewbox="0 0 32 32"><path d="M24,3H8A5,5,0,0,0,3,8V24a5,5,0,0,0,5,5H24a5,5,0,0,0,5-5V8A5,5,0,0,0,24,3Zm3,21a3,3,0,0,1-3,3H8a3,3,0,0,1-3-3V8A3,3,0,0,1,8,5H24a3,3,0,0,1,3,3Z"></path><path d="M11,14a1,1,0,0,0-1,1v6a1,1,0,0,0,2,0V15A1,1,0,0,0,11,14Z"></path><path d="M19,13a4,4,0,0,0-4,4v4a1,1,0,0,0,2,0V17a2,2,0,0,1,4,0v4a1,1,0,0,0,2,0V17A4,4,0,0,0,19,13Z"></path><circle cx="11" cy="11" r="1"></circle></svg></a></li><li><a aria-label="Twitter" class="link" href="https://twitter.com/CriticalPeds"><svg class="c-1" viewbox="0 0 32 32"><path d="M13.35,28A13.66,13.66,0,0,1,2.18,22.16a1,1,0,0,1,.69-1.56l2.84-.39A12,12,0,0,1,5.44,4.35a1,1,0,0,1,1.7.31,9.87,9.87,0,0,0,5.33,5.68,7.39,7.39,0,0,1,7.24-6.15,7.29,7.29,0,0,1,5.88,3H29a1,1,0,0,1,.9.56,1,1,0,0,1-.11,1.06L27,12.27c0,.14,0,.28-.05.41a12.46,12.46,0,0,1,.09,1.43A13.82,13.82,0,0,1,13.35,28ZM4.9,22.34A11.63,11.63,0,0,0,13.35,26,11.82,11.82,0,0,0,25.07,14.11,11.42,11.42,0,0,0,25,12.77a1.11,1.11,0,0,1,0-.26c0-.22.05-.43.06-.65a1,1,0,0,1,.22-.58l1.67-2.11H25.06a1,1,0,0,1-.85-.47,5.3,5.3,0,0,0-4.5-2.51,5.41,5.41,0,0,0-5.36,5.45,1.07,1.07,0,0,1-.4.83,1,1,0,0,1-.87.2A11.83,11.83,0,0,1,6,7,10,10,0,0,0,8.57,20.12a1,1,0,0,1,.37,1.05,1,1,0,0,1-.83.74Z"></path></svg></a></li></ul></div><div class="details"><p class="name">Ajay Agade | DNB(Pediatrics), FNB(Pediatric Intensive Care), Fellowship in Pediatric pulmonology and LTV</p><p class="about">Ajay is a Paediatric Intensivist, currently working in Pediatric Pulmonology & LTV at Great Ormond Street Hospital NHS, London</p></div></div></section>Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-18455270231762034532015-03-12T21:14:00.006+00:002021-01-02T13:41:56.950+00:00Capnography interpretation super simplified<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: blue; font-size: medium;"><span style="text-align: left;"><span style="font-family: "sketch block"; font-size: large;">It is always usefull to start by asking: Is there any EtCO2? Is it normal or abnormal? and what is the trend?</span></span></span><br />
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<span style="color: blue; font-size: small;"><span style="text-align: left;"><span style="color: #666666;"><span style="font-family: "verdana" , sans-serif;">John H. Eichhorn. University of Mississippi school of medicine/Medical centre, Jackson, Mississippi.</span></span></span></span></div>
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This is a Second post on capnography focusing on how to simply understand abnormal capnograph. This is more of theoretical post, coming up is a graphical post on how to make interpretation in cardiac arrest, mechanical ventilation, sedation and other scenarios.<br />
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We discussed the anatomy of normal capnograph in the previous post already.</div>
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<span style="color: blue; font-family: "sketch block"; font-size: 22px;">Never forget:</span></div>
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Most frequent abnormal capnograms results from technical problems like improper calibration, loose connection, cracks in connector of circuits specially in side stream capnography. These need to be ruled out before hand in case of sudden changes in trend and no correlation clinically or in relation with blood gases.<br />
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<span style="language: en-us; line-height: normal; mso-ascii-font-family: 'Sketch Block'; mso-bidi-font-family: 'Times New Roman'; mso-color-index: 1; mso-fareast-font-family: +mj-ea; mso-font-kerning: 12.0pt; text-align: left;"><span style="font-family: "sketch block";"><span style="color: blue; font-size: 32px;">CHECKLIST FOR INTERPRETATION</span></span></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgMQuDC4r2pqLOzPO-D4jtpRFjAMCe_LUi_hy3ZN5vCYZsi0K2GWRBy78yvYUQSNC7ia_8swt7xNrcZSd8Uovi7p-sD4uDipmMvHUHYdkbt0av-pJQBDkpwTqpo_WlxtztPK3sFW5QuJ8U/s1600/Capnograph+anatomy.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="725" data-original-width="1024" height="451" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgMQuDC4r2pqLOzPO-D4jtpRFjAMCe_LUi_hy3ZN5vCYZsi0K2GWRBy78yvYUQSNC7ia_8swt7xNrcZSd8Uovi7p-sD4uDipmMvHUHYdkbt0av-pJQBDkpwTqpo_WlxtztPK3sFW5QuJ8U/s640/Capnograph+anatomy.jpg" width="640" /></a></div>
(Normal Anatomy of capnogrph is discussed in previous posts here)</div>
<strong>Phase I – Deadspace Gas</strong><br />
Rebreathing? (1)<br />
Deadspace seem right?<br />
<strong>Phase II – Transitional Phase</strong><br />
Transition from upper to lower airways Should be steep. (3)<br />
Represents changes in perfusion.<br />
<strong>Phase III – Alveolar Gas Exchange</strong><br />
Changes in gas distribution.<br />
Increased slope = mal-distribution of gas delivery. (5)<br />
End of Phase III is the PETCO2. (6)<br />
Area under the curve represents the volume of expired CO2 (VCO2). (7)<br />
<strong>Total Exhaled volume</strong> (8)
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<span style="color: blue; font-family: "sketch block"; font-size: 30px;">CAUSES ALTERED ETCO2</span></div>
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<b style="font-family: "sketch block"; font-size: 25px;"><u>High EtCO2</u></b><br />
<strong style="text-align: left;"><span style="font-family: "kg second chances sketch"; font-size: medium;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiCdNOGXmOzFXTp00gms99djG1D9aO5VEuDjCL5CzruT497pVmkgxRysyLuxokXShzKiqodgeqOTYaUgGa_G99x06W8JiRBdxEw8tO_VslPD_nRzpzbvytBzHyeObyeYQxuLBFXv2H1OZE/s1600-h/capnography%252520simpified%2525202%25255B3%25255D.jpg" style="font-family: "Times New Roman"; font-size: medium; font-weight: normal;"><img alt="capnography simpified 2" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhiHDxcvDImOdGGtj6tL0EJQHbbjs-q0c13agWp1yHp183K6Alf0mH3ON6OSCPm13wZ-2b_y7tunt4ot-QybYp6ECZRTXb0TPuuMhctCWuDdpiFoRD7Zgp91_6xmnv9xEBaanL2c68zeSQ/?imgmax=800" height="110" style="background-image: none; border-width: 0px; display: inline; padding-left: 0px; padding-right: 0px; padding-top: 0px;" title="capnography simpified 2" width="400" /></a></span></strong></div>
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<strong>1. Decreased alveolar ventilation.</strong> </div>
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eg. V/Q missmatch, decreased respiratory effort due to disease or sedation, decrease in tidal volume because of inappropriate ventilator settings or reduced compliance, partially obstructed airway due to secretion or kinks. </div>
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<strong>2. Increased rebreathing of CO2.</strong> </div>
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eg. Abnormally functioning exhalation valve, Inadequate inspiratory flow. Insufficient expiratory time, Malfunction of a CO2 absorber system (exhausted sodalime), Partial rebreathing circuits </div>
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<strong>3. Increased CO2 production.</strong> </div>
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eg. Fever, sepsis, malignant hyperthermia. </div>
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<strong>4. Sodium bicarbonate infusion.</strong> </div>
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Bicarbonate given for acidosis dissociates into CO2, if adequate arrangement for CO2 washout is not made, it may adversely can cause acidosis. </div>
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<span style="font-family: "sketch block"; font-size: 25px;"><b><u>LOW EtCO2</u></b></span> </div>
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<strong>1. Increased alveolar ventilation.</strong> </div>
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eg. Increase in RR or TV, Hyperventilation from any cause, DKA, </div>
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<strong>2. No gaseous exchange.</strong> </div>
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eg. Apnoea, complete obstruction of upper airway. </div>
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<strong>3. Mechanical causes</strong> </div>
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eg. leak in circuit, broken sampling tube, dislodgement of ET tube. </div>
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<strong>4. Decreased CO2 production.</strong> </div>
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eg. Hypothermia, decrease muscular activity like use of muscle relaxant. </div>
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<strong>5. Decreased pulmonary circulation. Less CO2 is brought to the lung for exchange so less is exhaled.</strong> </div>
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eg. Low cardiac output states, Cardiac arrest, Pulmonary embolism, Inadequate chest compression while CPR. </div>
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<strong>Exponential decrease in PETCO2 reflects a catastrophic event in the patient’s cardiopulmonary system.</strong><br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjozMSoDw3kVklfJp9J3fxmqMFywKL30IHGjIpKKnvnyCFlKQrzg8yQSFXe_p18_0OCmBLpAGWpCnuYIHfckLTHbY-FTvs1U7wF8tTKZF4LSCml2FIeDVKu86iG0EKzaeUIHtG1gbH_3fc/s1600-h/capnography%252520simplified%25255B4%25255D.jpg"><img alt="capnography simplified" border="0" height="65" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhAzEPEIGpswQEkb49bDFEnCUgywA-EDXCl1H_KHXy7p_TnfhbsL1dzm8fP6sxOEZ6nwUibxL7WNX9Av-w5RJA8vZ8xoHUnbWmOCrikLkFRnOyMJFaDRLGdp7sGpZva1-xlgBs1ir6nr4o/?imgmax=800" title="capnography simplified" width="246" /></a><br />
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Sudden Hypotension/massive blood loss<br />
Circulatory arrest with continued ventilation<br />
Pulmonary embolism<br />
Cardiopulmonary Bypass</blockquote>
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<strong>Gradual decrease in PETCO2 indicates a decreasing CO2 production, or decreasing systemic or pulmonary perfusion.</strong><br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjqnj5ncLu7Awzo_wmEmCxtnfFYGbFnKR8QWKBU51_9VYmNsayPoJmxLJmjITnbgBBxMwwDV8eHlYwA2GRBXR_35XBaqzNUv01ObTsG-goo3fVxWv4qpVnmnaUgBKRzb5nELA8lSISUMGU/s1600-h/capnography%252520simplified1%25255B3%25255D.jpg"><img alt="capnography simplified1" border="0" height="44" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgBs2Fh0Z8_vnmOgu_a3ALEl3Iu6GT_Nc75PLbqm55YBulkA5tcsyt0HrrAzKLcki7OzsepbeYCzg6HzCjarIaLvG0zbo5jlS-ls0I6d5I1-rgruEN-ot0g2m7D4rbbLmNTtbOiHigciIY/?imgmax=800" title="capnography simplified1" width="285" /></a> <br />
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Hypothermia<br />
Sedation like thiopental coma (also might cause increasing trend by hypoventilating)<br />
Hyperventilation<br />
Hypovolemia<br />
Decreasing Cardiac Output.</blockquote>
<span style="color: blue; font-family: "sketch block"; font-size: 18pt;">Using a-ETCO2 GRADIENT:</span></div>
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Read basics of gradient between arterial and PEtCO2 in previous post on capnography <span style="color: blue;"><span style="font-family: "kg second chances sketch";"><strong><a href="https://www.criticalpediatrics.org/2015/01/capnography-supersimplified-basics.html"><span style="font-size: small;">here.</span></a></strong></span></span> Decrease in cardiac output and pulmonary blood flow causes decrease in PETCO2 but the arterial PaCO2 remains same therefore the difference between them increases causing high <strong>a-EtCO2</strong> gradient. Thus if ventilation kept same, this gradient can be used for monitoring pulmonary blood flow or indirectly the cardiac output (Details in following post on capnography for cardiac arrest) </div>
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<strong>Increased alveolar dead space</strong> </div>
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1. Low cardiac output <br />
2. Pulmonary embolism <br />
3. Other causes, Obstructive lung disease, Excessive lung inflation <br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj4YFxegaYWZLn-f8PtktCl3ArUheTLMfarM3uax948Q2OmHx-QN36-d-DAnd1SZ3cuajAoR6rnzCUlUpbu9Myw5Z4-NW4mUWdm0_G8ygD7cjIp5mu7-hjmqz2fi4GDzrZgzN9ap_7xLqw/s1600-h/image%25255B5%25255D.png"><img alt="image" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEghRLa2ij0hX8_HxXyVjYnFWQaYgFcuFe7XPCQtlSWQfkrCUeXzGLwOP_Wbz5BmqPAbz-n9WajiN7H6kGhCPVXInLRPEXB_2KyE1hmpXOP_XDT_wVdRNYZugO6nRtgy2wXEKzo5sw-sKfY/?imgmax=800" height="123" style="background-image: none; border-width: 0px; display: block; float: none; margin-left: auto; margin-right: auto; padding-left: 0px; padding-right: 0px; padding-top: 0px;" title="image" width="429" /></a><br />
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This study in respiratory care in 2005 concluded presence of moderate to strong positive linear correlation between PETCO2 and PaCO2 difference for all ratios of dead space to tidal volume (VD/VT) ranges, although the strength of the correlation decreased slightly as VD/VT increased. As expected physiologically, the absolute difference between PETCO2 and PaCO2 consistently increased with increasing VD/VT.</div>
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<span style="color: blue; font-family: "sketch block"; font-size: x-large;">ETCO2 and Metabolc acidosis</span></div>
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EtCO2 tracks serum HCO3 & degree of acidosis ( Decreasing EtCO2 = Increasing metabolic acidosis)<br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgIEKp7lijKIkQsIBE5_UUEOld_DW9_JwAApoMKigdlkue0D5vqZjLcgjRaAWoJ8V7pN4BddnrwliuXlF5-dQWZv6_5tqVUSU7wqj_cUmWjZ260v8dRX2xR9JN78BU5i6ldAsowJvsJSLs/s1600-h/image%25255B9%25255D.png"><img alt="image" border="0" height="300" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiakJSm5LE19YCH9T0SzZVzyaPrzk1eD_ltisqEveNBrBtJq_OfExvqkHW7Wm7ahEI6pASGlKeKlZ_BvvlhN-ZIubMntLH7dtJU2foTKCWs1HHCIGdAEggYJkROuglc657b6ZS8HZidAHk/?imgmax=800" title="image" width="400" /></a><br />
Thus helps to distinguish DKA from NKHHC and dehydration.<br />
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<strong>ETCO2 and Synypnea</strong><br />
ETCO2 can help in distinguishing those patient with actual hyperventilation with same respiratory rate. ETCO2 is much more accurate than the RR. The RR is just a measure of how many times someone is breathing. The ETCO2 is how they are ventilating.<br />
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<b>There is lot more to make use of ETCO2 ! </b></div>
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<b><br /></b>
1. During Apnea Testing in Brain-dead patients.<br />
<span style="color: blue;"><u>(Eur</u> J <u>Anaesthesia</u> Oct 2007, 24(10):868-75)</span><br />
2. Evaluating DKA in children. No patients with a PETCO2 >30 had DKA.<br />
<span style="color: blue;">(J Paeditr Child Health Oct 2007, 43(10):677-680)</span> <br />
3. Vd/Vt ratio and ARDS Mortality. Elevated Vd/Vt early in the course of ARDS was correlated with increased mortality.<br />
<span style="color: blue;">(Chest Sep 2007, 132(3): 836-842)</span><br />
4. PCA Administration “Continuous respiratory monitoring is optimal for the safe administration of PCA, because any RD event can progress to respiratory arrest if undetected.”<br />
<span style="color: blue;">(Anesth Analg Aug 2007, 105(2):412-8)</span></blockquote>
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<span style="color: red; font-family: "sketch block"; font-size: 35px;">Trends </span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjvP7SPIl-cSAVXM1rL9bw3YieYHJwuzMBNQZDAaSlg58c-O2glJNSrqb1fG7fF6FSze743BT-JUQ9XoGTaTaoZm6HUqxixmVC7MfYRu4oJmDuflOLM2CHuBK4hPGavS45swpna0L5VF1Y/s1600-h/capnography%252520supersimplified%2525204%25255B3%25255D.jpg"><img alt="capnography supersimplified 4" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg6mYfY-h5sTbxGeyNBJH0pDchnk6kfsaoACEmH0hGDuIc1xESBbDl9jJHNX-9FemZ5M7vV3UKE_ItEkElAGJFeopZhT3L8mOaoyc6eoVSXssKL9NaqrQ57whFfVOdQQO8e6crn5EucSOQ/?imgmax=800" height="121" style="background-image: none; border-width: 0px; display: inline; float: left; margin: 0px 17px 0px 0px; padding-left: 0px; padding-right: 0px; padding-top: 0px; text-align: left;" title="capnography supersimplified 4" width="240" /></a><span style="text-align: left;">Trends are very important and gives a idea of changes in airway status, ventilation, and perfusion of lung as well as mechanical issues in critically ill children over a period of time.</span></div>
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It also can be utilized to audit the case in retrospect. </div>
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A time capnogram may be recorded at two speeds. A high speed capnogram (about 7mm/sec) gives detailed information about each breath whereas the overall CO<sub>2</sub> changes <strong>(trend)</strong> can be followed at a slow (about 0.7 mm/sec) speed. </div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi3Vl7O1bS1IYNzGy4d3zn7m1445MLCh6fIETAXqMbrY3CLgIbE0ErkY9dU63c3oOYrUIX_w8KSa8PH7szHWdObli_IzfifDNLm_gOrSFAg9DBGMY6OZ48SjeNUFO6oKZNY0iiTRU1W7js/s1600-h/capnography%252520supersimplified%2525205%25255B3%25255D.jpg"><img alt="capnography supersimplified 5" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjsKZe_Cy7IFMVPXnsYpjpR7tTtJi78hpraAAZhnSskkGwvXFQTcRzbPyTJ5oN2vUxSO2fYORGC1HDI_0abfBiWP-rJIN_TLrPL-8b3JQmVVNBAZ9S6HW12peqEx2cUsTDvuKJ-JPLFuCo/?imgmax=800" height="154" style="background-image: none; border-width: 0px; display: inline; float: left; margin: 0px 16px 0px 0px; padding-left: 0px; padding-right: 0px; padding-top: 0px; text-align: left;" title="capnography supersimplified 5" width="240" /></a><br />
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<span style="text-align: left;">This image depicts the </span><strong style="text-align: left;">trend</strong><span style="text-align: left;"> of capnography showing events that caused an decrease in end tidal CO2 as discussed above and possible causes including acute onset hypotension, circulatory collapse and pulmonary embolism can be suspected.</span></div>
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References:<br />
1. www.capnography.com<br />
2. S David McSwain MD et al, End-Tidal and Arterial Carbon Dioxide Measurements Correlate Across All Levels of Physiologic Dead Space. Respiratory care, march 2010 VOL 55 NO 3.<br />
3. Madati PJ1, Bachur R.Development of an emergency department triage tool to predict acidosis among children with gastroenteritis. Pediatr Emerg Care. 2008 Dec;24(12):822-30.<br />
4. Fearon DM, Steele DW. End-tidal carbon dioxide predicts the presence and severity of acidosis in children with diabetes. Acad Emerg Med. 2002 Dec;9(12):1373-8. PubMed PMID: 12460840.<br />
5. D’MELLO, BUTANI. Indian J. Anaesth. 2002; 46 (4) : 269-278.</div>
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<img alt="" "" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg9SpsekuG1K1PsFBOT9P8sr1TQfwS0yrgpZtXaUEdQdyxviuLzKGsLtdG1o2BL20sH7UE0xARVk57DUOCANfBcaQA7yKt5-SoEliE68LHzDlaaoeomrfCiMWVXIwvS3aEyHDt4rc9dSMU/?imgmax=650" height="260" title="" width="520" /></div>
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Flow dynamics and its application in critical care</h3>
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Fluid dynamics has a wide range of applications in critical care, starting from high flow nasal cannula to high frequency ventilations, I am going to simplify the concept as i understood during my residency in pediatric intensive care</div>
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Lets start with some basic terminology</div>
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Fluid dynamics is a subdiscipline of fluid mechanics that study fluid flow.</div>
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Dynamics is a science of fluids (liquids and gases) in motion.</div>
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Rheology is the study of the flow of matter, primarily in the liquid state.</div>
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Terminologies: 4 basic terms</h1>
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1. Velocity</div>
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2. Pressure</div>
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3. Density</div>
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4. Temperature</div>
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Types of flow: Lamellar vs Turbulence</h1>
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An object moving through a gas or liquid experiences a force in direction opposite to its motion.<br />
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<img alt="" "" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhieX91np1ixd9zVYB73yMpww7NXcU88aSUCXmtQCN006sFpcHuzVeJPd8N45AB_wuS5c3VyU45Z2gYoF41L3qI97SHtYVyWWypH8SINbO49GFF7pm2NIJuQHF_6QM9Rosla1GI8XtFz2Q/?imgmax=800" title="" /></div>
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Image source: Google images</div>
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<strong>Laminar flow</strong> </div>
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occurs when a fluid flows in parallel layers, with no disruption between the layers. At low velocities the fluid tends to flow without lateral mixing, and adjacent layers slide past one another like playing cards. </div>
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There are no cross currents perpendicular to the direction of flow.</div>
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In laminar flow the motion of the particles of fluid is very orderly with all particles moving in straight lines parallel to the pipe walls (Parabolic velocity profile). </div>
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In fluid dynamics, laminar flow is a flow regime characterized by <strong>high momentum of diffusion</strong> and <strong>low momentum convection.</strong></div>
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<img alt="lamellar flow" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiHUJKf4IZZ6bmvE8VKN7OGL0iJKo5uQNMhme9eyLiyQYJS7iqiO5vfVkPpgyHYQeGADMHVaTjhRb64IcBoZtMIbmtXeozkUZvLTFiteAIzi4r6Ms7713Gds0ODpf09g6PFPilq572_eLU/?imgmax=800" style="background-image: none; border: 0px currentcolor;" title="" /></div>
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Image source:unknown</div>
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This flow profile of a fluid in a pipe shows that the fluid acts in layers and slides over one another.</div>
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Arrow shows adhesive forces between fluid and surface and relatively stationary flow at surface. Flow velocity increases towards the center gradually.</div>
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How to decide which type of flow ?:</h1>
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Laminar and Turbulent flows is characterized and <strong>quantified</strong> by using Reynolds Number established by Osborne Reynolds and is given as</div>
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<img alt="reynolds number" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjP8oQrVZukEbUh59VRMCfW8_lL8ru2QpIU8ZFkRour7NXBeQWVUAF8d8NSBeooX5T509nmvkfRnsAMYx1kdDe2lpCUomLuZJvSG7vNnUC6bjxt0PGRUcv_ex5LpLjCFmKVjnPYLwOzxRw/?imgmax=800" style="background-image: none; border: 0px currentcolor;" title="" /></div>
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Where v = mean velocity, D = vessel diameter, ρ = blood density, and η = blood viscosity</div>
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If NR &lt; 2000 – laminar flow</div>
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NR &gt; 4000 – Turbulent flow</div>
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Thus Higher velocity and lower viscosity favours the lamellar flow, The <span style="color: navy;">GOOD FLOW</span></div>
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<strong><span style="color: navy;">Dont be surprise, we are intelligent cause Reynolds number for Blood flow in brain ~ 100 and Blood flow in aorta ~ 1000</span></strong></div>
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Application:</h1>
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1) AIRWAY OBSTRUCTION</h2>
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Flow in the large airways is turbulent, and the resistance in thE flow is density dependent. In cases of extreme large-airway obstruction, the resistance can be reduced by reducing the density of the gas with the use of a mixture of helium and O2 (Heliox). </div>
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This reduction may help to relieve obstruction such that intubation of the patient is avoided. The primary limitation is the O2 requirement of the patient that dilutes the helium in the mixture.</div>
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2) HIGH FREQUENCY VENTILATION</h2>
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From estimates of the Reynolds number and the dimensions of the airways obtained flow in the larger airways is turbulent. Laminar flow becomes established between the 4th and the 15th generation of airways, depending on the flow rate of the gas.</div>
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If the gas in a long, straight tube is moved in a laminar fashion by a sinusoidal pressure generator, the flow profile has to reverse with each cycle. The gas in the center of the tube will reverse velocity greater than that close to the wall. This type of flow movement is responsible for gas mixing in HFOV</div>
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3) VENTILATION</h2>
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Airway resistance is also affected by the aerodynamics of flow through tubes. Flow through the airways is driven by a pressure drop between the alveoli and the endotracheal tube <span style="color: navy;"><strong>(Bernoulli's principle)</strong>.</span> In laminar flow, the gas has a precisely ordered velocity profile, and has the least possible pressure drop or energy dissipation for a given flow and tube diameter therefore unnecessary kinks in vent tubes as well as inappropriate tube diameter should be avoided.</div>
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It is also relevant in small endotracheal tubes for newborns during conventional ventilation of &gt;60 breaths/min, when the inertia of the gas can cause an underestimation of airway pressure of several cm H2O.</div>
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4) CARDIOVASCULAR BLOOD FLOW</h2>
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No turbulence occurs until the velocity of flow becomes high enough to break flow lamina. Therefore, as blood flow velocity increases in a blood vessel or across a heart valve. there is not a gradual increase in turbulence, Instead, turbulence occurs suddenly when a specific Reynolds number (Re) is reached.</div>
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<img alt="cardiovascular flow dynamics" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgQFVWzDfOiG0xm9MzQvjOBiKV2f58jLJyQc16Vn74Y57d0KO1AqSLj4kH6XgdGx7_x9yZ0Waz9rwtxRCjQuxI2qkv3P_3fzRpBSGl1DNI6Pq_cPSk-dv-r7pb2bNhaObnC47NXcXHfoj8/?imgmax=800" title="" /></div>
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Image source:cvsphysiology.com</div>
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In large arteries at branch points, in diseased and narrow arteries and across stenotic heart valves laminar flow can be disrupted and become turbulent. When this occurs, blood does not flow linearly and smoothly in adjacent layers, but instead in chaotic fashion, this can also occur in ascending aorta cause of high flow velocity.</div>
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Constriction of an artery also increases the velocity of blood flow through the constriction, producing turbulence and sound. Examples are bruits over constricted arteries and the Korotkoff sounds. </div>
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Turbulence occurs more frequently in anemia because of lower viscosity. This may be the explanation of the systolic murmurs that are common in anemia.</div>
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Elevated cardiac outputs, even across anatomically normal aortic valves, can cause physiological murmurs because of turbulence.</div>
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PERFUSION PRESSURE AND TUERBULENT FLOW</h2>
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<img alt="" "" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEglo872rY5yuagmzexElsGAQHr0G4aUjS6dGcWKuNHQUn9pEX1BMBdX-iZWKkTQmSyrE33xCgbTAvusXGG0IFEmNcNnBY4BYLt_fqxvwpgTjRKPSOhKoedSJdfhPiCSNGpOLBjzFlbYsqE/?imgmax=800" height="220" style="background-image: none; border: 0px currentcolor;" title="" width="320" /></div>
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Image source:cvsphysiology.com</div>
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Turbulence increases the energy required to drive blood flow by increasing the loss of energy in the form of friction, which also generates heat.</div>
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When plotting a pressure-flow relationship (see figure above), turbulence increases the perfusion pressure required to drive a given flow. <strong><span style="color: navy;">Alternatively, saying at a given perfusion pressure, turbulence leads to a decrease in flow.</span></strong></div>
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NEWTONIAN AND NON-NEWTONIAN FLUID</h1>
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Newtonian fluid obeys the law that viscosity of fluid remains constant regardless of any external stress that is placed upon it, at constant temperature and pressure.</div>
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For, Non-newtonian fluids, flow is affected by their viscosity and affected differently for different fluid due to different coefficient of viscosity (n).</div>
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What generates Viscosity ?</h2>
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When fluids flow they have a certain amount of internal friction called viscosity. It exists in both liquids and gases.</div>
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Whats is coefficient of viscosity?</h2>
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Fluid in contact with surface is held to that surface by adhesive forces between the molecules of the fluid and surface. Therefore, the molecules at the surface of the stationary wall are at rest and the molecules at the surface of the moving plate will be moving with velocity v.</div>
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The layer of fluid in contact with the stationary wall will retard the flow of the layer just near to it. This layer will retard the layer near and so on. The max flow velocity will be present in centre. With different adhesive forces for different fluid, the velocity will vary. This is coefficient of viscosity (n).</div>
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Different fluid have different coefficient of viscosity. It is one of the several determinants of flow rate of gases and blood in body.</div>
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Earlier, blood was treated as a Newtonian fluid. However <strong>Thurston </strong>reported that The viscoelastic properties which make human blood non- Newtonian depend on the elastic behavior of red blood cells.</div>
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“Blood is not a Newtonian fluid. (<strong>Viscosity differs constantly).</strong> The viscosity depends strongly on the fraction of volume occupied by red cells (Hematocrit).”</div>
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Viscosity of blood increases with</h3>
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Increased hematocrit</div>
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Constrictions in vessels</div>
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Decrease flow rate of blood through vessel (RBCs adhere to each other, and the vessel walls.)</div>
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Viscosity of blood decreases with</h3>
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Increased flow velocity</div>
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Vessel diameter below 300 μm (Reduced η when RBCs get aligned in small vessels. (This is called as <strong>Fahraeus-Lindqvist effect</strong>.)</div>
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In very small vessels (&lt; 20 μm), η increases as RBCs fill the capillaries, “tractor tread” motion.</div>
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DYNAMICS OF BLOOD FLOW (RHEOLOGY)</h1>
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The macroscopic rheologic properties of blood are determined by its constituents.</div>
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In large arteries, the shear stress exerted on blood elements is linear and blood behaves as a newtonian fluid. In the smaller arteries, the shear stress acting on blood elements is not linear and therefore it become non-newtonia</div>
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APPLIED PHYSIOLOGY</h2>
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The aorta and arteries have a low resistance to blood flow compared with the arterioles and capillaries.</div>
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When the ventricle contracts, a volume of blood is rapidly ejected into the arterial vessels. Since the outflow to the arteriole is relatively slow because of their high resistance to flow, the arteries are inflated to accommodate the extra blood volume. During diastole, the elastic recoil of the arteries forces the blood forward into the arterioles.</div>
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Thus, the elastic properties of the arteries help to convert the pulsatile flow of blood from the heart into a more continuous flow through the rest of the circulation.</div>
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<strong>The Moens-Kortweg wave speed</strong></div>
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<strong><img alt="moens kortweg wave" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh0yd4jNqXyilfVF5FzfI78E5CiGTv-grBDrpNn8U9M7QGfAtxWEptLGHKiWilSCGSaiVQUXa9spWTCY8MF8JhUoVZxQogvkobN5Rnvc5Dl0NfNDhC4MCUcVw0HOnjD6vcq6R36pQg6ncs/?imgmax=800" title="" /></strong></div>
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(Steeping of pressure pulse with increasing distance away from heart)</div>
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Concept was obtained by Thomas Young in 1808, and is known as the Moens-Kortweg wave speed. Steepening of the pressure front as it travels from the heart toward the peripheral circulation . Wave speed also varies with age because of the decrease in the elasticity of arteries and increasing intramural pressure. </div>
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INVASIVE BP WAVEFORM</h2>
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The arteries are not infinitely long, and it is possible for the wave to reflect from the distal end and can travel back up the artery to add to the pressure. </div>
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In patient with high blood pressure there can be increase reading in systolic BP than actual BP called as pressure augmentation due to above effect</div>
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FLOW IN CURVED TUBES</h2>
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<img alt="blood flow in major vessels" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgzbh9Gu6TFqMoGkSEIdOe25touThA58x3dAa1jmfCWImdvZe2eIEgYOd1vZf3OwrJaJuaLz47O_kn4ur_SBsp_fpuDzsyIELs_gQN3LWu_wnDU1Q-hI5g7Bv7apEVw7uEgKKkYoL9yxiw/?imgmax=800" title="" /></div>
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The arteries and veins are generally not straight but have some curvature, especially the aorta, which has a complex three-dimensional curved geometry.</div>
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Effect of curvature on blood flow, can be understood by a steady laminar flow in a plane curved tube . </div>
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When a steady fluid flow enters a curved pipe in the horizontal plane, all of its elements are subjected to a centripetal acceleration relative to their original directions and directed toward the bend center. (SEE ABOVE IMAGE)</div>
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Branching is clearly an important contributor to the measured pressures in the major arteries. (HIGH)</div>
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FLOW IN MICROCIRCULATION</h2>
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Concept of a closed circuit for the circulation was established by Harvey (1578–1657). The experiments of Hagen (1839) and Poiseuille (1840) were performed in an attempt to explain the flow resistance of the human microcirculation.</div>
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The term “microcirculation” is for vessels with internal diameter that is multiple of major diameter of the RBC. This definition includes primarily the arterioles, the capillaries, and the postcapillary venules.</div>
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The capillaries are of particular interest because they are generally from 6 to 10 μm in diameter, which is about the same size as the RBC. In the larger vessels, RBC may tumble and interact with one another and start moving streamlined as they travel down the vessel. In contrast, in the microcirculation the RBC must travel in single file through true capillaries. </div>
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Therefore,</div>
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<span style="color: #400080;">The viscosity of blood has a primary influence on flow in the larger arteries</span>, <span style="color: red;">while the elasticity, which resides in the elastic deformability of red blood cells, has primary influence in the arterioles and the capillaries.</span></div>
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If you like this post, or suggest any additions comment below, share too ! See you for the next post</div>
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<strong>References:</strong></div>
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<span style="font-size: x-small;">1. Ganongs Review of medical physiology</span></div>
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<span style="font-size: x-small;">2. Wikipedia for images</span></div>
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<span style="font-size: x-small;">3. Fluid flow, viscosity, poiseuille's law. visual physics. school of physics university of SydneyAustralia.</span></div>
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<span style="font-size: x-small;"><a href="https:/#">4. www.ncbi.nlm.nih.gov/pmc/articles/PMC3614720/</a></span></div>
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<span style="font-size: x-small;"><a href="https:/#">5. https://udel.edu/~inamdar/EGTE215/Laminar_turbulent.pdf</a></span></div>
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<span style="font-size: x-small;"><a href="https:/#">6. https://www.cvphysiology.com/Hemodynamics/H007.htm</a></span></div>
Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-75244074119516149852015-01-30T17:54:00.004+00:002021-01-02T13:38:04.275+00:00Capnography basics super simplified <h3>
<span style="text-align: justify;"><b>CAPNOGRAPHY</b></span></h3>
<span style="text-align: left;"> </span> <span style="text-align: left;">is synonymous with patient safety during anesthesia and sedation, and a must during CPR. Since the first infrared CO2 measuring and recording apparatus by Luft in 1943, capnography has evolved into an essential component of standard anesthesia monitoring armamentarium. </span><br />
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<span style="text-align: left;">I</span>n 1978, Holland was the first country to adopt capnography as a standard of monitoring during anesthesia.<br />
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WHY CAPNOGRAPHY ? IN PICU </blockquote>
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<span style="color: #444444;">Beware the falsely reassuring statement " He must be breating, sats are ok " </span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhQMBuETGzQq-Sd9-mNFalHcrMzd4pdwM5L-k_vJMf5Sidj8hb-3VB5LZLzkGq1-mDol15iiT-W4B_nVzkZ40tLSP5PyncvOwvH_ldslETDw192m6ntvfgHh_bI5lSSkLTl4LJymJHVbUo/s1600-h/Picture1%25255B1%25255D.png" style="margin-left: 1em; margin-right: 1em;"><img alt="Picture1" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgNztd6KesM2GGuWwKWWBhjdTYmqEntFgAZxg5x9Svq-4kAr4QMnZO9n5U86_ptWpa-Lbd49_HmTn5Kix4ufUnF1uQpPa3QV4JiU9jo8hqGZHzcjF9yUegujLGnTvfqG5umfLMMWnWdVUw/?imgmax=800" height="211" style="background-image: none; border-color: initial; border-style: initial; border-width: 0px; display: inline; padding-left: 0px; padding-right: 0px; padding-top: 0px;" title="Picture1" width="276" /></a></div>
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The risk of encountering major airway complication in ICU,s is about 66 times more often than OT/OR because of lack of continuous capnogarphy monitoring.<span style="text-align: left;"> Pules ox can identify the oxygenation failure but not the ventilatory failure, this is specially important during sedation procedures.</span></div>
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<li style="text-align: left;">Differential diagnosis of hypoxia to enable remedial measures to be taken before hypoxia results in an irreversible brain damage.</li>
<li style="text-align: left;">Provides information about Co2 production, pulmonary perfusion, alveolar ventilation, respiratory patterns, and elimination of Co2 from the anesthesia circuit and ventilator.</li>
<li style="text-align: left;">Effective in the early detection of adverse respiratory events.</li>
<li style="text-align: left;">Capnography and pulse oximetry together could have helped in the prevention of 93% of avoidable anesthesia mishaps according to ASA closed claim study.</li>
<li style="text-align: left;">Better detection of potentially life-threatening problems than clinical judgment alone.</li>
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<blockquote class="tr_bq" style="text-align: center;">
What is Capnography <span style="text-align: left;">= Measurement of Co2 during expiration</span></blockquote>
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<b><u>PHYSICS</u></b></h3>
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Infrared absorption of CO2 is a principle of operation. It uses <strong>Beer-Lambert law.</strong> A known concentration of infrared light is traverses through the exhaled gases. Carbon dioxide, being a poly atomic gas, absorbs infrared light. The remaining beam of light is detected by sensors and exhaled CO2 values are computed. </div>
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Carbon dioxide selectively absorbs specific wavelength of infrared light 4.3 micrometer. The ammount of light is proportional to ammount of Co2 molecule, the measured absorbence is compared with standard absorbence and the Co2 at ET is calculated.<br />
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<b><u>TYPES</u></b></h3>
A) Main-stream capnography<br />
<ol>
<li>A sample cell or cuvette, airway adapter, is inserted directly in the airway.</li>
<li>A lightweight infrared sensor, emitted light is detected by a photo detector located on the opposite side of the airway.</li>
<li>Produces waveforms that reflect real-time CO measurements during a respiratory cycle without a delay.</li>
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B) Side-stream capnography</div>
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<li>Sensor located in the main unit , away from the patient, and a pump aspirates gas samples from the patient’s airway into the main processing unit.</li>
<li>The capnographs will have a delay in displaying co2 concentration</li>
<li>A main problem encountered in the ICU setting is the blockage of the sampling tubes</li>
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Advantage of side-stream capnography is that expiratory gases can be obtained from the nasal cavity using nasal adaptors or with a simple modification of the standard nasal cannula.</div>
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These devices are<br />
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<li>Easy to connect, </li>
<li>No sterilization as they are disposable</li>
<li>Can also be used in spont breathing patients.</li>
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<tr> <td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgop9iED5lOUpDaEH8v-q0zRo_fZnivZIXObbGy3e9CUI6Szsx_GbwT0ZS7iTWf2QmTAfN0IGn2DOEadd6drue2cRITjJycjU6aGFGshT-zSezoS9SyWuckYQAplRw8ZKXzG2hZh7eQYwE/s1600/Modified+nasal+cannula+for+sidestream+capnography.JPG" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgop9iED5lOUpDaEH8v-q0zRo_fZnivZIXObbGy3e9CUI6Szsx_GbwT0ZS7iTWf2QmTAfN0IGn2DOEadd6drue2cRITjJycjU6aGFGshT-zSezoS9SyWuckYQAplRw8ZKXzG2hZh7eQYwE/s1600/Modified+nasal+cannula+for+sidestream+capnography.JPG" /></a></td></tr>
<tr> <td class="tr-caption" style="text-align: center;"><span style="font-size: 12px;">Image source: Reference 2</span></td></tr>
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Real time main stream capnogarphy vs sidestream with delayed reflection of respiratory cycle</div>
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C) Qualitative CO2 measurement</div>
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Quick and simple method of determining if an endotracheal tube has been placed properly. Devise contains filter paper that is impregnated with a PH-sensitive indicator that changes colour on exposure to <span style="text-align: left;">CO2. The outer perimeter of the device contains colour coded section indicating the concentration of exhaled CO2 associated with each colour change</span></div>
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<tr> <td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgXVOEYtvPorhuNF_q1Suxeg-a_8HduSxkUlRHt6I4UW1PR5EOR8WyJ0w5Mfhhyphenhyphen6kiKZExdWnozq5uaa2n0SHktQOyACblV0YGysEA8NEuSS5gPVr82PlQnRSaelrVydO__xzGszWO9qys/s1600/calorimetric+capnography.png" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="174" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgXVOEYtvPorhuNF_q1Suxeg-a_8HduSxkUlRHt6I4UW1PR5EOR8WyJ0w5Mfhhyphenhyphen6kiKZExdWnozq5uaa2n0SHktQOyACblV0YGysEA8NEuSS5gPVr82PlQnRSaelrVydO__xzGszWO9qys/s1600/calorimetric+capnography.png" width="200" /></a></td></tr>
<tr> <td class="tr-caption" style="text-align: center;">Image source: Reference 2</td></tr>
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TERMINOLOGY</h3>
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<strong>1. Capnometry:</strong></div>
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The measurement and display of CO2 on a digitial or analogue monitor. Maximum inspiratory and expiratory CO2concentrations during a respiratory cycle are displayed.</div>
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<strong>2. Capnography:</strong></div>
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A graphic display of instantaneous CO2 concentration during a respiratory cycle (CO2 waveform or capnogram)</div>
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<strong>3. Capnograms:</strong> <span style="text-align: left;">Time and Volume</span></div>
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<span style="text-align: left;"><span style="text-align: justify;">Can be of two types: ETCO2 can be plotted against expired volume or against time (time capnogram) during a respiratory cycle.</span></span></div>
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<strong>4. PETCO2:</strong>Partial pressure of CO2 at the end of expiration</div>
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<strong>5. (a-ET)PCO2:</strong>Arterial to end-tidal CO2 tension/pressure difference or gradient</div>
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<span style="font-family: "sketch block";"><span style="language: en-us; mso-ascii-font-family: 'Sketch Block'; mso-bidi-font-family: 'Times New Roman'; mso-color-index: 1; mso-fareast-font-family: +mn-ea; mso-font-kerning: 12.0pt;"><span style="font-size: 30pt;">Waveform phases</span></span></span></div>
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Little bit of lung physiology will help understanding typical waveform, so during expiration the first air the sensor breaths is from deadspace which contains very low co2. This air is then mixed with the air from conducting zone and then Co2 content increases rapidly, lastly followed by air in alveoli with highest concentration of co2.</div>
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<tr> <td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEicbnzMW9SSrE9VrJFZ7hU1SiW8QT0SaTLVNT1SjcD1tt06tZKj2QmLCorfNnMXBcDL50q-AnVhucIcuY4zbYdhJfYQaeXM1FmUW-BYZKh5axsIcsvXYWfYe87z9QhKnLNFt1_OcoNx9kE/s1600-h/Picture3%25255B5%25255D.png" style="margin-left: auto; margin-right: auto;"><img alt="Picture3" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgxcEwwGzhXxttCgHlgir44jhJnTufCHmRmLLQAvLz96f8yz_p8ntEKhcAlXTZBvPYfJQ81Nx3yJw9iYYROfP5uGR04AQMZH3ehN_gMmdqxxqlC05Jp_r3gICYdGm8k5hkwrAjIdxYcgGk/?imgmax=800" height="228" style="background-image: none; border-bottom-width: 0px; border-left-width: 0px; border-right-width: 0px; border-top-width: 0px; display: block; float: none; margin-left: auto; margin-right: auto; padding-left: 0px; padding-right: 0px; padding-top: 0px;" title="Picture3" width="363" /></a></td></tr>
<tr> <td class="tr-caption" style="text-align: center;">Image Source: Reference 6</td></tr>
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A time capnogram can be divided into inspiratory and expiratory segments. The inspiratory segment (phase 0) is further divided into three phases</div>
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<span style="color: #073763;"><span style="color: #073763;"><strong>phase I :</strong> </span>Sensor starts detecting the Co2 from <span style="color: #073763;">a</span>natomical dead space gases</span></div>
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<span style="color: #073763;"><strong><span style="color: #073763;">phase II : Rapid rise</span></strong>, Mixture of Anatomical dead space and Physiological dead space Co2</span></div>
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<span style="color: #073763;"><span style="color: #073763;"><strong><span style="color: blue;">Alpha angle</span></strong> : </span>Angle bewteen phase 2 and phase 3</span></div>
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<span style="color: #073763;"><span style="color: #073763;"><strong>phase III : Alveolar Plateau</strong> </span>The sensor detects Co2 rich gas from alveoli and has a mild positive upslope. This positive up slope is not clearly seen in a time capnogram. In Volume capnogram, the positive slope is prominent as CO concentration is plotted against evolving expiratory volume.</span></div>
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<span style="color: #073763;"><strong><span style="color: #073763;">Beta angle :</span></strong> Angle between phase three and descending limb</span></div>
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<span style="color: #073763;"><strong><span style="color: #073763;">Phase 0 :</span></strong> Fresh Co2 free gas is inhaled and CO2 concentration falls rapidly to zero giving rise to 90 degree angle between phase III and Phase 0</span></div>
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<span style="text-align: left;">Magnified Capnograph of a mechanical breath showing various phases mentioned above where ETCO2 is plotted </span><span style="text-align: left;">against time.</span><br />
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ANGLES </h3>
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<span style="font-weight: normal;"><u>Alpha angle</u></span></div>
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Increases in alpha angle (angle between phase II and phase III) and the slope of phase III are a good refection of V/Q perfusion status of the lung. </div>
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In asthma or any obstructive airway, the slope of phase III is increases together with an increase in the alpha angle. </div>
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<span style="font-weight: normal;"><u>Beta angle</u></span></div>
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Its a 90 degrees angle between phase III and the descending limb of capnogram. Increases in case of re-breathing in circuit due to failure of exhalation valve.</div>
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<h3 style="text-align: left;">
VOLUME CAPNOGRAPHY</h3>
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The volume capnogram can be related to components of tidal volume; physiological dead space and alveolar ventilation . </div>
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<strong>A noninvasive estimate of physiological dead space can be obtained from volume capnography</strong></div>
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEijqjCKDRDc9B0Lfz3EEF9jKLjwVQlLhgqFIEa4GlxRYHmYMaeZ5lbt2Q0h4cxtEtBOZuUtBW4LLoq-PuRCtjrz3aqc75lhrdfHfxTgxeu-7f_Fmt8aCY_EftgjCy_Z6dmp4DKg7fw6OYc/s1600/Capture_thumb%255B8%255D" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" data-original-height="270" data-original-width="373" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEijqjCKDRDc9B0Lfz3EEF9jKLjwVQlLhgqFIEa4GlxRYHmYMaeZ5lbt2Q0h4cxtEtBOZuUtBW4LLoq-PuRCtjrz3aqc75lhrdfHfxTgxeu-7f_Fmt8aCY_EftgjCy_Z6dmp4DKg7fw6OYc/s1600/Capture_thumb%255B8%255D" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Capnograph where ETCO2 is plotted against Tidal volume</td></tr>
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Image shows virtual spaces occupied by various volumes when volume capnograph is plotted.</div>
<blockquote class="tr_bq" style="text-align: left;">
X is total exhaled volume<br />
Y is alveolar dead space and reflects quantitative V/Q mismatch<br />
Z is anatomical dead space</blockquote>
<h3 style="text-align: left;">
a-EtCo2 GRADIENT </h3>
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The gas exchange in lungs is not a perfect model and there are always mixing defect of gases wiht the blood in capillaries, as a result the PaCo2 is always higher than the Normally ETCO2 by 2-5. The changed in this can be used to assess the alveloar dead space. The more the difference more is the dead space. </div>
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On mechanical ventilator worsening of this gradient can be taken as increasing dead space while decrease from previous values can be taken as improvement of disease or response to the therapy like bronchodilators in asthma </div>
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<span style="font-family: "calibri"; font-size: medium;">IIn</span><span style="background-color: transparent; font-family: "calibri"; font-size: medium; text-align: left; text-indent: -0.38in;"><span style="mso-spacerun: yes;"> In Children, the (a-et)pco2 gradient is Smaller (0.65-3 mm hg) than adults. This is due to a better V/Q matching, and hence a lower alveolar dead space in children. Therefore, changes in alveolar dead space correlate well With changes in (a-et)pco2 “Hence (a-et)pco2 is an Indirect estimate of V/Q mismatching of the lung.</span></span></div>
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<b>Increased anatomical dead space</b></div>
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Open vent circuit</div>
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Shallow breathing</div>
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<b>Increased alveolar dead space</b></div>
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<span style="text-indent: -0.38in;">Obstructive lung disease</span></div>
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Excessive lung inflation</div>
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Low cardiac output</div>
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Pulmonary embolism</div>
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<h3 style="text-align: left;">
MEASUREMENT ERRORS</h3>
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Before interpreting abnromal capnograph and EtCo2, first think about</div>
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<ol>
<li style="text-align: left;">Sampling error</li>
<li style="text-align: left;">Calibration error</li>
<li style="text-align: left;">Leaks or occlusion in sampling lines</li>
<li style="text-align: left;">Difficulty in obtaining a true end-tidal CO2</li>
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<span style="font-size: x-small;"><b>References</b></span></div>
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<div style="text-align: left;">
<span style="font-size: x-small;">1.The ICU book by Paul Marino</span></div>
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<div style="text-align: left;">
<span style="font-size: x-small;">2.Kodali, Bhavani Shankar Anesthesiology. 118(1):192-201, January 2013.</span></div>
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<span style="font-size: x-small;">3.National audit project</span></div>
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<span style="font-size: x-small;">4.Quick guide to capnography philips</span></div>
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<div>
<div style="text-align: left;">
<span style="font-size: x-small;">5.Capnography in pediatric Intensive care medicine, Ajay Desai, Great Ormond Street Hospital, London</span></div>
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Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-19209330949382438782014-07-05T12:37:00.004+01:002021-01-02T13:18:21.910+00:00Journal scan 3: Lorazepam vs Diazepam for Pediatric Status Epilepticus: Which is better?<div dir="ltr" style="text-align: left;" trbidi="on">
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Here is the study of 259 patients was publisheed in JAMA in 2014, by James M. Chamberlain, on efficacy of Lorazepam vs diazepam for pediatric status epilepticus, it was a randomized clinical trial.<br />
<a name='more'></a><br />
<b>Background</b><br />
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Both Diazepam and lorazepam are benzodiazepines used in treatment of status epilepticus. They differ in potency and in the time-course of their action. As a sedative, diazepam 10 mg is equivalent to lorazepam 2–2.5 mg. Diazepam is better absorbed after oral than after i.m. administrations but this does not apply to lorazepam. The clinical effect and amnesia begin more rapidly with diazepam, but last longer following lorazepam. <br />
<br />
Diazepam but not lorazepam is approved by the US Food and Drug Administration for status epilepticus in children, although both drugs are widely used for this purpose.<br />
<br />
Importance<br />
<br />
Benzodiazepines are considered first-line therapy for pediatric status epilepticus. Some studies suggest that lorazepam may be more effective or safer than diazepam, but lorazepam is not Food and Drug Administration approved for this indication.<br />
<br />
Objective<br />
<br />
The hypothesis that lorazepam has better efficacy and safety than diazepam for treating pediatric status epilepticus was tested.<br />
<br />
The Pediatric Emergency Care Applied Research Network (PECARN) conducted a double-blind randomized clinical trial at 11 pediatric emergency departments. This double-blind, randomized clinical trial was conducted on patients aged 3 months to younger than 18 years with convulsive status epilepticus . There were 273 patients; 140 randomized to diazepam and 133 to lorazepam.<br />
Interventions Patients received either 0.2 mg/kg of diazepam or 0.1 mg/kg of lorazepam intravenously, with half this dose repeated at 5 minutes if necessary. If status epilepticus continued at 12 minutes, fosphenytoin was administered.<br />
<br />
Outcomes<br />
<br />
The primary efficacy outcome was cessation of status epilepticus by 10 minutes without recurrence within 30 minutes. Secondary outcomes included rates of seizure recurrence and sedation and times to cessation of status epilepticus and return to baseline mental status. Outcomes were measured 4 hours after study medication administration.<br />
<br />
Results<br />
<br />
Cessation of status epilepticus for 10 minutes without recurrence within 30 minutes occurred in 72.1% in the diazepam group and 72.9% in the lorazepam group. There were no statistically significant differences in secondary outcomes except that lorazepam patients were more likely to be sedated.<br />
<br />
Conclusions<br />
<br />
Among pediatric patients with convulsive status epilepticus, treatment with lorazepam did not result in improved efficacy or safety compared with diazepam. These findings do not support the preferential use of lorazepam for pediatric status epilepticus.<br />
<br />
Review<br />
<br />
The RAMPART (Rapid Anticonvulsant Medication Prior to Arrival Trial)<br />
<br />
Both adults and children studied, overall, intramuscular midazolam initiated in the prehospital setting stopped more seizures at arrival to the emergency department than intravenous lorazepam (73% vs 63%). However, a subgroup analysis of the 149 children enrolled showed no difference results for the 2 medications (70% vs 68%, respectively).<br />
<br />
However, following studies supported that lorazepam as a better choice than diazepam for status epilepticus although these were not pediatric specific studies.<br />
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This study published in NEJM in 2001 by Brian K. Alldredge for comparison of lorazepam, diazepam, and placebo for the treatment of out-of-hospital status epilepticus concluded that Lorazepam is likely to be a better therapy than diazepam.<br />
<br />
Another study by Kameshwar Prasad in 2007 on Anticonvulsant therapy for status epilepticus published in British Journal of Clinical Pharmacology concluded that Lorazepam is better than diazepam or phenytoin alone for cessation of seizures and carries a lower risk of continuation of status epilepticus requiring a different drug or general anaesthesia.<br />
<br />
Reference <br />
<br />
1. James M. Chamberlain, MD Lorazepam vs diazepam for pediatric status epilepticus: a randomized clinical trial. JAMA. 2014 Apr 23-30;311(16):1652-60. doi: 10.1001/jama.2014.2625.<br />
2. Dundee JW, McGowan WA, Lilburn JK, McKay AC, Hegarty JE. Comparison of the actions of diazepam and lorazepam.<br />
3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3211107/<br />
4. N Engl J Med. 2001 Aug 30;345(9):631-7.<br />
5. Kameshwar Prasad Anticonvulsant therapy for status epilepticus. British Journal of Clinical Pharmacology. Volume 63, Issue 6, pages 640–647, June 2007</div>
Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-34979728999209220552014-06-17T21:13:00.002+01:002020-09-20T22:45:16.063+01:00Drug Review: Levosimendan<div dir="ltr" style="text-align: left;" trbidi="on">
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<br />
<a name='more'></a><br />
<strong>Introduction</strong><br />
Levosimendan is a novel positive inotropic agent belonging to the category of “inodilators”, which increases cardiac contractility along with vasodilatatory action . It improves myocardial contractility by its calcium-sensitizing action, without increasing myocardial oxygen demand and causes vasodilatation by opening ATP-sensitive potassium channels. It also has potentially anti-ischemic effects by opening mitochondrial adenosine triphosphate (ATP)-sensitive potassium channels.<br />
Levosimendan helps in de-escalating catecholamine infusions, by its non-β-adrenergic actions, which decreases the tolerance to these drugs. <br />
<br />
<b><u>Mechanism of Action</u></b><br />
<br />
Levosimendan is a pyridazole dinitrate derivative. It is a weak acid with a two basic mode of action. One, it exerts positive inotropic effects by binding calcium dependent to troponin C during systole only.<br />
<br />
Levosimendan, prolongs the cross-bridging time of actin-myosin filaments and acts on troponin C only when intracellular calcium levels are high, i.e., during systole. During diastole, when intracellular calcium levels are low, it has no effect on troponin C. Thus it improves systolic and diastolic myocardial function. <br />
<br />
Drugs like digoxin, dobutamine, amrinone and milrinone, act by facilitating calcium binding to the protein troponin-C of the striated cardiac muscle, thereby activating the cardiac contractile proteins. The force of the heart’s contraction is thus dependent on the amount of free calcium in the myocyte cytoplasm during systole.<br />
<br />
Cardiac troponin C can bind up to three calcium ions. The increasing calcium influx into the myoplasm results in excess of calcium in the sarcoplasmic reticulum and subsequent arrhythmias.<br />
<br />
Unlike the catecholamines and the phosphodiesterase III inhibitors, levosimendan does not increase the level of intra-cardiomyocyte calcium and thus does not result in undesirable side effects like increased myocyte oxygen consumption and arrhythmias.<br />
<br />
Secondly, Levosimendan is a potent vasodilator of arteries, veins and coronary vasculature. This effect is achieved by opening of ATP sensitive K channels in vascular smooth muscle cells, cardiac myocytes, and in mitochondria.<br />
<br />
<b><u>PK and PD</u></b><br />
<br />
The drug is 95–98% is protein bound, mainly to albumin. Approximately 5% of a dose is converted in the intestines to a highly active metabolite, OR-1896. The elimination half-life of OR-1896 is 75–80 h (compared to 1 hour elimination half-life for levosimendan itself ).<br />
<br />
This metabolite reaches a peak plasma concentration about 2- 5 days after the termination of a 24 hour infusion and exhibits hemodynamic effects similar to those of levosimendan. The long half-life of the active metabolite, OR-1896, ensure these effects last for up to 7 to 9 days after discontinuation of a 24-hour infusion of levosimendan.<br />
<br />
<b><u>Caution</u></b><br />
<br />
Elimination of unchanged drug and its metabolites was significantly decreased in patients with mild-tomoderate renal failure, indicating a requirement for caution in these patients . Elimination of the active metabolite is prolonged in patients with liver and renal disease failure thus levosimendan should be used with caution here.<br />
<br />
Levosimendan should be used with caution when used with other intravenous vasoactive drugs, like milrinone, due to the increased risk of hypotension. No pharmacokinetic interactions have been observed in patients receiving digoxin and levosimendan infusion.<br />
<br />
Levosimendan is usually well tolerated and no increase in heart rate is reported in dose up to 1mg (i.e. 12mcg/kg). The drug has been shown to increase the cardiac output and ejection fraction, dose dependently. The increase in ejection fraction at low doses is due to an increase in stroke volume. The hemodynamic efficacy was not associated with an increase in myocardial oxygen consumption. <br />
<br />
<b><u>Dosage</u></b><br />
<br />
The usual dosage of intravenous levosimendan is 6-12mcg/kg loading dose over 10 minutes followed by a continuous infusion at 0.05-0.2mcg/kg/min in 5% dextrose. The dose and duration of infusion should be individualized. If the patient develops hypotension or tachycardia the dose can be reduced to 0.05mcg/kg/min.<br />
<br />
If the dose is tolerated and an increased hemodynamic response is required, the infusion rate can be increased to a max of 0.2mcg/kg/min. Infusions longer than 24 hours are not recommended in view of side effects. <br />
<br />
<b><u>Monitoring</u></b><br />
<br />
While the patient is receiving continuous infusion of levosimendan, heart rate, ECG, blood pressure and urine<br />
output should be closely monitored. Invasive monitoring has been recommended during continuous infusion.<br />
Non-invasive monitoring is required for 72 hours after discontinuing the infusion. levosimendan is also available as oral preparation.<br />
<br />
<b><u>Side Effects and Contraindications:</u></b><br />
<br />
The adverse effects are dose related and due to its vasodilator effect. Headache, dizziness, hypotension, and tachycardia are reported along with GI symptomps like nausea, vomiting, constipation and diarrhea. Rarely arrhythmias have been reported.<br />
<br />
Other adverse effects reported with levosimendan include insomnia, decreased hemoglobin and hypokalemia. Levosimendan is contraindicated in patients with mechanical obstruction affecting ventricular filling/ outflow; severe hypotension and tachycardia, severe renal, hepatic failure; or history of Torsades de Pointes.<br />
<br />
<b>Evidence:</b><br />
<br />
<strong>Pediatr Crit Care Med 2006:</strong><br />
<strong>A small study, 15 children, Retrospective cohort design </strong>published in March 2017 in PCCM demonstrated that levosimendan, can be safely administered to infants and children with severe heart failure. The study also proved that levosimendan allowed substantial reductions in catecholamine infusions and produced improvement in myocardial performance.<br />
<br />
<strong>LIDO study</strong> (Levosimendan Infusion versus Dobutamine) study designed to compare the clinical and hemodynamic effects of levosimendan and dobutamine. The study showed that levosimendan improved hemodynamic performance more effectively than dobutamine. The benefit was accompanied by lower mortality in the levosimendan group.<br />
<br />
<strong>RUSSLAN study</strong><br />
The study concluded that levosimendan at doses of 0.1-0.2mcg/kg/min did not induce hypotension or ischemia and reduced the risk of worsening heart failure and death in patients with left ventricular failure complicating acute myocardial infarction. <br />
<br />
<b>CASINO study </b><br />
(Calcium sensitizer or inotrope or none in low-output heart failure) <br />
Survival benefit as compared to dobutamine and placebo. The mortality benefit in favor of the levosimendan group.<br />
<br />
<strong>The REVIVE-II</strong><br />
The study revealed that on the 5th day, more than 33% patients in the levosimendan group had improved and fewer than 30% in the levosimendan group worsened compared to the patients in the control group. The study however failed to demonstrate a survival benefit.<br />
<br />
<b>SURVIVE</b><br />
survival of patients with acute heart failure in need of intravenous inotropic support) study.<br />
This was the first study, which used mortality as an end point in evaluating the efficacy. The study failed to demonstrate mortality benefits with levosimendan and also raised concerns over the apparent increased incidence of deleterious side effects.<br />
<br />
<strong>References</strong><br />
<ol>
<li>Marino P, Sutin KM. Acute heart failure syndromes. Chapter 14. The ICU Book. 3rd Edition. Philadelphia. Lippincott Williams and Wilkins Publications; 2006. p. 265. </li>
<li>Yokoshiki H, Katsube Y, Sunagawa M, et al. Levosimendan, a Ca2+ sensitizer, activates the glibenclamide-sensitive K+ channel in rat arterial myocytes. Eur J Pharmacol 1997; 333: 249-259.</li>
<li>Kamath SR, Jaykumar I, Matha S. Levosimendan. Ind Pediatr. 2009; 46: 593-596.</li>
<li>Puttonen J, Kantele S, Kivikko M, et al. Effect of severe renal failure and haemodialysis on the pharmacokinetics of levosimendan and its metabolites. Clin Pharmacokinet 2007; 46: 235-246</li>
<li>Namachivayam P, Crossland DS, Butt WW, Shekerdemian LS. Early experience with levosimendan in children with ventricular dysfunction. Pediatr Crit Care Med 2006; 7: 445- 448.</li>
<li>Follath F, Cleland JG, Just H, et al. Efficacy and safety of intravenous levosimendan compared with dobutamine in severe low output cardiac failure (the LIDO study): a randomized double blind trial. Lancet 2002; 360:196-202.</li>
<li>Moiseyev VS, Poder P, Andrejevs N, et al; Safety and efficacy of a novel calcium sensitizer, levosimendan, in patients with left ventricular failure due to an acute myocardial infarction. A randomized, placebocontrolled, double-blind study (RUSSLAN). Eur HeartJ 2002; 23: 1422- 1432.</li>
<li>Zairis MN, Apostolatos C, Anastasiadis P, et al. The effect of a calcium sensitizer or an inotrope or none</li>
<li>in chronic low output decompensated heart failure: results from the calcium sensitizer or inotrope or none in low output heart failure study (CASINO). Program and abstracts from the American College of Cardiology Annual Scientific Sessions 2004; March 7-10, 2004; New Orleans, Louisiana. Abstract 835- 836.</li>
<li>Garratt C, Packer M, Colucci W, et al. Development of a comprehensive new endpoint for the evaluation of new treatments for acute decompensated heart failure: results with levosimendan in the REVIVE I study. Crit Care 2004; 8 (Suppl 1): P89.</li>
<li>Mebazaa A, Nieminen M, Packer M, et al. Levosimendan vs dobutamine for patients with acute decompensated heart failure: the SURVIVE randomized trial. JAMA 2007; 297: 1883–1891.</li>
</ol>
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Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-88689653005122731512014-06-13T17:08:00.002+01:002020-09-20T22:45:55.652+01:00Med Gadget Review: Glucomix<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi1-niHa8-3d2NUjGwIU4QIV4l01HO2MpYNTyjP0xIdQ0xvT2oX5OwkoiSyL6gaP39uRuUmcVknhyphenhypheneyV2XvZslToh9xCyVsqS4SFvnvI2AsJjidNWufLcqtamtPiWTIsKDB4fNTfh77SVs/s1600/glucomix+app+review.JPG"><img height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi1-niHa8-3d2NUjGwIU4QIV4l01HO2MpYNTyjP0xIdQ0xvT2oX5OwkoiSyL6gaP39uRuUmcVknhyphenhypheneyV2XvZslToh9xCyVsqS4SFvnvI2AsJjidNWufLcqtamtPiWTIsKDB4fNTfh77SVs/s1600/glucomix+app+review.JPG" width="292" /></a></div>
<strong>Overview:</strong><br />
<blockquote>
Glucose homoeostasis is amongst most important issues to be addressed in both PICU and NICU. Both hyperglycemia and hypoglycemia occur in ICUs and has been strongly associated with increased morbidity and mortality rates in children. </blockquote>
<br />
<a name='more'></a>Glycemic control was shown to reduce morbidity and mortality rates. The frequent changes in sugars value of kids mandate change of glucose content in IVF and modify Glucose infusion rate of fluids repeatedly. These can be done by using pre manufactured solution containing dextrose with various percentage but the desired glucose percent may not be available to target specific GIR everywhere. <br />
<br />
Manually calculating the quantity of two fluid with different dextrose percent to be mixed to get desired dextrose percent may at times not practical in busy schedule of ICU.<br />
<br />
<strong>Medical Gadget: Glucomix</strong><br />
Glucomix is a simple free android application which helps to calculate ammount of two fluids to be mixed to obtain desired dextrose concentration for target GIR.<br />
The interface is very simple. Initially we have to put desired concentration, Highest and lowest concentration of available fluids and then desired amount of fluid for example 100 ml for neonates and 500 ml for pediatric patients. Glucomix calculates the desired amount of fluids to be mixed at the snap of finger.<br />
<br />
<strong>Final words:</strong><br />
Free, simple yet useful android app to mix and make desired dextrose concentration of the fluid.<br />
PS: It occupies a very tiny space.</div>
Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-19319311523321487952014-06-08T19:50:00.006+01:002021-01-02T13:18:33.868+00:00Pediatric traumatic brain injury<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjdjxBH-eClLStabDwjTMZxieXGWKNlkOhGKGJm6abc33GDCvAgtxz1cHLOdggyMwJw8-s-3UgZ1amweImRSov4z1mArsSnvhzUn-n3-Dt_CnP1xfJhuVRdDUd73cJTkIu6T-o_EhyR6wQ/s1600/Traumatic+brain+injury+2012+guidelines.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="329" data-original-width="640" height="328" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjdjxBH-eClLStabDwjTMZxieXGWKNlkOhGKGJm6abc33GDCvAgtxz1cHLOdggyMwJw8-s-3UgZ1amweImRSov4z1mArsSnvhzUn-n3-Dt_CnP1xfJhuVRdDUd73cJTkIu6T-o_EhyR6wQ/s640/Traumatic+brain+injury+2012+guidelines.jpg" width="640" /></a></div>
Guidelines for the management of severe traumatic brain injury in infants, children, and adolescents.<br />
<a name='more'></a><br />
The second edition of guidelines for acute medical management of Traumatic Brain Injury in infant, children and adolescent was published by Brain trauma foundation in 2012. Almost 8 years ago in 2003 the first edition of these guidelines was published.<br />
<blockquote class="tr_bq">
Major changes are in Hyperosmolar therapy: Use of 3% saline in preference ("should be considered for treatment"). The targets of serum osmolarity with regards to mannitol therapy are discarded. Details about inducing moderate hypothermia are included. Etomidate to control severe intracranial hypertension and use of prophylactic phenytoin to reduce incidence of early post-traumatic seizures are also emphasized. </blockquote>
<blockquote class="tr_bq">
These are the major excerpts from guidelines, in short. </blockquote>
<br />
<table border="1" cellpadding="5" cellspacing="2">
<tbody>
<tr>
<td valign="top" width="40%">Icp monitoring</td>
<td valign="top"><b>Level II </b><br />
There are insufficient data to support a level II recommendation for this topic.<br />
<b>Level III </b><br />
Use of intracranial pressure (ICP)monitoring may be considered in infants and children with severe traumatic braininjury (TBI) </td>
</tr>
<tr>
<td valign="top">Threshold for treating Intracranial hypertension </td>
<td valign="top"><b>Level III </b><br />
Treatment of intracranial pressure (ICP) may be considered at a threshold of 20 mm Hg.<br />
Cerebral perfusion pressure threshold</td>
</tr>
<tr>
<td valign="top">Cerebral perfusion pressure<br />
threshold </td>
<td valign="top"><b>Level III </b><br />
A minimum cerebral perfusion pressure (CPP) of 40 mm Hg may be considered in children with traumatic brain injury(TBI). A CPP threshold 40–50 mm Hg may be considered. There may be age-specific thresholds with infants at the lower end and adolescents at the upper end of this range.</td>
</tr>
<tr>
<td valign="top">Advanced neuromonitoring</td>
<td valign="top"><b>Level III </b><br />
If brain oxygenation monitoring is used, maintenance of partial pressure of brain tissue oxygen (PbtO2) 10 mm Hg may be considered.<br />
Neuroimaging (repeat CT)</td>
</tr>
<tr>
<td valign="top">Neuroimaging (repeat CT)</td>
<td valign="top"><b>Level III</b><br />
In the absence of neurologic deterioration or increasing intracranial pressure (ICP), obtaining a routine repeat CT scan 24 hrs after the admission and initial follow-up study may not be indicated for decisions about neurosurgical intervention.</td>
</tr>
<tr>
<td valign="top">Hyperosmolar therapy</td>
<td valign="top"><b>Level II</b><br />
Hypertonic saline should be considered for the treatment of severe pediatric traumatic brain injury (TBI) associated with intracranial hypertension. Effective doses for acute use range between 6.5 and 10 mL/kg.<br />
<b>Level III</b><br />
Hypertonic saline should be considered for the treatment of severe pediatric TBI associated with intracranial hypertension. Effective doses as a continuous infusion of 3% saline range between 0.1 and 1.0 mL/kg of body weight per hour administered on a sliding scale. The minimum dose needed to maintain intracranial pressure (ICP) 20 mm Hg should be used. Serum osmolarity should be maintained 360 mOsm/L. </td>
</tr>
<tr>
<td valign="top">Temperature control</td>
<td valign="top"><b>Level II</b><br />
Moderate hypothermia (32–33°C) beginning early after severe traumatic brain injury (TBI) for only 24 hrs’ duration should be avoided. Moderate hypothermia (32–33°C) beginning within 8 hrs after severe TBI for up to 48 hrs’ duration should be considered to reduce intracranial hypertension. If hypothermia is induced for any indication, rewarming at a rate of > 0.5°C/hr should be avoided.<br />
<b>Level III </b><br />
Moderate hypothermia (32–33°C) beginning early after severe TBI for 48 hrs, duration may be considered.</td>
</tr>
<tr>
<td valign="top">CSF drainage</td>
<td valign="top"><b>Level III</b><br />
Cerebrospinal fluid (CSF) drainage through an external ventricular drain may be considered in the management of increased intracranial pressure (ICP) in children with severe traumatic brain injury (TBI). <br />
<b>Level III </b><br />
The addition of a lumbar drain may be considered in the case of refractory intracranial hypertension with a functioning external ventricular drain, open basal cisterns, and no evidence of a mass lesion or shift on imaging studies. </td>
</tr>
<tr>
<td valign="top">Use of Barbiturates.</td>
<td valign="top"><b>Level III</b><br />
High-dose barbiturate therapy may be considered in hemodynamically stable patients with refractory intracranial hypertension despite maximal medical and surgical management.<br />
When high-dose barbiturate therapy is used to treat refractory intracranial hypertension, continuous arterial blood pressure monitoring and cardiovascular support to maintain adequate cerebral perfusion pressure are required.</td>
</tr>
</tbody>
</table>
<div>
Full article<b><a href="https://www.braintrauma.org/pdf/protected/guidelines_pediatric2.pdf"> here</a></b><br />
<span style="font-family: "verdana" , sans-serif; font-size: x-small;"><b>Reference:</b> Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents--second edition. Pediatr Crit Care Med. 2012 Mar;13(2):252.</span></div>
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Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-4828985958534459292014-06-03T22:11:00.004+01:002021-01-02T13:18:47.259+00:00Cardiovascular effects of ventilation<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgQHeJUbISND_vA5eT-bKa7fV1LF4bcuOSmDkyvgxmpWZlA51UEfXG237VcOaDFawfdcD6mj_ZnjYJiq6en_AZ4h18p4qzWqbZsEQXZMmCBpKaSPiE__BqY5fccw426casVxhVwD47lTSQ/s1600/Cardiovascular+effects+of+mechanical+ventilation++++Shekerdemian+and+Bohn+CP+INTERACTION.png"><img height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgQHeJUbISND_vA5eT-bKa7fV1LF4bcuOSmDkyvgxmpWZlA51UEfXG237VcOaDFawfdcD6mj_ZnjYJiq6en_AZ4h18p4qzWqbZsEQXZMmCBpKaSPiE__BqY5fccw426casVxhVwD47lTSQ/s1600/Cardiovascular+effects+of+mechanical+ventilation++++Shekerdemian+and+Bohn+CP+INTERACTION.png" width="311" /></a></div>
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<strong>By Lara Shekerdemian, Desmond Bohn</strong></div>
<blockquote>
The heart and lungs work closely to meet the tissue’s oxygen demands. An essential part of critical care is to maintain optimal cardiopulmonary function with the help of pharmacotherapy ,fluid management, and respiratory support. </blockquote>
<br />
<a name='more'></a>Cardiopulmonary interactions (the effects of spontaneous and mechanical ventilation on the circulation) were first documented in 1733, when <strong>Stephen Hales</strong> showed that the blood pressure of healthy people fell during spontaneous inspiration. Over a century later <strong>Kussmaul</strong> described pulsus paradoxus (the inspiratory absence of the radial pulse) in patients with tuberculous pericarditis.
<br />
<br />
This article provides an overview of this broad topic, describes how simple ventilator interventions can sometimes be used to obviate the unnecessary escalation of pharmacological support, and have how in
other situations, anticipatory management with fluids or vasoactive agents can minimize cardiovascular compromise during mechanical ventilation. Mechanical ventilation plays a crucial role in the hemodynamic management of critically ill children, and application of the principles that have been described are an essential part of intensive care management.<br />
<br />
This is one of the best and simple descriptive article, Full article <a href="https://adc.bmj.com/content/archdischild/80/5/475.full.pdf" rel="nofollow" target="_blank">here</a></div>
Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-2973205308700349052014-06-02T19:59:00.002+01:002020-09-20T22:47:39.176+01:00Approach to Elevated Lactate Levels<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEivrEHhxWCZaUJ_R6SGz2GX8xaHdBpKmJgFwMo8-Avy0vYJL4MkRh1NG9tCdew9pUBcYLGsPwKFejzzIc9S3B9p8mULIEASjBVzwabZ2rO5hUfgBg7RoKn4vG0_96xkTE1EcO0QJBhgxYM/s1600/approach+to+elevated+lactate.png"><img height="250" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEivrEHhxWCZaUJ_R6SGz2GX8xaHdBpKmJgFwMo8-Avy0vYJL4MkRh1NG9tCdew9pUBcYLGsPwKFejzzIc9S3B9p8mULIEASjBVzwabZ2rO5hUfgBg7RoKn4vG0_96xkTE1EcO0QJBhgxYM/s400/approach+to+elevated+lactate.png" width="400" /></a></div>
<b>Review:</b> Etiology and Therapeutic Approach to Elevated Lactate Levels.<br />
<blockquote class="tr_bq">
An elevated lactate is associated with increased mortality. If the lactate is cleared it is associated with better outcome. Lactate is the best means to screen for occult severe sepsis. In the River’s Trial, almost 1/5 of the patients with severe sepsis had a completely normal blood pressure (MAP > 100), Almost ½ of the patients didn’t have a SBP < 90 when their lactate was discovered to be high.<br />
This article from Mayo clinic is a detail review of etiology and therapeutic approach to elevated lactate levels.</blockquote>
<b></b><br />
<a name='more'></a><b>Article highlights following points.</b><br />
<ol>
<li>Lactate levels can be caused by variety of conditions including shock, sepsis, cardiac arrest, trauma, seizure, ischemia, diabetic ketoacidosis, thiamine deficiency, Malignancy, liver dysfunction, genetic disorders, toxins and medications.</li>
<li>Elvated lactate levels have been associated with increased mortality rates in 3 variety of diseases, such as sepsis, trauma and cardiac arrest. </li>
<li>Decreased lactate clearance has been found to be associated with increased mortallty rates in sepsis, pose-cardiac arrest, trauma, burns, and other conditions. </li>
<li>The use of lactate clearance as an end point of resuscitation might prove beneficial, but further research is warranted. <br />When approaching the patient with an elevated lactate Ievels, the possibility of a multifactorial etiology must be considered. </li>
<li>Despite its Imperfect sensitivity and specificity lactate assay remains clinically useful test that can alert a clinician to un- derlying hypoperfusion in need of Immediate treatment or an etiology not readily apparent on initial evaluation.</li>
</ol>
Good Read! Link for full article <b><a href="https://www.mayoclinicproceedings.org/article/S0025-6196(13)00555-7/pdf" rel="nofollow" target="_blank">Here</a></b></div>
Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-58240701458507133002014-05-25T19:05:00.003+01:002020-09-20T22:50:17.971+01:00Journal scan 2<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiExTyL-GzatJm8oSV3oyjdeT2N7hQSZYR3Ct38C-yl6dMravT47EVNoXXWly6t7bca3tSVyMv4QqLG49Rgu7jGv_NBImBhp8pLkiayxgo9Nx6s6cAjqEwmFX7pDp4udF7AUjeWGVXo7zk/s1600/neonatal+Intubation.jpeg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="399" data-original-width="600" height="212" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiExTyL-GzatJm8oSV3oyjdeT2N7hQSZYR3Ct38C-yl6dMravT47EVNoXXWly6t7bca3tSVyMv4QqLG49Rgu7jGv_NBImBhp8pLkiayxgo9Nx6s6cAjqEwmFX7pDp4udF7AUjeWGVXo7zk/s320/neonatal+Intubation.jpeg" width="320" /></a></div>
<b>Study:</b><br />
<blockquote class="tr_bq">
Digital palpation of endotracheal tube tip as a method of confirming endotracheal tube position in neonates: an open-label, three-armed randomized controlled trial. Saboo AR, Dutta S, Sodhi KS. Pediatric Anesthesia 23 (2013) 934–939</blockquote>
<br />
After neonatal intubation, chances of dislocation of the tracheal tube are fairly high. A technique was studied at PGIMER, India involving palpation of the tube tip in the suprasternal notch. This is a small but interesting study.<br />
<a name='more'></a><br />
<b>Design: </b>The chances of malposition after insertion length based on a weight-based nomogram against malposition after insertion based on palpation of tube in suprasternal notch was studied. <br />
The suprasternal notch was chosen because it anatomically corresponds to vertebral level <strong>T2,</strong> close to the optimal position at the mid-tracheal point. Correct position on the chest radiograph was defined as any position <0.5 cm above the interclavicular midpoint and more than 1 cm above the carina.<br />
<br />
<b>Conclusions:</b> The authors concluded that Suprasternal palpation shows promise as a simple, safe, and teachable method of confirming ETT position in neonates.<br />
Read full PDF article <a href="https://eurekamag.com/pdf.php?pdf=036821122" target="_blank">here</a></div>
Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0tag:blogger.com,1999:blog-3681218115501698781.post-89035640281462906422014-05-24T20:10:00.006+01:002020-09-20T22:50:32.366+01:00Journal scan 1<div dir="ltr" style="text-align: left;" trbidi="on">
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<blockquote class="tr_bq">
Protocolized versus non-protocolized weaning for reducing the duration of invasive mechanical ventilation in critically ill paediatric patients</blockquote>
<br />
<b>Author</b>: Bronagh Blackwood
<br />
<br />
<b>Objective</b>: was to compare the total duration of mechanical ventilation of critically ill children who are weaned using protocols versus those weaned through usual (non protocolized) practice and to detect any differences between protocolized weaning and usual care in terms of mortality, adverse events, length of stay and quality of life.<br />
<a name='more'></a><br />
<b>What is new? </b><br />
This is the first published systematic review comparing protocolized weaning with usual care in <strong>critically ill children</strong> in intensive care.
<br />
<br />
<b>Conclusion</b>: The authors concluded that there is limited evidence suggesting reduction in duration of mechanical ventilation and the available evidence is inadequate to determine whether achievement of shorter duration of ventilation causes children benefit or harm.
<br />
The article is available full and free <a href="https://onlinelibrary.wiley.com/doi/10.1002/14651858.CD009082.pub2/pdf">here</a></div>
Ajay Agadehttp://www.blogger.com/profile/02483478977846082818noreply@blogger.com0