Aortic Stenosis in the Emergency Department 


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A Resident Pearl by Dr. Eric Plant

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Dr. Eric Plant, FM PGY1

Dalhousie Medicine New Brunswick, Saint John

Reviewed By Dr. David Lewis

Copyedited by Dr. David Lewis


The Quick Pearls You Came Here For

  • Aortic stenosis (AS) is very common and severe AS, especially when paired with an acute drop in preload or new onset tachydysrhythmia, can cause cardiogenic shock.
  • Features of severe AS can and should be caught on a routine emergency department (ED) cardiac exam
  • Differentiating from mitral regurgitation (MR) is clinically important and can be aided by PoCUS.
  • Management of cardiogenic shock from severe AS is challenging and relies on achieving euvolemia, normotension, optimizing oxygenation, and maintaining perfusion with a heart rate on the lower end of normal.
  • Dropping the preload of someone with severe AS can cause them to go into cardiogenic shock so everyone who gets nitroglycerine should have their heart auscultated first
  • Goals of managing severe AS in the ED are identification and stabilization until definitive care from a mechanical assist device and or valve replacement can be offered.
  • Identification of symptomatic AS and early referral can be lifesaving whether the patient is in cardiogenic shock or not.

Outline

  • Overview of aortic stenosis
  • Overview of shock and cardiogenic shock
  • Differential diagnosis
  • History features
  • Physical exam
  • Diagnostics
  • Treatment
  • Conclusion

Brief Overview of Aortic Stenosis

AS is the most common valvular heart disease, and in Canada, typically develops from chronic calcification over a course of decades.5

Typically, people will develop progressive exertional symptoms which can ultimately lead to heart failure, syncope, and acute myocardial infarctions. While not commonly discussed in emergency medicine resources, valvular disease is very common and can either be the primary reason for an ED visit or complicate another presenting cardiac complaint. 3 Nearly 30% of people over 65 have some degree AS and 2-9% of patients greater than 75 have severe AS.6 Congenital bicuspid valves are the most common etiology in the developed world in patients less than 65.6 Finally, in the developing world, Rheumatic valve disease is the most common cause.6

Calcified AS progressively increases afterload over the course of decades which causes left ventricular hypertrophy.6 The compensatory hypertrophy causes the ventricle to become stiffer and less contractile. As heart failure slowly develops from this progressive left ventricular (LV) outflow obstruction, a person’s ability to maintain cardiac output becomes more and more dependent on synchronicity of the heart and preload. As a heart with AS becomes more larger and stiffer due to compensatory changes, it develops both diastolic and systolic dysfunction.4

 

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GIF 1 from gfycat.com

 

It is important to note that severity of AS has a wide range from having low clinical significance to life-threatening. While it is not necessary to try to accurately grade the severity of aortic stenosis in the ED, it is important to know that most patients with aortic stenosis are asymptomatic. For those patients who are asymptomatic, without typical symptoms of decreased exercise tolerance or an audible murmur, their AS is very unlikely to be the etiology of any cardiogenic shock they develop. However, AS should be considered as the etiology of cardiogenic shock for those patients who have known severe aortic stenosis and/or who have a loud characteristic murmur.

Full grading criteria for AS are complicated and can be found here. A more simplified chart is provided below.

 

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Figure 1 From the European Society of Cardiology, 2018

 

Cardiogenic shock in severe AS can cause a spiralling of instability.7 An acute episode of cardiogenic shock due to AS is typically because a there has been an exacerbating incident that decreases the heart’s ability to overcome the increased afterload that AS causes.7 Most commonly this is a loss of preload (sepsis, DKA, sever dehydration, excessive nitroglycerine spray) or an episode of a tachydysrhythmia (most commonly rapid atrial fibrillation).3 The spiral begins when the resulting heart failure leads to a drop in coronary perfusion pressure, which causes myocardial ischemia and infarct, which further impede the heart’s ability to overcome the afterload and ultimately causes the patient to crash.

 

PEARL: AS is very common and severe AS, especially when paired with an acute drop in preload or new onset tachydysrhythmia, can cause cardiogenic shock.

 

If you prefer a good video to learn cardiac physiology, I’d recommend one of the following:


Brief Overview of Cardiogenic Shock

Shock is most simply defined as impairment in end organ perfusion.7 Cardiogenic shock takes place when the heart fails to provide the necessary pressure to maintain this perfusion. There are several variations of the definition of cardiogenic shock that rely on specific values and metrics. Unfortunately, these definitions were developed as inclusion/exclusion criteria in academic studies and too cumbersome to be utilized at the bedside in a resuscitation.

 

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Figure 2 (left) from the Taming the SRU Blog, Figure 3 (right) from the Journal of Cardiovascular Pharmacology and Therapeutics

 

In an emergent resuscitation many of these numbers are not available and/or somewhat unreliable therefore it is easiest to evaluate perfusion clinically with a combination of basic vitals, physical exam, and PoCUS. The simplest ways to assess end organ perfusion is simply to examine the patient’s mental status and skin. Extremities in cardiogenic shock will be cool, with pale or mottled skin, and peripheral pulses will be weak or absent. An altered mental status without another cause suggests that the brain is not receiving adequate perfusion. In the case that either of these features are present, the patient is in serious trouble, and you should assume that all end organs are currently ischemic and being damaged.

Many of us remember the classic chart depicting the Forrester classifications of heart failure. Cardiogenic shock is represented in the bottom, higher mortality, half of the graphic.

 

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Figure 4 from emcrit.org

 

As we see represented in figure 1, true cardiogenic shock typically takes place in the highest mortality area of “wet and cold,” meaning that the patient’s skin is cold and systolic dysfunction is causing pulmonary edema. Some cardiogenic shock patients can exist in the cold and dry lower left box but this requires volume depletion or the elusive euvolemic state.

 

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Figure 5 from the Handbook of ICU Therapy


Assessment: History

Many people with severe AS will know they have a history of aortic valve disease. If they’re not aware or able to give you the history, they may have previous echocardiogram reports on record demonstrating AS. Without these history features being gifted to you in one of the previous ways, people with severe AS may present with typical history of angina, decreased exercise tolerance or exertional dyspnea, and presyncope/syncope.6 Syncope is a particularly important history feature as patient with severe aortic stenosis and a history of syncope have a poorer prognosis.6

Given that AS develops slowly over time while the heart compensates, cardiogenic shock caused by AS requires an acute insult to precipitate a crisis.3 Typically, these insults come as either a sudden onset of an arrythmia (namely atrial fibrillation) or an acute drop in preload.3 Common causes of a sudden drop in preload could be sepsis, dehydration (secondary to DKA, diarrheal illness, etc.), excessive use of nitroglycerine for treatment of angina, or acute hemorrhage.

 

PEARL: Dropping the preload of someone with severe aortic stenosis can cause them to go into cardiogenic shock so make sure to auscultate before administering nitroglycerine to a patient with suspected angina or CHF exacerbation.

 

Finally, a patient with severe AS may present with new onset or an exacerbation of heart failure. These patients can pose a treatment dilemma that we will discuss later. If the patient is on heart failure medications, hopefully you’ll be able to find an echo report at least!

Risk factors for disease progression include many of the classic cardiac risk factors: age, smoking, hypertension, obesity, dyslipidemia, and renal insufficiency.5

History Pearls:

  • Aortic stenosis presents with typical features of angina, exertional dyspnea, and presyncope/syncope.
  • Cardiogenic shock from aortic stenosis requires an insult which is typically a new arrythmia (particularly rapid atrial fibrillation) or a sudden drop in preload.
  • Aortic stenosis takes time to develop, and the patient may be aware of their condition.

Assessment: Physical Exam

Inspection:

A simple glimpse can tell a lot about a patient’s perfusion status. People in cardiogenic shock do not look well. On general inspection they are pale, look distressed, may be lethargic with abnormal eye opening, probably experiencing dyspnea, and may be visually diaphoretic. It is important to assess for volume status by examining mucous membranes. You may also see:

  • Skin mottling
  • Elevated or decreased JVP (elevated indicating heart failure, decreased indicating a possible hypovolemia precipitating the crisis)

Palpation:

The highest yield exam for assessing cardiogenic shock will simply be assessing the skin of the extremities for temperature and peripheral pulses.6 People with cool and clammy extremities with weak or absent peripheral pulses are in shock until proven otherwise. You may also start to assess volume status with crude indicators like skin turgor or axillary moisture. Finally, if you have the hands of a cardiologist, you may also feel:

  • Pulsus parvus (slow) et tardus (late)
  • Displacement of apex from 5th intercostal space in midclavicular
  • Heaves or thrills

Auscultation:

Auscultating murmurs is difficult, and while most of us are happy to be able to distinguish systolic from diastolic in the ED, it is especially important clinically to distinguish AS from MR as our goals of resuscitation are different. Both conditions have a systolic murmur and differentiating in an emergency is difficult. Below are some links to videos which demonstrate these differences.

  • Aortic stenosis: harsh, crescendo-decrescendo, mid-late systolic, best heard at right upper sternal border, that radiates bilaterally to the carotids, decrease in intensity with increased afterload, increase in intensity with increased preload

Aortic Stenosis - Heart Sounds - MEDZCOOL

Video 1 from the MEDZCOOL YouTube channel

 

  • Mitral regurgitation: soft, decrescendo, holosystolic, best heard at cardiac apex, does not radiate, increase in intensity with increased afterload, decrease in intensity with increased preload

Mitral Regurgitation (MR) - Heart Auscultation - Episode 4

Video 2 from the AMBOSS: Medical Knowledge Distilled YouTube channel

  • You may also hear:
  • Pulmonary edema (crackles)
  • S3 or S4 – S3 vs S4 Heart Sound
  • Early systolic ejection “click”
  • A softer S2

Special tests: Getting the patient to perform a two-hand grip test for 30 seconds while auscultating a patient’s murmur may help distinguish between aortic stenosis and mitral regurgitation. The two-hand grip test is supposed to increase afterload which should increase regurgitant murmurs and decrease stenotic murmurs.


Assessment: PoCUS

While this article will not go into detail on the ultrasound features of AS, it is useful to know the basic of features of AS on PoCUS. As you place your probe on the patient it is always important to remember the 5 F’s of ED echocardiography because ruling out other common causes of cardiogenic shock is just as valuable as identifying potential aortic valve disease.1 The graphic below from provides an excellent summary but a full PDF of the The Five F’s of Focused Echocardiography in Shock publication from Dr. Atkinson, Dr. Peach, and Dr. Lewis in the Just the Facts section of CJEM can be found here.

 

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Figure taken from Just the Facts: The Five F’s of Focused Echocardiography in Shock

 

It is important to note that aortic stenosis should not be ruled in or out with ER PoCUS at our level. Proper measurements need to be taken from a transthoracic echocardiogram and interpreted by an expert. For our purposes, PoCUS is being used as an extension of the physical exam and to help see some features that further support your diagnosis. For a more comprehensive overview of the PoCUS features of AS you can watch these two excellent videos by Dr. Katie Wiskar. The following GIF images were made from clips from the first video.

Point-of-Care Echo: Aortic Stenosis vs. Sclerosis (9mins)

Basic Valve Evaluation with POCUS (20mins)

For comparison’s sake, below is an example of normal aortic valve function in a parasternal long-axis view. You can see that the hypogenic valve leaflets are thin and mobile with a wide lumen when they open.

 

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GIF created with frames from Point-of-Care Echo: Aortic Stenosis vs. Sclerosis, Parasternal long-axis graphic from Introduction to transthoracic echocardiography by Philips Ultrasound

 

In the two images below, we can see that the valve leaflets are thick and surrounded by sclerotic tissue. In the second more zoomed in image the opening of the valve is very narrow.

 

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GIFs created with frames from Point-of-Care Echo: Aortic Stenosis vs. Sclerosis

 

The above images only evaluate the valve in 2D however it is important to note that more experienced practitioners will add doppler, either colour flow or spectral, to examine for regurgitant jets and attempt to measure gradients across the valves. This is not addressed in this article as it is an advanced skill which is prone is error without the appropriate training.

While assessing the heart for AS, it is clinically important to look for MR. As stated before, distinguishing between AS and MR is tricky during a resuscitation but clinically important.4 Features of MR on PoCUS that are pertinent negatives would be left atrial enlargement or a poorly functioning/prolapsing mitral valve. Although a proper diagnosis of MR also requires formal echocardiography, finding an obvious regurgitant jet as seen below could explain that systolic murmur you think you’ve found when auscultating.

PEARL: Differentiating from mitral regurgitation is clinically important and can be aided by PoCUS.

This is an obvious regurgitant jet seen in the parasternal long-axis view. It is worth noting that MR is commonly underestimated in parasternal long view.

 

GIF created with frames from Point-of-Care Echo: Aortic Stenosis vs. Sclerosis

 

Therefore, it is ideal to achieve a good apical four-chamber view and evaluate the mitral valve from there. Below is another obvious regurgitant jet seen from the apical four-chamber view

 

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GIF created with frames from Point-of-Care Echo: Aortic Stenosis vs. Sclerosis , Apical four-chamber graphic from Introduction to transthoracic echocardiography by Philips Ultrasound


Assessment: Investigations

Below are some of the investigations that you should order for work up a person presenting with aortic stenosis and/or cardiogenic shock.

CXR: Boot-shaped heart, pulmonary edema

ECG: LVH, possible STE elevation or depression with concomitant infarct/ischemia

Labs: troponin, BNP, extended electrolytes including magnesium and calcium, blood gas, creatinine, and blood cultures if you suspect sepsis as the culprit of dropping the patient’s preload.

Echocardiogram: Definitive diagnosis is made from a formal cardiac echo.

Angiogram: Many patients presenting in cardiogenic shock will be sent to the cath lab with ACS in mind. Conveniently the left ventriculogram will allow for measurement of LVEDP and aortic valve gradients during the same procedure.


Differential Diagnosis

Once we have identified cardiogenic shock, our differential diagnosis has eliminated the other causes of shock: obstructive, distributive (sometimes subdivided into septic and neurogenic), and hypovolemic. However, there are still numerous etiologies of cardiogenic shock with some important differences in clinical management. Below are the three most important differential diagnoses to consider:

Mitral regurgitation: Severe MR can cause a systolic murmur and cardiogenic shock. Additionally, these patients may tell you that they have “valve problems” on history. Careful physical exam and PoCUS can help differentiate these two but ultimately, they will need a formal echocardiogram.

Acute coronary syndrome: When a patient presents in cardiogenic shock the first thing on everyone’s mind is acute coronary syndrome. Furthermore, patients in cardiogenic shock from severe AS can suffer an acute myocardial infarction secondary to their cardiogenic shock. On initial assessment it can be difficult to determine whether the etiology of their ischemia is atherosclerosis or the decrease in coronary perfusion pressure resulting from severe AS. Therefore, someone with severe AS and normal coronary arteries can still present with increase troponins and ST changes due to myocardial injury.

Hypertrophic cardiomyopathy: Another presentation of LVOT obstruction, this can also present with cardiogenic shock or syncope. Although possible, a systolic murmur is much less common in HOCM. Luckily the demographics of people presenting with HOCM may help eliminate this as they are typically younger than even the younger aortic stenosis patients that present with a bicuspid etiology.

Extended differential diagnosis:

  • Congestive heart failure
  • COPD
  • Pulmonary embolism
  • Supravalvular and subvalvular LVOT pathologies

Treatment: Severe AS with Cardiogenic Shock

Patients with severe AS causing cardiogenic shock are very sick and tricky to manage. Primary goals of resuscitation are:

  • Oxygen: Simple intervention but optimizing O2 in these patients is a great first step. In the state of cardiogenic shock, it is ok to aim for high SPO­­­2 because our concern is oxygen delivery to ischemic end organs and not O2 toxicity. Once resuscitated they can be titrated back to normal SPO­2.
  • Euvolemia: Given that a sudden drop in preload is a common precipitating factor for cardiogenic shock in severe AS, correcting a decreased volume status should improve their shock status. Unfortunately, someone with severe AS is always in danger of heart failure from fluid overload, so the goal should be careful fluid resuscitation with frequent reassessments.3
    • Bolus of fluid with frequent reassessments
  • Normal Sinus Rhythm: Sudden onset of arrythmia can put someone with severe aortic stenosis into cardiogenic shock because the lack of synchronicity between the atria and ventricle deprives the left ventricle of the atrial kick.7
    • Rhythms such as SVT or rapid afib should be corrected aggressively with electrical cardioversion
  • Normotension: People with aortic stenosis do not tolerate hypotension or hypertension very well. Hypertension increases the afterload so peripheral vasoconstrictors should be used sparingly. Unfortunately, soft BPs are also a huge problem because can reduce preload and drop coronary perfusion pressure which can cause the final collapse. The goal is once again, in the middle.
    • Aim for MAP of 65-80
    • In a crashing patient, lifting their legs and administering phenylephrine can be good first steps.
    • Norepinephrine is a good first choice in a case of that doesn’t improve with fluid administration
  • Lower end of normal heart rate: Even those severe AS patients in NS rhythm will do better with lower HRs rather than high rates. This is because the longer the diastolic cycle, the greater the left ventricular preload will be. High HRs with short diastolic periods can have trouble overcoming the increased afterload of AS.3
  • Improving cardiac contractility: Inotropes like dobutamine or milrinone can be added but the above avenues of resuscitation should be explored first.

 

PEARL: Management of cardiogenic shock from severe AS is challenging and relies on achieving euvolemia, normotension, optimizing oxygenation, and maintaining perfusion with a heart rate on the lower end of normal. Early consultation with cardiology/cardiac surgery is key and arterial and central line insertion should be priorities after initial resuscitation.

 

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Figure 5 From: EM Crit 327 – Acute Valve Disasters Part 2 – Management of Critical Aortic Stenosis

 

Definitive treatment of these patients is aortic valve replacement. Some may require mechanical assistance from a device like an intra-aortic balloon pump to bridge them until this procedure can be done. Either way early consultation from cardiology/cardiac surgery and critical care should be prioritized. Once resuscitated, they should have early insertion of arterial and central lines to allow for more accurate and frequent assessment of their hemodynamics.

A full breakdown of treatment and resuscitation for these patients is beyond the scope of this article but can be found at these two excellent resources below:


Treatment: Hemodynamically Stable

Identification of AS as the reason for a person’s syncope, angina, or heart failure in a hemodynamically stable patient can still save their life. Referral to the appropriate service in your system (cardiac surgery or cardiology) is the best thing you can do for these patients.5 People with symptomatic AS have a poor prognosis and should be referred urgently for aortic valve replacement.5 These patients are at risk for sudden cardiac death and their pathology can be missed completely if simple things like auscultation are not done. Prognosis is improved significantly with aortic valve replacement and the increasing prevalence of transcatheter aortic valve implantation (TAVI) is expanding access to valve replacement into older and more complicated patient populations.5 Therefore, identification and referral for further evaluation itself can significantly improve patient care.

 

PEARL: Identification of symptomatic AS and early referral can be lifesaving whether the patient is in cardiogenic shock or not.

 


Conclusion

Aortic stenosis is common and can be the primary etiology of a person’s presenting complaint or a complicating factor. Identification of the characteristic murmur in a hemodynamically stable patient who presents after an episode of angina or syncope should prompt an urgent consult to cardiology/cardiac surgery and echocardiogram. Some of these patients will have severe AS and valve replacement will significantly improve their length and quality of life. Patients in cardiogenic shock secondary to severe AS have probably undergone a recent insult that has dropped their preload or caused asynchrony of the cardiac rhythm and can be very tricky to manage. It is clinically important to try to differentiate quickly between AS and MR because patients with MR tolerate tachycardia well while patients with AS do much better with lower heart rates. Resuscitation of patients in cardiogenic shock due to severe AS should target euvolemia, aggressive correction of arrythmias, and normotension.


References

  1. Atkinson, P., Peach, M., & Lewis, D. (n.d.). Just the facts: The five F S of focused echocardiography in shock – CAEP. Canadian Association of Emergency Physicians. Retrieved September 25, 2022, from https://caep.ca/periodicals/Volume_22_Issue_5/Vol_22_Issue_5_Page_655_-_657_Atkinson.pdf
  2. Helman, A. Hedayati, T, Tillmann, B. Cardiogenic Shock. Emergency Medicine Cases. January 2022. https://emergencymedicinecases.com/cardiogenic-shock. Accessed July 7th, 2022
  3. Lebowitz, D. (2017, April 21). Management of the crashing aortic stenosis patient. emDOCs.net – Emergency Medicine Education. Retrieved September 25, 2022, from http://www.emdocs.net/management-of-the-crashing-aortic-stenosis-patient/
  4. Messika-Zeitoun, D., & Lloyd, G. (n.d.). Aortic valve stenosis: Evaluation and management of patients with discordant grading. European Society of Cardiology. Retrieved September 25, 2022, from https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/Aortic-valve-stenosis-evaluation-and-management-of-patients-with-discordant-grading https://emcrit.org/emcrit/critical-aortic-stenosis/
  5. Pujari, S. H., & Agasthi, P. (n.d.). Aortic stenosis – statpearls – NCBI bookshelf. Retrieved September 25, 2022, from https://www.ncbi.nlm.nih.gov/books/NBK557628/
  6. Pellikka, P.A., Otto, C. M., Yeon, S. B, Natural history, epidemiology, and prognosis of aortic stenosis. In: UpToDate, Shefner JM (Ed), UpToDate, Waltham, MA. (Accessed on September 25, 2022)
  7. White, C. W., Freed, D. H., Zieroth, S. R., & Singal, R. K. (2015). Heart Failure. In Handbook of ICU therapy. essay, Cambridge University Press. Retrieved from https://www.cambridge.org/core/books/abs/handbook-of-icu-therapy/heart-failure/7B6068B9FC128E16F7250A1D2BC0D4EC. Media
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An EM Approach to Syncope in Adults

 

Medical Student Pearl

Samarth Fageria

Med 3

Memorial University of Newfoundland Class of 2024

Reviewed by Dr. J Gross

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ An EM Approach to Syncope by SFargeria

 


Case

A 60-year-old male presented to the ED after experiencing recurrent episodes of syncope. The first episode occurred at a convenience store in an upright position. He denied prodrome and exertional activity at the time of syncope. After a transient loss of consciousness, he woke up confused with urinary incontinence. He felt nauseous and had emesis in the ambulance on the way to ED. He had two more episodes of syncope over the span of two hours. On assessment in the ED, he endorsed a past history of light-headedness preceded by laughing and holding his breath. He denied dyspnea and chest pain. He had no significant past medical history. There was no family history of cardiovascular disease and syncope, and social history was unremarkable.

 

On examination, he was alert and oriented. He had a minor laceration on his forehead from the fall. His respiratory and cardiovascular exams were unremarkable, neurological exam was normal. In the ED, his blood work was unremarkable. He was placed on telemetry when he had two more episodes of syncope. The monitor showed 20-second-long sinus pauses corresponding with the syncopal episodes. Cardiology was consulted and he was temporarily placed on intermittent transcutaneous pacing.

 

 


Differential Diagnosis of Syncope2

True Syncope

1. Reflex (autonomic hypersensitivity)

  • Vasovagal, carotid sinus hypersensitivity, situational

2. Orthostatic hypotension

  • Volume depletion, autonomic failure

3. Cardiac

  • Valvular (aortic stenosis, mitral stenosis), dysrhythmias (bradyarrhythmia, ventricular tachyarrhythmia, supraventricular tachyarrhythmia), mechanical (pacemaker dysfunction), cardiomyopathy, infiltrative (eg. hemochromatosis, sarcoidosis, amyloidosis), acute MI, ARVC, cardiac tamponade, acute aortic dissection

Other Causes

1. Medication/ Drug-induced

  • Anti-hypertensives, QT prolonging meds, insulin, alcohol, anti-depressants, anti-glycemic agents, diuretics, anti-anginal agents, etc

2. Transient Loss of Consciousness (TLOC)

    • Traumatic brain injury, seizure disorders, intoxications, hindbrain TIA, conversion disorders and metabolic abnormalities

 


Background

Syncope is defined as a brief, sudden, transient loss of consciousness due to cerebral hypoperfusion1. The three broad categories of syncope are reflex, orthostatic and cardiac syncope. The most common cause of cardiac syncope includes dysrhythmias1. A good past medical history of cardiovascular disease is important as it is 85-94% sensitive and 64-83% specific in predicting a cardiac etiology of syncope1.


Diagnostic Workup

Diagnostic workup for syncope requires a thorough history, physical exam, and a 12-lead ECG. Cardiac monitoring is necessary in patients that present to ER with an acute presentation of syncope, and a strong suspicion for cardiac etiology2. History should consist of identifying high-risk features that warrant a prompt cardiology consult2. A detailed HPI should consist of asking about an absence of a prodrome, exertional or supine syncope, concomitant trauma, past medical history of cardiovascular disease and family history of sudden cardiac death (<50 years)2. Low-risk features include presence of a prodrome, specific triggers (eg. dehydration, stress, laughter), syncope while upright and the absence of cardiovascular disease2. Vital signs and a cardiac exam should be completed2. If cardiac causes of syncope cannot be ruled out on first assessment, a 12-lead ECG should be placed to assess for dysrhythmias or conduction disease, and serial troponin values should be collected2.

 

Though there are multiple clinical decision rules for syncope, the following have been externally validated: Evaluation of Guidelines in Syncope Study (EGSYS), San Francisco Syncope Rule and Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL)1. Patients that are stratified as high risk require admission for further evaluation. EGSYS predicts the probability of cardiac syncope at two years based on abnormal ECG findings (eg. BBB, sinus bradycardia), heart disease (eg. ischemic, structural), palpitations before syncope, as well exertional and positional syncope, symptoms of prodrome (nausea/vomiting) and predisposing/precipitating factors1. An admission is warranted if the patient scores a three or higher as there is a 21% mortality risk at two years1. The OESIL risk score estimates a 1-year all-cause mortality in patients presenting with syncope1. The factors include age (>65), history of cardiovascular disease, lack of prodrome and abnormal ECG characteristics (eg. BBB, AV conduction disorders and hypertrophy)1. Admission is warranted for one or more variables1. The Canadian Syncope Risk Score can be used in patients presenting to ER with syncope to predict a 30-day serious adverse events2.  It consists of factors such as abnormal QRS axis, corrected QT interval >480 ms, elevated troponin (>99th percentile of normal population) and ED diagnosis based on evaluation to stratify patients into risk categories: very low (-3 to -2), low (-1 to 0), medium (1 to 3), high (4 to 5) and very high (6 to 11)2.

The Canadian Journal of Cardiology recommends a disposition algorithm for patients presenting to ER with syncope that is based on history of a serious medical condition and high-risk features3. Figure 1 illustrates an approach to disposition from the ER. Patients that have an unclear etiology and intermediate risk should be considered for an urgent cardiology assessment.

 

Figure 1: A disposition plan for patients presenting to the ER with syncope (Canadian Cardiovascular Society 2020).


Best Practice for Treatment

Given the benign course, treatment for vasovagal syncope is based on lifestyle modification, education and reassurance2. Lifestyle modification consists of educating patients on identifying and managing prodromes early and managing triggers (eg. dehydration, defecation, micturition, laughing, coughing and crowded environments)2.

Treatment for orthostatic syncope also relies on lifestyle modification, education and reassurance2. Lifestyle modification consists of re-adjusting diuretics, ACE-inhibitors, angiotensin receptor blockers, calcium channel and beta blockers to ensure optimal blood pressure and hydration control2.

Managing cardiac syncope requires addressing the underlying etiology through antiarrhythmic medications (eg. tachyarrhythmias), cardiac pacing (eg. bradyarrhythmias), catheter-directed ablation and ICD insertion1. Cardiac pacemaker therapy is indicated for patients that have intermittent sinus node disease if correlation is identified between sinus pauses on ECG and syncope3. Selected patients that are diagnosed with the bradycardia-tachycardia form of sick sinus syndrome, can benefit from a percutaneous cardiac ablative technique3.  Dual-chamber pacing is recommended for patients with sinus node dysfunction provided there is an increased risk of AV block4.


Case continued

The patient was admitted and had no further asystole after receiving atropine and intermittent transcutaneous pacing. He was accepted for a dual-chamber pacemaker insertion and was discharged with the diagnosis of syncope with sinus arrest and vagal overtones.


Take Home Points

  1. Patients presenting to the ER with new-onset syncope require a thorough history and physical exam to rule out cardiogenic causes.
  2. Validated clinical decision-making tools can be helpful to supplement clinical judgement for assessing the risk of a future cardiac event, identifying the need for a cardiology consult and creating a disposition plan.

References

  1. Runser LA, Gauer RL, Houser A. Syncope: Evaluation and Differential Diagnosis. Am Fam Physician. 2017;95(5):303-312. https://www.aafp.org/pubs/afp/issues/2017/0301/p303.html#:~:text=A%20standardized%20approach%20to%20syncope,%2C%20physical%20examination%2C%20and%20electrocardiography
  2. UpToDate. www.uptodate.com. https://www.uptodate.com/contents/syncope-in-adults-clinical-manifestations-and-initial-diagnostic-evaluation
  3. Sandhu RK, Raj SR, et al. Canadian Cardiovascular Society Clinical Practice Update on the Assessment and Management of Syncope. Can J Cardiol. 2020;36(8):1167-1177. doi:10.1016/j.cjca.2019.12.023 https://www.onlinecjc.ca/article/S0828-282X(19)31549-1/fulltext
  4. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J. 2018;39(21):1883-1948. doi:10.1093/eurheartj/ehy037https://academic.oup.com/eurheartj/article/39/21/1883/4939241?login=false
  5. Dakkak W, Doukky R. Sick Sinus Syndrome. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 18, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470599/

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Unvexing the VExUS Score – An Overview

Unvexing the VExUS Score – An Overview

 

PoCUS Clinical Pearl

Dr Steven Chen

DalEM PoCUS Elective

PGY2 Internal Medicine, University of Toronto

Reviewed: Dr David Lewis

Copyedited: Dr David Lewis


Introduction:

The pursuit of a rapid and objective measure of volume status has always been a vexing problem for clinicians as proper fluid management is pivotal for patient outcomes. In recent years, there has been increased attention towards the concept of “fluid-responsive” as liberal fluid boluses can often be associated with poor outcomes as a result of systemic congestion. 1

In the POCUS community, while Inferior Vena Cava (IVC) measurements have promise in assessing central venous pressure, the subsequent translation towards “volume responsiveness” has been met with many other limitations. For one, it did not account for venous congestion at other organ levels such as the pulmonary, renal, or hepatic systems. 2,3

Venous excess ultrasound (VExUS) is a growing bedside ultrasound-based approach that aims to provide a more comprehensive assessment of venous congestion. This was initially described by Beaubien-Souligny et al. (2020) from a post-hoc analysis correlating ultrasound grading parameters with risk in development of AKI in cardiac surgery patients.4 The protocol serves to assess multiple sites of venous congestion, including the IVC, hepatic veins, portal veins and intrarenal veins. By assessing congestion in these multiple sites, the VExUS score has gained attraction in providing a more comprehensive assessment of systemic congestion. 4,5

View Acquisition:

The VExUS protocol is composed of four main components outlined below:

  • IVC diameter
  • Hepatic Vein Doppler Assessment
  • Hepatic Portal Vein Doppler Assessment
  • Intrarenal Vein Doppler Assessment

This can be performed using either the curvilinear probe (preferred) or the phased array probe. The patient should be positioned flat and supine on the bed to acquire the views. The table below depicts some suggested views where larger regions of the veins may be accessible for pulse wave doppler gating in reference to standardized sonography protocols. 6,7

Note: Reviewing the basics of pulse wave doppler will be needed prior to completing VExUS scans (not covered in this article).

 

 

 

 

 

Interpretation:

Interpretation of the VExUS grading system is well summarized in diagram below (sourced from POCUS1018) and takes some practice to differentiate normal from abnormal waveforms. Pulse wave doppler assessment is pursued only if the inferior vena cava is found plethoric, defined as greater or equal to 2cm. 4,5

Each of the hepatic, portal and renal veins are subsequently examined and classified as normal, mildly congested, or severely congested. The VExUS system has four grades: Grade 0 represents no congestion in any organ, Grade 1 represents only mild congestive findings, Grade 2 represents severe congestive findings in only one organ, and Grade 3 represents severe congestive findings in at least two out of three organ systems. 4,5

Source: POCUS1018

Some sample waveforms are shown below with comments to help with distinguishing normal from abnormal waveforms.

 

Evidence:

VExUS has also been shown to be reliable and reproducible, with good interobserver agreement in trained individuals and correlation with other measures of volume status such as central venous pressure.4,5 As the technique is growing in the POCUS literature, below is a table summarizing several recent studies exploring its application across numerous settings.

Study Purpose Results
Beaubien-Souligny W, et al. (2020)4

 

Post-hoc analysis of a single centre prospective study in 145 patients

 

 

 

Initial model of VExUS grading system looking at association in development of AKI in cardiac surgery population Association with subsequent AKI:

 

HR: 3.69 CI 1.65–8.24 p = 0.001;

+LR: 6.37 CI 2.19–18.50 when detected at ICU admission, which outperformed central venous pressure measurements

 

Bhardwaj V, et al. (2020)9

 

Prospective cohort study of 30 patients in ICU setting

 

Prospective study on application of VExUS scoring on staging of AKI in patients with cardiorenal syndrome Resolution of AKI injury significantly correlated with improvement in VExUS grade (p 0.003).

 

There was significant association between changes in VExUS grade and fluid balance (p value 0.006).

Varudo R, et al. (2022)10

 

Case report of ICU patient with hyponatremia

Application of VExUS in case report as rapid tool to help with volume status assessment in patient with complex hyponatremia Overall VExUS grade 2, prompting strategy for diuresis with improvement
Rolston D, et al. (2022)11

 

Observational study of 150 septic patients in single centre

VExUS score performed on ED septic patients prior to receiving fluids with chart review done to determine if there is association with poorer outcomes Composite outcome (mortality, ICU admission or rapid response activation):

 

VExUS score of 0: 31.6% of patients

VExUS score of 1: 47.6% of patients

VExUS score >1: 67.7% of patients

(p: 0.0015)

Guinot, PG, et al. (2022)12

Prospective observational study of 81 ICU patients started on loop diuretic therapy

Evaluation of multiple scores to predict appropriate diuretic-induced fluid depletion (portal pulsatility index, renal venous impedance index, VExUS) Baseline portal pulsatility index and renal venous impedance index were found to be superior predictors compared to VExUS.

 

The baseline VExUS score (AUC of 0.66 CI95% 0.53–0.79, p = 0.012) was poorly predictive of appropriate response to diuretic-induced fluid depletion.

Menéndez‐Suso JJ, et al. (2023)13

 

Cross-sectional pilot study of 33 children in pediatric ICU setting

Association of VExUS score with CVP in pediatric ICU VExUS score severity was strongly associated with CVP (p<0.001) in critically ill children.
Longino A, et al. (2023)14

 

Prospective validation study in 56 critically ill patients

Validation looking at association of VExUS grade with right atrial pressure. VExUS had a favorable AUC for prediction of a RAP ≥ 12 mmHg (0.99, 95% CI 0.96-1) compared to IVC

diameter (0.79, 95% CI 0.65–0.92).

Pitfalls:

It should be kept in mind that numerous factors may affect interpretation of VExUS gradings.

For the IVC component, increased intra-abdominal pressure can affect measurements independently of the pressure in the right atrium or may be affected by chronic pulmonary hypertension. The hepatic vein may not show significant changes even in severe tricuspid regurgitation if the right atrium can still expand and contract normally. In thin healthy people and those with arteriovenous malformations, the portal vein can have a pulsatile flow without venous congestion. It is also important to note that for patients with underlying disease renal or liver parenchymal disease, venous doppler recordings may be less reliable. 3-5

Outside of physiologic factors, another limitation is the need for adequate training and familiarity in performing and interpreting the technique. While VExUS is fairly well protocolized, it requires proficiency with pulse wave doppler to perform accurately. As with any new technique, there is a risk of variability in technique and interpretation. To avoid misinterpretation, it is important to consider repeat tracings to ensure consistency of results and to consider findings within the overall clinical context of the patient.

Bottom line:

VExUS is a non-invasive ultrasound method for assessing venous congestion across multiple organ systems. While there are several physiologic limitations and results need to be used in adjunct with the clinical picture, studies have shown promise for VExUS to be incorporated as part of a physician’s toolkit to help with clinical decision making. 3-5

References

  1. Atkinson P, Bowra J, Milne J, Lewis D, Lambert M, Jarman B, Noble VE, Lamprecht H, Harris T, Connolly J, Kessler R. International Federation for Emergency Medicine Consensus Statement: Sonography in hypotension and cardiac arrest (SHoC): An international consensus on the use of point of care ultrasound for undifferentiated hypotension and during cardiac arrest. Canadian Journal of Emergency Medicine. 2017 Nov;19(6):459-70.
  2. Corl KA, George NR, Romanoff J, Levinson AT, Chheng DB, Merchant RC, Levy MM, Napoli AM. Inferior vena cava collapsibility detects fluid responsiveness among spontaneously breathing critically-ill patients. Journal of critical care. 2017 Oct 1;41:130-7.
  3. Koratala A, Reisinger N. Venous excess doppler ultrasound for the nephrologist: Pearls and pitfalls. Kidney Medicine. 2022 May 19:100482.
  4. Beaubien-Souligny W, Rola P, Haycock K, Bouchard J, Lamarche Y, Spiegel R, Denault AY. Quantifying systemic congestion with point-of-care ultrasound: development of the venous excess ultrasound grading system. The Ultrasound Journal. 2020 Dec;12:1-2.
  5. Rola P, Miralles-Aguiar F, Argaiz E, Beaubien-Souligny W, Haycock K, Karimov T, Dinh VA, Spiegel R. Clinical applications of the venous excess ultrasound (VExUS) score: conceptual review and case series. The Ultrasound Journal. 2021 Dec;13(1):1-0.
  6. Mattoon JS, Berry CR, Nyland TG. Abdominal ultrasound scanning techniques. Small Animal Diagnostic Ultrasound-E-Book. 2014 Dec 2;94(6):93-112.
  7. Standardized method of abdominal ultrasound [Internet]. Japanese society of sonographers. [cited 2023Apr12]. Available from: https://www.jss.org/english/standard/abdominal.html#Longitudinal%20scanning_2
  8. Dinh V. POCUS101 Vexus ultrasound score–fluid overload and venous congestion assessment.
  9. Bhardwaj V, Vikneswaran G, Rola P, Raju S, Bhat RS, Jayakumar A, Alva A. Combination of inferior vena cava diameter, hepatic venous flow, and portal vein pulsatility index: venous excess ultrasound score (VExUS score) in predicting acute kidney injury in patients with cardiorenal syndrome: a prospective cohort study. Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine. 2020 Sep;24(9):783.
  10. Varudo R, Pimenta I, Blanco JB, Gonzalez FA. Use of Venous Excess UltraSound (VExUS) score in hyponatraemia management in critically ill patient. BMJ Case Reports CP. 2022 Feb 1;15(2):e246995.
  11. Rolston D, Li T, Huang H, Johnson A, van Loveren K, Kearney E, Pettit D, Haverty J, Nelson M, Cohen A. 204 A Higher Initial VExUS Score Is Associated With Inferior Outcomes in Septic Emergency Department Patients. Annals of Emergency Medicine. 2021 Oct 1;78(4):S82.
  12. Guinot PG, Bahr PA, Andrei S, Popescu BA, Caruso V, Mertes PM, Berthoud V, Nguyen M, Bouhemad B. Doppler study of portal vein and renal venous velocity predict the appropriate fluid response to diuretic in ICU: a prospective observational echocardiographic evaluation. Critical Care. 2022 Dec;26(1):1-1.
  13. Menéndez‐Suso JJ, Rodríguez‐Álvarez D, Sánchez‐Martín M. Feasibility and Utility of the Venous Excess Ultrasound Score to Detect and Grade Central Venous Pressure Elevation in Critically Ill Children. Journal of Ultrasound in Medicine. 2023 Jan;42(1):211-20.
  14. Longino A, Martin K, Leyba K, Siegel G, Gill E, Douglas I, Burke J. Prospective Validation of the Venous Excess Ultrasound “(VExUS)” Score.

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Bicuspid Aortic Valve – An important incidental PoCUS finding?

Bicuspid Aortic Valve – An important incidental PoCUS finding?

Medical Student Pearl

 

Khoi Thien Dao

MD Candidate – Class of 2023

Dalhousie Medicine New Brunswick

Reviewed by: Dr. David Lewis


Case:

A 58-year-old male presents to Emergency Department with sudden onset of chest pain that is radiating to the back. He was also having shortness of breath at the same time of chest pain. The patient later reveals that his past medical history only consists of “bicuspid valve”, and he takes no medication. On examination, he was uncomfortable, but no signs of acute distress. His respiratory and cardiac exam were unremarkable for reduced air sound, adventitious sound, heart murmur, or extra heart sound. ECG was normal and initial cardiac markers were within normal range. His chest x-ray is normal.

You are aware that with his medical presentation and a history of bicuspid aortic valve, you need to consider associated concerning diagnosis (aortic root aneurysm and aortic dissection) within the differential (myocardial infarct, congestive heart failure, pneumonia, etc.).


Bicuspid Aortic Valve

Bicuspid aortic valve is one of the most common types of congenital heart disease that affects approximately one percent of population. There is a strong heritable component to the disease. Bicuspid aortic valve occurs when two leaflets fused (commonly right and left coronary leaflets) and form a raphe, a fibrous ridge1. The fusion of the leaflets can be partial, or complete, with the presence or absence of a raphe1. Bicuspid aortic valve disease is associated with increasing risks for valve calcification, which lead to aortic stenosis or regurgitation secondary to premature degeneration1. This congenital heart defect is also a well-known risks factor for aortic dissection and aortic dilatation. Reports have estimated prevalence of aortic dilation in patients with bicuspid aortic valve ranging between 20 to 80 percent, and that the risks of aortic dilation increase with age2. Increases risk of aortic dilatation in bicuspid valve disease also leads to a significantly greater risk for aortic dissection2.3.

The majority of patients with bicuspid aortic valve are asymptomatic with relatively normal valve function and therefore can remain undiagnosed for many years. However, most patients with bicuspid aortic valve will develop complications and eventually require valve surgery within their lifetime. Early diagnosis, while asymptomatic, can enable close follow-up for complications and early intervention with better outcomes. However, asymptomatic individuals are rarely referred for echocardiography.

With increasing use of cardiac PoCUS by Emergency Physicians, there are two scenarios where increased awareness of the appearance of bicuspid aortic valve and its complications may be of benefit.

  1. Known bicuspid aortic valve patients presenting with possible associated complications
  2. Undiagnosed bicuspid aortic valve patients presenting with unrelated symptoms undergoing routine cardiac PoCUS

This clinical pearl provides a review of the clinical approach to bicuspid aortic valve and its associated complications and provides guide to enhancing clinical assessment with PoCUS.


Clinical Approach:

Although bicuspid aortic valve commonly presents as asymptomatic, a detailed focused cardiac history can assess for clinical signs and symptoms related to valve dysfunction and its associated disease, such as reduced exercise capacity, angina, syncope, or exertional dizziness1. Information about family history with relation to cardiac disease is essential for a clinician’s suspicion of heritable cardiovascular disease. Red flag symptoms that shouldn’t be missed such as chest pain, back pain, hypertensive crisis, etc. should be specifically identified. They are indicators for possible emergent pathologies that should not be missed (for example: acute MI, aortic dissection, ruptured aortic aneurysm, etc.)

Physical examination findings in patients with bicuspid aortic valve include, but not limited to, ejection sound or click at cardiac apex/base, murmurs that have features of crescendo-decrescendo or holosystolic. Clinical signs of congestive heart failure such as dyspnea, abnormal JVP elevation, and peripheral edema may also be present.


Core Cardiac PoCUS:

With cardiac PoCUS, it is important to obtain images from different planes and windows to increase the complexity of the exam and to be able to be confidently interpreting the exam. There are four standard cardiac view that can be obtained: parasternal short axis (PSSA), parasternal long axis (PSLA), subxiphoid (sub-X), and apical 4-chamber view (A4C). Each cardiac view has specific benefits.

Parasternal Long Axis

With the PSLA, the phased-array transducer is placed to the left sternum at 3rd or 4th intercostal with transducer orientation pointing toward patient’s right shoulder. Key structures that should be seen are Aortic Valve (AV), Mitral Valve (MV), Left Ventricle (LV), pericardium, Right Ventricle (RV), Left Ventricular Outflow Tract (LVOT), and portion of ascending and descending aorta8. It is primarily used to assess left ventricular size and function, aortic and mitral valves, left atrial size8. Furthermore, pericardial effusions and left ventricular systolic function can be assessed.

Parasternal Long Axis

 

Parasternal Short Axis

Using the same transducer position as the PSLA the transducer can be centered to the mitral valve and rotated 90 degrees clockwise to a point where the transducer marker points to patient’s left shoulder to obtain the PSSA. With this orientation, one can assess for global LV function and LV wall motion8. Furthermore, with five different imaging planes that can be utilized with this view, aortic valve can be visualized in specific clinical contexts.

Parasternal Short Axis

 

Apical 4-Chamber

The apical 4-chamber view is generated by placing the transducer at the apex, which is landmarked just inferolateral to left nipple in men and underneath inferolateral of left breast in women. This view helps the clinician to assess RV systolic function and size relative to the LV8.

Apical 4-Chamber

 

Subxiphoid

The subxiphoid view can be visualized by placing a transducer (phased-array or curvilinear) immediately below the xiphoid process with the transducer marker points to patient’s right. The movements of rocking, tilting, and rotation are required to generate an optimal 4-chamber subcostal view. A “7” sign, which consists of visualizing the border between liver and pericardium, the septum, and the RV and LV that looks like number 7. This view allows user to assess RV functions, pericardial effusion, and valve functions8. In emergency setting, it can be used for rapid assessments in cardiac arrest, cardiac tamponade, and global LV dysfunction8.

From –  the PoCUS Atlas

Subxiphoid labelled

 

7 Sign


PoCUS Views for Aortic Valve Assessment

In assessing the aortic valve, the PSSA and PSLA can be best used to obtain different information, depending on clinical indications. Both views can be used to assess blood flows to assess stenosis or regurgitation. However, the PSLA view includes the aorta where clinician can look for aortic valve prolapse or doming as signs of stenosis and its complications, like aortic dilatation. On the other hand, PSSA are beneficial when assessing the aortic valve anatomy.

Parasternal Long Axis

From PoCUS 101

Parasternal Short Axis

From – the PoCUS Atlas


PoCUS Appearance of Normal Aortic Valve (Tricuspid) vs Bicuspid Aortic Valve

With PSSA view, the normal aortic valve will have three uniformly leaflets that open and form a circular orifice during most of systole. During diastole, it will form a three point stars with slight thickening at central closing point. The normal aortic valve is commonly referred to as the Mercedes Benz sign.

Parasternal Short Axis – Normal Tricuspid AV – Mercedes Benz Sign and 3 cusp opening

Pitfall

However, the Mercedes Benz Sign sign can be misleading bicuspid valve disease when three commissure lines are misinterpreted due to the presence of a raphe. A raphe is a fibrous band formed when two leaflets are fused together. It is therefore important to visualize the aortic valve when closed and during opening, to ensure all 3 cusps are mobile. Visualization of The Mercedes Benz sign is not enough on its own to exclude Bicuspid Aortic Valve.

Apparent Mercedes sign when AV closed due to presence of raphe. Fish mouth appearance of the same valve when open confirming bicuspid aortic valve

Bicuspid Aortic Valve

Identification requires optimal valve visualization during opening (systole). Appearance will depend on the degree of cusp fusion. In general a ‘fish mouth’ appearance is typical for bicuspid aortic valve.

Parasternal Short Axis – Fish Mouth Opening – Fusion L & R Coronary Cusps – Bicuspid Aortic Valve

In the parasternal long axis view the aortic valve can form a dome shape during systole, and prolapse during diastole, rather than opening parallel to the aorta. This is called systolic doming. Another sign that can be seen in PSLA view is valve prolapse, when either right or non-coronary aortic valve cusps showed backward bowing towards the left ventricle beyond the attachment of the aortic valve leaflets to the annulus. This can be estimated by drawing a line joining the points of the attachment.

Systolic doming

 

Diastolic prolapse and systolic doming

 

 

 


PoCUS Appearance of the Complications of Bicuspid Valve Disease

In patients presenting with chest/back pain, shock or severe dyspnea who have either known or newly diagnosed bicuspid valve disease, PoCUS assessment for potential complications can be helpful in guiding subsequent management.

Complications of bicuspid aortic valve include aortic dilatation at root or ascending (above 3.8cm) and aortic dissection 5-9.

Dilated aortic root, from – sonomojo.com

Aortic root dilatation – Normal maximum = 40mm

 

Aortic root dilatation with dissection

Valve vegetations or signs of infective endocarditis are among the complications of severe bicuspid valve5-9

Aortic valve vegetations


General Management of Patients with Bicuspid Valve in the Emergency Department

Management of bicuspid aortic valve disease is dependent on the severity of the disease and associated findings.

For a patient with suspicious diagnosis of bicuspid valve disease, a further evaluation of echocardiography should be arranged, and patient should be monitored for progressive aortic valve dysfunction as well as risk of aortic aneurysm and dissection. Surgical intervention is indicated with evidence of severe aortic stenosis, regurgitation, aneurysm that is > 5.5cm, or dissection1.


How accurate is PoCUS for Aortic Valve assessment?

Bicuspid aortic valve disease is usually diagnosed with transthoracic echocardiography, when physical examination has revealed cardiac murmurs that prompt for further investigation. However, patients with bicuspid valve disease frequently remain asymptomatic for a prolonged periods. Michelena et al. (2014) suggested that auscultatory abnormalities account for 60 to 70% diagnostic echocardiograms for BAV in community10.

While there are no published studies on the utility of PoCUS for the diagnosis of bicuspid aortic valve, there are studies on the use of PoCUS as part of the general cardiac exam. Kimura (2017) published a review that reported early detection of cardiac pathology when PoCUS was used as part of the physical exam 9. Abe et al. (2013) found that PoCUS operated by expert sonographer to screen for aortic stenosis has a sensitivity of 84% and a specificity of 90% in 130 patients 11. In another study by Kobal et al. (2004), they found that PoCUS has a specificity of 93% and sensitivity of 82% in diagnosing mild regurgitation12.

There are also limitations of using PoCUS to assess for bicuspid aortic valve disease, or valve disease in general. Obtaining images from ultrasound and interpretation are highly dependent on user’s experiences to assess for the valve9. Furthermore, research is needed to investigate the use of PoCUS in lesser valvular pathology.

 

When a new diagnosis of bicuspid aortic valve is suspected, a formal echocardiogram should be arranged, and follow-up is recommended.


Summary 

  • Bicuspid aortic valve is often asymptomatic and undiagnosed until later in life
  • Patients with known bicuspid aortic valve disease are closely followed and may require surgical intervention in the event of complications
  • Diagnosis of bicuspid aortic valve requires careful visualization of valve closing and opening during diastole and systole
  • The increased use of PoCUS by Emergency Physicians as an adjunct to cardiac examination may result in increased diagnosis of bicuspid  aortic valve. These may be related to the presentation or incidental findings
  • In patients presenting to the Emergency Department with known or newly diagnosed bicuspid aortic valve disease, consider if a complication is related to their presentation
  • In patient with incidental finding of bicuspid aortic valve disease refer for cardiology follow up

 


References

  1. Braverman, A. C., & Cheng, A. (2013). The bicuspid aortic valve and associated aortic disease. Valvular heart disease. Philadelphia: Elsevier, 179-218.
  2. Verma, S., & Siu, S. C. (2014). Aortic dilatation in patients with bicuspid aortic valve. N Engl J Med370, 1920-1929.
  3. Della Corte, A., Bancone, C., Quarto, C., Dialetto, G., Covino, F. E., Scardone, M., … & Cotrufo, M. (2007). Predictors of ascending aortic dilatation with bicuspid aortic valve: a wide spectrum of disease expression. European Journal of Cardio-Thoracic Surgery31(3), 397-405.
  4. Tirrito, S. J., & Kerut, E. K. (2005). How not to miss a bicuspid aortic valve in the echocardiography laboratory. Echocardiography: A Journal of Cardiovascular Ultrasound and Allied Techniques22(1), 53-55.
  5. Baumgartner, H., Donal, E., Orwat, S., Schmermund, A., Rosenhek, R., & Maintz, D. (2015). Chapter 10: Aortic valve stenosis. The ESC textbook of cardiovascular imaging. European Society of Cardiology.
  6. Fowles, R. E., Martin, R. P., Abrams, J. M., Schapira, J. N., French, J. W., & Popp, R. L. (1979). Two-dimensional echocardiographic features of bicuspid aortic valve. Chest75(4), 434-440.
  7. Shapiro, L. M., Thwaites, B., Westgate, C., & Donaldson, R. (1985). Prevalence and clinical significance of aortic valve prolapse. Heart54(2), 179-183.
  8. Gebhardt, C., Hegazy, A.F., Arntfield, R. (2015). Chapter 16: Valves. Point-of-Care Ultrasound. Philadelphia: Elsevier, 119-125.
  9. Kimura, B. J. (2017). Point-of-care cardiac ultrasound techniques in the physical examination: better at the bedside. Heart103(13), 987-994.
  10. Michelena, H. I., Prakash, S. K., Della Corte, A., Bissell, M. M., Anavekar, N., Mathieu, P., … & Body, S. C. (2014). Bicuspid aortic valve: identifying knowledge gaps and rising to the challenge from the International Bicuspid Aortic Valve Consortium (BAVCon). Circulation129(25), 2691-2704.
  11. Abe, Y., Ito, M., Tanaka, C., Ito, K., Naruko, T., Itoh, A., … & Yoshikawa, J. (2013). A novel and simple method using pocket-sized echocardiography to screen for aortic stenosis. Journal of the American Society of Echocardiography26(6), 589-596.
  12. Kobal, S. L., Tolstrup, K., Luo, H., Neuman, Y., Miyamoto, T., Mirocha, J., … & Siegel, R. J. (2004). Usefulness of a hand-carried cardiac ultrasound device to detect clinically significant valvular regurgitation in hospitalized patients. The American journal of cardiology93(8), 1069-1072.
  13. Le Polain De Waroux, J. B., Pouleur, A. C., Goffinet, C., Vancraeynest, D., Van Dyck, M., Robert, A., … & Vanoverschelde, J. L. J. (2007). Functional anatomy of aortic regurgitation: accuracy, prediction of surgical repairability, and outcome implications of transesophageal echocardiography. Circulation116(11_supplement), I-264.
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Management of Supraventricular Tachycardia (SVT) in Pregnancy

 

Management of Supraventricular Tachycardia (SVT) in Pregnancy

Medical Student Clinical Pearl

 

Tyson Fitzherbert, DMNB Class of 2024

Reviewed by Dr. Luke Taylor and Dr. David Lewis

 


Case:

A 30-year-old pregnant (32 weeks) female presents to the emergency department with palpitations and chest discomfort. On ECG they are diagnosed with supraventricular tachycardia, a narrow complex arrythmia – how would you proceed?

 


Introduction:

Pregnant women have a higher incidence of cardiac arrhythmias. The exact mechanism of increased arrhythmia burden during pregnancy is unclear, but has been attributed to hemodynamic, hormonal, and autonomic changes related to pregnancy. A common arrhythmia in pregnancy is supraventricular tachycardia (SVT). SVT is a dysrhythmia originating at or above the atrioventricular (AV) node and is defined by a narrow complex (QRS < 120 milliseconds) at a rate > 100 beats per minute (bpm). The presentations of SVT in pregnancy are the same as the nonpregnant state and include symptoms of palpitations that may be associated with presyncope, syncope, dyspnea, and/or chest pain. Diagnosis is confirmed by electrocardiogram (ECG).

 


Figure 1: Rhythm strip demonstrating a regular, narrow-complex tachycardia, or supraventricular tachycardia (SVT).

In general, the approach to the treatment of arrhythmias in pregnancy is similar to that in the nonpregnant patient. However, due to the theoretical or known adverse effects of antiarrhythmic drugs on the fetus, antiarrhythmic drugs are often reserved for the treatment of arrhythmias associated with clinically significant symptoms or hemodynamic compromise. Below is a detailed description of the management of SVT in pregnancy.

 


Management:

Figure 2: Treatment algorithm for SVT in pregnancy.

 


General Considerations:

  • Non‐pharmacological treatment including vagal manoeuvres such as carotid massage and Valsalva manoeuvre are well tolerated and aid in management.
  • Intravenous adenosine can be used in all three trimesters, including labor.
  • Electrical cardioversion is an effective treatment method for hemodynamically unstable or drug-refractory patients, which has proven to be safe in all three trimesters, including labor. There are some examples of this leading to pre-term labor in the third trimester.
  • AV nodal blocking agents and anti-arrhythmic agents may be considered for cardioversion; see table below for effects in pregnancy and breast feeding.

 

 


Case Continued:

A modified Valsalva manoeuvre is performed with resolution to sinus rhythm after 2 attempts. The patient is discharged with OBGYN follow-up.

https://sjrhem.ca/modified-valsalva-maneuver-in-the-treatment-of-svt-revert-trial/

 


Further Reading


References:

  1. Patti L, Ashurst JV. Supraventricular Tachycardia. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www-ncbi-nlm-nih-gov.ezproxy.library.dal.ca/books/NBK441972/
  2. UpToDate – https://www.uptodate.com/contents/supraventricular-arrhythmias-during-pregnancy#H11407709
  3. Ibetoh CN, Stratulat E, Liu F, Wuni GY, Bahuva R, Shafiq MA, Gattas BS, Gordon DK. Supraventricular Tachycardia in Pregnancy: Gestational and Labor Differences in Treatment. Cureus. 2021 Oct 4;13(10):e18479. doi: 10.7759/cureus.18479. PMID: 34659918; PMCID: PMC8494174. https://www-ncbi-nlm-nih-gov.ezproxy.library.dal.ca/pmc/articles/PMC8494174/
  4. Ramlakhan KP, Kauling RM, Schenkelaars N, et al, Supraventricular arrhythmia in pregnancy, Heart 2022;108:1674-1681. https://heart.bmj.com/content/early/2022/01/26/heartjnl-2021-320451#T2
  5. Goyal A, Hill J, Singhal M. Pharmacological Cardioversion. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www-ncbi-nlm-nih-gov.ezproxy.library.dal.ca/books/NBK470536/
  6. Vaibhav R. Vaidya, Nandini S. Mehra, Alan M. Sugrue, Samuel J. Asirvatham, Chapter 60 – Supraventricular tachycardia in pregnancy, Sex and Cardiac Electrophysiology. https://www-sciencedirect-com.ezproxy.library.dal.ca/science/article/pii/B9780128177280000607

 

 

 

 

 

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Volume Status Assessment in ED: Beyond the Vitals

Dr. Rawan Alrashed (@rawalrashed)

PEM Physician

PoCUS Fellow

Reviewed and edited by: Dr. David Lewis

Case

A 55 year old man known to have hypertension, diabetes, atrial fibrillation, chronic kidney disease presenting with 1 week H/O fever, SOB, chest pain, cough, fatigability, looking distressed on exam with HR 110, SpO2 of 86% on RA and BP of 87/45. No audible crackles or gallop rhythm, bilateral pitting edema noticed.

So, you are asking yourself should your next step be Fluids or Diuresis ??

Background

Patient presenting to the emergency department as critically ill with shock status presents a challenge in the initial hour to balance their fluid requirements with their volume status to reach an improvement in hemodynamics without causing harm.

Volume status assessment and fluid responsiveness have been investigated using multiple measures ranging from physical examination to laboratory work up to invasive measures. Despite all that, no single or multiple factor have been sensitive or specific enough to guide further fluid management. Currently, PoCUS is progressing widely in aiding the emergency physician to take a decision in assessing patient’s  fluid vs vasopressor vs diuretic needs and guide further resuscitation. PoCUS is noninvasive, readily available, reproducible test that can be augmented with other measures to guide fluid management (1).

 

Pathophysiology

To simplify fluid responsiveness, patients are assessed on accordance of the Frank-Starling curve. Patients will respond to fluid administration if they are on the ascending portion of the Starling curve and no benefit will be added if they are at a plateau where more harm can occur which is difficult to be predict form physical examination solely (2).

 

Figure 1: Frank Starling Law

 

Fluid Challenge

Traditionally volume responsiveness has been assessed by small fluid bolus challenge. A safer alternative to this is passive leg raise (PLR) which is an autotransfusion where you mobilize about 300-500 ml of intravascular volume from the lower limb to the heart by raising the patient legs from 0o to 45o. A Pre-Post assessment of stroke volume within 30-90 sec from PLR can be done to measure the difference where change of 10% consider to be responsive.

This have been shown to have a sensitivity of 77% to 100%, and a specificity of 88% and 99% (1).

 

Figure 2: Passive Leg raising technique (uptodate)

 

Volume Status Assessment

PoCUS have been used in volume status assessment and fluid responsiveness using multiple surrogates which can be classified as follows for simplification:

  1. Cardiac PoCUS: core and advanced.
  2. Stroke volume Assessment: VTI of LVOT/Carotid artery.
  3. Vascular Assessment: IVC, IJV.
  4. Venous Congestion: Hepatic, portal, & intra-renal doppler.
  5. Lung PoCUS.

 

1) Cardiac PoCUS

The target of Cardiac PoCUS is to assess for possible causes of hypotension and shock status using the RUSH or SHoC protocol (3).

 

Figure 3: SHoC Protocol (3).

 

2) Cardiac Output Assessment

Two measures can be used to assess fluid responsiveness: the left ventricular outlet tract (LVOT) and the carotid artery where you assess the velocity time integral (VTI) representing the column of blood passing through the vessel through time. This can be used as surrogate of fluid responsiveness before and after the PLR where a change of 10-15% consider as fluid responsive (4).

 

a. LVOT measurements

Cardiac output variation of greater than 14% has a high positive predictive value for the patient being fluid responsive while values less than 10% are associated with a high negative predictive value (1)

Cardiac output (mL/min) = Stroke Volume (mL/cycle) x Heart Rate (bpm)

Stroke Volume= LVOT area    x    LVOT VTI

 

PoCUS Technique (4)

  • Using the cardiac phased array probe to get apical 5 chamber view and parasternal long axis view.
  • Apical five chamber view, with visualization of the LVOT (A).
  • Pulsed wave Doppler interrogation of the LVOT. The interrogation window is placed just above the aortic valve, and the line of interrogation is positioned parallel to the long-axis of the LVOT itself (B).
  • Measuring the area under the curve of the LVOT Doppler waveform to derive the velocity time integral (C) .
  • Diameter of the LVOT, measured from a parasternal long-axis view (D)

Figure 4: Stroke volume measurement at the LVOT.

 

 

b. Common Carotid Artery

Two measurement are applied to the carotid artery: the carotid blood flow and the corrected carotid flow time index. These measure are recently established in the field of cardiac output assessment and accuracy is still under debate with further studies needed.

 

  • The carotid blood flow is the integral of blood volume that is ejected through the carotid artery with each cardiac cycle. An increase of carotid blood flow by 20% after PLR is indicative of fluid responsiveness with a sensitivity of 94% and specificity of 86% (6).

 

  • The corrected carotid flow time index  (CFTI) representing the flow time between the onset of systole and the closure of the aortic valve as the duration of the full cardiac cycle. A change in the CFTI of 25% following PLR was found to have high specificity but a low sensitivity accordingly a cutoff values of 10% to 15% are more typical, still further studies are needed to specify the accurate cut off value (4).

 

PoCUS Technique (4,5)

a. The linear transducer is placed at approximately at the level of the thyroid cartilage, with the orientation marker pointed toward the patient’s head (A).

b. The Carotid artery identified in long-axis and the bulb before the bifurcation visualized and the doppler is applied within 2–3 cm proximal to the carotid bulb, interrogation line (green) has also been angled to make it more parallel to the long-axis of the artery.

c. The Doppler angle correction cursor is placed parallel to the direction of blood flow with insonation angles <60° .

d. Carotid artery Doppler waveform with measurement of the systolic flow time (SFT) and total cycle time (CCT).

e. Calculate the corrected flow time index using the following formula (Figure-5):

                                           CFTI=SFT/√CCT

f. Calculate the carotid blood flow using velocity time integral tracing and carotid diameter (Intima to intima)  then apply it in this formula (Figure-6):

                                     blood flow=π×(carotid diameter)2/4×VTI×heart rate

 

Figure-5: Corrected Carotid Flow Time Index Measurement (4).

 

Figure-6: Carotid Blood Flow measurement (5).

 

 

 

3) Vascular Assessment

a. Inferior vena cava (IVC)

Measurements of IVC diameter and respiratory variation with the collapsibility index as a predictor of fluid responsiveness was found to be having pooled sensitivity and specificity of 63% and 73% respectively (7).  

PoCUS Technique (8)

  • Use the curvilinear or phased array probe.
  • placed in the sub-xiphoid space with the transducer flat against the abdomen identifying RA and gradually fanning the probe until the intrahepatic IVC can be identified.
  • The probe is then rotated 90 degrees with the marker toward patient head to obtain the IVC in long axis view.
  • IVC diameter is measured 2 cm inferior to the cavo-atrial junction or about 1 cm inferior to the branching of the hepatic veins (Figure 7).
  • M-mode can be used to track IVC collapse during inspiration in spontaneously breathing patients.

Figure-7: IVC and measurement of respiratory variation (Collapsibility Index)

 

Measurements:

Collapsibility Index (Caval Index)

The collapsibility index=(maximal vessel diameter – minimal vessel diameter)÷maximal vessel diameter

It has been demonstrated that venous collapsibility may be inversely proportional to CVP: a 1 mmHg change in central venous pressure correlates to about 3.3% change in IVC collapsibility (9).

 

IVC diameter (cm) CI (%) CVP (mmHg)
<1.5 100% <0-5 Volume depleted
1.5-2.5 >50% <10 Less predictive of responsiveness
1.5-2.5 <50 >10
>2.5 0% >20 Volume overload

 

Important to note that sole interpretation of the IVC for volume assessment was found to be poorly correlating and thus should be used in conjunction with  other measures and integrated on patient presentation (9).

 

b. Internal Jugular Vein (IJV)

Internal jugular vein is used for the assessment of the central venous pressure in comparable way to IVC. A small study of non-ventilated patients who were simultaneously undergoing CVP monitoring, a mean IJV diameter of 7 mm correlated with a CVP of 10 mmHg (8). 

Collapsibility index of the IJV with change of 39% consider the patient as volume depleted but this carries a limitation of the intrabdominal/ intrathoracic pressure effects (4).

PoCUS Technique

  • Use the linear Probe
  • Identify the IJV in transverse plane then rotate the probe 90o toward the patient head.
  • Image of IJV is obtained where it narrows into a paintbrush appearance (Figure 8).
  • The height where the IJV tapers correlates with jugular venous distension.
  • The IJV diameter is measured using M-mode through several respiratory cycles, and the end expiratory diameter is used as the final measurement.

Figure-8: Internal Jugular vein

 

4)Venous Congestion (VEXUS):

This includes assessment of the Hepatic/Portal/Intrarenal veins wave forms which has been correlated to the level of venous congestion thus estimating the end organ volume effects.

Hepatic Vein Doppler mainly reflects the right atrium filling pattern, portal and intrarenal venous Doppler provide additional information about right atrial filling pressure and its correlation with congestive organ injury (10).

 

PoCUS Technique (9)

Hepatic Vein Doppler

  • The probe is placed over the liver in the subcostal position to visualize the middle hepatic vein. Pulsed-wave Doppler is used 2-4 cm from where the hepatic vein drains into the IVC.

Findings: The waveform of the hepatic vein is reversed with higher velocities seen in diastole in states of volume overload. In severe volume overload, retrograde flow is seen in systole (Figure 9)

 

Figure-9: Hepatic vein doppler different wave forms (11).

 

Portal Vein Doppler

  • Moving towards the portal vein, the transducer is placed in the right mid-axillary line

Findings: Flow through the portal vein is normally monophasic, but in the presence of hypervolemia, pulsatility will be present. This can be quantified using the pulsatility index where a pulsatility index greater than 50% indicates severe volume overload.

 

Figure 10: Portal vein doppler wave forms (11).

 

Intra-renal Doppler

  • The curvilinear transducer is placed on the posterior axillary line

Findings: A normal Doppler waveform is continuous. With increasing venous congestion, there is a decrease in the systolic component of the wave with progression to biphasic (systolic/diastolic phases), and with severe renal congestion, there is complete absence of systolic flow showing only diastolic phase.

 

Figure 11: Intra-renal doppler wave forms (11).

 

Figure-12: the change in the venous doppler according to progression of venous congestion (10).

 

Figure -13: VExUS grading system for venous congestion using IVC and different venous doppler wave form for categorization.

 

5)Lung Ultrasound 

A meta-analysis showed that LUS is 88% sensitive and 90% specific for acutely decompensated heart failure and was more sensitive at detecting pulmonary edema than CXR (8).

Another meta-analysis determined the sensitivity and specificity of ultrasound for detection of pleural effusions as 93% and 96% respectively. The sensitivity approaches 100% with pleural effusions >100 mL in volume (8).

PoCUS Technique

  • Use the linear or curvilinear probe.
  • In longitudinal plane, along the midclavicular, midaxillary line then the posterior-lateral point.

Findings:

  • B-lines are hyperechoic vertical lines extending from the pleura down to the bottom of the US image (Figure 14). Two or fewer B-lines in each section is considered normal
  • Pleural effusion can be identified with presence of V-sign (extension of vertebral line proximal to the diaphragm (Figure-15) .  

 

Figure 14: B-Lines

Figure 15: Pleural effusion

 

 

 

 

 

 

 

 

 

 

Case Conclusion

Patient was found to have reduced LV function with Dilated IVC and CI of 15%, VExUS grade 2. Assessment of COP after PLR didn’t show a proper change thus patient was started on diuretic and respiratory support with consideration of inotropic support. 

Conclusion

The table below (8) shows a summary of the evidence related to the different used marker for volume assessment from physical exam to the use of PoCUS. Thus, it is imperative that we do not rely on one single tool, but rather integrate both pertinent physical examination and POCUS findings for better probability of coming to the right decision.

 

 

References

  1. Pourmand A, Pyle M, Yamane D, Sumon K, Frasure SE. The utility of point-of-care ultrasound in the assessment of volume status in acute and critically ill patients. World J Emerg Med. 2019;10(4):232-238. doi:10.5847/wjem.j.1920-8642.2019.04.007.
  2. Praveen P., Shanmugam L., Prasath, P. A review of role of lung ultrasound and clinical congestion score in acute left ventricular failure. International Journal of Advances in Medicine. 2020;7. 720. 10.18203/2349-3933.ijam20201130.
  3. Atkinson P, Bowra J, Milne J, et al. International Federation for Emergency Medicine Consensus Statement: Sonography in hypotension and cardiac arrest (SHoC): An international consensus on the use of point of care ultrasound for undifferentiated hypotension and during cardiac arrest – CORRIGENDUM. CJEM. 2017;19(4):327. doi:10.1017/cem.2017.31.
  4. Millington SJ, Wiskar K, Hobbs H, Koenig S. Risks and Benefits of Fluid Administration as Assessed by Ultrasound. Chest. 2021;160(6):2196-2208. doi:10.1016/j.chest.2021.06.041.
  5. Ma IWY, Caplin JD, Azad A, et al. Correlation of carotid blood flow and corrected carotid flow time with invasive cardiac output measurements. Crit Ultrasound J. 2017;9(1):10. doi:10.1186/s13089-017-0065-0.
  6. Marik PE LA, Young A, Andrews L. The use of bioreactance and carotid Doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients. Chest. 2013;143(2):364-370. doi:10.1378/chest.12-1274.
  7. Long E, Oakley E, Duke T, Babl FE. Does Respiratory Variation in Inferior Vena Cava Diameter Predict Fluid Responsiveness: A Systematic Review and Meta-Analysis. Shock (Augusta, Ga). 2017;47(5):550-559.
  8. Kearney, D., Reisinger, N., & Lohani, S. (2022). Integrative Volume Status Assessment. POCUS Journal7(Kidney), 65–77.
  9. Argaiz Eduardo R, Koratal A., Reisinger N. Comprehensive Assessment of Fluid Status by Point-of-Care Ultrasonography. Kidney360
  10. Galindo P, Gasca C, Argaiz ER, Koratala A. Point of care venous Doppler ultrasound: Exploring the missing piece of bedside hemodynamic assessment. World J Crit Care Med. 2021;10(6):310-322. Published 2021 Nov 9. doi:10.5492/wjccm.v10.i6.310.
  11. Dinh, V. (n.d.). Vexus ultrasound score – fluid overload and venous congestion assessment. POCUS 101. Retrieved March 29, 2022, from https://www.pocus101.com/vexus-ultrasound-score-fluid-overload-and-venous-congestion-assessment/. 

 

 

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Murmurs for the Learners: An approach to pediatric heart murmurs

Murmurs for the Learners: An approach to pediatric heart murmurs – A Medical Student Clinical Pearl

Luke MacLeod, Med IV

DMNB Class of 2022

Reviewed by Dr. Tushar Pishe

Copyedited by Dr. Mandy Peach

Case:

You are a senior medical student working in the emergency department and are asked to see Charlie, a 3-year-old boy who had a fall.  He is accompanied by his uncle Kevin, who gives you the history.  About one hour ago, Charlie was climbing onto a chair when he fell off and hit his head.  The chair was only a few feet off the ground and the floor was covered with a rug.  Charlie cried for several minutes after the fall, but there was no loss of consciousness or vomiting following the event.

Kevin tells you that Charlie is a healthy boy with no known medical issues or surgical history. There have been no concerns with his growth or development thus far.  He has no allergies, does not take any medications, and is up to date on his immunizations.  Kevin is unable to tell you much about Charlie’s family history.  He recently adopted Charlie, whose biological parents are no longer involved.

On exam, you observe an active and responsive 3-year-old.  He is afebrile with stable vital signs.  He has normal colour and shows no signs of respiratory distress.  There is a small bump on the top of his head, but no other injuries are noted.  His neurological exam reveals no focal neurological deficits.  To complete the exam, you feel his abdomen, which is soft and non-tender with no organomegaly, and auscultate his heart and lungs.  His lungs are clear with no crackles or wheeze. On auscultation of the heart, you detect a soft, non-radiating systolic murmur that seems to go away with inspiration.

You are reassured from the history and exam that Charlie’s head injury was very minor and that no further investigations or interventions are necessary, but you wonder about the significance of his heart murmur.

 

What is a heart murmur?

 

A heart murmur is an additional sound, often described as whooshing or blowing noise, heard between heart beats that is generated by turbulent blood flow in or near the heart.1,2  Heart murmurs are very common, with up to 90% of children having one either during infancy or later in childhood.  However, less than 1% of these murmurs are due to congenital heart disease.3  If the heart murmur is related to a serious underlying condition, the child may have signs or symptoms such as cyanosis, cough, shortness of breath, or light-headedness.1  Most murmurs are asymptomatic, but the absence of symptoms does not always mean that the murmur is benign.3 In some cases a murmur may be the only sign of an underlying heart condition.4

 

How to describe a murmur

 

Before picking up your stethoscope, you’ll want to make sure you have clean ear canals so you can pick up subtle murmurs.  The characteristics use to describe a murmur can be remembered with the pneumonic Q-TIP ROLS (note: this is not a recommendation to clean your ears with cotton swabs).

 

Quality

The quality of a murmur can be described as harsh, blowing, musical, rumbling, or vibrating.3

 

Timing

Timing describes when the murmur occurs in the cardiac cycle.  A systolic murmur occurs between S1 and S2.  These can be further categorized into four sub-types:

  • Early systolic: heard with or immediately after S1 and ends about halfway through systole.
  • Mid-systolic/systolic ejection murmur: heard midway between S1 and S2. Increases then decreases in volume (crescendo-decrescendo).
  • Mid-to-late systolic: heard about halfway through systole and ends before S2
  • Holosystolic/pansystolic: heard throughout systole.

Click here to listen to a holosystolic murmur: https://www.youtube.com/watch?v=MzORJbyHTT0

 

A diastolic murmur occurs between S2 and S1.  These can be further categorized into three sub-types:

  • Early diastolic: a high-pitched murmur heard with or immediately after S2.
  • Mid-diastolic: heard soon after S2 and ends before S1.
  • Late diastolic/presystolic: heard just before S1.

 

A continuous murmur is heard throughout the cardiac cycle.3

 

Intensity

A grading system from 1-6 is used to describe a murmur’s intensity, with higher values representing greater volumes.3  The following table details what each grade indicates:5

Pitch

A murmur can have low, medium, or high pitch.  High pitch murmurs are best detected using the diaphragm of the stethoscope, while low pitch murmurs are easier to hear using the bell.3

 

Radiation

This is the furthest point from the location (see below) where the murmur can still be detected.3

 

Other sounds

S3: heard in early diastole (shortly after S2).  S3 can be present in hyperdynamic states or with a large VSD.  This sound is best heard with the bell over the apex (for blood flow to the left ventricle) or the lower left sternal border (for blood flow to the right ventricle). When an S3 is present, the heart beat cadence is often described using the word “Kentucky” where “Ken” is S1, “tuc” is S2, and “ky” is S3.5

 

S4: heard late in diastole (just before S1) when there is turbulent blood flow into a stiff ventricle, such as in hypertrophic cardiomyopathy, myocardial dysfunction, semilunar valve stenosis, or tachycardia-induced cardiomyopathy.  S4 is best heard with the bell and is a pathologic exam finding.  When an S4 is present, the heart beat cadence is often described using the word “Tennessee,” where “Ten” is S4, “nes” is S1, and “see” is S2.5

 

Click below to listen to S3 and S4 heart sounds

https://www.youtube.com/watch?v=o8eqYHCy7dw

 

Ejection clicks

These are high pitch sounds that are often generated by abnormal heart valves.  The affected valve is determined based on the location, timing, and nature of the click as shown in the table below:5

Pericardial friction rub

A coarse grinding sound heard with pericarditis. This is best heard along the left sternal border.5

 

Location

This is the point where the murmur is most easily heard.3

 

Shape

Shape describes a murmur’s volume pattern. A few examples are shown below:6

What are the characteristics of benign and pathological murmurs?

 

Some red flag characteristics of pathologic murmurs are listed below.4,7

  • Holosystolic
  • Diastolic
  • Grade 3 or higher
  • Harsh quality
  • Systolic click
  • Max intensity at upper left sternal border
  • Abnormal S2
  • Greater intensity with standing

 

Characteristics of benign murmurs can be remembered using The Seven S’s.4,8

  • Systolic
  • Soft
  • Short (not holosystolic)
  • Small (non-radiating)
  • Sweet (not harsh)
  • Single (no clicks or gallops)
  • Sensitive (changes with position or respiration)

 

Click below to listen to an innocent heart murmur

https://www.youtube.com/watch?v=uFyWHPfrRak

 

Here are some examples to practice differentiating innocent from pathological murmurs:

https://teachingheartauscultation.com/pediatric-murmur-recognition-program-intro

 

What are some of the more common pediatric heart murmurs?

 

Innocent9

  • Classic vibratory parasternal-precordial stills murmur
  • Pulmonary ejection murmur
  • Systolic murmur of pulmonary flow in neonates
  • Venous hum
  • Carotid bruit

 

Pathologic4

  • Ventricular septal defect
  • Atrial septal defect (example: https://www.youtube.com/watch?v=W8gg2S-mvSQ)
  • Patent ductus arteriosus
  • Teratology of Fallot
  • Pulmonary stenosis
  • Coarctation of the aorta
  • Aortic stenosis
  • Transposition of the great arteries

 

Next steps

 

In patients with a heart murmur and an abnormal chest X-ray or ECG, an echocardiogram is indicated.  The echocardiogram is the gold standard test to diagnose congenital heart defects.  While the chest X-ray and ECG are low cost tests and can help rule out other diagnoses, they are not particularly useful in identifying the cause of a heart murmur. 3

An innocent heart murmur in an asymptomatic patient with an otherwise normal exam does not require referral to cardiology.  However, the patient should be followed by their family physician to monitor the murmur.

Patients who are symptomatic, have a pathologic murmur, and/or have other concerning exam findings should be referred to a pediatric cardiologist.10

 

Case Conclusion

 

Charlie’s heart murmur lacked any of the red flag characteristics.  It was soft (grade 2) systolic murmur that did not radiate and changed with inspiration, which are all reassuring signs.  He was also asymptomatic and had an otherwise normal exam.

You explain to Kevin that Charlie looks well and that there are no signs of serious head trauma.  You mention that you did notice a heart murmur that is likely benign.  Charlie does not need to see a specialist, but you recommend that he have a follow up appointment with his family doctor in the next few weeks to monitor the heart murmur.

 

 

References:

  1. Heart Pulse Sound Wave Icon Stock Vector – Illustration of blood, healthcare: 91331428. Accessed November 19, 2021. https://www.dreamstime.com/stock-illustration-heart-pulse-sound-wave-icon-background-image91331428
  2. Heart Murmur | NHLBI, NIH. Accessed November 18, 2021. https://www.nhlbi.nih.gov/health-topics/heart-murmur
  3. Heart murmurs: MedlinePlus Medical Encyclopedia. Accessed November 18, 2021. https://medlineplus.gov/ency/article/003266.htm
  4. Pediatric Heart Murmurs: Evaluation and management in primary care. Accessed November 18, 2021. https://oce-ovid-com.ezproxy.library.dal.ca/article/00006205-201103000-00006/HTML
  5. Frank JE, Jacobe KM. Evaluation and Management of Heart Murmurs in Children. Am Fam Physician. 2011;84(7):793-800.
  6. Approach to the infant or child with a cardiac murmur – UpToDate. Accessed November 18, 2021. https://www.uptodate.com/contents/approach-to-the-infant-or-child-with-a-cardiac-murmur?search=heart%20murmurs&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
  7. Physical Examination – Textbook of Cardiology. Accessed November 18, 2021. https://www.textbookofcardiology.org/wiki/Physical_Examination
  8. Pediatric Heart Murmur Recognition Program intro. Teaching Heart Auscultation to Health Professionals. Accessed November 19, 2021. https://teachingheartauscultation.com/pediatric-murmur-recognition-program-intro
  9. Bronzetti G, Corzani A. The Seven “S” Murmurs: an alliteration about innocent murmurs in cardiac auscultation. Clin Pediatr (Phila). 2010;49(7):713. doi:10.1177/0009922810365101
  10. Begic E, Begic Z. Accidental Heart Murmurs. Med Arch. 2017;71(4):284-287. doi:10.5455/medarh.2017.71.284-287
  11. McConnell ME, Adkins SB, Hannon DW. Heart murmurs in pediatric patients: When do you refer? Am Fam Physician. 1999;60(2):558-565.

 

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QUICK TIPS on STEMI equivalents

QUICK TIPS on STEMI equivalents – A Medical Student Clinical Pearl

Ilya Abelev

MD Candidate, Class of 2022

Dalhousie Medical School New Brunswick

Reviewed by Dr. Jay Mekwan

Copyedited by Dr. Mandy Peach

 

Why recognize STEMI’s?2

STEMI’s indicate an infarction pattern on ECG, and can guide emergency physicians to identify patients who would benefit from emergent catheterization and revascularization.

What is a STEMI?

(S-T Segment Elevation Myocardial Infarction)

A patient presents with clinical symptoms consistent with an acute coronary syndrome together with S-T segment elevation (STE) on ECG or a new LBBB.

What is a STEMI equivalent?

A STEMI equivalent is an ECG pattern suggestive of ischemia that should trigger emergency physicians to consult specialists such as interventional cardiologists for revascularization interventions – similar to a STEMI.

MI Definition1

• ≥ 2.5 mm STE in V2-V3 for males < 40 years*
• ≥ 2 mm STE in V2- V3 for males ≥ 40 years*
• ≥ 1.5 mm STE in V2-V3 for females regardless of age*
• ≥ 1 mm STE all other leads

• New J-point elevation ≥ 1 mm from prior ECG should be considered ischemic
• The J-point is defined as the junction between the QRS termination and the ST-segment onset, and the ST-segment should be measured against the isoelectric TP segment (assuming a stable baseline)3

J point in a) normal; b) c) J point elevation; d) J point depression; e) with J wave (Osborn wave)

Osborn wave: Characteristically seen in hypothermia (typically T < 30C), but they are not pathognomonic (4)

Mnemonic for Stemi Equivalents – PTSD (5)

  1. Posterior MI
  2. T wave Abnormalities
  3. Sgarbossa Criteria
  4. Diffuse ST depression with ST elevation in AVR

Posterior MI (1,6)

“Posterior MIs are easily missed because of the absence of any ST elevation. Posterior involvement is estimated to occur in 15-21% of all acute myocardial infarctions and in isolation ~3% of the time, typically due to occlusion of the left circumflex or right coronary arteries.”

More Information(7)

“As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3.”

Posterior MI is suggested by the following changes in V1-3:

  1. Horizontal ST depression
  2. Tall, broad R waves (>30ms)
  3. Upright T waves
  4. Dominant R wave (R/S ratio > 1) in V2” (7)

Image illustrating reciprocal changes in V2 and how a ST depression in V2 can appear like a STEMI when flipped (reciprocal)

Where to expect reciprocal changes?

PAILS (8)

Posterior MI – anterior reciprocal changes
Anterior MI – inferior reciprocal changes
Inferior MI – lateral reciprocal changes

Lateral MI <-> inferior or septal reciprocal changes*** exception to mnemonic
Septal MI – posterior reciprocal changes

 

T wave abnormalities

de Winter T-waves (9,10)

Key 12-Lead Features

  1. “J-Point depression with up-sloping ST segments.
  2. Tall, prominent, symmetric T waves in the precordial leads.
  3. Upsloping ST segment depression > 1mm at the J-point in the precordial leads.
  4. Absence of ST elevation in the precordial leads.
  5. ST segment elevation (0.5mm-1mm) in aVR.
  6. “Normal” STEMI morphology may precede or follow the DeWinter pattern.”

 

Wellens Syndrome(11)

Rhinehart et al (2002) describe the following Diagnostic criteria(12) for Wellens syndrome:

• “Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
• ECG pattern present in pain-free state
• Isoelectric or minimally-elevated ST segment (< 1mm)
• No precordial Q waves
• Preserved precordial R wave progression
• Recent history of angina
• Normal or slightly elevated serum cardiac markers”

“There are two patterns of T-wave abnormality in Wellens syndrome:

Type A/1 – Biphasic, with initial positivity and terminal negativity (25% of cases)
Type B/2 – Deeply and symmetrically inverted (75% of cases)”

Sgarbossa Criteria(13,14)

In patients with left bundle branch block (LBBB) or ventricular paced rhythm, infarct diagnosis based on the ECG can be difficult
Abnormal depolarisation should be followed by abnormal repolarisation, manifesting as ST-segment and T-wave deviations that do not necessarily indicate acute ischaemia (“appropriate discordance”)

  1. Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)

  1. Concordant ST depression > 1 mm in V1-V3 (score 3)

  1. Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2)

“These criteria are specific, but not sensitive (36%) for myocardial infarction. A total score of ≥ 3 is reported to have a specificity of 90% for diagnosing myocardial infarction.”(13)

Diffuse ST depression with ST elevation in AVR(1)

“STE ≥ 1 mm in aVR or V1 with STD ≥ 1 mm in ≥ 6 leads can suggest left main coronary artery insufficiency, proximal LAD insufficiency, or triple vessel disease, especially if accompanied by pathologic Q-waves, hemodynamic compromise, and/or refractory symptoms.”

• Widespread deep ST depression involving V2-6, I, II, aVL
• ST elevation in aVR > V1

 

Examples of STEMI Equivalents(16): Resource to test knowledge of STEMI equivalents

Conclusion:

  1. Definition of MI varies by age and sex
  2. Use PTSD mnemonic to remember the STEMI equivalents.
    a. Use PAILS to remember appropriate location of reciprocal changes
  3. Initiate appropriate consultation to revascularize/ stent for both STEMI and STEMI equivalents

 

References

  1. Daniel Kreider; Jeremy Berberian. STEMI Equivalents: Can’t-Miss Patterns EMRA [Internet]. [cited 2022 Feb 19]. Available from: https://www.emra.org/emresident/article/stemi-equivalents/
  2. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, et al. Fourth Universal Definition of Myocardial Infarction (2018). Circulation. 2018 Nov 13;138(20):e618–51.
  3. J point ECG Interval • LITFL • ECG Library Basics [Internet]. [cited 2022 Feb 19]. Available from: https://litfl.com/j-point-ecg-library/
  4. Slovis C, Jenkins R. Conditions not primarily affecting the heart. BMJ. 2002;
  5. STEMI Equivalents for ECGs – YouTube [Internet]. [cited 2022 Feb 19]. Available from: https://www.youtube.com/watch?v=lH19cYBdvaQ
  6. van Gorselen EOF, Verheugt FWA, Meursing BTJ, Oude Ophuis AJM. Posterior myocardial infarction: the dark side of the moon. Neth Heart J. 2007;
  7. Posterior Myocardial Infarction • LITFL • ECG Library Diagnosis [Internet]. [cited 2022 Feb 19]. Available from: https://litfl.com/posterior-myocardial-infarction-ecg-library/
  8. Tiny Tips: STEMI? Don’t forget your PAILS! – CanadiEM [Internet]. [cited 2022 Feb 19]. Available from: https://canadiem.org/chest-pain-pails/
  9. de Winter RJ, Verouden NJW, Wellens HJJ, Wilde AAM. A New ECG Sign of Proximal LAD Occlusion. N Engl J Med. 2008;
  10. DeWinter’s T-Waves [Internet]. [cited 2022 Feb 19]. Available from: https://handbook.bcehs.ca/clinical-practice-guidelines/pr-clinical-procedure-guide/pr16-12-lead-ecgs/stemis-equivalents-imposters/stemi-equivalents/dewinters-t-waves/
  11. Wellens Syndrome: A Historical Literature Review – Dr. Jason West [Internet]. [cited 2022 Feb 19]. Available from: https://jacobiem.org/wellens-syndrome-a-historical-literature-review-dr-jason-west/
  12. Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med. 2002;
  13. Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce LA. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified sgarbossa rule. Ann Emerg Med. 2012;
  14. Sgarbossa Criteria • LITFL • ECG Library Diagnosis [Internet]. [cited 2022 Feb 19]. Available from: https://litfl.com/sgarbossa-criteria-ecg-library/
  15. Sgarbossa Criteria – MEDZCOOL – YouTube [Internet]. [cited 2022 Feb 19]. Available from: https://www.youtube.com/watch?v=oLFJy1e9WWI&t=135s
  16. STEMI Equivalents — Maimonides Emergency Medicine Residency [Internet]. [cited 2022 Feb 19]. Available from: https://www.maimonidesem.org/blog/stemi-equivalents-1

 

 

 

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Allergic Acute Coronary Syndrome (Kounis Syndrome)

Allergic Acute Coronary Syndrome (Kounis Syndrome) – A Medical Student Clinical Pearl

Amar Bhardwaj CC3

Dalhousie Medicine New Brunswick

Class of 2022

Reviewed and edited by Dr. Kavish Chandra

Copyedited by Dr. Mandy Peach

 

Case presentation

A 52-year-old female presents to the ED with sudden onset left sided chest with radiation to her left arm shortly after eating.  The patient is diaphoretic and has been experiencing exertional dyspnea since her meal.  Patient also noted they developed an itchy red rash on their face and torso. There was no evidence of angioedema or other classical clinical signs or symptoms of anaphylaxis.

The patient is otherwise healthy and has a family ischemic heart disease.

Her vitals are BP 160/90, temperature 36.4, HR: 152, RR: 20, Sats:98% O2 on room air. The cardiovascular and respiratory exam are otherwise normal. The ECG shows sinus tachycardia without evidence of other abnormalities.

 

Image source: Burns, Ed. “Sinus Tachycardia • LITFL • ECG Library Diagnosis.” Life in the Fast Lane • LITFL, 7 Feb. 2021, litfl.com/sinus-tachycardia-ecg-library/.

Her hsTnT is 8 and the repeat marker is unchanged and the diagnosis of Kounis syndrome is considered.

 

Kounis syndrome

Kounis syndrome is defined as a concurrent acute coronary syndrome (ACS) in the setting of mast cell activation, which can be spontaneous or secondary to an allergic reaction (Lerner et al. 2017).  Kounis syndrome can be triggered by food, insect stings, drugs, environmental exposure and underlying medical conditions (Rodrigues et al. 2013). Allergen induced mast cell activation and release of inflammatory mediators leads to vasospasms, intimal thickening, and upregulation of proinflammatory cytokines that affect the coronary arteries and potential for occlusion progressing to an acute MI. The epidemiology remains scarce, and thus the prevalence is not entirely known as it is often missed or under diagnosed (Kounis, 2013; Kounis 2016).

Patients with Kounis syndrome can present with dyspnea, angioedema, pruritis, urticaria, gastrointestinal distress and hemodynamic instability. Airway compromise is of high importance in severe anaphylactic reactions with the potential to progress to anaphylactic shock. Along with an anaphylactic response, the coronary arterial effect can accelerate plaque rupture and cause symptoms indistinguishable from ACS.

Kounis Syndrome can be classified into three types (Kounis 2013)

Type I:

Acute coronary syndrome with normal or near-normal coronary arteries.

Type II:

Pre-existing atherosclerotic disease with syndrome causing coronary artery spasm, plaque rupture or erosion leading to acute MI.

Type III:

Coronary artery stent thrombosis with evidence of aspirated thrombus specimens containing eosinophils and mast cells respectively.

 

Presentation

Patients with this Kounis syndrome typically present with anaphylactic signs and symptoms accompanied with chest pain and associated signs and symptoms of acute coronary syndrome.  Table 1 depicts pertinent signs and symptoms that may point you in the right direction.

Table 1. Clinical and laboratory findings in Kounis syndrome (Adapted from Kounis 2016)

 

Kounis syndrome is a clinical diagnosis.

Management

There are no guidelines addressing the management of Kounis syndrome. However, treatment needs to address any hemodynamic instability as well as the cardiac and allergic concerns. Involvement of cardiology and allergy specialists can be helpful.

Concurrent management of anaphylaxis does not generally interfere with management of ACS however careful analysis of the risks and benefits of epinephrine administration to treat anaphylaxis without exacerbating cardiac ischemia. Case reports describe the successful treatment of Kounis syndrome patients with intramuscular epinephrine (Lerner et al. 2017). Other agents that have shown to aid symptomatically in allergic responses are H1 and H2 blockers as well as systemic corticosteroids for prevention of potential delayed phase reactions.

ACS management may be guided by cardiology and does not differ from traditional management with the exception that aspirin may be omitted due to its potential role propagating anaphylaxis (Lerner et. 2017). Other anti-platelets can be administered however beta-blockers are avoided as analgesics like morphine (further histamine release; Lerner et al. 2017). The timing and role of cardiac catheterization will be guided by cardiology and may involve intracoronary vasodilator infusion or thrombus evacuation (Carr and Helman, 2016).

Summary

In a patient presenting with ACS and severe allergic reaction/anaphylaxis, consider Kounis syndrome. There are no guidelines to assist in the management but the key aspects of managing ACS and anaphylaxis are critical in treating Kounis syndrome as well early consultation with cardiology and allergy.

References:
Carr, D. Helman A. Anaphylaxis and Anaphylactic Shock. Emergency Medicine Cases. February, 2016. https://emergencymedicinecases.com/anaphylaxis-anaphylactic-shock.

Kounis, N. G. (2016). Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management. Clinical Chemistry and Laboratory Medicine (CCLM), 54(10), 1545-1559
Kounis, N. G. (2013). Coronary hypersensitivity disorder: the Kounis syndrome. Clinical therapeutics, 35(5), 563-571.

Lerner M, Pal RS, Borici-Mazi R. Kounis syndrome and systemic mastocytosis in a 52-year-old man having surgery. CMAJ. 2017 Feb 6;189(5):E208-E211. doi: 10.1503/cmaj.151314. Epub 2016 Aug 2. PMID: 27486207; PMCID: PMC5289872.

Mattu, A. Demeester, S. Cardiology Corner: Kounis Syndrome. EMRAP. June, 2021. https://www.emrap.org/episode/emrap2021june1/cardiology

Rodrigues MC, Coelho D, Granja C. Drugs that may provoke Kounis syndrome. Braz J Anesthesiol. 2013 Sep-Oct;63(5):426-8. doi: 10.1016/j.bjan.2013.04.006. PMID: 24263049.

 

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A Case of Pediatric Cardiac Arrest

A Case of Pediatric Cardiac Arrest – EM Reflections November 2021

Authored and Copyedited by Dr. Mandy Peach

Big thanks to Dr. Paul Page for leading this month’s discussions

All cases are imaginary but highlight important learning points.

Case

You are working a day shift at a tertiary hospital that sees both adult and pediatric patients. You receive dispatch for a 2 year-old female with potential sepsis. Parents report high fevers for 4 days and poor intake. EMS report a somnolent child, febrile and tachycardic. ETA of 5 minutes.

On arrival the child appears mottled and drowsy, paramedics have placed a non-rebreather and are supporting the airway. You rapidly complete an assessment while the patient is being placed on cardiorespiratory monitoring and nurses attempt access. The patient responds to voice with whimpers. A paramedic is performing a jaw thrust while another bags. Breathing is shallow and rapid. She is mottled with cool extremities and delayed capillary refill.

Vitals: BP 60 SBP, HR 160 sinus tachycardia, T 39.7 RR 50 O2 88% on 100% NRB.

Gulp. You ask the nurse to page the pediatrician on call as you are worried about this patient.

Pediatric vitals are interpreted by weight or age, but you don’t need a table to see that these vitals are abnormal and this kid is altered. Frankly, this patient is pre-arrest if intervention doesn’t take place soon.

Not so sick kid? Here’s a reminder of expected vitals per age1.

Pediatric patients tend to compensate and compensate – until finally they don’t. Are there earlier signs of sepsis to be on alert for when assessing a patient1?

  • tachycardia out of proportion to fever – fever can give an expected increase in HR by 10 bpm,
  • tachypnea – RR tends to increase by 5 breaths/min for every 1 deg over 38°C.
  • poor perfusion – this can range from poor cap refill to altered level of consciousness.

When it’s later stages – it’s obvious. But sepsis doesn’t always have all these signs – a high suspicion is needed to recognize sepsis before it gets to critical stages.

What is the most concerning vital sign of our patient1?

Hypotension – this is a late sign of sepsis and if untreated the patient will arrest.

You suspect this child has septic shock given the brief history and temperature. Currently, their airway is being well managed by paramedics who have added NC under the mask and with continued jaw thrust they have improved oxygen saturation – but this is temporary.

You want to initiate management for sepsis and potentially need to intubate this child.

But before any of that can occur you need IV access.

Nurses have attempted twice and failed – it’s been 2 minutes. What next?

Do not hesitate to move to intraosseous (IO). This child may imminently arrest. Fluid resuscitation and administration of antibiotics are vital. If you can’t obtain IV access in 60 secs – obtain IO1

Preferred sites in pediatric patients (altered from EMdocs.net)2

Worried about hurting the child? Flush lidocaine through the IO – evidence suggests pain is more from infusions and medications through the IO than the insertion itself.1

Have more time with a relatively stable patient? Consider using PoCUS to help obtain peripheral lines

You obtain IO access and immediately request fluids. You want them to run in as fast as possible, but the child is too small for a level 1 infuser. What’s your approach?

First, choose the fluid type. Normal saline or Ringer’s lactate is fine to start. 20cc/kg is the typically starting bolus over the first 5 minutes of resuscitation. This can be repeated twice more up to 60cc/kg in the first hour. For this patient, and any patient under 2, load a 30-60cc syringe with crystalloid and manually bolus.

Signs of fluid overload?

Hepatomegaly and crackles auscultated in the lungs

A better sign – pulmonary edema seen on PoCUS3.

Normal vs B lines

IO assess has been obtained in both tibia, a nurse is pushing fluid manually while another asked you what antibiotics you want drawn up.

What are the broad-spectrum antibiotics suggested by age1?

You go back to reassess the patient’s airway. They are now satting 92% on 100% NRB + 5L NC. There is still some spontaneous whimpering. You estimate the GCS to be 9: E- 3 V- 2 M -4. This patient’s respiratory status is worsening and they have a low GCS. You feel they need intubation. Repeat vitals are obtained after first bolus.

BP 64 SBP, HR 158 sinus tach, T 39.8, RR 48 O2 as above.

Do you immediately intubate?

This patient is in profound shock, their catecholamine surge is deplete and any induction agents, even ketamine, would likely still worsen their hypotension and potentially precipitate arrest. If successfully intubated there is then the complication of increasing intrathoracic pressure – thus reducing blood flow back to the heart and decreasing cardiac output1.

The principle of resuscitate before you intubate is especially true in this situation.

You order repeat bolus of fluid to be manually given while antibiotics are being infused in the other IO. A nurse has now achieved peripheral IV access.

You prepare drugs and airway equipment for RSI – you plan to intubate once fluid boluses are complete if vitals have improved.

What drugs will you use? What drugs would you avoid5,6,7,8,9?

Avoiding worsening hypotension is key – ketamine is the drug of choice for sedation in children as it is considered hemodynamically neutral, but again expect drop in BP when the body is in shock. Ketamine also preserves airway reflexes and ventilatory drive.
Conversely propofol creates vasodilation and suppresses the myocardium – causing hypotension. It also can cause respiratory depression and apnea.

There is some evidence that etomidate is associated with less adverse events in septic patients, specifically hypotension. In one observational study in an adult population, ketamine was shown to be complicated by post-intubation hypotension more frequently when compared to etomidate.

In the pediatrics population etomidate for intubation in the ED setting has also been shown to be associated with minimal change in blood pressure – but this was a small, retrospective study. Currently etomidate is not recommended in patients < age 10 and more evidence is needed. One could also consider the potential for adrenal suppression post etomidate (etomidate inhibits functioning of an enzyme required to make cortisol, aldosterone and corticosterone). There are various studies – some in pediatric patients showing decreased plasma cortisol levels at 24 hours post etomidate. A similar effect was seen in other critically ill adult patients. The CORTICUS trial indicated a higher 28 day mortality in patients who received a single dose etomidate vs those that did not, regardless of being given exogeneous steroid.

For paralytics succinylcholine should be used cautiously in pediatric patients – it can precipitate hyperkalemia, bradycardia and even arrest. Rocuronium does have fewer side effects and contraindications, but it’s duration of action lasts approximately 50 mins – compared to approximately 6-10 minutes with succinylcholine. So strongly consider your choice – if you feel this is a ‘can’t intubate, can’t ventilate’ situation rocuronium is a dangerous choice.

You decide to go with ketamine and rocuronium and the drugs are being drawn up – what doses will you use?

In an adult population a safe choice in the shocked patient is to half the sedative and double the paralytic. The reason being even with ketamine you can get myocardial suppression and potential apnea.

For the paralytics use higher dose as the onset of action will be slower – double the dose.

For pediatric patients there is no evidence in the literature to support this practice, currently practice is to choose agents that have the least effect on hemodynamics – typically ketamine and rocuronium.

The RT is asking what size tube and airway equipment you would like.

Quick answer – Broslow tape. In this unstable patient this is the easiest way to get what you need without having to do any mental math. You request a cuffed tube – decreases the need  for ET tube changes4.

While airway equipment is being set up you move now to prepare the patient. How do you position this 2 year old5,10?

Children have larger heads that naturally lies in flexion when supine. To align the mouth, larynx and trachea often the position has to be changed. You can roll up a towel to help with placement. As a rule of thumb:

Keeping a patient supine can also worsen hypoxemia as children have increased chest wall compliance and therefore increased work at baseline to maintain tidal volume. This can eventually lead to intrapulmonary shunting.

So although this patient doesn’t require additional positioning with a towel based on age we would still put the head of the bed up.

Someone asks if they can remove the additional oxygen mask or nasal cannula in preparation for intubation so it’s out of your way. Your response5?

No – pre-oxygenation is vital in the intubation of any patient, especially a child as they desaturate so quickly. In this 2 year old patient we expect a time of less than 4 minutes to desaturate to 90%. Children have much less surface area or ventilation channels as the alveoli continue to develop until the age of 8. In this patient with potential underlying respiratory illness there could be areas of atelectasis, worsening lung ventilation.

What other airway considerations are going through your head for a pediatric patient10?

Remember CHILD

For a great overall review see this infographic5

 

 

You are about to reassess the airway and obtain new vitals when the patient’s breathing changes to agonal and her whimpering has ceased. There is cardiac activity on the monitor, it be appears to be tachycardia with a widened QRS. Someone yells – check a pulse!

Do you need a pulse to initiate CPR in this patient?4

No – given the frequency of bradycardia and hypovolemia, pulse checks are not reliable. If apnea and unresponsive, initiate CPR.

At what rate should CPR be initiated in this patient4?

Use the encircling hands technique for infant CPR – it is shown to give better hemodynamics. Push hard (>1/3 AP diameter of chest) and fast (100-120 bpm), minimizing interruptions and allowing full recoil of the chest between compressions.

As this is an in-hospital cardiac arrest an LMA is immediately inserted to prevent interruption in compressions and to provide oxygenation.

Aim for 20-30 breaths/minute when an advanced airway is in place.

Out of hospital cardiac arrest4? Resuscitation with bag valve mask results in the same resuscitation outcomes as advanced airways -don’t underestimate the value of a good seal and a 2 person technique.

CPR is ongoing, an LMA has been inserted. The initial rhythm did not appear to be shockable. This is a PEA arrest.

What is your priority?

Determining the cause and in the meantime administering epinephrine – early administration within 5 minutes of non-shockable rhythms increases survival4.

You review your H’s and T’s.

You are pushing fluids for hypovolemia, the patient maintained oxygenation throughout with 2 sources of oxygen and had a normal oxygen saturation before arrest, the patient could be acidotic – but you are drawn to hypoglycemia. You rack your brain but can’t remember the glucose. You verbalize to the room, but no one knows if a glucose was done.

You quickly obtain one – 0.5.

You must correct glucose rapidly:

5cc/kg D10W IV push followed by an infusion of D10NS at 5cc/kg/hr (max at 250cc/hr)11

After the correction of glucose and additional round of CPR you get ROSC.

Obtaining a glucose is VITAL in any pediatric patient – something you know but failed to recognize as you had an unstable patient in front of you.

ABC + DEFG = ABC and DON’T EVER FORGET GLUCOSE1

What other metabolic abnormality must you consider1?

Hypocalcemia is commonly seen in critically ill pediatric patients, even without clinical signs like seizure or arrythmia it is recommended to treat.

Calcium gluconate 10% 0.5-1 cc/kg slowly over 5 minutes (max of 20 cc)

You reassess the vitals and the patient is still hypotensive and tachycardic despite 3 boluses and fluid circulating throughout the arrest. The oxygen saturation is 100%. The RT is still bagging via LMA. Clinically they appear cool and mottled with pulses weaker distally.

The patient is in cold shock. What is the vasopressor of choice11?

You initiate epinephrine at 0.05 mcg/kg/min IV and titrate up by 0.02 mcg/kg/min.

You assess cardiac function and lung fields via bedside ultrasound – the heart is hyperdynamic, lung fields are clear. You continue another bolus.

The patient’s GCS post arrest is back to 9. They are being easily bagged. You plan to wait until vitals have stabilized to switch out the tube.

At this point a pediatric attending arrives and you give an update.Immediately the staff begins verbalizing orders to the room for pressors, fluids and antibiotics. They begin questioning RT and direct them to intubate. The staff look to you for direction.

What do you do at this point?

This can be an uncomfortable situation to be in – this patient is still your patient; they are still unstable at this point and you have been guiding resuscitation. You have developed a sense of trust with your team and more than one leader can often lead to confusion.

You ask the attending to step out and together you review the management up to that point. This was a complex case with a lot of intervention. You discuss each medication given and the outcome. You make your suggestions on pressor support and fluid and reinforce what has been given. Together you are on the same page and go back in to reassess with the team.

It’s important to respectfully gain additional input from consultants and work together to ensure optimum care, but still realize that you are running the room. In other cases you may be at a loss for what to do and need guidance for what to do next – but again, once a plan is decided with your consultant it’s important that you verbalize to the room and give clear instruction to your team.

Overwhelmed and need to pass off? No problem – once you have help verbalize to the room that the consultant will now be leading resuscitation and stay nearby to assist and learn.

Lastly, what other medication should you consider if the patient’s hemodynamics or clinical picture do not improve1?

Steroid – up to 25% of pediatric patients with septic shock have adrenal insufficiency. This may be from the infectious process itself, from previous steroid use or from primary adrenal insufficiency.

You administer hydrocortisone 2mg/kg IV.

What markers of a successful resuscitation will you look for1?

  • Capillary refill < two seconds
  • Normal blood pressure
  • Normal pulses with no differential betweencentral and peripheral pulses
  • Warm extremities
  • Urine output > 1 ml/kg/hr
  • Normal mental status
  • Normal lactate

The patient gets admitted to the ICU for Pneumococcal sepsis and after a prolonged admission does well.

 

Pediatric patients are scary – use the resources you have, verbalize your thought process to the room and ask for help. Continuously reassess 

ABC + DEFG = ABC and DON’T EVER FORGET GLUCOSE1

 

References and further reading:

  1. EM Cases Digest – Vol 2. Pediatric Emergencies. Chapter 2: Sepsis and septic shock. Helmon, A. Lloyd, T. 2016. Toronto, ON.
  2. Image altered from http://www.emdocs.net/feelin-it-in-my-bones-a-review-of-intraosseous-access-in-the-emergency-department/
  3. Images from https://www.thepocusatlas.com/
  4. Highlights of the 2020 American Heart Association Guidelines for CPR and ECC
  5. Tolmie, A 2021. PEM Pearls01: Pediatric Airway Differences. CanadiEM. Retrieved Jan 20, 2022 from https://canadiem.org/pem-pearls-01-pediatric-airway-differences/
  6. Scheirer, O. 2018. CRACKCastE192 – Airway. CanadiEM. Retrieved Jan 20, 2022 from https://canadiem.org/crackcast-e192-airway-9th-edition/
  7. Mohr NM, Pape SG, Runde D, Kaji AH, Walls RM, Brown CA 3rd. Etomidate Use Is Associated With Less Hypotension Than Ketamine for Emergency Department Sepsis Intubations: A NEAR Cohort Study. Acad Emerg Med. 2020 Nov;27(11):1140-1149. doi: 10.1111/acem.14070. Epub 2020 Jul 20. PMID: 32602974; PMCID: PMC8711033.
  8. Guldner G, Schultz J, Sexton P, Fortner C, Richmond M. Etomidate for rapid-sequence intubation in young children: hemodynamic effects and adverse events. Acad Emerg Med. 2003 Feb;10(2):134-9. doi: 10.1111/j.1553-2712.2003.tb00030.x. PMID: 12574010.
  9. Sprung CL, Annane D, Keh D, Moreno R, Singer M, Freivogel K, Weiss YG, Benbenishty J, Kalenka A, Forst H, Laterre PF, Reinhart K, Cuthbertson BH, Payen D, Briegel J; CORTICUS Study Group. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008 Jan 10;358(2):111-24. doi: 10.1056/NEJMoa071366. PMID: 18184957.
  10. Hsu, J. 2021. Tiny Tips: Pediatric Airway Anatomy Considerations CanadiEM. Retrieved Jan 20, 2022 from https://canadiem.org/tiny-tips-pediatric-airway-anatomy-considerations/
  11. Pediatric Severe Sepsis Algorithm 2018. A PedsPac from Translating Emergency Knowledge for Kids (TREKK).

 

 

 

 

 

 

 

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It’s Not Over Till It’s Over – ECMO Resuscitation in the ED

It’s Not Over Till It’s Over – ECMO Resuscitation in the ED: A Medical Student Clinical Pearl

Ryan Buyting

Med III, Class of 2022

Dalhousie Medicine New Brunswick (DMNB)

Reviewed by Dr. Luke Taylor

Copyedited by Dr. Mandy Peach

Extracorporeal Membrane Oxygenation (ECMO), also sometimes referred to as extracorporeal life support (ECLS), employs components from traditional cardiopulmonary bypass machines to augment a patient’s heart and/or lung capacity for a prolonged duration of days to weeks. Importantly, ECMO is not a treatment but a bridge to native heart/lung recovery or durable organ replacement. 1

 

ECMO has been a hot topic of discussion over the past year based on its role in supporting patients with severe COVID-19 infections. The Extracorporeal Life Support Organization (ELSO), the World Health Organization and the Surviving Sepsis Campaign (SSC) Guidelines recommend considering ECMO, in specialized centers, for patients with COVID-19 who develop severe acute respiratory distress syndrome (ARDS). 2 Many of these cases made use of veno-venous ECMO, which exclusively provides pulmonary bypass for severe respiratory failure.

 

This article will focus on veno-arterial ECMO (which provides both cardiac and pulmonary bypass) and seeks to provide readers with an overview of the following:

  • What is an Extracorporeal Cardiopulmonary Resuscitation (ECPR) code?
  • Which patients should be considered for acute ECMO initiation?
  • What care will patients need in the ED post-circuit initiation?
  • What is the evidence for the use of ECPR?

 

 

Calling an ECPR Code and Patient Selection

An ECPR code essentially mobilizes the cannulation team to initiate an ECMO circuit in a previously high-functioning patient. The goal is to restore end-organ perfusion, buying time to investigate the underlying causative pathology, with hopes of improving long-term survival and neurological outcomes. Emergency physicians should consider calling an ECPR code for severe cardiac and/or pulmonary failure deemed refractory to conventional therapies. 3 Patients in cardiac arrest are potential candidates for ECPR if they meet the following:

  • reversible cause of arrest
  • witnessed arrest with bystander CPR
  • total chest compression time < 60 minutes
  • no known preexisting terminal illnesses

 

Review the reversible causes of cardiac arrest or see the image below outlining the “Hs and Ts” mnemonic.

Figure 1: The Hs and Ts / Reversible Causes of Cardiac Arrest 4

The timing at which an ECPR code should be initiated is (at present) left to physician discretion, but often depends on the availability of the cannulation team. ECMO as an option for a given patient should be anticipated and considered early amid a code to allow the team and equipment to be assembled. Most often the procedure is performed by a cardiac surgeon, however there is growing interest and involvement from vascular, general, and trauma surgeons. 5

 

The initiation of ECMO is divided into 3 stages:

(1) vascular access,

(2) insertion of ECMO cannulas and connection to the circuit once the patient is determined to be an ECMO candidate,

(3) pump initiation.

 

In emergent situations, unilateral peripheral cannulation is the preferred and most expedient method. 6 This approach also allows for the continuation of high-quality CPR while access is obtained. Either through surgical exposure or under ultrasound guidance, a venous drainage cannula is placed in the femoral vein. Blood is returned from the machine through a similarly placed cannula in the adjacent femoral artery. Several alternative circuits are possible in extenuating circumstances depending upon patient injuries or characteristics. 1

Figure 2: Veno-arterial peripheral ECMO via unilateral femoral-arterial and femoral-venous cannulation. 7

 

Post-Circuit Initiation Critical Care

After the circuit has been initiated, the lines should be closely examined; the venous drainage blood should be dark red and the arterial return blood should be bright red. Given the proximity of the vessels and the fact that these procedures are often done with ongoing CPR, this confirmation of placement is crucial.

 

Next, it is important to reassess the patient’s rhythm; if the patient is in VFIB, defibrillation should be repeated after a few minutes on circuit as it is important to have an ejecting left ventricle on ECMO to prevent distention. 8

 

At this point, the team should obtain a right radial arterial line (for accurate measurement of the MAP) and an ABG (to assess for adequate oxygenation and the need for setting adjustments). Vasopressors and/or inotropes should be initiated as required to meet a target MAP of 60-80mmHg. If LV distention (as assessed based on arterial line pulsatility >10mmHg or POCUS) is not improved with these medications on board, an LV vent (such as an Impella or intra-aortic balloon pump) may be needed. 8

 

Important next steps in the process include the initiation of therapeutic hypothermia, planning for the placement of a distal perfusion catheter to prevent leg ischemia, and, based on the etiology of the arrest, any other appropriate treatment (such as transfer to the cardiac catheterization laboratory for acute coronary syndrome).

 

Current Evidence for ECPR

No randomized trials concerning the use of ECPR have been published to date. Sonneville and Schmidt recently summarized the four most robust observational studies comparing the use of ECPR versus conventional CPR in patients with out-of-hospital cardiac arrest. 9 They describe a large study that reported similar low survival rates between 525 patients managed with ECPR and 12,666 patients with conventional CPR, with no significant effect of ECPR on outcomes after adjusting for confounders. 10 However, more recently, after instituting very strict patient selection criteria, Bartos et al. reported a relative risk reduction of 29% for death or poor neurological outcome (95% CI, 18%–41%) for patients receiving between 20 and 59 minutes of CPR and 19% (95% CI, 10%–27%) for patients receiving more than 60 minutes of CPR. 11 This group has since published the University of Minnesota ECPR Protocol here. 12

 

Until results from randomized trials become available, it is likely that difficult continuation decisions will need to be made on a case-by-case basis at physician discretion. Protocols requiring objective data input such as specific time periods, lactate level and oxygenation status upon arrival, may help ease this burden in the meantime, if only marginally.

 

References

  1. Badulak JH, Shinar Z. Extracorporeal Membrane Oxygenation in the Emergency Department. Emerg Med Clin North Am. 2020;38(4):945-959. doi:10.1016/j.emc.2020.06.015
  2. Ramanathan K, Shekar K, Ling RR, et al. Extracorporeal membrane oxygenation for COVID-19: a systematic review and meta-analysis. Crit Care. 2021;25(1):211. doi:10.1186/s13054-021-03634-1
  3. Extracorporeal Life Support Organization (ELSO). Guidelines. Accessed August 29, 2021. https://www.elso.org/Portals/0/ELSO%20Guidelines%20General%20All%20ECLS%20Version%201_4.pdf
  4. @lightssirensaction. Hs and Ts. Accessed August 28, 2021. https://www.instagram.com/p/CA4MMdVBy8V/
  5. McCallister D, Pilon L, Forrester J, et al. Clinical and Administrative Steps to the ECMO Program Development. IntechOpen; 2019. doi:10.5772/intechopen.84838
  6. Stoecklein H, Slack S, Tonna JE, Youngquist ST. ECMO & ECPR. JEMS. Published December 2, 2017. Accessed August 28, 2021. https://www.jems.com/patient-care/ecmo-ecpr/
  7. Lawler PR, Silver DA, Scirica BM, Couper GS, Weinhouse GL, Camp PC. Extracorporeal Membrane Oxygenation in Adults With Cardiogenic Shock. Circulation. 2015;131(7):676-680. doi:10.1161/CIRCULATIONAHA.114.006647
  8. Cevasco M, Takayama H, Ando M, Garan AR, Naka Y, Takeda K. Left ventricular distension and venting strategies for patients on venoarterial extracorporeal membrane oxygenation. J Thorac Dis. 2019;11(4):1676-1683. doi:10.21037/jtd.2019.03.29
  9. Sonneville R, Schmidt M. Extracorporeal Cardiopulmonary Resuscitation for Adults With Refractory Out-of-Hospital Cardiac Arrest. Circulation. 2020;141(11):887-890. doi:10.1161/CIRCULATIONAHA.119.044969
  10. Bougouin W, Dumas F, Lamhaut L, et al. Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest: a registry study. Eur Heart J. 2020;41(21):1961-1971. doi:10.1093/eurheartj/ehz753
  11. Bartos JA, Grunau B, Carlson C, et al. Improved Survival With Extracorporeal Cardiopulmonary Resuscitation Despite Progressive Metabolic Derangement Associated With Prolonged Resuscitation. Circulation. 2020;141(11):877-886. doi:10.1161/CIRCULATIONAHA.119.042173
  12. Yannopoulos D, Bartos JA, Martin C, et al. Minnesota Resuscitation Consortium’s Advanced Perfusion and Reperfusion Cardiac Life Support Strategy for Out‐of‐Hospital Refractory Ventricular Fibrillation. J Am Heart Assoc. 5(6):e003732. doi:10.1161/JAHA.116.003732
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