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.


  • 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


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


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


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)


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


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.



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.


  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
  2. Helman, A. Hedayati, T, Tillmann, B. Cardiogenic Shock. Emergency Medicine Cases. January 2022. Accessed July 7th, 2022
  3. Lebowitz, D. (2017, April 21). Management of the crashing aortic stenosis patient. – Emergency Medicine Education. Retrieved September 25, 2022, from
  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
  5. Pujari, S. H., & Agasthi, P. (n.d.). Aortic stenosis – statpearls – NCBI bookshelf. Retrieved September 25, 2022, from
  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 Media
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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


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).



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



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:


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



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


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



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


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



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



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


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


What are some of the more common pediatric heart murmurs?



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



  • Ventricular septal defect
  • Atrial septal defect (example:
  • 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.




  1. Heart Pulse Sound Wave Icon Stock Vector – Illustration of blood, healthcare: 91331428. Accessed November 19, 2021.
  2. Heart Murmur | NHLBI, NIH. Accessed November 18, 2021.
  3. Heart murmurs: MedlinePlus Medical Encyclopedia. Accessed November 18, 2021.
  4. Pediatric Heart Murmurs: Evaluation and management in primary care. Accessed November 18, 2021.
  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.
  7. Physical Examination – Textbook of Cardiology. Accessed November 18, 2021.
  8. Pediatric Heart Murmur Recognition Program intro. Teaching Heart Auscultation to Health Professionals. Accessed November 19, 2021.
  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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Modified Valsalva maneuver in the treatment of SVT – REVERT Trial

Falling heels over head: you make my heart skip a beat

Resident Clinical Pearl (RCP) November 2019


Patricia Marks – PGY1 (FRCPC) Dalhousie University, Halifax, NS

Reviewed by Dr David Lewis




Supraventricular tachycardias (SVT) is a common presentation to the emergency room, and most patients will require treatment with adenosine or electrical cardioversion, as vagal maneuvers are less than 20% of the time in clinical practice. Adenosine and electrical cardioversion both require additional hospital resources, and adenosine is poorly tolerated by patients.


The REVERT trial published in 2015 in the Lancet by Appelboam et al. proposed a modified Valsalva maneuver in the treatment of SVT.  The study was a multicentre randomized control trial in England involving 433 patients with stable SVT. According to an intention to treat analysis, the authors found a 43% success rate of conversion to sinus rhythm with the modified Valsalva maneuver compared to 17% with standard Valsalva. No significant dangerous adverse effects occurred in this study.


Modified Valsalva: The How-To

  1. Patient identification:

    1. Is my patient eligible for Valsalva?
      • Stable SVT
      • Age > 18 years
      • Able to perform Valsalva
      • Able to lie flat and have legs lifted
    2. Contraindications:
      • Unstable or indication for immediate cardioversion
      • Atrial fibrillation, atrial flutter, sinus tachycardia
      • Recent MI
      • Aortic stenosis
      • Glaucoma
      • Retinopathy
      • Third trimester of pregnancy
  2. Materials

      • 10cc syringe
      • Manometer (optional)
  3. Performing the modified Valsalva maneuver

    1. Position the patient in a semi-recumbent position (45º)
    2. Instruct the patient to blow into the tip of a 10cc syringe for 15 seconds. The patient should be targeting a pressure reading on the manometer of 40mmHg, or blowing hard enough to move the plunger tip*
    3. Lower the patient flat and passively raise their legs to a 45º angle for 15 seconds
    4. Return the patient to a semi-recumbent position for an additional 45 seconds
    5. Assess the rhythm
    6. Repeat x1 if unsuccessful before moving on to adenosine or electrical cardioversion (provided the patient remains stable)

*The REVERT trial used a manometer to measure 40mmHg of pressure, however Smith and Boyle have demonstrated that 40mmHg of pressure is generated when a patient is instructed to blow into a 10cc syringe until the plunger moves

Image obtained from on February 21, 2020.


Watch the REVERT authors perform the maneuver:



Benefits of this method:

  • Easy to instruct patients; can try at home
  • Higher success rate than standard Valsalva
  • Similar ED length of stay compared to standard Valsalva
  • Less patients require adenosine or cardioversion

Additional considerations

  • No formal studies exist for pediatric patients, however a recent case report by Rayburn and Wagers did demonstrate successful conversion to sinus rhythm with this maneuver


Bottom Line 

In adults with stable SVT, the modified Valsalva maneuver as published in the REVERT trial achieves a high rate of conversion to sinus rhythm with a NNT of 3.8 and without significant adverse effects. In patients without contraindications, the modified Valsalva maneuver is a low-cost and easy to teach strategy that should be trialled to convert patients in SVT prior to adenosine or electrical cardioversion.




  • Appelboam A, Reuben A, Mann C, Gagg J, Ewings P, Barton A, Lobban T, Dayer M, Vickery J, Benger J; REVERT trial collaborators. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet. 2015 Oct 31;386(10005):1747-53. doi: 10.1016/S0140-6736(15)61485-4.
  • Rayburn D, Wagers B. Modified Valsalva Maneuver for Pediatric Supraventricular Tachycardia. Pediatr Emerg Care. 2020 Jan;36(1):e8-e9. doi: 10.1097/PEC.0000000000002023
  • Smith G, Boyle MJ. The 10 mL syringe is useful in generating the recommended standard of 40 mmHg intrathoracic pressure for the Valsalva manoeuvre. Emerg Med  Australas. 2009 Dec;21(6):449-54. doi: 10.1111/j.1742-6723.2009.01228.x
  • Smith GD, Fry MM, Taylor D, Morgans A, Cantwell K. Effectiveness of the Valsalva Manoeuvre for reversion of supraventricular tachycardia. Cochrane Database of Systematic Reviews 2015, Issue 2. Art. No.: CD009502. DOI: 10.1002/14651858.CD009502.pub3
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PoCUS in Pericardial Effusion

Medical Student Clinical Pearl – October 2019


Alex Pupek

Faculty of Medicine
Dalhousie University
Class of 2020

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


A 70F with a history of bladder CA, HTN and 4.9cm AAA presented to the Emergency Department (ED) and was Triaged as Level 3 with a chief complaint of generalized weakness. Initial assessment was significant for hypotension and low-grade fever with dysuria elicited on history; she was started on Ceftriaxone with a working diagnosis of urosepsis. Bloodwork and imaging studies were sent to rule out other potential sources of infection.

She had a mild leukocytosis of 12.4, pH of 7.23 and a lactate of 5.0. Point-of-care urinalysis was unremarkable. The chest x-ray revealed an enlarged cardiothoracic ratio of 0.62 compared to 0.46 ten months previously, concerning for a pericardial effusion.

Upon reassessment, the patient appeared unwell with slight mottling to the skin, cool extremities and tenuous blood pressure; point of care ultrasound revealed a large pericardial effusion.  Interventional cardiology was paged; the patient was moved to the trauma area and an emergent pericardiocentesis was performed: 360cc of bloody fluid was removed. The pericardial drain was left in situ.

Post-procedure bloodwork included a troponin of 216 and CK of 204. The patient was admitted to the Cardiac Care Unit and discharged within a week’s time.


Pericardial Effusions and The Role of Point-of-Care Ultrasound (POCUS)

The normal pericardial sac contains up to 50 mL of plasma ultrafiltrate [1]. Any disease affecting the pericardium can contribute to the accumulation of fluid beyond 50mL, termed a pericardial effusion. The most commonly identified causes of pericardial effusions include malignancy and infection (Table 1).


Table 1 – UpToDate, 2019 – Diagnosis and Treatment of Pericardial Effusions


Evaluation of the pericardium with point-of-care ultrasound includes one of four standard views: parasternal long axis, parasternal short axis, subxiphoid and apical (Figure 1). A pericardial effusion appears as an anechoic stripe or accumulation surrounding the heart. Larger effusions may completely surround the heart while smaller fluid collections form only a thin stripe layering out posteriorly with gravity. Seen most commonly post-cardiac surgery, pericardial effusions may be loculated and compress only a portion of the heart. [1,2] (Table 2)

Figure 1[1]

Table 2 [2]


Both the pericardial fat pad and pleural effusions can be mistaken for pericardial effusions. The parasternal long-axis view is most helpful to accurately define the effusion with the descending aorta, posterior to the mitral valve and left atrium, serving as a landmark: the posterior pericardial reflection is located anterior to this structure. Fluid anterior to the posterior pericardial wall is pericardial, whereas a pleural effusion will lie posterior. The pericardial fat pad is an isolated dark area with bright speckles, located anteriorly; unlike fluid, it is not gravity dependent. Rather than competing with the cardiac chambers for space within the pericardial sac, the fat pad moves synchronously with the myocardium throughout the cardiac cycle. [1,2] (Figure 2)

Figure 2[1]

A pericardial effusion discovered on POCUS in the ED may be mistaken for tamponade, leading to inappropriate and invasive management in the form of pericardiocentesis.[2]

Patient tolerance of pericardial effusions depends on the rate by which they accumulate. As little as 150-200 mL of rapidly accumulating effusion can cause tamponade whereas much larger amounts of slowly accumulating fluid can be well tolerated. Pericardial effusions formed gradually are accommodated by adaptations in pericardial compliance. A tamponade physiology is reached once the intrapericardial pressure overcomes the pericardial stretch limit.[2] (Figure 3)

Figure 3[2]

The core echocardiographic findings of pericardial tamponade consist of:

  • a pericardial effusion
  • diastolic right ventricular collapse (high specificity)
  • systolic right atrial collapse (earliest sign)
  • a plethoric inferior vena cava with minimal respiratory variation (high sensitivity)
  • exaggerated respiratory cycle changes in mitral and tricuspid valve in-flow velocities as a surrogate for pulsus paradoxus

In the unstable patient with clinical and echocardiographic findings of tamponade, an emergent pericardiocentesis is indicated.[2]

A retrospective cohort study of non-trauma emergency department patients with large pericardial effusions or tamponade, ultimately undergoing pericardiocentesis, found that effusions identified by POCUS in the ED rather than incidentally or by other means saw a decreased time to drainage procedures, (11.3 vs 70.2 hours, p=0.055).[3]

Point of care ultrasound is a valuable tool during the initial evaluation of the undifferentiated hypotensive emergency department patient but should be interpreted judiciously and within clinical context to avoid unnecessary emergency procedures.

Additional Images

From GrepMed





  1. Goodman, A., Perera, P., Mailhot, T., & Mandavia, D. (2012). The role of bedside ultrasound in the diagnosis of pericardial effusion and cardiac tamponade. Journal of emergencies, trauma, and shock, 5(1), 72.
  2. Alerhand, S., & Carter, J. M. (2019). What echocardiographic findings suggest a pericardial effusion is causing tamponade?. The American journal of emergency medicine, 37(2), 321-326.
  3. Alpert, E. A., Amit, U., Guranda, L., Mahagna, R., Grossman, S. A., & Bentancur, A. (2017). Emergency department point-of-care ultrasonography improves time to pericardiocentesis for clinically significant effusions. Clinical and experimental emergency medicine, 4(3), 128.


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EM Reflections – December 2019

Thanks to Dr Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 

Discussion Topics

  1. Cardiopulmonary Resuscitation In Patients With Mechanical Circulatory Support

    • Patient with mechanical circulatory support devices have unique clinical signs of cardiac arrest
    • Understanding the function of these devices ids critical to the management of these complex cases
  2. Aortic Dissection

    • Remains a commonly missed or delayed diagnosis
    • Once diagnosed, meeting the therapeutic goals requires a careful and considered approach

Cardiopulmonary Resuscitation In Patients With Mechanical Circulatory Support


A 70yr male presents with cardiac arrest. He has an LVAD. What are the implications for emergency management and cardiopulmonary resuscitation?


Cardiac arrest in patients on mechanical support is a new phenomenon brought about by the increased use of this therapy in patients with end-stage heart failure.

It is important to understand the difference between blood flow and perfusion when assessing any patient with suspected cardiovascular hemodynamic instability, especially patients with an LVAD, in whom the peripheral arterial pulse is not a reliable indicator. Flow represents the forward movement of blood through the systemic circulation. It can be either adequate or inadequate to provide sufficient oxygen delivery to sustain tissue per- fusion. Assessment of adequate tissue perfusion is the most important factor in determining the need for circu- latory assistance such as chest compressions.

What is a Left Ventricular Assist Device?

With an LVAD, blood enters the device from the LV and is pumped to the central aortic circulation, “assisting” the heart.  The outflow cannula is typically anastomosed to the ascending aorta, just above the aortic valve. RA/RV still working


Blue Arrow – Important point as patients often present with iGel in place…


Unique Patient Properties

  • Pulses often absent
    • BP measured manually with a Doppler – MAP (50-90)
  • SpO2 may not be measurable
  • Anticoagulated
  • Need power!
  • Very reliant on RV function/preload
  • Leading cause of death – sepsis and stroke

Further Reading

Cardiopulmonary Resuscitation in Adults and Children With Mechanical Circulatory Support. A Scientific Statement From the American Heart Association

Aortic Dissection

Aortic dissection remains difficult to diagnosis with 1 in 6 being missed at the initial ED visit. Why? The diagnosis is rare with and incidence of only 2.9/100,000/year, and the presentation is often atypical mimicking other more common diagnoses such as ACS and stroke.

View The SJRHEM  – Aortic Dissection – Resident Clinical Pearl here:

Aortic Dissection


The most common initial misdiagnoses are acute coronary syndrome, pulmonary embolism, and stroke. Patients with these suspected diagnoses should also be screened for high-risk features of acute aortic dissection. If none are present, they are unlikely to have an acute aortic dissection. If high-risk features are present, balance your clinical suspicion for an aortic dissection with the likelihood of an alternative diagnosis using an approach such as RAPID

How Do I rule Out Aortic Dissection – Just the Facts – CJEM


Early Screening for Aortic Dissection With Point‐of‐Care Ultrasound by Emergency Physicians

A total of 127 patients were enrolled: 72 in the US group and 55 in the control group. In the US group, compared with CTA, the sensitivity of EP POCUS was 86.4%, and the specificity was 100.0%.



Treatment Goals



Further Reading

Episode 92 – Aortic Dissection Live from The EM Cases Course


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Palpitations – A Paroxysmal Pearl

Palpitations – A Paroxysmal Pearl

Medical Student Clinical Pearl

Scott Fenwick

Class of 2021

Faculty of Medicine
Dalhousie University

Reviewed and Edited by Dr. David Lewis

Case Presentation:

A 49-year-old female presented with palpitations for the past 2 hours. She had two similar episodes in the last 2 weeks, both of which resolved within 1-2 minutes. She had no other symptoms. She was otherwise healthy, with no past medical history. She was a non-smoke and non-drinker who leads an active lifestyle. She denied weight loss, diarrhea, and heat intolerance.

On physical exam, she was tachycardic at 130bpm with an irregularly irregular pulse. She did not display any tremor or diaphoresis. On auscultation, S1 and S2 were audible, with no murmurs or extra sounds. Respiratory and abdominal exams were unremarkable.

What to ask on History?

Common Symptoms: palpitations, tachycardia, fatigue, weakness, dizziness, light-headedness, reduced exercise capacity, mild dyspnea, and polyuria. It is essential to know when exactly the symptoms started. AF that presents before 48 hours can be safely rhythm controlled without anticoagulation.(1)

Severe/Secondary Symptoms: angina, dyspnea at rest, presyncope and, uncommonly, syncope. Embolic events and heart failure can be severe complications of AF.

Past Medical History: cardiovascular or cerebrovascular disease, diabetes, hypertension, COPD, obstructive sleep apnea, and hyperthyroidism.

What to look for On Examination?

ABCs and vitals: particularly pulse rate and rhythm.

General Assessment: look for signs of thyroid disease, PE, pulmonary disease, alcohol withdrawal, and signs of liver disease from excessive alcohol ingestion.

CVS: precordial scars from prior cardiac surgery, JVP, peripheral edema, and auscultation for murmurs or additional sounds that might suggest valvular AF. There is often an apical-radial pulse deficit where not every apical beat has an associated radial beat due to lack of left ventricular stroke volume.(2)

Case Continued – Testing:

The patient was put on a cardiac monitor and an ECG was performed, demonstrating atrial fibrillation. There was also a right bundle branch block that was consistent with a previous ECG performed in 2017. Laboratory testing was unremarkable.

Depending on clinical suspicion, initial testing may include CBC, electrolytes, blood glucose, PT/INR, creatinine, BUN, TSH, cardiac enzymes, LFTs, and chest x-ray.2

See Basic ECG interpretation Pearl for a great guide to ECGs

Basic ECG Interpretation


Classifying Atrial Fibrillation:

AF is classically described as an irregularly irregular heartbeat, as can be observed from the variable RR intervals in the ECG above. In AF, there are no distinct P-waves due to the uncoordinated atrial activity. Broadly, AF can be divided into valvular and non-valvular subtypes. Non-valvular AF can be classified into the following categories:(1)

  • Paroxysmal – AF terminates spontaneously or with intervention within 7 days of onset.
  • Persistent – AF fails to terminate within 7 days of onset; often a progressive disease.
  • Long-Standing Persistent – AF has persisted for greater than 12 months.
  • Permanent – Joint decision between patient and provider to no longer pursue rhythm control.

AF commonly progresses from paroxysmal to persistent states. The above classification only refers to primary atrial fibrillation, not AF that is secondary to cardiac surgery, pericarditis, myocardial infarction, valvulopathy, hyperthyroidism, pulmonary embolism, pulmonary disease, or other reversible causes.

For persistent and permanent AF, the CHADS2 score can be used to estimate a patient’s 1-year risk of ischemic stroke without anticoagulation (0 = low risk, 1-2 = moderate risk, 3+ = high risk).(1)

Calculate it here


CAEP and CCS now recommend using the CHAD-65 Score to determine anticoagulation requirement.




DC and chemical (e.g. procainamide) cardioversion are two well-described methods of treating uncomplicated AF. The goal of treatment is to return patients to NSR. Some important points about the two methods include:

  • DC cardioversion can be administered at an initial energy dose of 100J and increased up to 360J as needed.(2)
  • Procainamide is often given in doses of 15-18mg/kg, or more simply, 1g over 60 minutes. Average time to cardioversion is about 1 hour.(1)
  • DC cardioversion requires procedural sedation; whereas, chemical cardioversion does not.
  • In a recent RCT, combination therapy achieved NSR in 99% of patients; Attempting DC cardioversion first decreased length of hospital stay by 1.2 hours.(3)
  • Both therapies are generally well-tolerated by patients.

Case Continued – Treatment:

The patient was diagnosed with paroxysmal atrial fibrillation. The arrhythmia did not spontaneously resolve in the ED. DC and chemical cardioversion methods were considered and discussed with the patient. Direct Current (DC) cardioversion was performed under procedural sedation with propofol and fentanyl. Shocks of 100J and 200J were unsuccessful in converting the patient into normal sinus rhythm (NSR). A third shock at 300J was ultimately successful. The following ECG was obtained demonstrating NSR. As in the initial ECG, there is a RBBB present.


CHADS2 score was 0. Therefore anticoagulation or antithrombotic therapy not indicated.


Case Conclusion:

The patient was discharged home within 4 hours of arriving to hospital, anticoagulation was not prescribed. It is likely that she will experience AF again and require anticoagulation later in life.



  1. January, C. T., Wann, L. S., Alpert, J. S., Calkins, H., Cigarroa, J. E., Cleveland, J. C., et al. (2014). 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: Executive summary. Journal of the American College of Cardiology, 64(21), 2246. doi:10.1016/j.jacc.2014.03.021
  2. Wakai, A., & Neill, J.O. (2003). Emergency management of atrial fibrillation. Postgrad Med J, 79(932), 313. doi:10.1136/pmj.79.932.313
  3. Scheuermeyer, F. X., Andolfatto, G., Christenson, J., Villa-Roel, C., & Rowe, B. (2019). A multicenter randomized trial to evaluate a chemical-first or electrical-first cardioversion strategy for patients with uncomplicated acute atrial fibrillation. Academic Emergency Medicine, 26(9), 969-981. doi:10.1111/acem.13669
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Color Flow Doppler to Assess Cardiac Valve Competence

Color Flow Doppler to Assess Cardiac Valve Competence

Resident Clinical Pearl (RCP) April 2019

Dr. Scott Foley – CCFP-EM PGY3 Dalhousie University, Halifax NS

Reviewed by Dr. David Lewis




When colour Doppler is initiated, the machine uses the principals of the Doppler effect to determine the direction of movement of the tissues off which it is reflecting.

The Doppler effect is the change in frequency of a wave in relation to an observer who is moving relative to a wave source. It was named after the Austrian physicist Christian Doppler who first described the phenomenon in 1842. The classic example is the change in pitch of a siren heard from an ambulance as it moves towards and away from an observer.

These principles are applied to POCUS in the form of colour Doppler where direction of flow is reflected by the colour (Red = moving towards the probe, Blue = moving away from the probe), and the velocity of the flow is reflected by the intensity of the colour (brighter colour = higher velocity).
*Note: the colour does not represent venous versus arterial flow.


The use of colour Doppler ultrasound can be useful in the emergency department to determine vascular flow in peripheral vessels as well as through the heart. It is one way to determine cardiac valve competency by focusing on flow through each valve.


Obtaining Views:

To optimize valve assessment, proper views of each valve must be obtained. It is best to have the direction of the ultrasound waves be parallel to the direction of flow. External landmarks for the views used are seen below:

  • Mitral Valve and Tricuspid Valve: The best view for each of these is the apical 4 chamber view. If unable to obtain this view, the mitral valve can be seen in parasternal long axis as well.
  • Aortic Valve: The best view is the apical 5 chamber or apical 3 chamber but are challenging to obtain. Instead, the parasternal long axis is frequently used.
  • Pulmonic Valve: Although not commonly assessed, the parasternal short axis can be used.
  • Visit for video instruction on obtaining views

Parasternal long axis: MV, AV

Parasternal short axis: PV, TV

Apical 4 chamber: TV, MV


Assessing Valvular Competency:

How to examine valvular competency:

  1. Get view and locate valve in question
  2. Visually examine valve: opening, closing, calcification
  3. Use colour Doppler:
    1. Place colour box over valve (as targeted as possible (resize select box) to not include other valves)
    2. Freeze image and scroll through images frame by frame
    3. Examine for pathologic colour jets in systole and diastole
  4. Estimating severity:
    1. Grade 1 – jet noticeable just at valve
    2. Grade 2 – jet extending out 1/3 of atrium/ventricle
    3. Grade 3 – jet extending out 2/3 of atrium/ventricle
    4. Grade 4 – jet filling entire atrium/ventricle

See video tutorial below for more

Mitral Regurgitation A4C

Tricuspid Regurgitation A4C

Aortic Stenosis PSLA

Bottom line:

Color flow Doppler on POCUS is a straightforward way to assess for valvular competency in the Emergency Department. A more detailed valvular assessment requires skill, knowledge and experience.


Useful Video Tutorials:

Mitral Regurgitation


Aortic Stenosis vs Sclerosis

Tricuspid Valve


  2. By Patrick J. Lynch and C. Carl Jaffe –, CC BY 2.5,
  4. ECCU ShoC 2018 powerpoint, Paul Atkinson, David Lewis
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EM Reflections – January 2018

Thanks to Dr Joanna Middleton for leading the discussion this month and providing these tips and references.

Edited by Dr David Lewis 


  1. Occult Fractures of the Upper Limb

  2. Door to Needle/Balloon Times

  3. Mycotic Aneurysms

  4. CME Quiz

Occult Fractures of the Upper Limb

In patients (particularly the elderly)who present with upper limb pain following a fall or other trauma, be careful not to miss an occult fracture. Localization may be impaired by dementia, acute confusion or other soft tissue injuries. Commonly missed fractures of the upper limb include:

  • Clavicle fracture
  • Supracondylar fracture
  • Radial Head/Neck fracture
  • Buckle fractures of the radius/ulna
  • Scaphoid fracture
  • Carpal dislocation
  • Any impacted fracture

Impacted fractures of the humeral neck may still allow some shoulder joint movement. Pain can be referred to the elbow (just as some hip injuries have pain referred to the knee).

When a fracture is strongly suspected ensure that the entire bone is included in the radiograph. If localization is impaired consider obtaining radiographs of the entire limb, starting with the most symptomatic area. Also follow the old mantra – “include the joint above and below” when ordering radiographs for suspected fracture.

Commonly missed fractures in the ED

Misses and Errors in Upper Limb Trauma Radiographs


Strategies to reduce door to ballon time

Delays in door to balloon time for the treatment of STEMI have been shown to increase mortality.



JACC 2006 Click on here for full text


BMJ 2009 – Click here for full text


This evidence has led to an international effort to establish strategies that can reduce door to balloon times

This rural program in the USA published their strategy for reducing door to ballon times below 90mins over a 4 year period. Their strategies included the following:

• Community hospital physicians visited by interventional cardiologist with recommendations to:

∘ Perform ECG within 10 min of arrival for chest pain patients

∘ Communicate with PCI center physicians via dedicated STEMI hotline

∘ Treat and triage patients without consulting with primary physicians

∘ Give aspirin 325 mg chewed, metoprolol 5 mg IV × 3 when not contraindicated, heparin 70 U/kg bolus without infusion, sublingual nitroglycerin or optional topical nitropaste without routine intravenous infusion, and clopidogrel 600 mg PO

∘ Eliminate intravenous infusions of heparin and nitroglycerin.

• Nurse coordinator hired to oversee program and communicate with emergency department personnel at all referring hospitals.

• Recommendations for medications listed above were formally endorsed for all STEMI patients.

• Formal next-day feedback provided to referring hospitals, including diagnostic and treatment intervals and patient outcomes.

• Quarterly “report cards” issued to each referring hospital emergency department.

• PCI hospital emergency physicians directly activated the interventional team (instead of discussing it first with the interventional cardiologist on call).

• A group page was implemented for simultaneous notification of all members of the interventional team and catheterization laboratory staff of an incoming STEMI patient.
ECG = electrocardiogram; IV = intravenous; PCI = percutaneous coronary intervention; PO = by mouth; STEMI = ST-segment elevation myocardial infarction.


However recent commentaries have highlighted the pitfall of this metric


The Challenges and Pitfalls of Door-to-Balloon Time as a Performance Metric


and further evidence has shown no improvement in mortality despite reducing door to balloon times. However, it should be noted that these centres were already achieving < 90 min.

This may be a result of multiple confounding factors:

total ischemic time may be a more important clinical variable than door-to-balloon time

it has been suggested that the association between door-to-balloon time and mortality may be affected by an “immigration bias” – healthier patients are likely to have shorter door-to-balloon times than are sicker patients with more complex conditions, for whom treatment may be delayed because of the time needed for medical stabilization


Whilst strategies to ever reduce door to balloon times may not be the correct focus to reduce overall mortality, it is clear that the presence of significant delays (>90mins) is associated with increased mortality.


Mycotic Aneurysms

Any kind of infected aneurysm, regardless of its pathogenesis. Such aneurysms may result from bacteremia and embolization of infectious material, which cause superinfection of a diseased and roughened atherosclerotic surface.


Aneurysmal degeneration of the arterial wall as a result of infection that may be due to bacteremia or septic embolization 

  • Symptoms:  pulsatile mass, bruit, fever
  • Risk Factors:  arterial injury, infection, atherosclerosis, IV drug use
  • #1 cause = staph, #2 = salmonella

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EM Reflections - Jan 18 - CME Quiz

EM Reflections – Jan 18 – CME Quiz

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ED Rounds – October 2015

This month ED Rounds were presented by Dr Mike Howlett  , Dr James French and Dr Wendy Alexander (Pediatrician SJRH).


Congestive Heart Failure – Dr Mike Howlett

Dr Howlett presented 4 cases that highlighted the differences in pathophysiology and approaches to treatment for CHF in the ED.

The definition of Congestive Heart Failure (ESC 2012 Guidelines)

a syndrome in which patients have typical symptoms (e.g. breathlessness, ankle swelling, and fatigue) and signs (e.g. elevated jugular venous pressure, pulmonary crackles, and displaced apex beat) resulting from an abnormality of cardiac structure or function

Diagnosis of CHF

The diagnosis of heart failure with reduced ejection fraction (Systolic) and Heart Failure with preserved ejection fraction (Diastolic) is summarised in the box below.

Diagnosis HF

The mortality of Diastolic and Systolic HF are similar


Dr Howlett’s full presentation can be downloaded / viewed below:

Download (PDF, 7.3MB)


How to be Awesome at Simulation – Dr James French

Dr French presented an interactive session that highlighted the important steps to designing, running and debriefing a simulation.

See our Simulation Program page for more details

Presentation to be uploaded here soon…


Pediatric Asthma – Dr Wendy Alexander

Dr Alexander presented pediatric pearls accumulated over her 25 years of practice.

See the SJRHEM Pediatric Asthma Guidelines





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ED Rounds – June 2015

Thanks to Dr Emily Love for preparing this useful post that summarizes the ED Rounds presentations for June 2015.

Resident Elective to South Africa.

Dr Leanne Hewitson and Dr Sarah Compeau

This was a great presentation. The girls talked about their work in several different hospitals in South Africa where they had an opportunity to assess and treat a large volume of trauma patients. In terms of some of the ways these hospitals differed from ours, there were often less resources (for example, there would be only so many suture trays for the night and they had to be careful not to use these up unnecessarily; also there were only two bags of O negative blood in the department in one of the hospitals – if they needed more they had to call a driver who would transport the blood from a facility 45 mins down the road).  

Another difference was staffing. There typically was not an attending staff on site, and they had a lot of independence in terms of diagnosing and treating their patients. they worked closely with a junior resident, a medical student and a senior physician who was not yet an attending (I can’t remember the name they assigned to this role).

Examples of hands-on opportunities: chest tube insertion, assessing and treating stab wounds and patients with multiple traumas

In terms of the discussion after the presentation, we talked about safety. In one of the cities, it was not safe to go out alone at night and was necessary to always have a route planned out so they would not get lost and end up in a dangerous area. The girls did feel  that with good planning and proper cautions the benefits of the experience outweighed the risks.  

Hands on experience: We talked about how valuable this experience was in terms of seeing a large volume of trauma patients, which we don’t see here in Canada. The girls both feel they are much more comfortable treating trauma patients here after their experience and would recommend it to other residents.

Teaching residents in other centers: Sarah and Leanne were able to both learn from house staff at the hospitals and also share some of their own skills. For example, they were able to teach ACLS protocols to the residents at one of the centers as they did not have formal  ACLS training as they did here.

Download (PDF, 7.5MB)

ST elevation in a 33 year old in RAZ

Dr Nicola Smith

This was a very interesting prevention and a good lesson to all of us on recognizing our own biases that may affect patient care.

When a 33 yo otherwise healthy female presented to RAZ with a headache, some potential biases were as follows

1- the triage note mentioned that she was quiet anxious but had settled

2-  she was in RAZ which gives the impression the patient is not acutely ill

3- it was the end of the day after a long busy day

The resident who saw this patient recognized these biases, and spent time with her to do a thorough history and physical. She was prompted to order an ECG which showed the ST elevations when the patient spoke about pain starting in her abdomen and moving up to her head and also left arm numbness.  

the patient turned out to have a pheochromocytoma. Lessons we learned about this are as follows:

1- close blood pressure and HR control are key before any surgery as there is a risk with surgery of further release of catecholamines and  a hypertensive emergency

2- these patients need close work-up for MENS syndromes

3 – there are some case studies reporting ST elevations in pheochromocytoma.

Download (PDF, 15.07MB)

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