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An EM Approach to Syncope in Adults

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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

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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?

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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 Med, 370, 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 Surgery, 31(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 Techniques, 22(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. Chest, 75(4), 434-440.
  7. Shapiro, L. M., Thwaites, B., Westgate, C., & Donaldson, R. (1985). Prevalence and clinical significance of aortic valve prolapse. Heart, 54(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. Heart, 103(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). Circulation, 129(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 Echocardiography, 26(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 cardiology, 93(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. Circulation, 116(11_supplement), I-264.
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Management of Supraventricular Tachycardia (SVT) in Pregnancy

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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

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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 Journal, 7(Kidney), 65–77.
  9. Argaiz Eduardo R, Koratal A., Reisinger N. Comprehensive Assessment of Fluid Status by Point-of-Care Ultrasonography. Kidney360 Aug 2021, 2 (8) 1326-1338; DOI: 10.34067/KID.0006482020. 
  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

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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

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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)

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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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