In this Part 2 of our 2-part podcast series on acute heart failure we dive into the diagnosis and management of the patient in cardiogenic shock and wrap up with some guidance to disposition decisions of the patient with acute heart failure in general. Thankfully, only about 10% of our heart failure patients will be in cardiogenic shock, but this a very challenging subgroup of patients with a high mortality rate of 30% that we need to be comfortable treating. With the help of Dr. Tarlan Hedayati and Dr. Bourke Tillmann we answer questions such as: what is the preferred order of vasopressors and ionotropes in the management of cardiogenic shock? In which patients would dobutamine be preferred over milrinone and vice versa? How can we best pick up occult cardiogenic shock before it floured shock kicks in? What are the best strategies to efficiently get the patient in cardiogenic shock to definitive care, whether that be the cath lab or the operating room? What is the evidence for intra-aortic balloon pumps, percutaneous ventricular assist devices and ECMO in the patient with cardiogenic shock? Which patients with acute heart are safe to send home in general? How useful is the Ottawa Heart Failure Risk Score in aiding in disposition decisions? and many more…
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Podcast production, sound design & editing by Anton Helman
Written Summary and blog post by Saswata Deb, edited by Anton Helman January 2022
Cite this podcast as: Helman, A. Hedayati, T, Tillmann, B. Cardiogenic Shock. Emergency Medicine Cases. January, 2022. https://emergencymedicinecases.com/cardiogenic-shock. Accessed [date]
Understanding the reduced contractility and assessment of end-organ perfusion is key to managing patients with cardiogenic shock
Reduced contractility is the keystone of cardiogenic shock
Cardiogenic shock is defined as systolic blood pressure (SBP) < 90mmHg or the need for pharmacological or mechanical support to maintain a SBP > 90mmHg and evidence of end-organ perfusion. Chronic heart failure progresses into cardiogenic shock when the reduced contractility of the ventricle impairs mean arterial pressures and cardiac output which results in decreased end-organ perfusion.
Assessment of end-organ perfusion is central to identifying occult cardiogenic shock
Patients with heart failure may have a lower baseline SBP due to heart-failure related pharmacotherapy which can make the diagnosis of cardiogenic shock difficult. A “soft” SBP may be the patients baseline or it may represent occult shock. Assessing for impaired end-organ perfusion in these patients can significantly aid in the identification of occult cardiogenic shock. On the other hand, a patient can be in a pre-cardiogenic shock, hypertensive state such as SCAPE (see Part 1). Again, assessment for impaired end-organ perfusion can be very helpful in diagnosis and management.
Assessment of end-organ perfusion involves assessment of the skin, mental status, urine output and PoCUS parameters. Assess the skin for 1. mottling 2. cool temperature 3. prolonged capillary refill time. Altered mental status and oliguria/anuria are often present. An elevated lactate is suggestive or poor end-organ perfusion although the specificity is poor. Advanced doppler PoCUS may aid in assessment of end organ perfusion (portal vein pulsatility index, renal doppler resistive index, splenic doppler resistive index). A central venous-arterial gap >6mmHg is an indicator of decreased systemic blood flow. It is the difference between PCO2 in central venous blood and PCO2 in arterial blood.
Clinical Pearl: The skin is a readily observable end-organ. Low cardiac output usually results in impaired perfusion to the skin which leads to mottled, cold extremities with a prolonged capillary refill time. In contrast, patients with sepsis, usually have warm extremities due to vasodilation.
PoCUS in the diagnosis and management of cardiogenic shock: Lung US, LV function & volume status
In addition to lung ultrasound looking for B-lines for pulmonary edema, PoCUS can be used to assess the overall LV function and volume status. Global LV function includes mitral valve movement (<1cm is normal), LV size (<5cm is normal) and LV contractility (≥ 1/3 the diameter is normal). Remember that the keystone for diagnosis of cardiogenic shock is reduced contractility. When it comes to volume status patients in cardiogenic shock may be hypovolemic, euvolemic or hypervolemic which will guide whether or not they require diuresis or volume replacement. Volume status assessment includes measuring LV size, jugular venous distention, and IVC size and collapsibility (diminished respiratory variation).
Clinical Pearl: It is important to determine the volume status of a patient in cardiogenic shock using clinical and PoCUS parameters because management differs based on volume status. For example, careful fluid bolus/infusion may be required if a patient is in cardiogenic shock and deemed to be intravascularly volume depleted.
PoCUS Cases on IVC for volume assessment
Treatment of the heart failure patient in cardiogenic shock
Goals of management in cardiogenic shock
The overall goal in the management of the heart failure patient in cardiogenic shock is to stabilize them by maintaining oxygenation with NIPPV, maintaining sufficient cardiac perfusion with vasopressors, improving cardiac contractility with ionotropes and optimizing volume status so that they can be safely transported to the cath lab or operating room for definitive management of the underlying mechanical lesion, if any. This usually involves 4 simple steps:
- Optimize oxygenation with NIPPV
- Optimize blood pressure with vasopressors (eg. norepinephrine) to maintain cardiac/end-organ perfusion targeting a MAP of 65-80
- Optimize contractility with ionotropes (eg. dobutamine, milrinone)
- Optimize volume status (crystalloid or diuretics)
Determining the cause of cardiogenic shock is essential to optimize management
Think of the causes of cardiogenic shock in 4 categories (keeping in mind that #1 and #2 require emergent mechanical repair):
- Acute coronary syndromes
- Mechanical (ie. severe aortic stenosis, endocarditis, ruptured valve, free wall rupture)
- Progressive non-ischemic chronic heart failure
See Part 1 for the full differential diagnosis of acute heart failure
Clinical Pearl: assess for papillary muscle rupture/severe mitral regurgitation/free wall rupture in patients with acute coronary syndromes who are in shock; listen for new cardiac murmur and look on PoCUS for obvious papillary muscle rupture/mitral regurgitation/free wall rupture as they require emergent cardiac surgery to replace the mitral valve or repair the free wall
Optimizing oxygenation in cardiogenic shock with carefully titrated NIPPV
Maintaining adequate tissue oxygenation is critical in patients with heart failure and cardiogenic shock, which is usually ideally achieved with NIPPV. It has the added benefit of decreasing preload and afterload. (see Part 1 for oxygenation strategies in heart failure)
Clinical pearl: avoid endotracheal intubation whenever possible in the patient in cardiogenic shock as removal of respiratory drive may lead to cardiovascular collapse
Clinical Pitfall: overshooting positive pressure ventilation in the patient with RV failure; positive pressure ventilation can potentially increase RV afterload and therefore should be used with caution in patients with cardiogenic shock resulting from acute RV failure
Optimize cardiac output by optimizing blood pressure, contractility and volume status
1.Optimizing blood pressure with norepinephrine +/- vasopressin: target a MAP of 65-80. This is required to augment end-organ/coronary perfusion. The preferred first line agent is norepinephrine. Vasopressin may be added as a second line agent. While epinephrine and norepinephrine both have been shown to improve MAP and cardiac indices, norepinephrine has a lower incidence of refractory shock compared to epinephrine.
2.Optimizing contractility with dobutamine or milrinone: while dobutamine is a Beta 1 and 2 agonist and milrinone is a phosphodiesterase 3 inhibitor, both agents are inotropes and vasodilators. A recent RCT showed no significant difference in in-hospital survival and major cardiac outcomes with dobutamine versus milrinone in patients in cardiogenic shock.
Our experts recommend starting with dobutamine as it is a shorter acting drug and can be titrated more easily compared to milrinone. However, for patients taking long-acting beta-blockers, milrinone may be the better first option as it works on a different receptor.
Clinical pitfall: giving an ionotrope before initiating a vasopressor may decrease BP further as they are vasodilators, which may lead to cardiovascular collapse; our experts suggest initiating norepinephrine prior to giving an ionotrope in heart failure patients with cardiogenic shock
Clinical pearl: for patients taking long acting beta-blockers milrinone may be the ionotrope of choice in patients with cardiogenic shock
3.Optimizing volume status: based on clinical and PoCUS assessment of intravascular volume, patients may require gentle and cautious crystalloid administration or diuresis with ongoing assessment of volume status.
Practical pearl: it is imperative to consult cardiology/CV surgery early in the resuscitation of patients with cardiogenic shock as there may be a need for emergent mechanical interventions
Cardiogenic shock caused by severe aortic stenosis – avoid tachycardia and maintain DBP in these high risk subset of patients
Patients with severe aortic stenosis and cardiogenic shock have an especially high mortality rate. Once identified by history of PoCUS, imminent consultation with both cardiology and cardiac surgery is important as definitive mechanical interventions are often life saving. These include percutaneous valvuloplasty, transcatheter aortic valve replacement (TAVR) or open aortic valve replacement. ECMO may be considered to bridge them to a percutaneous or surgical intervention.
Avoidance of tachycardia and maintenance of diastolic BP are essential in the management of patients with cardiogenic shock caused by severe aortic stenosis. The fixed lesion at the aortic valve causes the left ventricle to chronically generate high pressures to overcome the high afterload. This leads to the LV hypertrophy requiring higher coronary perfusion pressures. Remember that coronary perfusion pressure (CPP) = diastolic blood pressure (DBP) minus left ventricular end diastolic pressure (LVEDP). Therefore, maintaining a higher DBP is important in order to maintain adequate coronary perfusion.
Clinical pitfall: rapidly decreasing the afterload which the aortic stenosis patient depends on for coronary/organ perfusion with high dose nitrates on ACE inhibitors may precipitate cardiovascular collapse; avoid high dose afterload-reducing medications in patients with aortic stenosis who are in cardiogenic shock or occult shock.
These patients will usually require an arterial line. If the blood pressure is very high, evidence from small a small study suggests that nitroprusside may be of benefit. If the blood pressure is low, consider fluids (often preload dependent), inotropes and/or vasopressors. Inotropes will need to be carefully titrated to ensure tachycardia is avoided.
Temporary mechanical circulatory support (MCS): ECMO, IAPBs and PVADs
The common types of MCS available include intra-aortic balloon pump (IABP), percutaneous ventricular assist devices (PVAD – Impella, Tandem Heart), and veno-arterial extracorporeal membrane oxygenation (VA-ECMO). These resources may be used to bridge a patient to percutaneous or surgical interventions, bridge to recovery (myocarditis), and sometimes a bridge to end-of-life decision making (a severe cardiogenic shock patient not improving with medical therapy, and no fixable lesion). There is a lack of robust evidence to suggest that utilization of MCS improves survival in cardiogenic shock patients (especially if there is no lesion to fix), however, it is an option considered in patients with cardiogenic shock who are refractory to medical therapy, and a discussion with interventional cardiology/CV surgery is apt in carefully selected patients.
Risk stratification, prognosis and disposition of patients with heart failure without cardiogenic shock
There is much regional variation when it comes to the proportion of patients with acute heart failure in the ED who are discharged home. In an attempt to standardize disposition and better risk stratify these patients, various scoring systems have been developed. The Ottawa Heart Failure Risk Score (OHFRS) evaluated the risk of 14 and 30-day adverse events among 1100 patients who presented with acute heart failure in 6 tertiary care EDs in Canada.
Patients with a score of < 1 according to the score should be considered for safe discharge home. An OHFRS score of 1 and O2 sat < 90% or any score > 2 should be considered for admission.
Disadvantages of this score are that it includes NT-ProBNP which has little evidence for benefit in the diagnosis of heart failure in the ED, and is not universally available in Canadian EDs; and it assumes that admission will prevent serious adverse events. The score was validated without the BNP, but was less sensitive. The walk test is a commonly used evidence-based test to help in disposition decisions of dyspneic ED patients that our experts find useful.
Another example of a risk score is the Emergency Heart failure Mortality Risk Guide for 7-day (EHMRG7) and 30-day (EHMRG30-ST) mortality. The variables of this score are age, SBP, heart rate, O2 saturation, Cr, K, transport by EMS, troponin positive, active cancer, on outpatient diuresis. The advantage of this score is that it does not require BNP.
Our experts do not routinely use these scores to decide on disposition because the scores do not incorporate the underlying cause of the heart failure which should weigh into your disposition decision. The patient who presents to the ED with acute heart failure because of dietary or medication indiscretion has an easily reversible cause whereas the patient with an unknown cause or mechanical cause is probably more likely to have a serious adverse event and/or require in-hospital treatments. These scores may help the emergency physician advocate for their patient whom they feel need to be admitted by calculating the score and communicating it to the consultant, or for the patient who would like to go home despite your advice to be admitted, especially for those patients who seem to improve during the ED stay.
It is important for patients and their families to understand the natural history and prognosis of chronic heart failure: it is a progressive disease; ED therapy for may lead to stabilization, however, months to years following the stability phase, the patient’s functional status may decline resulting in multiple hospitalizations and eventually the condition may become refractory to treatment.
See Episode 4: Acute Congestive Heart Failure for an overview on acute heart failure
See Part 1 for an updated approach to Acute Heart Failure ED Management
Take home points for the diagnosis and management of cardiogenic shock
- Understanding the reduced contractility and clinical/PoCUS/lab assessment of end-organ perfusion is key to diagnosing and managing patients with cardiogenic shock
- Patients may present in occult cardiogenic shock with a near normal blood pressure making it challenging to diagnose; this stresses the importance of a thorough assessment of end-organ perfusion
- Effective management of cardiogenic shock requires early recognition of the etiology (eg. ACS, valvular, myocarditis, progressive non-ischemic chronic heart failure)
- Early consultation with cardiology/CV surgery is important to consider, especially in patients with a potentially reversible mechanical cause and in those patients who may benefit from temporary mechanical circulatory support (ECMO, PVADs, IAPBs)
- Resuscitation is a bridge to definitive therapy and includes optimization of: oxygenation with NIPPV, blood pressure with vasopressors (eg. norepinephrine) to maintain cardiac/end-organ perfusion targeting a MAP of 65-80, contractility with ionotropes (eg. dobutamine, milrinone) and volume status (crystalloid or diuretics)
- Patients with severe aortic stenosis in cardiogenic shock have a high risk of mortality, require mechanical definitive management urgently, and careful attention should be paid to maintaining DBP and avoiding tachycardia
- Various risk scores exist to help guide disposition in patients with acute heart failure, but they do not take into account the underlying cause of heart failure; nonetheless they may be useful to calculate and communicate to the consultant and/or patient for the patient who you feel should be admitted
- Yandrapalli S, Sanaani A, Harikrishnan P, Aronow WS, Frishman WH, Lanier GM, et al. Cardiogenic shock during heart failure hospitalizations: Age-, sex-, and race-stratified trends in incidence and outcomes. Am Heart J. 2019;213:18-29.
- Abraham J, Blumer V, Burkhoff D, Pahuja M, Sinha SS, Rosner C, et al. Heart Failure-Related Cardiogenic Shock: Pathophysiology, Evaluation and Management Considerations: Review of Heart Failure-Related Cardiogenic Shock. J Card Fail. 2021;27(10):1126-40.
- Corradi F, Via G, Tavazzi G. What’s new in ultrasound-based assessment of organ perfusion in the critically ill: expanding the bedside clinical monitoring window for hypoperfusion in shock. Intensive Care Med. 2020 Apr;46(4):775-779.
- Levy B, Clere-Jehl R, Legras A, Morichau-Beauchant T, Leone M, Frederique G, et al. Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction. Journal of the American College of Cardiology. 2018;72(2):173-82.
- Mathew R, Di Santo P, Jung RG, Marbach JA, Hutson J, Simard T, et al. Milrinone as Compared with Dobutamine in the Treatment of Cardiogenic Shock. New England Journal of Medicine. 2021;385(6):516-25.
- Khot UN, Novaro GM, Popović ZB, Mills RM, Thomas JD, Tuzcu EM, et al. Nitroprusside in Critically Ill Patients with Left Ventricular Dysfunction and Aortic Stenosis. New England Journal of Medicine. 2003;348(18):1756-63.
- Aksoy O, O’Brien BL, Menon V. Options for managing severe aortic stenosis: a case-based review. Cleve Clin J Med. 2013;80(4):243-52.
- Beck DL. Feature | An Update on Acute Mechanical Circulatory Support in Cardiogenic Shock. Absence of Evidence Base Supports a Patient-Centered Team Approach. American College of Cardiology Magazine [Internet]. 2020 Accessed Dec 20, 2021. Available from: https://www.acc.org/latest-in-cardiology/articles/2020/07/01/12/42/an-update-on-acute-mechanical-circulatory-support-in-cardiogenic-shock.
- Ezekowitz JA, O’Meara E, McDonald MA, Abrams H, Chan M, Ducharme A, et al. 2017 Comprehensive Update of the Canadian Cardiovascular Society Guidelines for the Management of Heart Failure. Can J Cardiol. 2017;33(11):1342-433.
- Collins SP, Pang PS. ACUTE Heart Failure Risk Stratification. Circulation. 2019;139(9):1157-61.
- Stiell IG, Perry JJ, Clement CM, Brison RJ, Rowe BH, Aaron SD, et al. Prospective and Explicit Clinical Validation of the Ottawa Heart Failure Risk Scale, With and Without Use of Quantitative NT-proBNP. Acad Emerg Med. 2017;24(3):316-27.
- Lee DS, Lee JS, Schull MJ, Borgundvaag B, Edmonds ML, Ivankovic M, et al. Prospective Validation of the Emergency Heart Failure Mortality Risk Grade for Acute Heart Failure. Circulation. 2019;139(9):1146-56.
- Pan AM, Stiell IG, Clement CM, Acheson J, Aaron SD. Feasibility of a structured 3-minute walk test as a clinical decision tool for patients presenting to the emergency department with acute dyspnoea. Emerg Med J. 2009 Apr;26(4):278-82.
Drs Helman, Hedayati and Tillman have no conflicts of interest to declare
what is your approach to patients with cardiogenic shock AND pulmonary edema? Do you think it is reasonable to use norepi+dobutamin and, after achieving better perfusion (MAP over 65), add nitro for better control of pulmonary edema? After that titrate catecholamines and nitro not to make the patient hypotensive.
Why not start with an inopressor like epi to keep MAP above 65 and then cautiously proceed with nitro and Lasix?
Basically, treat cardiogenic shock like SCAPE after assuring adequate contractility and MAP with epi.