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    Cardiogenic Shock

    Cardinal Presentations / Presenting Problems, Cardiovascular, Critical Care / Resuscitation

    Last Updated Oct 12, 2022
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    The First 5 Minutes

    • Look for hypotension on monitor.
    • Look for hypoxia on O2 sat and often wet lungs (to auscultation and on CXR).
    • Look for signs hypoperfusion.
    • Look at your ECG for ACS.
    • Look with your ultrasound.


    Incidence of shock:

    Distributive 66% , Hypovolemic 16%, Cardiogenic 16%, Obstructive 2%.


    Types of Shock:
    Cold & Wet – Most common. Cold extremities, wet lungs.
    Cold & Dry – Cold extremities, euvolemic (seen in diuretic-responsive with chronic CHF who present with an acute exacerbation).
    Warm & Wet – Warm extremities, wet lungs (seen in some of those who have a SIRS-type response to ACS causing more vasodilation than vasoconstriction).

    Primary Cause is ACS, including mechanical complications of ACS (rupture of papillary muscle, rupture of free wall or septum). *Elevation in aVR is an independent predictor.

    Other causes include: Aortic Stenosis, Endocarditis, CHF, Cardiomyopathy, Myocarditis, Myocardial contusion, Dysrhythmias, Toxins (Beta-blockers, Calcium-Channel blocker), Pulmonary Hypertension.

    Diagnostic Process

    • Is there a recommended decision aid?
    • If so, what is it and how do you use it?
    • If no decision aid, what investigative process do you recommend?
    • Important limitations or pitfalls of testing/interpretation of test results.
    • Look for hypotension, often with narrow pulse pressure due to low stroke volume (systolic -diastolic= <25% of systolic).
    • Look for hypoxia and often wet lungs (to auscultation and on CXR).
    • Look for signs hypoperfusion (cool extremities, altered mental status, decreased urine output, AKI, elevated lactate, and LFTs).
    • Look at your ECG.
    • Look with your ultrasound.

    Ultrasound findings in Cardiogenic Shock

    • IVC: enlarged or normal (in dry &wet type).
    • Lung: B lines.
    • Heart: decreased LVEF, RV dilation in patients with RV failure.


    Recommended Treatment

    • Non-drug including surgical treatments.
    • Preferred or recommended drugs and dosages.
    • Treatments to avoid (i.e., often used but shown to not be effective).

    Stabilize for Definitive Treatment


    • NIPPV if tolerated (*not in RV failure as will increase RV afterload).
    • Intubation if necessary (*removal of respiratory drive can lead to cardiovascular collapse).

    Blood Pressure

    • Norepinephrine is ideal pressor choice.
    • Consider Vasopressin in RV failure (doesn’t cause pulmonary vasoconstriction, though no RCT).
    • Not recommended: Epinephrine (increased refractory cardiogenic shock in Optima CC trail, 2018), Dopamine (increased mortality in Soap II trial, 2010), Phenylephrine (unopposed alpha receptor agonism leads to decreased contractility, no RCT).


    • All inotropes can worsen hypotension, so consider inotropy only if refractory hypoperfusion despite pressor support.
    • Milrinone and Dobutamine- no significant difference between the two (DoReMi trial, 2021).
    • Dobutamine is more rapidly titratable, so may be preferable in the ED setting.

    Definitive Treatment

    • Emergent Revascularization of the culprit coronary artery is the only intervention shown to reduce mortality (Shock trial, 1999).
    • No role for Intraaortic Balloon Pump (IABP SHOCK II trial, 2012).
    • No role for multi-vessel revascularization (CULPRIT-SHOCK trial, 2017).
    • ECMO, Impella – no significant impact on outcome, but may serve as a bridge for patients with reversible causes (awaiting valve repair, heart transplant candidate, etc.)
    • Thrombolytics- No change in mortality, but might be worth a try if long delay to revascularization (>6-8hrs).

    Criteria For Hospital Admission

    All admitted to ICU or CCU setting with appropriate consults which may require consultation.

    Quality Of Evidence?


    Limited but increasing number of studies.


    Related Information


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