#41 Cardiogenic Shock

Written By Nick Mark

If you thought ARDS was a long episode... get ready for a marathon! This week on Critical Care Time, Cyrus and Nick take on the unenviable task of trying to cover everything you need to know about cardiogenic shock - at least in broad strokes - in ONE episode! That's right, this is your one-stop-shop for all things cardiogenic shock. While we will have some deep dives on RV and LV failure, as well as ECMO and other mechanical circulatory support options - this episode has a little bit of it all to wet your whistle and then some! We deconstruct the epidemiology of cardiogenic shock, do a deep dive on the SCAI classes of cardiogenic shock, talk pathophysiology (duh!) and then move on to treatment considerations - both medical and mechanical - followed finally by some cases to cement all the learning. We know this is a long one so feel free to listen/watch in chunks. However you decide to enjoy it, we are certain you will walk away from it ready to conquer the next CGS case you come across! Once you've finished this epic - leave us a review and let us know how we did!


Introduction to Cardiogenic Shock

Cardiogenic shock (CS) is a critical condition resulting from the heart's inability to pump blood effectively, leading to inadequate tissue perfusion and organ dysfunction. It can arise from left ventricular (LV) or right ventricular (RV) failure, or both, and may coexist with other shock states (e.g., septic shock). Understanding its pathophysiology, classification, and management is crucial in critical care.

SCAI stages of cardiogenic shock.

Source: Society for Cardiovascular Angiography and Interventions (SCAI).

Pathophysiology and Classification

  • Pathophysiology: Cardiogenic shock often begins with an acute insult (e.g., acute coronary syndrome, decompensated heart failure) leading to decreased cardiac output (CO). The compensatory mechanisms, including increased systemic vascular resistance (SVR) and tachycardia, eventually fail, exacerbating myocardial strain and worsening perfusion.

  • SCAI Staging of Cardiogenic Shock:

    • Stage A: At risk (e.g., large MI, early decompensation).

    • Stage B: Beginning shock (mild hypotension or tachycardia without hypoperfusion).

    • Stage C: Classic shock with hypoperfusion requiring active support.

    • Stage D: Deteriorating shock despite interventions.

    • Stage E: Extremis, often requiring heroic measures such as VA-ECMO or CPR.

  • Clinical Features

    • LV Failure: Often presents with hypotension, pulmonary edema (crackles), cool extremities, oliguria, and elevated biomarkers like lactate and BNP.

    • RV Failure: May manifest with elevated central venous pressure (CVP), hepatomegaly, RUQ pain, and ascites.

    • Bi-Ventricular Failure: Combines features of both LV and RV failure and is often associated with septic cardiomyopathy.

  • Key Metrics:

    • Cardiac Output (CO) and Cardiac Index (CI): Indexed to body size; CI < 2.2 L/min/m² indicates severe dysfunction.

    • Pulmonary Artery Pulsatility Index (PAPI): Differentiates RV dysfunction (<0.9 suggests RV failure).

    • Cardiac Power Output (CPO): Reflects myocardial function; CPO < 0.6 W is highly indicative of cardiogenic shock.

Cardiac Power Output (CPO)

  • Cardiac power output (CPO) is a holistic measure of the heart's pumping ability, calculated by multiplying cardiac output (blood flow) by mean arterial pressure (blood pressure), essentially representing the rate of energy produced by the heart as it pumps blood throughout the body. This is analogous to the basic hydraulic flow formula power = pressure x flow. CPO is considered a more comprehensive indicator of cardiac function compared to cardiac output alone, as it considers both pressure and flow.

  • Power is defined as work done per unit time. In the case of the heart, work is typically expressed as ventricular stroke work (VSW), which is the area under the pressure volume curve. The product of VSW and heart rate (HR) is cardiac power output (CPO).

  • A normal cardiac power output (CPO) is between 0.8 and 1.1 watts.

  • A CPO less than 0.6 watts is a sign of hemodynamic compromise and is associated with a higher risk of mortality. This is used as a threshold for consideration of MCS.

Cardiac Power Output Calculator

Cardiac Power Output Calculator

You can embed this calculators in your own site and check out the source code here.

Pulmonary Artery Pulsatility Index (PAPI)

  • The Pulmonary Artery Pulsatility Index (PAPI) is related to - but is not a direct measure of - right ventricular function. Several factors influence PAPI including RV stroke volume, Pulmonary artery compliance, Right Atrial Pressure (RAP), and Pulmonary Artery Wedge Pressure (PCWP).

  • A PAPI < 0.9 is suggestive of Right Ventricular Failure. A PAPI < 0.9 is also associated with an increased risk mortality or requiring RV mechanical circulatory support.

Pulmonary Artery Pulsatility Index (PAPI) Calculator

Pulmonary Artery Pulsatility Index (PAPI) Calculator

A pulmonary artery pulsatility index (PAPI) < 0.9 is indicative of right ventricular dysfunction and is associated with increased risk of RV mechanical support and mortality.


Initial Stabilization

  • ABCs (Airway, Breathing, Circulation): Manage hypoxemia and respiratory failure with high-flow nasal cannula (HFNC), non-invasive ventilation (NIV), or intubation as needed.

    • NIPPV is beneficial for several reasons. It can improve cardiac output due to a pressure gradient from chest to abdomen/head. It can also improve oxygenation when pulmonary edema is present

  • Hemodynamic Goals: Target MAP > 65 mmHg, CI > 2.5 L/min/m², and adequate end-organ perfusion (normal capillary refill, urine output > 0.5 ml/kg/hr, lactate clearing, mentation intact, etc)

Pharmacologic Therapy

  • Inotropes:

    • Dobutamine: Improves contractility; used for LV dysfunction.

    • Milrinone: Reduces pulmonary vascular resistance (PVR); helpful for RV failure.

  • Vasopressors:

    • Norepinephrine: First-line for maintaining MAP.

    • Vasopressin or Angiotensin II: Adjuncts in refractory cases.

  • Pulmonary Vasodilators (e.g., inhaled nitric oxide): Reduce RV afterload in RV failure.

  • Volume Management:

    • Diuresis is preferred in volume-overloaded patients.

    • Cautious fluid resuscitation in RV dysfunction to optimize preload.

  • Related episodes:

Mechanical Circulatory Support (MCS)

  • Intra-Aortic Balloon Pump (IABP): Decreases afterload and improves coronary perfusion. No mortality benefit in routine use (IABP-SHOCK II trial) but remains an option in select patients.

    • IABP-SHOCK II Trial

      • Population: ~600 patients with AMI-induced cardiogenic shock.

      • Key Findings:

        • No significant mortality benefit of intra-aortic balloon pump (IABP) at 30 days, 1 year, or 6 years compared to medical therapy alone.

        • Highlighted limited routine benefit of IABP in cardiogenic shock.

      • Impact: Guidelines downgraded routine use of IABP but recognized it may be helpful in specific scenarios.

Intra-aortic Balloon Pump (IABP) by ICU OnePager

  • Impella: A temporary ventricular assist device providing partial to near-complete support (e.g., Impella RP for RV support).

    • DanGer Shock Trial (2024)

      • Population: Patients with STEMI and cardiogenic shock randomized to optimized Impella therapy or standard care.

      • Key Findings:

        • Impella group showed significant reduction in 180-day mortality (45.8% vs. 58.5%; p = 0.04).

        • Higher complications (24% vs. 6.2%), including bleeding, limb ischemia, and hemolysis.

      • Impact: Supported targeted use of Impella in carefully selected patients, emphasizing early removal to minimize complications.

Impella OnePager by ICU OnePager

  • VA-ECMO: Provides full cardiopulmonary support; used in extremis or refractory cases despite complications like bleeding and limb ischemia.

    • ECLS-SHOCK Trial (2023)

      • Population: Patients with AMI and refractory cardiogenic shock randomized to VA-ECMO or standard care.

      • Key Findings:

        • No significant mortality benefit at 30 days (47.8% vs. 49%).

        • VA-ECMO group had higher complications, including bleeding and limb ischemia.

      • Impact: Questioned routine VA-ECMO use, emphasizing selective application in carefully chosen patients.

    • Lancet Meta-Analysis (2023)

      • Scope: Pooled data from four RCTs on VA-ECMO for infarct-related cardiogenic shock.

      • Key Findings:

        • No survival benefit at 30 days (mortality: 45.7% VA-ECMO vs. 47.7% standard care).

      • Impact: Reinforced findings from ECLS-SHOCK, discouraging routine VA-ECMO use but supporting its role in extremis.

Advanced Diagnostics

  • Pulmonary Artery Catheter (PAC): Provides real-time hemodynamic data, including CI, CVP, and PAPI. Crucial for guiding therapy in complex or refractory cases.

    • PACMAN Trial (2005)

      • Population: 1,041 ICU patients where clinicians considered pulmonary artery catheter (PAC) use.

      • Key Findings:

        • No difference in mortality (66% vs. 68%) between PAC and non-PAC groups.

        • High complication rates (10%) with PAC placement in the study.

        • Limited inclusion of cardiogenic shock patients (~11%).

      • Impact: Misinterpreted as evidence against PAC use; highlights the importance of patient selection and modern PAC techniques.

    • ESCAPE Trial (2005)

      • Population: Patients with advanced heart failure randomized to PAC vs. clinical assessment alone.

      • Key Findings:

        • No survival benefit of PAC in advanced heart failure.

      • Impact: Findings limited to heart failure without shock and should not be extrapolated to cardiogenic shock.

  • Point-of-Care Ultrasound (POCUS): Assesses ventricular function and fluid status but has limitations in critically ill patients with poor imaging windows.

  • Transthoracic Echo (TTE): may provide better continuous imaging in critically ill patients.

  • Cardiac catherization: very useful when ischemic causes are under consideration




Nick Mark
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