Tom Wade MD

For an outstanding brief review of this topic please see also

EMCrit 259 – Cardiogenic Shock — The Next Level & Mechanical Circulatory Support with Jenelle Badulak. November 13, 2019 by Scott Weingart, MD FCCM.*

*Scott Weingart, MD FCCM. EMCrit 259 – Cardiogenic Shock — The Next Level & Mechanical Circulatory Support with Jenelle Badulak. EMCrit Blog. Published on November 13, 2019. Accessed on August 1st 2021. Available at [https://emcrit.org/emcrit/cardiogenic-shock-2-mcs/ ].

In this post, I link to and excerpt from Contemporary Management of
Cardiogenic Shock: A Scientific Statement From the American Heart Association [PubMed Abstract] [Full-Text HTML] [Full-Text PDF]. Circulation. 2017 Oct 17;136(16):e232-e268.

The above article has been cited 179 articles inPubMed.

All that follows is from the above article.

ABSTRACT: Cardiogenic shock is a high-acuity, potentially complex, and hemodynamically diverse state of end-organ hypoperfusion that is frequently associated with multisystem organ failure. Despite improving survival in recent years, patient morbidity and mortality remain high, and there are few evidence-based therapeutic interventions known to clearly
improve patient outcomes. This scientific statement on cardiogenic shock summarizes the epidemiology, pathophysiology, causes, and outcomes of cardiogenic shock; reviews contemporary best medical, surgical, mechanical circulatory support, and palliative care practices; advocates
for the development of regionalized systems of care; and outlines future research priorities.

DEFINITION OF CS

Acute cardiac hemodynamic instability may result from disorders that impair function of the myocardium, valves, conduction system, or pericardium, either in isolation or in combination. CS is pragmatically defined as a state in which ineffective cardiac output caused by a primary cardiac disorder results in both clinical and biochemical manifestations of inadequate tissue perfusion. The clinical presentation is typically characterized by persistent hypotension unresponsive to volume replacement and is accompanied by clinical features of end-organ hypoperfusion requiring intervention with pharmacological or mechanical support. Although not mandated, objective hemodynamic parameters for CS can help
confirm the diagnosis and enable comparison across
cohorts and clinical trials. Definitions in clinical practice
guidelines and operationalized definitions used in the
SHOCK (Should We Emergently Revascularize Occluded
Coronaries for Cardiogenic Shock) and IABP-SHOCK II
(Intraaortic Balloon Pump in Cardiogenic Shock II) trials
are presented in Table 1.1,9,15*

*For the most current definitions of Cardiogenic Shock, please see SCAI clinical expert consensus statement on the classification of cardiogenic shock [PubMed Abstract] [Full-Text HTML] [Full-Text PDF]. Catheter Cardiovasc Interv. 2019 Jul 1;94(1):29-37.

PATHOPHYSIOLOGY

HEMODYNAMIC PHENOTYPES

Early reports of CS described patients with HF and elevated central venous pressures (CVPs).34 With the advent of invasive hemodynamic measurements, patients with CS were further characterized by a low CI, an elevated systemic vascular resistance, and a high PCWP.35 This classic “cold and wet” (Figure 2) profile is the most frequent CS phenotype, accounting for nearly two thirds of patients with MI-associated CS.36

Euvolemic or “cold and dry” CS typically describes a diuretic-responsive patient with chronic HF with a subacute decompensation but also represents a reported 28% of patientswith MIassociated CS.36,40 Compared with patients with classic CS, those with euvolemic CS were less likely to have
had a previous MI or chronic kidney disease and had significantly lower PCWPs.36

Overlaid on this framework are 2 uncommon but hemodynamically distinct entities of normotensive CS
and right ventricular (RV) CS.

In the SHOCK trial registry, 5.2% of patients were normotensive with peripheral hypoperfusion despite an SBP >90 mmHg.50 This group had comparable CIs, PWCPs, and LV ejection fractions but higher systemic vascular resistance compared with hypotensive patients with CS, thus highlighting the risk of relative hypotension and the potential for hypoperfusion without profound hypotension.

The reported prevalence of RV CS is 5.3% among
patients with MI-induced CS. For these patients, the
severity of shock may depend on the degree of both
RV and LV ischemia, given a shared septum and the
importance of ventricular interdependence on RV
function.51–53 Hemodynamically, this cohort is characterized by relatively higher CVPs, LV ejection fractions,
and lower pulmonary artery systolic pressures, with no
differences in CI or PCWP.

PATHOGENESIS

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