Cardiogenic shock (CS) is a common cause of mortality, and management remains challenging despite advances in therapeutic options. CS is caused by severe impairment of myocardial performance that results in diminished cardiac output, end‐organ hypoperfusion, and hypoxia.1 Clinically this presents as hypotension refractory to volume resuscitation with features of end‐organ hypoperfusion requiring pharmacological or mechanical intervention.1 Acute myocardial infarction (MI) accounts for 81% of patient in CS.2
Contemporary trials and guidelines (Table 1)3, 4, 5, 6, 7 outline clinical criteria for defining CS and are limited by lack of uniformity. The SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) and intra‐aortic balloon pump (IABP)‐SHOCK II trials used systolic blood pressure (SBP) measurements of <90 mm Hg for ≥30 minutes or use of pharmacological and/or mechanical support to maintain an SBP ≥90 mm Hg.1, 3, 4 Evidence of end‐organ hypoperfusion varied between the trials but typically included urine output of <30 mL/h, cool extremities, altered mental status, and/or serum lactate >2.0 mmol/L.1, 3, 4 The SHOCK Trial included cardiac index (CI) of ≤2.2 L/min per m2 and a pulmonary capillary wedge pressure (PCWP) of ≥15 mm Hg.3 An SBP <90 mm Hg that is refractory to fluid resuscitation with clinical and laboratory evidence of end‐organ dysfunction, in the setting of suspected cardiac dysfunction, is essential to the definition of CS. However, CS is a continuum that extends from pre‐shock to refractory shock states, which influence the timely considerations of various interventions.8 Acknowledging this continuum in future trials would likely facilitate the unification of clinical and hemodynamic criteria in defining CS.

Various forms of cardiac dysfunction can cause cardiogenic shock. The most common causes of cardiogenic shock include:

Acute myocardial ischemia
Mechanical defect: acute mitral regurgitation (papillary muscle rupture), ventricular wall rupture (septal or free wall), cardiac tamponade, left ventricular outflow obstruction (hypertrophic obstructive cardiomyopathy [HOCM], aortic stenosis [AS]), Left ventricular inflow obstruction (MS, atrial myxoma)

Contractility defect: ischemic and non-ischemic cardiomyopathy, arrhythmias, septic shock with myocardial depression, myocarditis
Pulmonary embolus (right ventricular with or without left ventricular failure)
Right ventricular failure
Aortic dissection
Other causes include cardiotoxic drugs (doxorubicin), medication overdose (beta/calcium channel blockers), metabolic derangements (acidosis), electrolyte abnormalities (calcium or phosphate)
Risk of Cardiogenic shock after ST-elevation myocardial infarction (STEMI):

Age more than 70 years
Systolic blood pressure less than 120 mmHg
Sinus tachycardia or bradycardia
A long duration of symptoms before treatment

Epidemiology

The incidence of cardiogenic shock is in decline, which can be attributed to increased rates of use of primary percutaneous coronary intervention (PCI) for acute MI. However, approximately 5% to 8% of STEMI and 2% to 3% of NON-STEMI cases can result in cardiogenic shock. This can translate to 40,000 to 50,000 cases per year in the United States.[6][7]

Cardiogenic shock has a higher incidence in the following classes of patients:
Elderly population
Patient population with diabetes
Prior history of left ventricular injury
Female gender
 The pathophysiology of cardiogenic shock is complex and not fully understood. Ischemia to the myocardium causes derangement to both systolic and diastolic left ventricular function, resulting in a profound depression of myocardial contractility. This, in turn, leads to a potentially catastrophic and vicious spiral of reduced cardiac output and low blood pressure, perpetuating further coronary ischemia and impairment of contractility. Several physiologic compensatory processes ensue.

                                        Journal of Perioperative Medicine