Cardiogenic Shock

Cardiogenic Shock

Navin K. Kapur MD

Daniel Steinberg MD, FSCAI


Cardiogenic shock (CS) is a major cause of global morbidity and mortality, and most commonly occurs after an acute myocardial infarction (AMI) or in patients with advanced heart failure (HF). Shock from any cause is characterized by tissue hypoperfusion leading to end-organ damage, and CS is defined as tissue hypoperfusion secondary to cardiac failure despite adequate circulatory volume and left ventricular (LV) filling pressure. Specifically, hemodynamic criteria for CS include: a systolic blood pressure <90 mm Hg for >30 minutes or a fall in mean arterial blood pressure greater than 30 mm Hg below baseline with a cardiac index (CI) of <1.8 L/min m2 without hemodynamic support or <2.2 L/min m2 with support and a pulmonary capillary wedge pressure (PCWP) >15 mm Hg (1, 2 and 3).

The incidence of CS after AMI has remained relatively stable over the past 30 years and ranges between 7% and 9% (4). A recent evaluation of the National Registry of Myocardial Infarction (NRMI) reported that CS occurred in 8.6% of patients presenting with AMI, defined as ST-segment elevation or new left bundle branch block, between June 1995 and May 2004 (5). In this study, only 29% of patients presented with CS, while 71% developed CS after admission.

Mortality associated with CS is high. In-hospital mortality in the SHOCK trial registry was reported to be 60% (6). This finding is consistent with in-hospital mortality rates observed by the NRMI, which ranged from 60.3% in 1995 to 47.9% in 2004 (5). Importantly, CS can develop after both ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI). The Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO)-IIb trial reported CS in 4.2% of STEMI and 2.5% of NSTEMI patients. The mean time to onset of CS after STEMI was 9.6 hours compared with 76.3 hours after NSTEMI (6). Despite variable times to onset, in-hospital mortality was not significantly different between the two groups.

Several historic classification schemes for CS after AMI include the Killip and Forrester classes (Table 20-1). Killip classes were first defined in 1967 from an observational series of 250 patients presenting with an AMI without cardiac arrest (7). CS was defined as Killip Class IV, and was associated with a 67% 30-day mortality rate. In 1977, Forrester and colleagues expanded the Killip definitions to include hemodynamic parameters such as PCWP and CI (8).

CS in the absence of AMI occurs most commonly in the presence of advanced HF. In the United States alone, over 7 million individuals suffer from HF. As a complex manifestation of acutely decompensated HF, CS is included among several HF classification systems (Table 20-2) (9). The New York Heart Association (NYHA) classifies HF severity based on symptoms. CS is categorized as a manifestation of NYHA Class IV HF. For patients with advanced HF (NYHA Class III or IV), the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) has defined seven clinical profiles before implantation of a LV assist device (LVAD) (10). CS is identified by INTERMACS profiles 1 and 2, where patients may be “crashing” despite aggressive therapy or “sliding fast on inotropes,” respectively. Both INTERMACS 1 and 2 subjects may be considered for temporary circulatory support as a bridge to recovery, surgical LVAD, or cardiac transplantation.



A common cause of CS is secondary to an AMI (Table 20-3). While thrombotic coronary artery occlusion can be well tolerated clinically, approximately 5% to 8% of AMI patients develop clinical manifestations of hemodynamic collapse (6, 11). The most common anatomic distribution of a coronary occlusion associated with CS is the proximal left anterior descending artery. Mean LV ejection fraction (LVEF) in patients with CS following an AMI is approximately 30% (12), and those who develop CS are generally older (age > 65) with a history of hypertension, prior infarction, or multivessel disease (13, 14). Early preclinical studies suggest that approximately 40% of the myocardium must be involved in an AMI to cause CS (15).

Post-Myocardial Infarction Complications

The timing of CS onset may influence clinical outcomes. In the Trandolapril Cardiac Evaluation (TRACE) registry, early development of CS within 48 hours of admission was associated with
significantly lower 30-day mortality than patients with late development of CS (16). This may be due to ventricular arrhythmias or mechanical complications such as papillary muscle dysfunction/rupture and acute mitral regurgitation, ventricular septal rupture, or ventricular free wall rupture.

TABLE 20-1 Classification Systems for Cardiogenic Shock in AMI

Killip Classification

Forrester Classification

Stage 1

No signs of cardiovascular decompensation

Stage 1

Normal perfusion and PCWP

Stage 2

Heart failure: rales (1/2 lung field), S3 gallop, pulmonary congestion

Stage 2

Poor perfusion and low PCWP

Stage 3

Severe heart failure. Diffuse rales

Stage 3

Normal perfusion and high PCWP

Stage 4

Cardiogenic shock. SBP < 90mm Hg; oliguria, cyanosis and sweating

Stage 4

Poor perfusion and high PCWP

TABLE 20-2 Classification systems for Advanced Heart Failure and Cardiogenic Shock






“Crash and burn,” emergent mechanical support



Intravenous inotropes, may need mechanical support



Stable, but inotrope dependent

IV (ambulatory)


Resting symptoms, oral therapy, peak Vo2 <12 L/min

IV (ambulatory)


ADL’s severely limited, peak Vo2 <12 L/min



ADL’s possible but limited



Advanced Class 3 symptoms


Structural disease, current or past symptoms


Structural disease, no symptoms


At risk, no structural disease or symptoms

Acute mitral regurgitation is an important mechanical complication of CS after an AMI, and may be due to papillary muscle dysfunction or rupture. In an analysis of 1,190 patients in the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? (SHOCK) registry, severe mitral regurgitation was considered the primary mechanism of shock in 98 (6.9%) (17). Several studies have reported that ischemic papillary muscle rupture occurs most commonly in patients presenting with their first AMI in the inferior territory since the posteromedial papillary muscle receives blood supply from the right coronary artery, while the anterolateral papillary muscle is supplied by both the left anterior descending and circumflex arteries (18, 19).

Ventricular septal rupture and free wall rupture are also important causes of CS after an AMI. Upon rupture of the ventricular septum, a sudden decrease in LV stroke volume occurs as an acute left-to-right shunt develops within the heart. Prior to the reperfusion era, septal rupture occurred in approximately 2% of patients (20, 21). Among 41,021 patients in the Global Utilization of Streptokinase and T-PA for Occluded Coronary Arteries (GUSTO) trial, 84 (0.2%) developed a ventricular septal rupture (22). In the SHOCK registry, 55 (3.9%) developed a ventricular septal rupture (17). Risk factors for development of a ventricular septal rupture include advanced age, female sex, and no prior symptoms of angina or prior myocardial infarction (23). Anterior myocardial infarctions are generally associated with anteroapical septal rupture, while inferior myocardial infarction (IMI) tends to occur in the posterobasal septum (24).

Ventricular free wall rupture can result in acute cardiac tamponade and CS. In these cases, hemopericardium commonly leads to pulseless electrical activity and sudden cardiac death (21). In the prethrombolytic era, free wall rupture was a common cause of death after an AMI. In modern day practice, free wall rupture is rare. In the SHOCK registry, cardiac tamponade from any cause (i.e., pericarditis or free wall rupture) accounted for only 20 (1.4%) of the 1,190 patients enrolled (17). Risk factors for free wall rupture include female sex, the extent of myocardial infarction, and the absence of prior coronary disease (21, 25, 26).

Right Ventricular Myocardial Infarction

Right ventricular (RV) myocardial infarction (RVMI) is another unique cause of CS after an AMI, and is associated with increased morbidity and mortality, including a higher likelihood of
CS, ventricular fibrillation, and high grade AV-conduction block (27, 28). The diagnosis of RVMI relies on clinical evidence of venous congestion, clear lung fields, and low cardiac output despite relatively preserved LV function. Echocardiographic evidence of RV dilatation or wall motion abnormalities may occur in up to 50% of subjects with acute IMI and may not correlate with clinical findings of RV failure (29). The RV receives blood from acute marginal branches of the right coronary artery and the posterior descending artery. RVMI occurs most commonly after acute proximal right coronary occlusion, but can occur after occlusion of a dominant circumflex artery (30, 31). RV ischemia leads to RV systolic failure and reduced LV preload. As RV pressure and volume overload develop, the interventricular septum shifts toward the LV cavity, further reducing LV stroke volume. Hemodynamic indices of RV failure in AMI include measurements of RV stroke work (RVSW), right atrial to PCWP (RA:PCWP) ratio of >0.8, and pulmonary artery pulse pressure (32). In the SHOCK registry, isolated RV failure accounted for 49 (5.3%) of the 933 patients with myocardial dysfunction as the primary mechanism underlying CS (33).

TABLE 20-3 Causes of Cardiogenic Shock




Acute myocardial infarction

Primary left ventricular failure

Severe sepsis

Chronic failure


Subarachnoid hemorrhage

Right ventricular infarction

Hypertrophic cardiomyopathy


Complications after AMI

Valvular heart disease


Myocardial contusion

Papillary muscle rupture

Stress cardiomyopathy

Ventricular septal rupture


Free wall rupture/tamponade

Valvular Heart Disease

May 28, 2016 | Posted by in CARDIOLOGY | Comments Off on Cardiogenic Shock

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