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Cardiogenic Shock - pathophysiology

Created: 25/9/2007
Updated: 9/10/2007
 

Cardiogenic Shock

Dr Andrew Walden MRCP, PhD
SpR in ICU medicine, John Radcliffe hospital, Oxford

Focus on definition of cardiogenic shock

Cardiogenic shock is sustained hypotension with inadequate tissue perfusion in spite of adequate left ventricular filling pressure. This is manifested with organ dysfunction such as oliguria, confusion, cool extremities and lactic acidosis.

Strict definitions are:

  • a systolic BP of <90mmHg for greater than 30 minutes
  • a cardiac index of <2.2L/min/m2 in the presence of a pulmonary capillary wedge pressure of >15mmHg.

Focus on causes of cardiogenic shock

The causes of cardiogenic shock are summarised in Table 1.


Table 1. Causes of Cardiogenic Shock

  • Acute Myocardial Infarction
    • Pump failure
      • Large Infarction
      • Smaller infarction with pre-existing disease
      • Right Ventricular failure
    • Mechanical complications
      • Papillary muscle rupture
      • Ventricular septal defect
      • Cardiac rupture
      • Tamponade
  • Other Condtions
    • Septic shock with myocardial depression
    • End-stage cardiomyopathy
    • Myocarditis
    • Drugs – eg beta-blocker overdose
    • Aortic dissection with acute aortic regurgitation
    • Myocardial contusion
    • Left ventricular outflow tract obstruction


By far the commonest cause is acute myocardial infarction – either large, involving much of the ventricular mass, or smaller on a previous background of impaired left ventricular dysfunction. This is believed to complicate 5-10% of all acute myocardial infarctions with a mortality rate approaching 80%. In the SHOCK trial registry in patients with myocardial infarction, 75% of the cases of shock were due to left ventricular failure with the other 25% being due to acute mitral regurgitation, ventricular septal defect, tamponade and caridac rupture. Of patients who develop cardiogenic shock following acute MI, 75% will occur within 24 hours of the infarct.

Focus on pathophysiology of cardiogenic shock

The shock paradigm is a complex and vicious circle of reduced coronary perfusion leading to worsening pump failure (figure 1). Once a critical ischaemic ventricular mass is affected then there is pump failure and reduction in cardiac output. This in turn leads to reduced coronary perfusion, lactic acidosis from reduced tissue perfusion and an increase in the left ventricular end diastolic volume. These factors all contribute to worsening afterload and contractility. The compensatory mechanisms of increased heart rate and increased contractility can further contribute to a worsening myocardial oxygen demand and ischaemia.




Areas around the edge of an acute infarct can extend and areas remote from the original infarction can become ischaemic. This in turn can lead to both systolic dysfunction and diastolic dysfunction due to reduced ventricular compliance.

Without intervention this process leads to myonecrosis and apoptosis with declining pump function and ultimately death. The process of breaking the vicious cycle requires mechanical augmentation and revascularisation/valve repair to remove the initiating insult.

Key learning points

  • Cardiogenic shock is defined as sustained hypotension with tissue hypoperfusion in spite of adequate left ventricular filling pressure
  • Cardiogenic shock complicates 5-10% of all acute myocardial infarctions and has a mortality approaching 80%
  • A vicious circle of poor coronary perfusion with worsening cardiac output occurs
  • It is essential to break the vicious circle with mechanical augementation and reversal of the underlying insult

Key References

Hollenberg SM
Recognition and treatment of cardiogenic shock.
Semin Respir Crit Care Med 2004; 25(6):661-71.

Hollenberg SM, Kavinsky CJ, Parrillo JE.
Cardiogenic Shock.
Annals of Internal Medicine 1999; 131(1):47-59

Hochman JS, Boland J, Sleeper LA, Porway A, Brinker J et al.
Current spectrum of cardiogenic shock and effect of early revascularisation on mortality. Results of an international registry.
Circulation 1995;91:873-81
ArticleDate:20070925
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