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Cardiogenic shock

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Systolic BP < 90 mm Hg, or 30 mm Hg below baseline for at least 30 mins, evidence of poor tissue perfusion and persistence of shock after correction of non-myocardial factors (eg hypovolaemia, hypoxia, acidosis, arrhythmias)



Compensatory mechanisms such as salt & water retention and peripheral vasoconstriction tend to exacerbate LV dysfunction. Also decreased perfusion pressure, especially in the presence of multi-vessel coronary disease leads to further depression of myocardial contractility.


  • Echo for all patients to exclude surgically correctable lesion and tamponade and to look for RV infarction
  • ECG: normal ECG virtually excludes possibility of cardiogenic shock caused by MI


  • optimize preload and afterload. Vasodilators should be given with extreme caution. Nitroprusside may cause coronary steal. Vasodilators particularly important when mitral regurgitation is a major contributing factor
  • inotropes. Dobutamine or levosimendan unless shock is profound in which case drugs with vasoconstrictor actions preferable. Phosphodiesterase inhibitors should be reserved for those in whom catecholamines have failed to improve cardiac performance or those in whom arrhythmia or ischaemia limits catecholamine dose
  • intra-aortic balloon pump. Only of value if subsequent revascularization is possible
  • thrombolysis. No definite evidence that this alters prognosis. May be less effective in patients with cardiogenic shock because of poor coronary blood flow. Combination of thrombolysis and IABP may be more effective. Mortality higher in those treated with t-PA compared to those treated with streptokinase
  • PTCA. Probably treatment of choice in cases due to IHD. Both PTCA and CABG need to be performed within first few hours (ideally within 2-4 h) of onset of symptoms. Result in improved survival at 6 months and 1 year although not at 30 days
  • CABG. May be of benefit if facilities immediately available. Operative mortality is high
  • Patients with RV infarction leading to cardiogenic shock particularly sensitive to volume depletion and prone to deterioration from bradycardia and loss of AV synchrony due to advanced heart block. Focus of therapy should be immediate restoration of adequate LV filling pressure, maintenance of sinus rhythm or synchronized pacing and use of dobutamine to stimulate RV systolic function


  • usual methods used to treat cardiogenic shock exacerbate obstruction
  • plasma volume expansion and IV titration of beta-blockers reduce ventricular outflow obstruction and improve cardiac output


  • poor
  • only about 1/3 of patients actively treated survive initial episode and many of the survivors have continuing angina, CCF and decreased exercise tolerance
  • approximately 1/2 with a surgically correctable lesion leave hospital
  • RV function usually returns to normal in survivors of cardiogenic shock associated with RV infarction
  • 50% of patients who require maximal therapy and IABP to come off bypass die. If ventricular assist device also required then only 35-45% survive. Functional prognosis for these survivors quite good
  • Mortality without aggressive highly technical care is 70-90%. Hospitals without the facilities for IABP or high-risk angioplasty and surgical intervention should begin initial resuscitative measures and then make a rapid decision about transfer to a hospital with the necessary resources

Myocardial stunning and hibernation

Myocardial stunning

Mechanical dysfunction of myocardium which persists despite absence of irreversible damage and restoration of normal or near-normal coronary flow and which recovers spontaneously.

Clinically important in 3 settings:

- after MI (especially after thrombolysis or primary angioplasty)

- after complicated coronary interventions (when myocardium may be ischaemic for long periods, particularly if there is pre-existing LV dysfunction)

- after cardiac surgery

Mechanical circulatory support may be preferable to inotropes for patients with stunned myocardium as inotropes may adversely influence recovery of potentially ischaemic segments

Hibernating myocardium

Myocardium with impaired function that is persistently impaired at rest due to decreased coronary blood flow but which demonstrates improved function when balance between oxygen supply and demand is improved.

Dobutamine echocardiography can be used to differentiate between stunned myocardium with a patent artery (­ function that persists during infusion) from stunned myocardium with a stenosed artery or hibernation (initial ­ followed by deterioration).


© Charles Gomersall July 1999, March 2006


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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