Cardiogenic Shock

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Cardiogenic shock occurs when there is failure of the pump action of the heart, resulting in a decrease in cardiac output causing reduced end-organ perfusion.[1] This leads to acute hypoperfusion and hypoxia of the tissues and organs, despite the presence of an adequate intravascular volume.

Cardiogenic shock can be defined as the presence of the following (despite adequate left ventricular filling pressure):

  • Sustained hypotension (systolic blood pressure (BP) <90 mm Hg for more than 30 minutes).
  • Tissue hypoperfusion (cold peripheries, or oliguria <30 ml/hour, or both).

Cardiogenic shock most commonly occurs as a complication of acute myocardial infarction (MI). It occurs in 7% of patients with ST-segment elevation MI and 3% with non ST-segment elevation MI.[2] It is a medical emergency requiring immediate resuscitation.

Cardiogenic shock is most often caused by acute MI, particularly affecting the anterior wall of the heart.[3] 

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Due to an intrinsic heart problem

  • MI.
  • Myocardial contusion (often from steering wheel impact).
  • Acute dysrhythmia compromising cardiac output.
  • Acute mitral regurgitation (usually as a complication of MI due to ruptured chordae tendinae).
  • Ventricular septal rupture (usually occurring as post-MI complication).
  • Cardiac rupture (rupture of the wall of the left ventricle can occur post-MI or due to cardiac trauma).
  • Hypertrophic obstructive cardiomyopathy or end-stage cardiomyopathy of other cause.
  • Myocarditis.
  • Post-cardiac surgery requiring prolonged cardioplegia and cardiopulmonary bypass.
  • Severe valvular heart disease, particularly aortic stenosis.

Due to other causes

  • Acute, severe pulmonary embolism (PE).
  • Pericardial tamponade or severe constrictive pericarditis.
  • Tension pneumothorax.
  • Myocardial suppression due to bacteraemia or sepsis (although, strictly speaking, this may be defined as septic shock).
  • Suppression of myocardial contractility by drugs (eg, beta-blockers) or due to metabolic disturbance (eg, acidosis, hypokalaemia or hyperkalaemia, hypocalcaemia).
  • Thyrotoxic crisis.

Risk factors

  • It is more likely to develop in the elderly and in those with diabetes.[4]
  • Anterior and right-ventricular MI are associated with an increased risk.
  • History of previous infarction, peripheral vascular disease, cerebrovascular disease and multi-vessel atheroma increases the likelihood of the development of cardiogenic shock.

Shock is due to an inability to perfuse vital organs and tissues adequately. The skin, brain, heart and kidneys are usually most severely affected by this. The symptoms and signs can present abruptly or develop insidiously over the course of many hours.

Symptoms

As many patients with cardiogenic shock have had an acute MI, symptoms can include:

  • Chest pain
  • Nausea and vomiting
  • Dyspnoea
  • Profuse sweating
  • Confusion/disorientation
  • Palpitations
  • Faintness/syncope

Signs

  • Pale, mottled, cold skin with slow capillary refill and poor peripheral pulses.
  • Hypotension (remember to check BP in both arms in case of aortic dissection).
  • Tachycardia/bradycardia.
  • Raised JVP/distension of neck veins.
  • Peripheral oedema.
  • Quiet heart sounds or presence of third and fourth heart sounds.
  • Heaves, thrills or murmurs may be present and may indicate the cause, such as valve dysfunction.
  • Bilateral basal pulmonary crackles or wheeze may occur.
  • Oliguria (catheterisation is a useful early monitoring intervention).
  • Altered mental state.
  • Potentially correctable underlying causes such as tension pneumothorax, massive PE, occult haemorrhage or hypovolaemia, sepsis, pericardial tamponade, anaphylaxis or respiratory failure should be kept in mind while assessment is carried out.
  • First-line investigations can help to determine the underlying cause of cardiogenic shock.
  • The aim of management is to make the diagnosis, prevent further ischaemia and treat the underlying cause.
  • Assess 'Airway and Breathing':
    • Intubation and mechanical ventilation may be needed; provide oxygen as adequate.
  • 'Circulation':
    • Gain venous access; patients often require central venous access as peripherally shut down - send bloods (see 'Investigations', below).
    • Intravenous fluids: 250 ml boluses should be used if any co-existent depletion of intravascular volume is present.
  • Monitoring:
    • Cardiac monitoring.
    • BP monitoring (usually via an arterial line).
    • Venous pressure monitoring via central venous pressure (CVP).
    • Insertion of a Swan-Ganz catheter (not performed routinely): allows monitoring of CVP and pulmonary capillary wedge pressure. This can guide the need for fluid resuscitation. Haemodynamic monitoring using a Swan-Ganz catheter can help to differentiate cardiogenic shock from other causes of shock such as hypovolaemia. (Arterial line, simple central venous line for CVP monitoring and a PiCCO® line are alternatives to a Swan-Ganz catheter.)
    • Urinary catheter.
  • Investigations:
    • U&Es and creatinine can assess renal function.
    • Urine pregnancy test in women.
    • LFTs.
    • FBC to exclude anaemia.
    • Cardiac enzymes, including troponins.
    • Arterial blood gases.
    • Brain natriuretic peptide (BNP): low BNP levels may help to rule out cardiogenic shock in the setting of hypotension but a high BNP level isn't diagnostic of cardiogenic shock (eg, there may be high BNP levels in PE, atrial fibrillation and sepsis).[5] BNP levels may be more practical in monitoring progression in CCU/ICU.
    • Perform an ECG early: this can show acute MI. ECG may be normal in other causes of cardiogenic shock.
    • CXR: can show tension pneumothorax, widened mediastinum in aortic dissection, signs of left ventricular failure.
    • CT pulmonary angiography (CTPA) or ventilation/perfusion lung scan (also known as V/Q scanning) to look for PE may be appropriate but only once the patient is stabilised (D-dimer is likely to be raised so less useful).
    • Echocardiography: this can establish the cause of cardiogenic shock - eg, acute ventricular septal defect, pericardial tamponade.
  • Consider pharmacological inotropic support (see directly below).
  • Provide symptom relief if needed - eg, opiate analgesia.
  • Treat any electrolyte abnormalities.
  • Treat any arrhythmias.
  • Treat any underlying causes - eg, usual management of acute MI, urgent valve repair.

Pharmacological inotropic support

  • Vasopressor/inotropic medications used include dopamine, dobutamine, enoximone, and milrinone.
  • Although inotropes increase cardiac output, they may also increase mortality due to increased tachycardia and myocardial oxygen consumption leading to arrhythmia and myocardial ischaemia.[6] 
  • There is currently no strong evidence to support a distinct inotropic or vasodilator drug-based therapy as best treatment to reduce mortality in haemodynamically unstable patients with cardiogenic shock or low cardiac output complicating acute MI.[7] 

Intra-aortic balloon pump (IABP) counterpulsation

  • IABP counterpulsation increases cardiac output and improves coronary artery blood flow.
  • Although evidence suggests that IABP may have a beneficial effect on some haemodynamic parameters, there is no strong evidence of survival benefits to support the use of IABP in infarct-related cardiogenic shock.[8] 

Revascularisation

  • Revascularisation with thrombolysis, percutaneous intervention or coronary artery bypass surgery should be considered.
  • The SHOCK trial (= SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK) found that early revascularisation (angioplasty or coronary artery bypass graft) improves one-year survival in patients under the age of 75 with acute MI and cardiogenic shock when compared with medical treatments (including thrombolysis and IABP). This survival advantage seems to persist at three and six years.[9]

See separate Acute Myocardial Infarction Management article.

  • Percutaneous mechanical support can provide substantial haemodynamic improvement in refractory cardiogenic shock.[10] 
  • Ventricular assist devices: these are essentially prosthetic ventricles that can support right and left ventricle performance. They may allow survival to cardiac transplantation. Ventricular assist devices have been shown to be a safe and effective therapy.[11]
  • Non-invasive positive pressure ventilation (NIPPV) may be helpful in mild-to-moderate cases of cardiogenic shock (provided the BP can support it).
  • Moderate hypothermia may improve parameters of cardiac function.[12] 
  • Cardiogenic shock is the leading cause of death in acute MI.
  • Mortality rates are variable but may be as high as 50%.[10] 
  • A recent study showed that, among patients with cardiogenic shock who survive for 30 days after an ST-segment elevation myocardial infarction (MI), annual mortality rates of 2% to 4% are approximately the same as those of patients without shock. Percutaneous revascularisation was associated with a reduced risk of death.[13]
  • Early coronary revascularisation in patients post-MI and adequate treatment of patients with structural heart disease may help to prevent cardiogenic shock.
  • Better treatment of acute coronary syndrome seems to be reducing the rates of cardiogenic shock.[14]

Further reading & references

  1. Acute Management of Myocardial Infarction with ST-Segment Elevation; Editors National Clinical Guideline Centre (UK), 2013.
  2. Ducas J, Grech ED; ABC of interventional cardiology. Percutaneous coronary intervention: cardiogenic shock. BMJ. 2003 Jun 28;326(7404):1450-2.
  3. Szymanski FM, Filipiak KJ; Cardiogenic shock - diagnostic and therapeutic options in the light of new scientific data. Anaesthesiol Intensive Ther. 2014 Sep-Oct;46(4):301-6. doi: 10.5603/AIT.2014.0049.
  4. Casella G, Savonitto S, Chiarella F, et al; Clinical characteristics and outcome of diabetic patients with acute myocardial infarction. Data from the BLITZ-1 study. Ital Heart J. 2005 May;6(5):374-83.
  5. Tung RH, Garcia C, Morss AM, et al; Utility of B-type natriuretic peptide for the evaluation of intensive care unit shock. Crit Care Med. 2004 Aug;32(8):1643-7.
  6. Francis GS, Bartos JA, Adatya S; Inotropes. J Am Coll Cardiol. 2014 May 27;63(20):2069-78. doi: 10.1016/j.jacc.2014.01.016. Epub 2014 Feb 12.
  7. Unverzagt S, Wachsmuth L, Hirsch K, et al; Inotropic agents and vasodilator strategies for acute myocardial infarction complicated by cardiogenic shock or low cardiac output syndrome. Cochrane Database Syst Rev. 2014 Jan 2;1:CD009669. doi: 10.1002/14651858.CD009669.pub2.
  8. Unverzagt S, Buerke M, de Waha A, et al; Intra-aortic balloon pump counterpulsation (IABP) for myocardial infarction complicated by cardiogenic shock. Cochrane Database Syst Rev. 2015 Mar 27;3:CD007398. doi: 10.1002/14651858.CD007398.pub3.
  9. Hochman JS, Sleeper LA, Webb JG, et al; Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction. JAMA. 2006 Jun 7;295(21):2511-5.
  10. Gilani FS, Farooqui S, Doddamani R, et al; Percutaneous Mechanical Support in Cardiogenic Shock: A Review. Clin Med Insights Cardiol. 2015 May 28;9(Suppl 2):23-8. doi: 10.4137/CMC.S19707. eCollection 2015.
  11. Leshnower BG, Gleason TG, O'Hara ML, et al; Safety and efficacy of left ventricular assist device support in postmyocardial infarction cardiogenic shock. Ann Thorac Surg. 2006 Apr;81(4):1365-70; discussion 1370-1.
  12. Schmidt-Schweda S, Ohler A, Post H, et al; Moderate hypothermia for severe cardiogenic shock (COOL Shock Study I & II). Resuscitation. 2013 Mar;84(3):319-25. doi: 10.1016/j.resuscitation.2012.09.034. Epub 2012 Oct 5.
  13. Singh M, White J, Hasdai D, et al; Long-term outcome and its predictors among patients with ST-segment elevation myocardial infarction complicated by shock: insights from the GUSTO-I trial. J Am Coll Cardiol. 2007 Oct 30;50(18):1752-8.
  14. Fox KA, Steg PG, Eagle KA, et al; Decline in rates of death and heart failure in acute coronary syndromes, 1999-2006. JAMA. 2007 May 2;297(17):1892-900.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Michelle Wright
Current Version:
Peer Reviewer:
Dr Hannah Gronow
Document ID:
1912 (v22)
Last Checked:
23/07/2015
Next Review:
21/07/2020

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