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Shock: cardiogenic


Synonym(s): Cardiogenic shock


  • Inadequate cellular metabolism secondary to cardiac dysfunction when there is adequate intravascular volume.
  • In some cases, the patient already has a disorder that has been previously diagnosed but some factor has caused an acute exacerbation of cardiac function, eg valvular endocardiosis with acute rupture of the chordae tendinae Heart: rupture of chordae tendinae , right atrial or heart base mass that has acutely bled causing pericardial tamponade or left atrial rupture.
  • In other cases, clinical condition may have not been previously diagnosed and clinical signs may be slow and gradual in onset, ie cough associated with left atrial enlargement, gradual decrease in exercise tolerance associated with dilative cardiomyopathy Heart: dilated cardiomyopathy (DCM) or dysrhythmias Heart: dysrhythmia , gradual development of cachexia and ascites seen with caval syndrome Caval Syndrome secondary to heartworm disease Cardiopulmonary dirofilariasis.
  • Cardiac dysfunction may occur secondary to other, indirectly related diseases such as reduced contractility due to high levels of inflammatory cytokines or dysrhythmias induced by electrolyte abnormalities.
  • Heart failure can be classified as:
    • Forward: left ventricular failure secondary to reduced forward flow into the systemic circulation; right ventricular failure secondary to reduced forward flow into the pulmonary circulation.
    • Backward (congestive): secondary to elevated venous pressures, usually secondary to increase in preload and will cause pulmonary edema with left sided failure and tissue bed edema/body cavity fluid accumulation with right sided failure.
Print off the owner factsheet Shock - how to recognise the signs to give to your client.



  • Clinical signs of cardiogenic shock associated with forward or backward failure.
  • Degree of severity depends on underlying cause and patients ability to compensate.



  • Associated with decreased cardiac output.
  • Primary determinants of cardiac output (CO) are heart rate and stroke volume.
  • Factors that influence stroke volume, or amount of blood expelled from left ventricle in one heartbeat, include:
    • Preload (filling of the chamber during relaxation).
    • Afterload (the 'load' on the arterial side that the heart has to push against).
    • Contractility (the strength/co-ordination of muscle contraction in the heart wall).
  • Knowledge of factors that influence cardiac output necessary to develop a multimodal plan for treatment.
  • Myocardial or pump failure causes decrease in contractile function of ventricle.
  • Body activates compensatory mechanisms to maintain cardiac output in the face of declining myocardial function.
  • Activation of renin-angiotensin-aldosterone axis increases cardiac preload by conserving sodium and water to further fill vasculature.
  • Causes increase in the stretch of the heart by increasing volume, resulting in an increase in contractility.
  • Also baroreceptors in the aortic arch and carotid body sense a decline in blood pressure associated with low cardiac output and neurohumoral mechanisms decrease vagal tone and allow a sympathetic mediated increase in heart rate.
  • Over time, increases in heart rate <150/160 beats/min are detrimental, as stroke volume decreases with an increasing heart rate, as does blood flow into the myocardium.
  • Additionally, as myocardial contractile function declines, the increase in circulating volume that originally served to increase preload and contractility eventually overwhelms left ventricular capacity, resulting in development of pulmonary edema Lung: pulmonary edema.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Côté E (2001) Cardiogenic shock and cardiac arrest. Vet Clin North Amer Sm Anim 31 (6), 1129-1145 PubMed.
  • Beardow A W (2000) The diagnostic and therapeutic approach to the patient in acute congestive heart failure. Clin Tech Sm Anim Pract 15 (2), 70-75 PubMed.
  • Bristow M R (2000) Beta-adrenergic receptor blockade in chronic heart failure. Circulation 101 (5), 558-569 PubMed.
  • Mann D G (1999) Mechanisms and models in heart failure: a combinatorial approach. Circulation 100 (9), 999-1008 PubMed.
  • Muir W W (1998) Shock. Comp Contin Educ Pract Vet 20 (5), 549-565 PubMed.

Other sources of information

  • Brown A J & Mandell D C (2015) Cardiogenic shock. In: Small Animal Critical Care Medicine. 2nd edn. Elsevier, Philadelphia. pp 210-213.

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