ISSN 2398-2977      

Cardiogenic shock

pequis

Synonym(s): Heart failure, Cardiac failure


Introduction

  • Cause: any condition in which the heart cannot pump enough blood to meet cellular demand.
  • Signs: similar to those for other classes of shock, specifically tachycardia with concurrent dysrhythmias or murmurs.
  • Diagnosis: identification of a cardiac condition AND evidence of systemic shock.
  • Treatment: depends on cause of heart dysfunction. In general, treatment goals are to supplement oxygen for heart and other organs, minimize work of the heart by decreasing preload and afterload (decrease intravascular volume and vasodilate, respectively), improving contractility of the heart, correcting underlying dysrhythmia if necessary, and removing excessive pericardial fluid.
  • Prognosis: depends on cause of heart dysfunction, but generally poor to guarded, unless this is due to a tachydysrhythmia or pericarditis, when the prognosis can be good to excellent.

Pathogenesis

Etiology

Predisposing factors

General

  • Progressive valvular disease, usually of the mitral valve.
  • Congenital defects.
  • SIRS and sepsis.

Specific

Pathophysiology

  • Any cardiac disease that decreases contractility will negatively affect stroke volume. A persistent inability to evacuate the heart properly with each stroke can lead to increased afterload and preload, which will further overload the heart and exacerbate the inability to pump enough blood out with each beat. Ultimately the alterations in preload, afterload, and contractility negatively affect cardiac output through diminished stroke volume.
  • Certain dysrhythmias may also lead to similar alterations in cardiac output due to significant tachycardia leading to poor ventricular filling and subsequent diminished stroke volume.
  • Decreases in cardiac output also decrease the delivery of oxygen to tissues leading to tissue dysfunction and ultimately death if prolonged. The result is multiple organ dysfunction syndrome (MODS) followed by death.
  • The body compensates typically responds to cardiovascular shock by increasing cardiac contractility and heart rate, increasing systemic vascular resistance (in an effort to redirect blood to the brain, heart, and kidneys, and away from the skin, muscle, and GI tract), and increasing blood volume through the actions of aldosterone and antidiuretic hormone (ADH).
  • However, in the case of cardiogenic shock, certain mechanisms may not be possible due the heart disease or could even be detrimental due to the increased burden placed on a poorly functioning heart.

Timecourse

  • Minutes to hours: ruptured chordae tendineae, severe congenital abnormalities.
  • Hours to days: pericardial effusion, ventricular or supraventricular tachycardia, congenital cardiac abnormalities.
  • Days to months: congestive heart failure, pericarditis, valvular disease, endocarditis, myocarditis.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Sleeper M M (2017) Equine cardiovascular therapeutics. Vet Clin North Am Equine Pract 33 (1), 163-179 PubMed.
  • Marr C M (2016) Cardiac and respiratory disease in aged horses. Vet Clin North Am Equine Pract 32 (2), 283-300 PubMed.
  • Schwarzwald C (2016) Heart disease in sports horses: Current recommendations of the 2014 ACVIM/ECEIM consensus statement. Schweiz Arch Tierheilkd 158 (10), 677-689 PubMed.

Other sources of information

  • Durando M & Corley K (2008) Monitoring and Treating the Cardiovascular System. In: The Equine Hospital Manual. Eds: Corley K & Stephen J. Wiley-Blackwell, UK. pp 417-456.

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