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The pathophysiology of shock ∗
Author(s) -
Skowronski George A.,
Shaw Editorial Advisory Panel John,
Brooks Peter M.,
McNeil John J.,
Moulds Robert F.W.,
Ravenscroft Peter J.,
Smith Anthony J.
Publication year - 1988
Publication title -
medical journal of australia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 131
eISSN - 1326-5377
pISSN - 0025-729X
DOI - 10.5694/j.1326-5377.1988.tb93816.x
Subject(s) - shock (circulatory) , inotrope , medicine , cardiogenic shock , septic shock , contractility , circulatory collapse , preload , afterload , sepsis , anesthesia , hemodynamics , myocardial infarction
Shock describes a group of circulatory syndromes, all of which result in generalized cellular hypoxia. This leads to the depletion of adenosine triphosphate, the failure of the sodium–potassium pump, mitochondrial dysfunction, and ultimately, the release of a variety of toxic substances. Eventually these give rise to irreversible cardiovascular collapse because of their effects on the microcirculation. Shock may arise due to a failure of preload (hypovolaemic shock), myocardial contractility (cardiogenic shock), afterload (septic shock) or combinations of these (for example, anaphylactic shock, traumatic shock and neurogenic shock). During shock, important physiological changes occur in the nervous, respiratory, renal and gastrointestinal systems, as well as in intermediary metabolism. Hypotension is not synonymous with shock, and emphasis should be placed on the detection of more subtle, early signs. Management requires a systematic approach in which diagnostic and therapeutic processes take place in parallel. Particular attention must be paid to ventilation, oxygenation, fluid and electrolyte therapy, haemodynamic monitoring and, where appropriate, inotropic drugs. Corticosteroid and opioid antagonist agents probably do not have a role, but other agents, such as thyroid hormones, are under investigation. (Med J Aust 1988; 148: 576‐583)