Shock

Any severe disease may progress to global hypoperfusion and shock. The most common causes of shock are grouped according to their pathologic mechanism:

• Cardiogenic (pump dysfunction): this may occur after myocardial infarction, due to cardiomyopathy, valvular abnormalities, or arrhythmias.[3]McDonagh TA, Metra M, Adamo M, et al. 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021 Sep 21;42(36):3599-726. https://academic.oup.com/eurheartj/article/42/36/3599/6358045 http://www.ncbi.nlm.nih.gov/pubmed/34447992?tool=bestpractice.com [15]Chioncel O, Parissis J, Mebazaa A, et al. Epidemiology, pathophysiology and contemporary management of cardiogenic shock - a position statement from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2020 Aug;22(8):1315-41. https://onlinelibrary.wiley.com/doi/10.1002/ejhf.1922 http://www.ncbi.nlm.nih.gov/pubmed/32469155?tool=bestpractice.com

• Hypovolemic (loss of intravascular volume): due to hemorrhage (trauma, gastrointestinal), third space losses, burns, heat stress, or gastrointestinal losses.[19]Rossaint R, Bouillon B, Cerny V, et al. The European guideline on management of major bleeding and coagulopathy following trauma: fourth edition. Crit Care. 2016 Apr 12;20:100. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4828865 http://www.ncbi.nlm.nih.gov/pubmed/27072503?tool=bestpractice.com [20]Cannon JW. Hemorrhagic shock. N Engl J Med. 2018 Jan 25;378(4):370-9. http://www.ncbi.nlm.nih.gov/pubmed/29365303?tool=bestpractice.com

• Distributive (failure of vasoregulation): sepsis, anaphylaxis, poisoning, injury of the brainstem or spine (neurogenic) or endocrine disease (adrenal, hypothyroid, or hypopituitarism).

• Obstructive shock (barriers to cardiac flow or filling): a pulmonary embolus may restrict pulmonary blood flow; cardiac tamponade and tension pneumothorax cause cardiac filling restriction.

Hypoperfusion is a lack of adequate oxygen delivery at a cellular level, due to decreased blood flow and oxygen delivery, or increased tissue oxygen demand without a homeostatic increase in blood flow to supply the required oxygen for organ tissue. When blood flow supply cannot meet demand, hypoperfusion results. Low oxygen delivery from poor blood flow or low blood oxygen saturation impairs basic metabolic functions of cells and organs.

Hypoperfusion triggers a systemic stress response, including tachycardia and peripheral vasoconstriction. Once physiologic compensation mechanisms are overwhelmed, organ dysfunction ensues, followed by organ failure, irreversible organ damage, and death.

In septic shock, pathologic peripheral vasodilation caused by the septic state may result in a relative loss of perfusion pressure due to loss of systemic vascular resistance (vascular regulation). This leads to secondary coronary ischemia and cardiac dysfunction. The resulting vascular and cardiac impairment may contribute to the progression of shock.

In cardiogenic shock, tissue hypoperfusion resulting from loss of cardiac output induces tissue (cellular) inflammation.[21]Geppert A, Steiner A, Zorn G, et al. Multiple organ failure in patients with cardiogenic shock is associated with high plasma levels of interleukin-6. Crit Care Med. 2002 Sep;30(9):1987-94. http://www.ncbi.nlm.nih.gov/pubmed/12352031?tool=bestpractice.com Shock may self-perpetuate by inducing additional cellular-level shock response such as cell-toxic cytokines, which results in systemic inflammatory response syndrome.

Low blood pressure is an indirect, imprecise measure of perfusion. This is illustrated by decreased cellular oxygen delivery in hypertensive crisis, where high arterial resistance actually reduces cardiac output and perfusion. Tissue hypoxia may be present without low blood pressure.[1]Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med. 2014 Dec;40(12):1795-815. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239778 http://www.ncbi.nlm.nih.gov/pubmed/25392034?tool=bestpractice.com

Pathologic mechanism

Shock is most commonly classified by cause.

• Cardiogenic (pump dysfunction): may occur after myocardial infarction, due to cardiomyopathy, arrhythmia, or cardiac valve pathology.[4]Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2022 May 3;79(17):e263-421. https://www.doi.org/10.1016/j.jacc.2021.12.012 http://www.ncbi.nlm.nih.gov/pubmed/35379503?tool=bestpractice.com

• Hypovolemic (loss of intravascular volume): due to hemorrhage, dehydration, gastrointestinal or third space losses.

• Distributive (failure of vasoregulation): results in a fall in systemic vascular resistance with vasodilation and, classically, warm peripheries, as occurs in sepsis and anaphylaxis.

• Obstructive (barriers to cardiac flow or filling): a pulmonary embolus may restrict flow; cardiac tamponade and tension pneumothorax cause a cardiac filling restriction.