Evaluation of shock

Diseases

Summary

Shock is best defined as a state of reduced end-organ oxygenation caused by an imbalance between tissue oxygen delivery and demand resulting in an oxygen debt.

Oxygen delivery is determined by cardiac output, vascular integrity, and oxygen content of the blood. Oxygen content is a composite of hemoglobin and arterial oxygen saturation, and the cardiac output is a product of stroke volume and heart rate. Stroke volume is affected by preload (filling), left ventricular contractility (pump function), and afterload as measured by the systemic vascular resistance.

Differences in the preload, afterload, and contractility generally differentiate the etiologies of shock. These are broadly classified into hypovolemic, cardiogenic, obstructive, and distributive types.[1]

Basic pathophysiology

Whatever the etiology, shock is characterized by release of cytokines and other inflammatory mediators that cause a systemic inflammatory response syndrome mediated by tissue hypoxia. This causes alterations in flow at the level of the microcirculation that can usually be reversed by intravascular volume resuscitation and, as appropriate, vasopressor and inotropic support.[2] [3] [4]

Outcome

Shock passes through an early reversible stage of compensated shock where the body's homeostatic mechanisms compensate for decreased perfusion by increasing the rate and force of contraction of the heart, initially maintaining arterial blood pressure. The circulation is centralized, due to peripheral vasoconstriction, so that blood flow to non-vital organs (commonly skin) is reduced. Respiratory rate increases to compensate for metabolic acidosis and urine output falls (to conserve fluid volume) as a result of release of antidiuretic hormone from the posterior pituitary. These adaptive responses may not be apparent to the casual observer. Unrecognized, this evolves to overt shock manifested by decreased blood pressure and altered mental status attributable to reduced cerebral blood flow. This usually occurs in the setting of an effective loss ≥30% of plasma volume and/or cardiac index of <2.2 L/minute/m². Untreated at this stage, it can cause irreversible cell death and organ damage.

The lack of tissue oxygenation leads to accumulation of products of anaerobic metabolism such as lactate. Significant tissue hypoxia leads to a systemic proinflammatory state with excess cytokine release; when prolonged (>6 to 12 hours) this causes irreversible cellular damage. This is clinically manifest as multiorgan dysfunction/failure with increased mortality.

Mortality from shock varies between 23% and 70%, depending on the type of shock and the duration of tissue hypoperfusion.[5] [6] [7]

Library

Sequential (or Sepsis-related) Organ Failure Assessment (SOFA) criteria
Parameters to differentiate between types of shock and examples

Citations

Key Articles

van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: a scientific statement from the American Heart Association. Circulation. 2017 Oct 17;136(16):e232-68.[Abstract][Full Text]
Shaker MS, Wallace DV, Golden DBK, et al. Anaphylaxis-a 2020 practice parameter update, systematic review, and Grading of Recommendations, Assessment, Development and Evaluation (GRADE) analysis. J Allergy Clin Immunol. 2020 Apr;145(4):1082-123.[Abstract][Full Text]
Campbell RL, Li JT, Nicklas RA, et al. Emergency department diagnosis and treatment of anaphylaxis: a practice parameter. Ann Allergy Asthma Immunol. 2014 Dec;113(6):599-608.[Abstract][Full Text]
Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International guidelines for management of sepsis and septic shock 2021. Crit Care Med. 2021 Nov 1;49(11):e1063-143.[Abstract][Full Text]
Seymour CW, Liu VX, Iwashyna TJ, et al. Assessment of clinical criteria for sepsis: for the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):762-74.[Abstract]

Referenced Articles

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