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 haemoglobin 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 aetiologies of shock. These are broadly classified into hypovolaemic, cardiogenic, obstructive, and distributive types.
Whatever the aetiology, shock is characterised 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.
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 centralised, 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. Unrecognised, this evolves to overt shock manifested by decreased BP 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 pro-inflammatory state with excess cytokine release; when prolonged ( >6 to 12 hours) this causes irreversible cellular damage. This is clinically manifest as multi-organ dysfunction and/or failure with increased mortality.
- Myocardial infarction
- Heart failure
- Beta-blocker and other drug-related toxicity
- Haemorrhage, external or internal from any site
- Trauma with external or internal haemorrhage
- Gastrointestinal fluid losses
- Intestinal obstruction with fluid third spacing
- Pancreatitis with fluid third spacing or haemorrhage
- Excessive renal loss
- Pulmonary embolism
- Septic shock
- Poisoning and adverse drug reaction
Samuel J. Stratton, MD, MPH
Fielding School of Public Health
The David Geffen School of Medicine
University of California
SJS declares that he has no competing interests.
Dr Samuel J. Stratton would like to gratefully acknowledge Dr Patrick Nee, Dr Joseph C. Farmer, and Dr Srikanth Hosur, the previous contributors to this topic. PN, JCF, and SH declare that they have no competing interests.
Armand Mekontso Dessap, MD, PhD
Medical Intensive Care Unit
Henri Mondor Hospital
AMD declares that he has no competing interests.
Ethan Cumbler, MD
Department of Internal Medicine
University of Colorado Health Sciences Center
EC declares that he has no competing interests.
Haibo Wang, MD, PhD
LSU Health Sciences Center
HW declares that he has no competing interests.
Karim Bendjelid, MD, PhD
Médecin Adjoint Agrégé
Intensive Care Division
Geneva University Hospitals
KB declares that he has no competing interests.
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