Shock is circulatory insufficiency that creates an imbalance between tissue oxygen supply (delivery) and oxygen demand (consumption). Such tissue hypoperfusion is associated with decreased venous oxygen content and metabolic acidosis (lactic acidosis). Shock is classified into four categories based on etiology: (a) hypovolemic, (b) cardiogenic, (c) distributive (e.g., neurogenic and anaphylactic), and (d) obstructive.
Factors that influence the clinical presentation of a patient in shock include the etiology, duration, and severity of the shock state and the underlying medical status of the patient. Often the precipitating cause of shock may be readily apparent (e.g., acute myocardial infarction, trauma, gastrointestinal [GI] bleeding, or anaphylaxis). It is not uncommon for the patient to present with nonspecific symptoms (e.g., generalized weakness, lethargy, or altered mental status). A targeted history of the presenting symptoms and previously existing conditions (e.g., cardiovascular disease, GI bleeding, adrenal insufficiency, or diabetes) will aid in identifying the cause and guide the initial treatment of shock. Drug use (prescribed and nonprescribed) is an essential element of the initial history. Medication use may be the cause or a contributing factor to the evolution of shock. For example, diuretics can lead to volume depletion and cardiovascular medications (e.g., β-blockers) can depress the pumping action of the heart. The possibility of drug toxicity and anaphylactic reactions to medications also should be considered.
Assessment of vital signs is a routine part of the physical examination; however, no single vital sign or value is diagnostic in the evaluation of the presence or absence of shock. The presence of hyperthermia or hypothermia may be a result of endogenous factors (e.g., infections or hypometabolic states) or exogenous causes (e.g., environmental exposures). The heart rate is typically elevated; however, bradycardia may be present with many conditions, such as excellent baseline physiologic status (young athletes), intraabdominal hemorrhage (secondary to vagal stimulation), cardiovascular medication use (e.g., β-blockers and digoxin), hypoglycemia, and preexisting cardiovascular disease.
The respiratory rate is frequently elevated early in shock. Increased minute ventilation, increased dead space, bronchospasm, and hypocapnia may be seen. As shock progresses, hypoventilation, respiratory failure, and respiratory distress syndrome may occur.
Shock is usually, but not always, associated with systemic arterial hypotension, defined as a systolic blood pressure (BP) below 90 mm Hg. The insensitivity of blood pressure to detect global tissue hypoperfusion has been repeatedly confirmed. Thus, shock may occur with a normal blood pressure, and hypotension may occur without shock. Early in shock, the systolic and diastolic BPs may initially be normal or elevated in response to a compensatory mechanism such as tachycardia and vasoconstriction. As the body’s compensatory mechanisms fail, BP typically falls. Postural changes in BP, commonly seen with hypovolemic states, will precede overt hypotension. The pulse pressure, the difference between systolic and diastolic BP measurements, may be a more sensitive indicator. The pulse pressure usually rises early in shock and then ...