critical care medicine
Shock
Etiology and Classification of Shock
There are several mechanisms of organ hypoperfusion and shock. Shock may be due to A low circulating volume (hypovolemic shock) Vasodilation (distributive shock) A primary decrease in cardiac output (both cardiogenic and obstructive shock) A combination Hypovolemic shock is caused by a critical decrease in intravascular volume. Diminished venous return (preload) results in decreased ventricular filling and reduced stroke volume. Unless compensated for by increased heart rate, cardiac output decreases. A common cause is bleeding (hemorrhagic shock), typically due to trauma, surgical interventions, peptic ulcer, esophageal varices, or ruptured aortic aneurysm. Bleeding may be overt (eg, hematemesis, melena) or concealed (eg, ruptured ectopic pregnancy). Hypovolemic shock may also follow increased losses of body fluids other than blood (see table Hypovolemic Shock Caused by Body Fluid Loss ). Site of Fluid Loss Site of Fluid Loss Mechanism of Loss Mechanism of Loss Skin Thermal or chemical Burns None Sweating due to excessive Overview of Heat Illness None Gastrointestinal tract Nausea and Vomiting , Kidneys Adrenal insufficiency Diabetes Mellitus (DM) , Polyuric phase after acute tubular damage Potent diuretic use Salt-losing nephritis Intravascular fluid lost to the extravascular space Increased capillary permeability secondary to inflammation, severe systemic hypoxia or ischemia, or traumatic injury (eg, crush), sepsis, bowel ischemia, acute pancreatitis Hypovolemic shock may be due to inadequate fluid intake (with or without increased fluid loss). Water may be unavailable, neurologic disability may impair the thirst mechanism, or physical disability may impair access. In hospitalized patients, hypovolemia can be compounded if early signs of circulatory insufficiency are incorrectly ascribed to heart failure and fluids are withheld or diuretics are given. Distributive shock results from a relative inadequacy of intravascular volume caused by arterial or venous vasodilation; circulating blood volume is normal. In some cases, cardiac output (and DO2) is high, but increased blood flow through arteriovenous shunts bypasses capillary beds; this bypass plus uncoupled cellular oxygen transport cause cellular hypoperfusion (shown by decreased oxygen consumption). In other situations, blood pools in venous capacitance beds and cardiac output falls. Distributive shock may be caused by Anaphylaxis (anaphylactic shock) Bacterial infection with endotoxin release ( Sepsis and Septic Shock ) or exotoxin release ( Severe injury to the spinal cord, usually above T4 (neurogenic shock) Ingestion of certain drugs or poisons, such as nitrates, opioids, and adrenergic blockers Anaphylactic shock and septic shock often have a component of hypovolemia as well. Hypotension and Cardiogenic Shock is a relative or absolute reduction in cardiac output due to a primary cardiac disorder. Obstructive shock is caused by mechanical factors that interfere with filling or emptying of the heart or great vessels. Causes are listed in the table Type Type Mechanism Mechanism Cause Cause Obstructive Mechanical interference with ventricular filling Pneumothorax (Tension) , cava compression, Interference with ventricular emptying Pulmonary Embolism (PE) None Cardiogenic Impaired myocardial contractility Myocardial ischemia or Acute Myocardial Infarction (MI) , Abnormalities of cardiac rhythm Tachycardia, bradycardia Cardiac structural disorder Acute Mitral Regurgitation or 