Pathophysiology – Shock

Vocabulary flashcards covering core terms and definitions related to the pathophysiology, types, mechanisms, clinical features, and complications of shock.

Shock

A medical emergency marked by inadequate tissue perfusion and an imbalance between cellular oxygen supply and demand.

Cardiogenic Shock

Shock caused by severe ventricular dysfunction that prevents effective cardiac pumping, often after myocardial infarction.

Obstructive Shock

Shock resulting from a mechanical blockage that prevents the heart from filling or ejecting blood, e.g., pulmonary embolism, cardiac tamponade.

Hypovolemic Shock

Shock due to inadequate circulating blood volume from hemorrhage, burns, or dehydration.

Distributive Shock

Shock characterized by loss of vascular tone causing peripheral pooling of blood; includes anaphylactic, neurogenic, and septic shock.

Impaired Tissue Oxygenation

Common consequence of all shock types in which low oxygen availability forces cells into anaerobic metabolism.

Compensatory Stage of Shock

Early phase where homeostatic mechanisms (SNS activation, vasoconstriction) maintain blood pressure despite falling cardiac output.

Progressive Stage of Shock

Phase where compensatory mechanisms fail, causing hypotension, tissue hypoxia, lactate buildup, and metabolic acidosis.

Refractory (Irreversible) Stage

Final stage of shock marked by widespread cellular death and organ failure unresponsive to therapy.

Sympathetic Nervous System (SNS) Activation

Physiologic response during early shock producing tachycardia, vasoconstriction, bronchodilation, and cool clammy skin.

Oxygen Free Radicals

Reactive molecules formed during oxygen deprivation that contribute to cellular injury in shock.

Inflammatory Cytokines

Mediators such as TNF-α and IL-1 released during shock that promote vasodilation and capillary leakage.

Lactic Acidosis

Metabolic acidosis produced when cells rely on anaerobic glycolysis during hypoxia.

Cardiogenic Shock Manifestations

Decreased cardiac output, elevated LV end-diastolic pressure, pulmonary edema, S3 heart sound, narrow pulse pressure.

Inotropic Agents

Medications that increase myocardial contractility to improve cardiac output in cardiogenic shock.

Afterload-Reducing Agents

Drugs (e.g., vasodilators) that lower systemic vascular resistance to ease ventricular ejection.

Preload-Reducing Agents

Therapies (e.g., diuretics, nitrates) that decrease ventricular filling pressures in cardiogenic shock.

Mechanical Assist Devices

Devices like Impella, ECMO, or ventricular assist devices that support cardiac output mechanically.

Baroreceptors

Pressure sensors in the aorta and carotids that trigger SNS responses when arterial pressure falls.

β1 Receptors

Cardiac adrenergic receptors whose stimulation raises heart rate and contractility during shock.

Pulmonary Embolism

A blockage of pulmonary arteries; a common cause of obstructive shock.

Tension Pneumothorax

Air accumulation under pressure in the pleural space causing mediastinal shift and obstructive shock.

Cardiac Tamponade

Compression of the heart by pericardial fluid, impeding filling and causing obstructive shock.

American College of Surgeons Classification

System dividing hemorrhagic shock into Classes I–IV based on blood-loss volume and clinical features.

Anaphylactic Shock

Distributive shock from excessive mast-cell degranulation following allergen exposure.

Neurogenic Shock

Shock due to loss of sympathetic tone, often after spinal or brain trauma.

Septic Shock

Distributive shock from severe systemic infection leading to profound vasodilation and hypotension.

Disseminated Intravascular Coagulation (DIC)

Complication of septic shock marked by widespread microvascular clotting and bleeding.

Sepsis

Systemic inflammatory response syndrome caused by bloodstream infection (bacteremia).

Systemic Inflammatory Response Syndrome (SIRS)

Body-wide inflammatory reaction to infection or injury, characterized by fever, tachycardia, tachypnea, and leukocytosis.

Nitric Oxide

Potent vasodilator overproduced in septic shock, contributing to peripheral pooling and hypotension.

Hemodynamic Monitoring

Use of invasive or non-invasive devices to measure cardiac output, preload, afterload, and oxygen delivery.

Cardiac Output (CO)

Volume of blood the heart pumps per minute; key determinant of tissue oxygenation.

Multiple Organ Dysfunction Syndrome (MODS)

Progressive dysfunction of two or more organ systems following severe shock or injury.

Acute Respiratory Distress Syndrome (ARDS)

Severe pulmonary complication of shock featuring non-cardiogenic pulmonary edema and hypoxemia.

Bicarbonate Buffer System

Primary extracellular buffer converting CO₂ and water to carbonic acid and bicarbonate to regulate pH.