NURS 4540 Module 8 – Shock Study Guide (Part 1)

Vocabulary flashcards covering key terms and concepts related to the pathophysiology, stages, assessment, and management of shock from NURS 4540 Module 8.

Shock

Life-threatening disorder of inadequate tissue perfusion that causes cellular hypoxia and altered metabolism.

Hypovolemic Shock

Shock caused by loss of circulating blood or fluid volume; the classic “fluid problem.”

Cardiogenic Shock

Shock produced by failure of the heart to pump effectively; the “pump problem.”

Distributive Shock

Shock in which excessive vasodilation causes relative hypovolemia and maldistribution of blood flow; the “pipes problem.”

Multiple Organ Dysfunction Syndrome (MODS)

Progressive failure of two or more organ systems following severe illness or shock.

Aerobic Metabolism

Oxygen-dependent energy pathway that yields ~38 ATP per glucose molecule.

Anaerobic Metabolism

Energy pathway used when oxygen is lacking; yields only 2 ATP per glucose and produces lactic acid.

Lactic Acid

Toxic by-product of anaerobic metabolism that leads to metabolic acidosis when elevated.

ATP (Adenosine Triphosphate)

Primary cellular energy molecule; depletion impairs essential cell functions.

Sodium–Potassium (Na⁺/K⁺) Pump

Membrane transport system that moves Na⁺ out and K⁺ in; failure causes Na⁺/water influx, cell swelling, and K⁺ loss.

Cellular Edema

Swelling of the cell caused by water following sodium into the cytoplasm after Na⁺/K⁺ pump failure.

Chemical Mediators

Inflammatory substances (e.g., histamine) released from injured cells that increase vascular permeability.

Histamine

Key inflammatory mediator that produces vasodilation and capillary leak, worsening edema in shock.

Initial Stage of Shock

Earliest phase with decreased cardiac output and cellular hypoperfusion; clinical signs are minimal.

Compensatory Stage of Shock

Stage where neural, hormonal, and chemical mechanisms attempt to maintain perfusion (e.g., SNS activation).

Progressive Stage of Shock

Phase in which compensatory mechanisms fail, leading to widespread hypoxia, massive edema, and organ dysfunction.

Refractory Stage of Shock

Irreversible phase marked by profound cell death and unresponsive MODS; death is imminent.

Baroreceptor Stimulation

Reflex triggered by hypotension that activates the sympathetic nervous system to raise BP.

Epinephrine

Adrenal catecholamine that increases heart rate and causes vasoconstriction during shock compensation.

Norepinephrine

Potent vasoconstrictor catecholamine released during SNS activation or given as a vasopressor.

Renin–Angiotensin–Aldosterone System (RAAS)

Hormonal cascade causing vasoconstriction and sodium/water retention to restore blood pressure.

Antidiuretic Hormone (ADH)

Posterior pituitary hormone that promotes renal water reabsorption, reducing urine output.

Chemoreceptor Stimulation

Response to acidosis/hypoxemia that increases respiratory drive to blow off CO₂.

Hyperventilation

Rapid, deep breathing that lowers PaCO₂ to compensate for metabolic acidosis.

Adrenocorticotropic Hormone (ACTH)

Pituitary hormone that stimulates glucocorticoid release, raising blood glucose for energy.

Hyperlactatemia

Elevated serum lactate indicating anaerobic metabolism and global tissue hypoxia.

Low Serum Bicarbonate

Reduction in HCO₃⁻ as it buffers excess acids; laboratory marker of metabolic acidosis in shock.

Mixed Venous Oxygen Saturation (SvO₂)

Percentage of oxygen remaining in venous blood; reflects the balance of oxygen delivery and consumption.

Mean Arterial Pressure (MAP)

Average arterial pressure; values < 60 mmHg signal global tissue hypoperfusion (shock state).

Vasopressor

Medication (e.g., norepinephrine, dopamine) that produces vasoconstriction to raise blood pressure after fluid resuscitation.

Inotrope

Drug that increases myocardial contractility (e.g., dobutamine) to improve cardiac output.

Third-Spacing

Leakage of fluid and protein from the intravascular space into interstitial tissues due to increased capillary permeability.

Oliguria

Urine output < 400 mL/24 h reflecting decreased renal perfusion.

Anuria

Complete absence of urine output, often indicating acute kidney injury in late shock.

Deep Vein Thrombosis (DVT) Prophylaxis

Interventions (anticoagulants, compression devices) to prevent venous thromboembolism in immobile patients.

Stress Ulcer Prophylaxis

Use of PPIs/H₂ blockers to prevent gastric mucosal injury caused by hypoperfusion and stress.

Skin Care in Shock

Nursing actions to prevent pressure injuries in poorly perfused, fragile tissue.

Infection Control

Strict aseptic measures to protect shock patients who are highly susceptible to infection.

Nutrition Support

Early enteral/parenteral feeding (within 24–48 h) to prevent catabolism and support immunity.

Glucose Control

Maintaining blood glucose < 180 mg/dL because hyperglycemia impairs immune function and wound healing.