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Comprehensive practice flashcards covering the etiology, pathophysiology, clinical manifestations, risk factors, and pharmacologic management of cardiogenic and noncardiogenic pulmonary edema.
Pulmonary edema
A restrictive pulmonary condition characterized by the abnormal accumulation of fluid in the extravascular, interstitial, and alveolar spaces of the lungs.
Restrictive pulmonary disorder
The pulmonary functional classification produced by pulmonary edema, characterized by restricted lung expansion and decreased lung compliance.
Interstitial edema
The pathologic fluid engorgement of the perivascular, peribronchial spaces, and alveolar wall interstitium that occurs early in pulmonary edema.
Alveolar flooding
The movement and spillover of edema fluid into the alveolar air spaces once the interstitial holding capacity is exceeded.
Alveolar surface tension
The inward pulling force at the air-liquid interface of the alveoli that increases as fluid swelling intensifies, predisposing alveoli to collapse.
Atelectasis
Alveolar shrinkage and collapse resulting from severe alveolar swelling and increased surface tension of alveolar fluids.
Frothy white or pink sputum
The characteristic tracheobronchial secretion formed when accumulated edema fluid is churned with air moving in and out of the lungs, often tinged with blood.
Cardiogenic pulmonary edema
Pulmonary edema resulting from elevated hydrostatic pressure in the pulmonary vasculature due to cardiac dysfunction, most frequently left ventricular failure.
Congestive heart failure (CHF)
Left-sided heart failure occurring when the left ventricle cannot pump an adequate amount of blood during ventricular contraction, representing the primary cause of cardiogenic pulmonary edema.
Left ventricular ejection fraction (LVEF)
A clinical diagnostic measurement used to assess the left ventricle's contractility and pumping effectiveness during each heartbeat.
Echocardiogram
An ultrasound imaging procedure used in pulmonary edema to examine cardiac structure, chamber dimensions, valve integrity, and left ventricular performance.
Coronary artery disease (CAD)
A condition involving plaque buildup and narrowing of the coronary arteries that compromises myocardial blood flow, serving as a primary etiology of cardiogenic pulmonary edema.
Cardiomyopathy
A disease of the heart muscle (such as viral cardiomyopathy) that impairs ventricular pumping ability and causes cardiogenic pulmonary edema.
Cardiac tamponade
An etiology of cardiogenic pulmonary edema characterized by compression of the heart due to pericardial fluid accumulation, preventing normal ventricular filling.
Rheumatic heart disease
An inflammatory condition of the heart, often presenting as myocarditis or valvular damage, identified as an etiology of cardiogenic pulmonary edema.
Age risk criteria for coronary heart disease
Demographic risk factors for coronary heart disease defined as males older than 45 years old and females older than 55 years old.
Family history risk criteria for CHD
A genetic risk factor defined as having a male relative with coronary heart disease diagnosed at <55 years old or a female relative diagnosed at <65 years old.
Hypertension (CHD risk factor)
A clinical cardiovascular risk factor defined as blood pressure >140/90mm Hg or being actively maintained on antihypertensive agents.
Low-density-lipoprotein cholesterol (LDL-C) threshold
The bad cholesterol threshold defined as a serum level >130mg/dL, indicating high risk for coronary heart disease.
High-density-lipoprotein cholesterol (HDL-C) threshold
The good cholesterol threshold defined as a serum level <35mg/dL, which confers increased risk for coronary heart disease.
Homocysteine risk threshold
An elevated serum amino acid level defined as >10mg/dL, functioning as an independent risk factor for coronary heart disease.
Serum lipid thresholds for CHD risk
Cardiovascular risk thresholds defined by total cholesterol levels >150 to 200mg/dL and triglyceride levels >200 to 300mg/dL.
Noncardiogenic pulmonary edema
Pulmonary edema occurring without elevated left-sided cardiac filling pressures, wherein fluid flows readily from the pulmonary capillaries into the alveoli due to altered vascular properties.
Increased capillary permeability
A major noncardiogenic mechanism where damage to the alveolar-capillary membrane from infectious, inflammatory, or toxic causes allows fluid to leak into the lung parenchyma.
Acute respiratory distress syndrome (ARDS)
A life-threatening condition causing widespread inflammation and dramatically increased pulmonary capillary permeability, leading to severe noncardiogenic pulmonary edema.
Toxic agent inhalation
The inhalation of harmful gases—including chlorine, sulfur dioxide, nitrogen dioxides, ammonia, and phosgene—that causes chemical injury and increased capillary permeability.
Cephalogenic pulmonary edema
A form of noncardiogenic pulmonary edema resulting from acute head injury or acute central nervous system trauma.
Lymphatic insufficiency
A mechanism of pulmonary edema in which decreased, obliterated, or distorted lymphatic drainage causes intravascular and extravascular fluid to pool in the lungs.
Lymphangitic carcinomatosis
A malignant condition where tumor cells obstruct the pulmonary lymphatic vessels, severely impairing lymph drainage and causing pulmonary edema.
Decreased intrapleural pressure
A noncardiogenic mechanism where extreme negative inspiratory pressures during severe airway obstruction exert a suction effect on pulmonary capillaries, pulling fluid into the alveoli.
Decompression pulmonary edema
A form of noncardiogenic pulmonary edema triggered by the sudden, rapid removal of a large volume of pleural effusion.
Normal oncotic pressure
The colloidal osmotic pressure exerted by blood proteins that normally measures 25 to 30mm Hg, maintaining fluid within the vascular compartment.
Normal hydrostatic pressure
The outward filtration pressure exerted by fluid against capillary walls, normally measuring 10 to 15mm Hg in the pulmonary microvasculature.
Decreased oncotic pressure mechanism
A rare cause of pulmonary edema occurring when oncotic pressure drops below the normal capillary hydrostatic pressure of 10 to 15mm Hg, causing fluid seepage into air spaces.
Hypoproteinemia
A marked deficiency of plasma proteins (e.g., caused by severe malnutrition) that lowers vascular oncotic pressure and promotes fluid movement into the lungs.
Uremia
A buildup of waste products in the blood associated with renal dysfunction that contributes to decreased oncotic pressure and pulmonary edema.
Acute nephritis
An acute inflammatory kidney disease that impairs protein regulation, cited as an etiology for decreased oncotic pressure pulmonary edema.
Polyarteritis nodosa
A systemic necrotizing vasculitis that affects systemic vessels, listed as a causative etiology of decreased oncotic pressure pulmonary edema.
High altitude pulmonary edema (HAPE)
A noncardiogenic pulmonary edema developing at high altitudes greater than 8000 to 10,000feet, theorized to involve hypoxic pulmonary vasoconstriction.
Transfusion-related acute lung injury (TRALI)
A severe noncardiogenic pulmonary edema reaction triggered by the transfusion of blood or blood products.
Cheyne-Stokes respiration
An abnormal, periodic breathing pattern characterized by alternating cycles of hyperpnea and apnea, presenting as a clinical manifestation of pulmonary edema.
Paroxysmal nocturnal dyspnea (PND)
Sudden awakening from sleep with severe dyspnea and coughing, typically caused by the reabsorption of dependent edema into the central circulation when recumbent.
Orthopnea
Difficulty breathing or shortness of breath that occurs when lying flat, compelling the patient to sit or stand upright to breathe comfortably.
Preload reduction
A therapeutic circulatory goal in cardiogenic pulmonary edema aimed at reducing venous return to the right heart and pulmonary circulation.
Afterload reduction
A therapeutic circulatory goal aimed at reducing systemic vascular resistance, thereby improving cardiac output and enhancing renal perfusion for diuresis.
Inotropic support
A therapeutic intervention utilizing pharmacological agents that produce vasodilation and increase myocardial contractility and cardiac output.
Loop diuretics (e.g., furosemide)
Rapid-acting diuretic medications classified as preload reducers that promote fluid excretion to decrease circulating volume in cardiogenic pulmonary edema.
Morphine sulfate
An opioid medication used as a preload reducer to decrease venous tone, reduce venous return to the heart, and alleviate patient anxiety.
Afterload reducers (ACE inhibitors & nitroprusside)
Vasodilating agents including captopril, enalapril (Vasotec), and nitroprusside (Nitropress) that lower systemic vascular resistance to improve ventricular emptying.
Fowler's position
An upright seated patient posture (often with legs and feet dangling over the bedside) used to decrease pulmonary capillary hydrostatic pressure and venous return.