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What is heart failure (HF)

A clinical syndrome in which the heart cannot maintain sufficient cardiac output to meet the body's metabolic demands; it is the end stage of many cardiac diseases.

What is the difference between forward failure and backward failure in HF

Forward failure = reduced cardiac output causing poor tissue perfusion (fatigue, oliguria, confusion). Backward failure = congestion of blood behind the failing ventricle.

What are the classic signs of left-sided heart failure

Bilateral crackles (rales), dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, cough, hypoxemia, and elevated left atrial pressure.

What causes the crackles heard in left-sided heart failure

Blood backs up into the pulmonary capillaries, forcing fluid into alveolar and interstitial spaces. Crackles result from air moving through partially fluid-filled alveoli.

What are the classic signs of right-sided heart failure

Jugular venous distention (JVD), peripheral/dependent edema (feet and ankles), hepatomegaly, ascites, splenomegaly, and gastrointestinal symptoms.

Why does right-sided heart failure cause peripheral edema

The failing right ventricle causes systemic venous congestion, increasing hydrostatic pressure in peripheral capillaries, forcing fluid into subcutaneous tissues.

What is biventricular heart failure

Failure of both the left and right ventricles, most commonly resulting from left-sided HF that progressed to right-sided HF; produces both pulmonary and systemic venous congestion.

What is HFrEF

Heart failure with reduced ejection fraction (<45%); indicates significant systolic dysfunction where the heart cannot contract forcefully enough to eject adequate blood volume.

What is HFpEF

Heart failure with preserved ejection fraction (>50%); diastolic dysfunction where the heart cannot relax and fill properly despite normal contractile ability.

What is a normal ejection fraction (EF)

60% to 80%.

What are the three main compensatory mechanisms in heart failure

(1) Sympathetic nervous system (SNS) activation, (2) increased preload via RAAS and fluid retention, and (3) myocardial hypertrophy.

How does the RAAS contribute to heart failure progression

Reduced cardiac output triggers RAAS, increasing aldosterone and causing sodium/water retention, which raises preload. Chronically, angiotensin II causes myocardial fibrosis and remodeling, worsening HF.

What is cardiac remodeling

The process of myocyte loss, hypertrophy of remaining cells, and interstitial fibrosis triggered by chronic neurohormonal stimulation; leads to progressive HF.

What is eccentric vs. concentric hypertrophy

Eccentric: muscle fibers grow longer (chamber dilates) due to high preload. Concentric: muscle fibers grow thicker (wall thickens) due to high afterload (e.g., hypertension).

What is the Frank-Starling mechanism

Increased preload stretches myocardial fibers, leading to a more forceful contraction. In HF, this curve is flattened and shifted right.

What is cor pulmonale

Right ventricular hypertrophy and eventual failure caused by pulmonary disease that increases pulmonary vascular resistance and right ventricular afterload.

What is the FACES acronym for heart failure

Fatigue, Activity limitation, Congestion, Edema, Shortness of breath — classic findings suggesting HF.

What medications are considered standard of care for HFrEF

ACE inhibitors (ACEIs) or ARBs, mineralocorticoid receptor antagonists (MRAs), and specific beta1-blockers.

What is the role of diuretics in heart failure treatment

Reduce intravascular volume, decrease preload, and alleviate congestive symptoms (edema, pulmonary congestion) without significantly reducing cardiac output.

What is blood pressure

The product of cardiac output (heart rate × stroke volume) and systemic vascular resistance (SVR).

What is the role of the baroreceptor reflex in blood pressure regulation

Baroreceptors in the carotid arteries and aortic arch detect pressure changes; a drop in pressure decreases baroreceptor firing, stimulating the SNS to increase HR and SVR.

What is primary (essential) hypertension

High blood pressure with no identifiable underlying cause; accounts for the majority of hypertension cases. Associated with genetic, lifestyle, and environmental factors.

What is secondary hypertension

Hypertension caused by an identifiable condition such as renal disease, aldosterone-producing tumors, or thyroid disorders.

How does the RAAS regulate blood pressure

Low renal perfusion → renin release → angiotensin I → angiotensin II (via ACE) → vasoconstriction + aldosterone release → sodium/water retention → increased blood volume and BP.

What is atherosclerosis

A progressive disease in which lipid-filled plaques develop within arterial walls, narrowing the lumen and reducing perfusion; the major cause of coronary artery disease.

What initiates atherosclerotic plaque formation

Endothelial injury from factors such as hypertension, smoking, hyperlipidemia, or toxins; leads to LDL insudation, macrophage recruitment, foam cell formation, and plaque development.

What is a foam cell

A lipid-filled macrophage that forms when macrophages engulf oxidized LDL in the vessel wall; foam cells accumulate to form fatty streaks, an early sign of atherosclerosis.

What is acute coronary syndrome (ACS)

A spectrum including unstable angina, NSTEMI, and STEMI caused by sudden partial or complete obstruction of a coronary artery, usually from vulnerable plaque rupture and thrombus formation.

What is the difference between stable and unstable angina

Stable angina: predictable chest pain with exertion that resolves with rest; caused by fixed atherosclerotic plaques. Unstable angina: pain at rest or with minimal exertion; associated with vulnerable plaque rupture.

What is a myocardial infarction (MI)

Irreversible necrosis of myocardial cells caused by prolonged ischemia; results in permanent loss of contractile tissue.

What are the four types of shock

Cardiogenic, obstructive, hypovolemic, and distributive shock.

What is cardiogenic shock

Shock resulting from heart disorders that cause inadequate cardiac output despite sufficient vascular volume (e.g., massive MI, cardiomyopathy).

What is the common cellular consequence of all types of shock

Impaired oxygen delivery to cells → switch from aerobic to anaerobic metabolism → lactic acid accumulation → cellular ATP depletion → ion pump failure → cell swelling and death.

What is hypovolemic shock

Shock caused by loss of blood volume through hemorrhage, vomiting, diarrhea, burns, or excessive diuresis.

What is distributive shock

Shock from inappropriate vasodilation causing expanded vascular space without fluid loss; includes anaphylactic, neurogenic, and septic shock.

What are the clinical signs of right-sided HF related to systemic venous congestion

JVD, hepatomegaly, splenomegaly, ascites, peripheral dependent edema, and decreased urine output.

What is the hepatojugular reflux test

Manual compression of the liver causes increased venous return; in right-sided HF, the jugular veins distend because the right heart cannot accommodate the increased volume.

What ECG finding is associated with right bundle branch block

Late R wave in lead V1 and an S wave in V6; the right ventricle depolarizes after the left ventricle.

What is ventricular fibrillation and how is it treated

Rapid, uncoordinated ventricular depolarization resulting in no effective contraction; treated immediately with CPR and defibrillation.

What is the difference between cardioversion and defibrillation

Cardioversion: synchronized electric shock timed to the R wave, lower energy. Defibrillation: unsynchronized shock at higher energy (200–350 J); used for ventricular fibrillation.

What is sinus tachycardia and what causes it

Heart rate >100 bpm initiated in the SA node; caused by SNS activation, fever, hypoxia, pain, or compensatory response to low cardiac output.

What is sinus bradycardia

Heart rate <60 bpm; caused by increased parasympathetic activity, sleep, drugs, or athletic conditioning.

What is atrial fibrillation

Disorganized, irregular atrial rhythm with variable ventricular response; loss of "atrial kick" reduces cardiac output; risk of atrial thrombus and stroke.

What is the BNP test used for in heart failure

B-type natriuretic peptide (BNP) is released by ventricular myocytes under increased wall stress; elevated levels help diagnose and assess the severity of HF.

What are the NYHA classes of heart failure severity

Class I: no symptoms with ordinary activity. Class II–III: symptoms with mild to moderate activity. Class IV: symptoms at rest.