Cardiovascular Disorders: Alterations in Cardiac Function, CAD, Valvular Disease, and Heart Failure

Comprehensive practice flashcards covering the pathophysiology, clinical manifestations, complications, and management of cardiac rhythm disturbances, coronary artery disease, valvular dysfunctions, heart failure, and cardiogenic shock.

What is tachycardia, and how does sympathetic nervous system (SNS) activation cause it?

Tachycardia is a heart rate faster than normal ($>100\,\text{beats/min}$). The SNS governs the "fight or flight" response and secretes epinephrine, which binds to beta receptors on the heart to increase heart rate.

How does hyperkalemia pathologically affect heart rate and rhythm?

Hyperkalemia causes hypopolarization of cardiac cells, which can trigger tachycardia and rhythm disturbances (dysrhythmias).

What is bradycardia, and how does parasympathetic nervous system (PNS) activation induce it?

Bradycardia is a heart rate slower than normal ($<60\,\text{beats/min}$). Via the vagus nerve, the PNS secretes acetylcholine, which acts on the heart to decrease heart rate.

Why can ischemia from a right coronary artery (RCA) narrowing or blockage cause bradycardia?

In most individuals, the RCA supplies blood to the sinoatrial (SA) node and atrioventricular (AV) node. Ischemia to these nodes impairs their ability to generate and conduct electrical impulses normally.

What are three primary causes of cardiac dysrhythmias?

1. Ischemic or infarcted tissue interfering with normal electrical impulse conduction.
2. Electrolyte imbalances, particularly potassium ($K^+$) derangements (hypokalemia and hyperkalemia).
3. Age-related wear and tear of the conduction system.

What is atrial fibrillation (Afib), and what are its common triggers?

Afib is a chaotic series of electrical impulses in the atria causing them to quiver ineffectively rather than contract smoothly. It commonly affects the elderly ($3\%$ of adults) and typically develops when the myocardium endures long-term hypoxic strain or chronic disease such as heart failure.

What is the "atrial kick," and what happens to it during atrial fibrillation?

The "atrial kick" is a coordinated contraction of the atria at the end of diastole that propels additional blood into the ventricles before ventricular systole. In Afib, ineffective quivering of the atria abolishes this kick, resulting in a small but sometimes significant decrease in cardiac output.

What are the two major embolic complications of blood pooling in atrial fibrillation depending on chamber origin?

1. Left atrium: Arterial thrombi form and can embolize to cerebral arteries, causing a stroke (manifested as one-sided weakness, confusion).
2. Right atrium: Venous thrombi form and can embolize to pulmonary arteries, causing a pulmonary embolism (manifested as shortness of breath, chest pain, hemoptysis, shock).

Why is ventricular fibrillation (Vfib) considered the deadliest dysrhythmia?

Vfib consists of chaotic electrical impulses causing the ventricles to quiver ineffectively, resulting in zero cardiac output, lack of cerebral perfusion, immediate unconsciousness, and death without immediate defibrillation.

How do right ventricular (RV) and left ventricular (LV) afterloads become pathologically increased?

RV afterload increases due to elevated pulmonary vascular resistance (PVR), such as from pulmonary artery vasoconstriction caused by chronic bronchitis. LV afterload increases due to elevated systemic vascular resistance (SVR), caused by hypertension, atherosclerosis of the aorta and systemic arteries, or peripheral vasoconstriction.

What pathophysiological state causes pathologically decreased LV afterload?

Massive peripheral arterial vasodilation, which occurs during distributive shock states such as anaphylactic shock (excessive inflammatory mediator release from allergic reaction) or septic shock (toxin-induced mediator release).

What roles do homocysteine and C-reactive protein (CRP) play in coronary artery disease (CAD)?

Elevated serum homocysteine causes oxidative damage to vessels similar to free radicals, promoting atherosclerosis. Elevated serum CRP serves as a marker linked directly to the inflammatory process of plaque formation within coronary arteries.

What are the classic characteristics of angina pectoris?

Described as tightness, heaviness ("elephant sitting on chest"), burning, or indigestion-like pain, often radiating to the left arm, jaw, or back; clenched fist over sternum (Levine sign); typically lasting $3\text{ to }5\,\text{minutes}$; exacerbated by exertion and relieved by rest or nitroglycerin.

How does collateral circulation develop in stable angina?

Slow, gradual development of an atherosclerotic plaque produces chronic, subtle ischemia that stimulates arteriogenesis (a form of angiogenesis). This establishes collateral circulation—new coronary branches that bypass and feed tissue distal to the occlusion.

What are the mechanisms of nitroglycerin (NTG) and aspirin in managing stable CAD?

Nitroglycerin dilates coronary arteries to enhance myocardial oxygen delivery and reduces cardiac workload. Aspirin acts as an anti-inflammatory to reduce plaque progression and inhibits platelet aggregation to prevent thrombus formation.

What three pathophysiologic events can precipitate Acute Coronary Syndrome (ACS)?

1. Sudden clot development within a coronary vessel.
2. An arterial embolus lodging in a narrowed coronary artery.
3. Rupture of an existing unstable plaque with luminal occlusion by its contents.

What distinguishes unstable angina from stable angina?

Unstable angina presents as a sudden worsening in the pattern of symptoms, including chest pain occurring at rest, increased pain severity, reduced or marginal responsiveness to previously effective doses of nitroglycerin, and acute ischemic changes on EKG due to partial arterial occlusion.

What are the key diagnostic laboratory biomarkers for myocardial infarction (MI)?

1. Creatine kinase (CK): A non-specific enzyme released by injured and necrotic cells throughout the body.
2. Troponin: A highly specific protein released exclusively by injured and dying myocardial cells, where higher serum titers indicate more extensive myocardial necrosis.

What signs and symptoms of low cardiac output and hypoperfusion commonly accompany ACS?

Fatigue, weakness, altered mental status or decreased responsiveness, hypotension, dyspnea, prolonged capillary refill ($>2\,\text{seconds}$), and low urine output (oliguria).

What acute medical and surgical interventions are commonly employed for hospital management of ACS?

Oxygen ($O_2$), IV nitroglycerin, IV morphine, IV heparin, IV platelet inhibitors, percutaneous transluminal coronary angioplasty (PTCA) with stenting, and coronary artery bypass graft (CABG) surgery.

What is the difference between valvular stenosis and valvular incompetence (regurgitation)?

Stenosis involves orifice constriction and stiffening that prevents full valve opening, creating turbulence as blood forces through. Incompetence (prolapse or insufficiency) involves valve leaflet floppiness preventing full closure, allowing backward regurgitation of blood into the preceding chamber.

What causes a cardiac murmur, and what are normal heart sounds?

A murmur is the audible sound of turbulent, non-smooth blood flow through stenotic or incompetent heart valves. Normal heart sounds consist solely of closing valves: "lub" (closure of atrioventricular valves) and "dub" (closure of semilunar valves).

What three basic pathological precipitants lead to heart failure (HF)?

1. Pump problem: Weakened myocardial contractility (e.g., from ischemia or MI).
2. Increased resistance: Pathologically elevated afterload (high SVR or PVR).
3. Increased preload: Fluid volume overload increasing the heart's workload.

Why is the renin-angiotensin-aldosterone system (RAAS) activation detrimental in heart failure?

The kidneys interpret low cardiac output as hypovolemia and activate RAAS. RAAS promotes fluid retention and vasoconstriction, which pathologically increases preload and afterload, forcing the already failing heart to work harder and worsening cardiac dysfunction.

What is the retrograde flow sequence and primary pulmonary symptoms seen in Left Heart Failure (LHF)?

Retrograde flow sequence: LV $\rightarrow$ LA $\rightarrow$ pulmonary veins $\rightarrow$ pulmonary capillaries $\rightarrow$ fluid transudation into alveoli (cardiogenic pulmonary edema). Signs include bilateral lung crackles, cough with pink frothy sputum (hemoptysis), tachypnea, orthopnea, and decreased $SO_2$.

Why do patients with Left Heart Failure experience orthopnea?

Assuming a supine position increases venous return to the heart and worsens hydrostatic back pressure into the pulmonary vasculature, intensifying alveolar pulmonary edema and shortness of breath.

What is the retrograde flow sequence and peripheral symptoms seen in Right Heart Failure (RHF)?

Retrograde flow sequence: RV $\rightarrow$ RA $\rightarrow$ superior vena cava (SVC) and inferior vena cava (IVC). Signs of peripheral venous congestion include jugular venous distention (JVD), hepatomegaly (liver congestion), ascites, and dependent peripheral edema of the legs and feet.

What is cor pulmonale, and how does chronic bronchitis cause it?

Cor pulmonale is right heart failure resulting specifically from pulmonary hypertension. Chronic bronchitis causes airway congestion and hypoxemia, which induces pulmonary arterial vasoconstriction; this elevates PVR, forcing the RV to pump against high afterload until it hypertrophies and fails.

What pharmacologic strategies are used to manage heart failure, based on underlying hemodynamic goals?

1. Positive inotropes (e.g., digoxin) to improve pump contractility.
2. Vasodilators (e.g., nitroglycerin) to decrease afterload (SVR/PVR).
3. ACE inhibitors to suppress the harmful compensatory actions of the RAAS.
4. Diuretics to reduce preload and relieve fluid congestion.

Why does serum B-type natriuretic peptide (BNP) become elevated in heart failure?

BNP is secreted by the ventricles in response to high intracardiac volume and myocardial stretch. The heart secretes BNP to promote renal diuresis of sodium and water; however, because the kidneys are overwhelmed by RAAS activation, BNP continues to rise frantically, serving as a diagnostic indicator of HF severity ($\approx 50\,\text{pg/mL}$ normal, $\approx 130\,\text{pg/mL}$ mild HF, $\approx 1000\,\text{pg/mL}$ severe HF).

What defines cardiogenic shock, and how is it treated pharmacologically?

Cardiogenic shock is inadequate tissue perfusion and cellular hypoxia driven by severe hypotension ($<90/60\,\text{mmHg}$) secondary to a primary cardiac pump failure. Treatment focuses on positive inotropic medications to augment contractility and peripheral vasodilators to diminish afterload.