Heart Failure Flashcards
What is Congestive Heart Failure (CHF)?
CHF occurs when the heart cannot maintain adequate output for metabolic demands or can only do so at elevated filling pressures.
What is the prevalence and mortality rate of CHF in the U.S.?
CHF affects 2% of the U.S. population and causes ~300,000 deaths annually.
CHF is characterized by what?
.CHF is characterized by diminished cardiac output (forward failure), accumulation of blood in the venous system (backward failure), or both.
What is the Frank-Starling Mechanism?
Increased filling pressures dilate the heart and thereby increase functional cross-bridges in the sarcomeres, enhancing contractility.
What is Myocardial Hypertrophy?
Increased expression of contractile proteins to sustain function.
What is Neurohumoral Activation?
Adrenergic stimulation → ↑ HR, contractility, vascular resistance. Renin-Angiotensin-Aldosterone activation → ↑ Blood volume, BP. Atrial natriuretic peptide released to counteract overload.
What are the downsides of compensation in CHF?
Eventually leads to cardiac damage (apoptosis, cytoskeletal changes, fibrosis).
What is Systolic Dysfunction?
Most common cause of CHF. ↓ Myocardial contractility (due to ischemia, valvular disease, or myocardial failure).
What is Diastolic Dysfunction?
Impaired relaxation & filling. Causes: Hypertrophy (most common), fibrosis, amyloid deposition, constrictive pericarditis. More common in women & elderly (>65 years).
What is the definition of Cardiac Hypertrophy?
Non-proliferating myocytes respond to stress by hypertrophy (larger, heavier heart).
What is Pressure-Overload Hypertrophy?
Sarcomeres in parallel → ↑ Wall thickness (e.g., hypertension, aortic stenosis).
What is Volume-Overload Hypertrophy?
Sarcomeres in series → Ventricular dilation (e.g., valvular insufficiency).
What are the consequences of Hypertrophy?
↑ Myocyte size but not capillary density → Ischemia risk. ↑ Interstitial fibrosis → ↓ Compliance. Associated with arrhythmic sudden death.
What is Physiologic Hypertrophy?
Aerobic exercise-induced hypertrophy is beneficial: ↑ Capillary density, ↓ Resting HR & BP.
What are the causes of Left-Sided Heart Failure (LSHF)?
Ischemic heart disease (IHD), Hypertension, Aortic/Mitral valve disease, Intrinsic myocardial disease.
What are the manifestations of LSHF?
Pulmonary congestion & edema → Dyspnea, orthopnea, rales. Left atrial dilation → Atrial fibrillation. Renal hypoperfusion → Salt/water retention, AKI, prerenal azotemia. Hypoxic encephalopathy → Confusion, irritability, coma.
What are the causes of Right-Sided Heart Failure (RSHF)?
Most common cause: Left-sided heart failure. Other causes: Tricuspid/Pulmonic valve disease, Pulmonary hypertension (Cor Pulmonale).
What are the manifestations of RSHF?
Right atrial/ventricular dilation & hypertrophy. Peripheral edema (feet, ankles, sacrum). Serous effusions (pericardial, pleural, peritoneal).
What are the liver and spleen effects of RSHF?
Hepatomegaly with nutmeg liver (chronic passive congestion). Severe hypoxia → Centrilobular necrosis, fibrosis. Congestive splenomegaly → Hemosiderin deposits, fibrosis.
What are the renal effects of RSHF?
More severe than LSHF. Congestion & AKI due to hypoxia.
What are the therapies for CHF?
Diuretics relieve fluid overload & congestion.
What do ACE Inhibitors/ARBs do in CHF treatment?
Blocks renin-angiotensin-aldosterone system → ↓ BP, ↓ Cardiac stress.
What is the role of Beta-Blockers in CHF?
↓ Adrenergic tone → ↓ HR, ↓ Oxygen demand.
What are advanced therapies for CHF?
Mechanical assist devices (e.g., LVADs). Cardiac resynchronization therapy for electrical efficiency.
When is Heart Transplantation indicated?
For end-stage CHF when other treatments fail.
What are the compensatory mechanisms attempt to maintain arterial pressure and organ perfusion?
.Frank-Starling mechanism
• Myocardial hypertrophy
• Activation of neurohumoral systems.
