Chapter 17_2 flashcards
(33 cards)
Heart Failure with Reduced Ejection Fraction (HFrEF / Systolic HF): Pathophysiology
Weakened LV has difficulty ejecting blood -> decreased SV & CO (LVEF <= 40%). Blood accumulates in LV -> increased LV pressure -> backup of hydrostatic pressure into LA, pulmonary veins, capillaries -> pulmonary edema. Detrimental activation of RAAS & SNS.
HFrEF: Common Etiologies
Coronary artery disease, ischemic heart disease, and acute myocardial infarction. [Text]
Heart Failure with Preserved Ejection Fraction (HFpEF / Diastolic HF): Pathophysiology
Ventricle has difficulty relaxing and is less elastic (stiff), so it cannot expand fully to fill with blood adequately during diastole. SV and CO can be reduced due to decreased end-diastolic volume, even though LVEF is >= 50%.
HFpEF: Common Etiologies
Long-standing hypertension (leading to LVH), atrial dysrhythmias, anemia, and chronic obstructive pulmonary disease (COPD). More common in older individuals and women. [Text]
Left Ventricular Failure (LVF): Backward Effects
Weak LV -> backup of hydrostatic pressure -> LA -> pulmonary veins -> pulmonary capillaries. Result: Pulmonary edema. Symptoms: Crackles on auscultation, cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND).
Left Ventricular Failure (LVF): Forward Effects & Compensatory Responses
Inadequate ejection of blood into aorta -> diminished systemic/organ perfusion. Kidneys sense low perfusion -> activate RAAS (increases blood volume & PVR). Baroreceptors sense low BP -> activate SNS (increases HR & PVR). Posterior pituitary releases ADH (increases water reabsorption). These worsen HF.
Orthopnea Classification
Classified based on the number of pillows the patient needs to elevate their head to breathe comfortably (e.g., “two-pillow orthopnea”).
Right Ventricular Failure (RVF): Backward Effects (Most Significant)
Weak RV -> backup of hydrostatic pressure -> RA -> SVC/IVC -> systemic venous system. Results in: Jugular Vein Distention (JVD), elevated CVP, hepatomegaly, splenomegaly, ascites, peripheral edema (ankle or sacral). Positive hepatojugular reflux.
Cor Pulmonale: Definition & Pathophysiology
Right ventricular failure caused by lung disease. Chronic hypoxia (e.g., from COPD) -> pulmonary arterial vasoconstriction (pulmonary HTN) -> increased resistance against RV -> RV hypertrophy -> RV ischemia & failure.
Biventricular Heart Failure
Dysfunction of one heart chamber eventually affects the other. Most patients clinically present with signs and symptoms of both LVF (pulmonary congestion) and RVF (systemic venous congestion).
Cardiomyopathy: Ischemic vs. Dilated
Ischemic Cardiomyopathy: Diffuse myocardial fibrosis and scarring due to coronary artery insufficiency and MI. Dilated Cardiomyopathy: Enlargement and hypertrophy of ventricles (often LV) leading to poor systolic function, dysrhythmias, and emboli risk.
Cardiomyopathy: Restrictive vs. Hypertrophic
Restrictive Cardiomyopathy (Box 17-5): Ventricle impeded from adequate filling due to stiffness (myocardial fibrosis, pericarditis). Hypertrophic Cardiomyopathy: LV muscle enlarged (often septum), stiff, may obstruct aortic outflow. Primary (genetic) or secondary (e.g., to HTN).
Heart Valve Abnormalities Causing HF: Mitral Regurgitation
Mitral valve doesn’t close completely during systole -> blood refluxes from LV to LA -> increased LA pressure -> backward pressure to pulmonary veins/capillaries -> pulmonary edema. Often post-MI due to papillary muscle rupture.
Heart Valve Abnormalities Causing HF: Aortic Stenosis
Narrowing of aortic valve (often due to age-related calcification/sclerosis) -> impedes blood ejection from LV to aorta -> increased resistance against LV -> LV hypertrophy -> LVF.
Diagnosis of HF: Framingham Criteria (Table 17-1)
Requires at least ONE Major criterion (e.g., PND, JVD, pulmonary crackles, cardiomegaly, S3 sound, increased CVP, hepatojugular reflux) AND TWO Minor criteria (e.g., bilateral extremity edema, nighttime cough, dyspnea on exertion, hepatomegaly, pleural effusion, tachycardia >120bpm, weight loss of >=4.5kg in 5 days with HF treatment).
Diagnosis of HF: B-type Natriuretic Peptide (BNP)
Secreted by ventricles when stretched by increased blood volume. Elevated levels (>500 pg/mL indicative of HF) in heart failure.
Diagnosis of HF: Chest X-Ray Findings
Cardiomegaly (enlarged heart). Pulmonary vascular congestion (increased opacity, Kerley A/B lines, “bat wing density” in pulmonary edema). Pleural effusion.
Diagnosis of HF: Echocardiogram
Estimates LVEF, shows size and function of ventricles, assesses valve structure and function.
Hemodynamic Measurements in LVF (Table 17-2)
Pulmonary Capillary Wedge Pressure (PCWP) is INCREASED (normal 12-15 mmHg). Left Ventricular Ejection Fraction (LVEF) is DECREASED (normal 50-70%; <40% indicative of LVF). Cardiac Output (CO) is DECREASED. Systemic BP often DECREASED.
Hemodynamic Measurements in RVF (Table 17-2)
Central Venous Pressure (CVP) is INCREASED (normal 1-5 mmHg).
NYHA Functional Classification of Heart Failure (Table 17-3)
Class I: No limitation of physical activity. Class II: Slight limitation; comfortable at rest, ordinary activity causes fatigue/palpitations/dyspnea. Class III: Marked limitation; comfortable at rest, less than ordinary activity causes symptoms. Class IV: Unable to carry on any physical activity without discomfort; symptoms at rest.
ACC/AHA Stages of Heart Failure (Table 17-4)
Stage A: At high risk for HF but no structural disease/symptoms. Stage B: Structural heart disease but no HF signs/symptoms. Stage C: Structural heart disease with prior/current HF symptoms. Stage D: Refractory HF requiring specialized interventions.
HF Treatment: Diuretics (e.g., Furosemide, Thiazides)
Enhance water loss, decrease blood volume, reduce edema. Loop diuretics for acute; thiazides for maintenance. Risk: Hypokalemia (increases digoxin toxicity risk).
HF Treatment: Aldosterone Antagonists (e.g., Spironolactone)
Potassium-sparing diuretic; inhibits Na+ and water reabsorption at nephron by blocking aldosterone. Risk: Hyperkalemia.
