Heart Failure 2024 Final Exam Questions With Answers

What is stage A Heart failure? - ANSWER- Patients at a high risk for developing heart failure such as hypertension, coronary artery disease or other atherosclerotic vascular disease, diabetes, obesity, metabolic syndrome What is stage B heart failure? - ANSWER- patients with structural heart disease (previous MI, left ventricular hypertrophy, low ejection fraction) but no signs and symptoms of heart failure What is stage C heart failure? - ANSWER- patients with structural heart disease and current or previous symptoms low or normal ejection fraction and symptoms such as dyspnea, fatigue, and reduced exercise tolerance What is stage D heart failure? - ANSWER- Refractory heart failure requiring specialized interventions, patients with treatment refractory symptoms at rest despite optimal guideline directed medical therapy (patients requiring recurrent hospitalization or cannot be discharged without mechanical assist devices or inotropic therapy) What is acute decompensating heart failure? - ANSWER- new or worsening signs and symptoms of heart failure such as volume overload or low cardiac output (hypo perfusion) which requires hospitalization usually presenting with the symptoms of dyspnea, edema, and fatigue What are the causes of acute decompensating heart failure? - ANSWER- refectory to guideline-directed management and therapy, medication noncompliance, other medical illnesses such as infections (pulmonary), acute coronary syndrome, hypertensive crisis, arrhythmias, pneumonia, MI or A.Fib What medications can precipitate/worsen ADHF? - ANSWER- negative inotropic effects- beta blockers, antiarrhythmic, Non-DHP CCB, itraconazole, Cardio toxic agents such as anthracyclines and cyclophosphamide Sodium and Water retention- NSAIDs, COX-2 inhibitors, salicylates, TZDs, Glucocorticoids, sodium containing medications (low concern) How do you evaluate clinical presentation? - ANSWER- review of systems, physical examination, clinical findings then evaluate volume status (wet or dry?) then cardiac output status (warm or cold?) What does the Frank-Sterling curve tell and what does it look like for heart failure patients? - ANSWER- it is a curve that represents cardiac inputs (stroke volume or cardiac output) vs left ventricular end diastolic pressure (preload) when one has heart failure the graph is shifted downward, the further down the curve is signifies hypoperfusion and the further to the right signifies congestion What is the forrester classification? - ANSWER- subset I- normal, warm and dry cardiac input is over 2.2 and PCWP is less than 18 Subset II- pulmonary congestion, warm and wet cardiac input is over 2.2 and PCWP is more than 18 Subset III- hypo perfusion, cold and dry cardiac input is less than 2.2 and PCWP is less than 18 Subset IV- hypo perfusion and pulmonary congestion, cold and wet cardiac input is less than 2.2 and greater than 18 *numbers are obtained through a swan-ganz catheter How do you treat the different subsets? - ANSWER- subset II- loop diuretics (+/- thiazides) and vasodilators Subset II- positive inotropic agents Subset IV- loop diuretics, vasodilators, positive inotropic agents What are the drug therapy goals in ADHF? - ANSWER- improve volume overload, improve cardiac output, optimize chronic therapy, symptom control, and minimize further cardiac damage What are the signs and symptoms of volume overload? - ANSWER- weight gain, dyspnea on exertion, orthopnea, tachypnea, JVD, crackles, hepatomegaly, lower extremity edema, abdominal distention, ascites, increased LFTs, S3 gallop, hypernatremia, elevated BNP What is BNP? - ANSWER- B-type Natriuretic peptide- released in response to increased ventricular volume and stress, binds to the type A natriuretic peptide receptor (NPR-A), leading to increased concentration of cGMP, vasodilation, this has a positive correlation with degree of left ventricular dysfunction (less than 100 excludes HF as etiology of dyspnea) What is the MOA of loop diuretics? - ANSWER- venodilation, reversibly binds to the sodium, potassium, chloride co-transport mechanism on the ascending loop of Henle and inhibits active reabsorption on the ATP dependent Na/K pump; sodium and chloride are not reabsorbed resulting in increased excretion of these ions What are the hemodynamic effects of loop diuretics? - ANSWER- decreased pulmonary congestion, peripheral edema, JVD, If CO is compromised due to fluid overload loops will improve CO What are the indications for loop diuretics? - ANSWER- fluid overload in ADHF subsets II and IV