CHF

Define the physiologic definition of CHF.

The inability of the heart to maintain circulatory demands without a rise in LV filling pressure

Clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or eject blood

List the most specific sign and symptom of CHF.

Most specific sign: S3 gallop

Most specific symptom: orthopnea/Paroxysmal Nocturnal Dyspnea.

Explain why dyspnea occurs in left-sided HF

Increased LA pressure is transmitted to pulmonary veins → pulmonary capillary pressure rises → pulmonary edema → dyspnea

Explain orthopnea physiologically.

Supine position increases venous return from legs → increased LV filling pressures → pulmonary congestion → SOB.

Explain paroxysmal nocturnal dyspnea.

Fluid redistribution during sleep increases LV filling pressures patient awakens gasping and improves when upright.

List signs of right-sided

HF. JVD, hepatomegaly, ascites, lower extremity edema

“By far, the greatest cause of right-sided heart failure is left-sided heart failure.”

Differentiate left- vs right-sided HF symptoms.

Left: dyspnea, orthopnea, PND, pulmonary edema.

Right: JVD, leg edema, ascites, hepatomegaly.

Define high-output vs low-output HF.__Discard

Low-output: AS, HTN, MI.

High-output: anemia, thyrotoxicosis, AVM, pregnancy. Vast majority is low-output.

Describe the “wet vs dry” and “warm vs cold” HF profiles.

Wet = congestion (orthopnea, PND, rales, JVD). Cold = low perfusion (cool extremities, narrow pulse pressure, renal dysfunction).

Explain LV remodeling after injury.

Reduced EF → LV dilates to maintain SV (↑EDV).

List causes of remodeling.

Myocardial insult → dysfunction → reduced perfusion → sympathetic/RAAS activation → altered gene expression → apoptosis → remodeling.

Describe sympathetic system effects in HF.

↑Automaticity, ↑Contractility, ↑Afterload, ↑Preload, chronic stimulation → myocyte death + arrhythmia.

Describe RAAS effects in HF.

Ang II → ↑Afterload, ↑Preload chronic → hypertrophy + ischemia.

Describe aldosterone effects in HF.

↑Afterload, ↑Preload, chronic → cardiac fibrosis.

Explain beta-1 receptor changes in HF.

Downregulated and desensitized due to chronic epinephrine stimulation (“less likely to stimulate cAMP production”).

Explain ANP release.

Atrial stretch from ↑LV filling pressures → ANP release → natriuresis, vasodilation.

Explain BNP release.

Ventricular tension/stretch → BNP release → natriuresis, ↓renin, ↓aldosterone, ↓preload/afterload.

State BNP’s diagnostic utility.

BNP elevation helps diagnose CHF

Define HFpEF, HFmrEF, HFrEF.

HFpEF ≥50%, HFmrEF 41–49%, HFrEF <40%

Describe HFpEF remodeling pattern.

Concentric hypertrophy: ↑mass, normal volume, ↓diastolic function, preserved systolic function. (think hypertrophy)

Describe HFrEF remodeling pattern.

Eccentric dilation: ↑volume, ↑mass, ↓systolic function, ↓diastolic function. (think dilated cardiomyopathy)

List causes of HFpEF(pressure overload) vs HFrEF(volume overload).

HFpEF: HTN, DM, Aortic stenosis (pressure overload). HFrEF: MI, alcohol, idiopathic (volume overload).

Define pulsus alternans and what it is a strong indicator of

Alternating strong/weak pulses; good indicator of HFrEF.

Define LV suction.

Elastic recoil during early diastole generates negative pressure → pulls blood from LA.

Explain impaired LV relaxation.

Slow relaxation prevents generation of low LV pressure → impaired suction → ↑LA pressure → exertional dyspnea.

Describe normal vs CHF filling pressures.

Normal: LV fills under low pressure. CHF: LV fills under high pressure → small SV increase with exercise.

Explain dependence on atrial kick.

As suction worsens, LV filling becomes more dependent on atrial contraction.

Does everyone with HF have diastolic dysfunction.

Yes! Everyone with HF—preserved or reduced EF—has abnormal diastolic filling.

List acute HF causes of increased preload.

Na/fluid intake, non-compliance, IV fluids, sympathetic stimulation.

List acute HF causes of increased afterload.

Na intake, non-compliance, sympathetic stimulation.

Explain acute HF treatment goals.

Decrease preload (diuretics-dec venous congestion, nitrates-dec pulm edema); decrease afterload/inc contractility(ACEi/ARB/hydralazine/nitroprusside)

State when beta-blockers are used in acute HF.

Not started until euvolemic, if already on them, continue at lower dose.

List chronic HF life-prolonging therapies.

ACEi/ARB/ARNI(ARB+ Neprilysin inhibitor), beta-blockers (carvedilol, metoprolol XL, bisoprolol), aldosterone antagonists(spironalactone)

Explain ARNI(ARB + Neprilysin Inhibitor) role.

Used in symptomatic HFrEF (Class II–III) improves outcomes.

Explain SGLT2 inhibitor role + Ex

Improves HF outcomes and survival (empagliflozin, dapagliflozin) by dec fluid and glucose

State ICD indications

LVEF EF ≤35% and no recovery after being on guideline directed therapy

Left sided HF sx

S3 gallop, Pulmonary edema, Dyspnea w exertion, orthopnea, Paroxysmal Nocturnal Dyspnea, fatigue, weakness

Treatment of Acute CHF meds

Diuresis(use furosemide(lasix)), Nitroglycerin to vasodilate and improve sx, and ACEi/ARBs, Hydralazine, Nitroprusside to inc stroke volume, and Dobutamine/milrinone to inc SV

Should you use Ca Channel Blockers in HF?

NO! Avoid Verapamil/diltiazem because they limit contractility

Treatment tree for HF

Initially start Beta blocker, ACEi/ARB, SGLT-2 inhibitor
Class III/IV: start aldosterone antagonist(spironalactone), maybe hydralazine nitrates

If EF <35% on meds»Use ICD + CRT