cardio: HF

What is heart failure?

A state in which the ventricles at normal filling pressures cannot maintain adequate cardiac output to meet the metabolic needs of peripheral tissues, or can do so only with elevated filling pressures.

What happens to preload, afterload, and contractility in heart failure?

Preload ↑; afterload ↑; myocardial contractility ↓ in HFrEF.

Why can blood pressure appear normal despite poor cardiac output in heart failure?

The body compensates for decreased cardiac output by increasing vascular resistance, which may maintain a normal-looking BP despite inadequate blood flow/cardiac output.

What is the most important epidemiologic risk factor for heart failure?

Age; >75% of HF occurs in patients >65 years old.

What commonly precedes the development of heart failure?

Hypertension; approximately 75% of patients have antecedent HTN.

What is HFrEF?

Heart failure with reduced ejection fraction; LVEF ≤40%. It represents impaired systolic contractility or a "weak pump."

What is HFmrEF?

Heart failure with mildly reduced EF; LVEF 41-49%.

What is HFpEF?

Heart failure with preserved EF; LVEF ≥50%. It represents impaired relaxation/filling or a "stiff ventricle."

What is HFimpEF?

Heart failure with improved EF; previous LVEF ≤40% with follow-up LVEF >40%.

What is the pathophysiology of HFrEF?

Impaired LV contractility → reduced stroke volume and cardiac output → progressive LV dilation/remodeling → activation of RAAS and SNS → further disease progression.

What are common causes of HFrEF?

CAD/prior MI, dilated cardiomyopathy, valvular heart disease, cardiotoxic drugs/alcohol, and myocarditis.

What is the major treatment concept for HFrEF?

Weak pump → reduced EF → Four Pillars of GDMT.

Why does neurohormonal activation worsen HFrEF over time?

Decreased cardiac output activates SNS and RAAS. Initially compensatory, chronic activation causes vasoconstriction, sodium/water retention, ventricular remodeling, and progressive HF.

How is HFmrEF generally treated?

Many patients benefit from therapies used for HFrEF, particularly SGLT2 inhibitors; benefit is especially considered when EF is closer to 40%.

Should GDMT be discontinued when HFrEF improves to HFimpEF?

No. Improved EF does NOT mean cured HF. Continue GDMT indefinitely to reduce relapse risk.

What is the pathophysiology of HFpEF?

The LV loses its ability to relax and fill normally → increased ventricular stiffness → elevated filling pressures despite preserved EF → reduced effective cardiac output and congestion.

Why can cardiac output be reduced in HFpEF despite a normal EF?

The heart ejects a normal percentage of its blood, but the stiff ventricle fills with less blood, so the total volume ejected can still be inadequate.

What are common risk factors for HFpEF?

HTN, obesity, diabetes mellitus, aging, CKD, and atrial fibrillation.

What is the easiest way to distinguish HFrEF from HFpEF?

HFrEF = weak pump/impaired contraction with EF ≤40%. HFpEF = stiff ventricle/impaired filling with EF ≥50%.

What is the most common etiology of HFrEF in the lecture?

Ischemic heart disease/CAD, approximately 50%.

What is the most common risk factor for HFpEF?

Hypertension.

What is the primary manifestation of left-sided heart failure?

Pulmonary congestion; think LEFT = LUNGS.

What is the most common symptom of left-sided heart failure?

Dyspnea.

How does dyspnea typically progress in left-sided HF?

DOE → orthopnea → paroxysmal nocturnal dyspnea → dyspnea at rest.

What symptoms are associated with left-sided heart failure?

Dyspnea, DOE, orthopnea, PND, pulmonary edema, chronic cough, nocturia, fatigue, and exercise intolerance.

What happens hemodynamically in left-sided HF?

↓ ventricular output → ↑ left atrial pressure → ↑ pulmonary venous pressure → pulmonary congestion.

What are causes of left-sided heart failure?

HTN, cardiomyopathy, CAD/MI, aortic stenosis, and other left-sided valvular disease.

What is the primary manifestation of right-sided heart failure?

Systemic venous congestion/fluid overload; think RIGHT = legs, liver, belly.

What are manifestations of right-sided heart failure?

JVD, peripheral edema, hepatic congestion, decreased appetite, nausea, ascites, abdominal fullness/bloating, and weight gain from fluid retention.

What is the major cause of right-sided heart failure?

Left-sided heart failure.

What other conditions can cause right-sided heart failure?

Pulmonary hypertension, right-sided valvular disease, chronic lung disease, pulmonary valvular stenosis, and multiple pulmonary emboli.

What happens hemodynamically in right-sided HF?

↓ RV output → ↑ right atrial/systemic venous pressure → systemic venous congestion.

What is biventricular heart failure?

Failure of both the right and left ventricles, producing both pulmonary congestion and systemic venous congestion.

What conditions can cause biventricular HF?

CAD and dilated cardiomyopathy.

What findings suggest biventricular HF?

Pulmonary edema plus peripheral edema/hepatic congestion/ascites, along with poor tissue perfusion such as fatigue, renal dysfunction, and cool extremities.

What is high-output heart failure?

HF in which cardiac output is elevated but still insufficient to meet abnormally high metabolic demands; characterized by an abnormally high pumping volume due to low systemic resistance.

What causes high-output heart failure?

Severe anemia, hyperthyroidism, AV fistulas, sepsis, and severe obesity.

AV fistulas: artery bypass capillaries and dump into veins : Because the blood is returning to the heart so fast and the resistance is so low

In obesity more to perfuse

What are clinical clues for high-output HF?

Warm extremities, bounding pulses, wide pulse pressure, tachycardia, and HF symptoms despite normal or elevated EF. Four bounding pulse think about how much fluid they have to push and low SVR

How are high-output HF and typical HF different on extremity examination?

High-output HF → warm extremities. Typical low-output HF → cool extremities.

How is high-output HF diagnosed?

Elevated cardiac output on echocardiography or right heart catheterization.

How is high-output HF treated?

Treat the underlying cause; use standard HF medications cautiously and avoid excessive vasodilation.

What is pulse pressure?

Systolic BP − diastolic BP.

What should be assessed in the history of a patient with suspected HF?

Symptom onset/severity/progression, medications and adherence, sodium/fluid intake, alcohol/tobacco/drugs, family history of cardiomyopathy or sudden cardiac death, and comorbidities.

What are common triggers of acute HF decompensation?

Medication nonadherence, excess sodium/fluid, arrhythmias especially AF, ACS/ischemia, PE, infection, uncontrolled HTN, and progression of underlying heart disease.

Why does nocturia occur in HF?

Fluid retained during the day is excreted when recumbent because renal perfusion improves.

What vital sign findings can occur in HF?

Tachycardia; hypotension is a late finding; hypoxemia may occur with pulmonary edema.

What does an S3 suggest in heart failure?

Volume overload; commonly associated with HFrEF.

What does an S4 suggest in heart failure?

A stiff ventricle; more commonly associated with HFpEF.

What does a displaced sustained apical impulse suggest in HF?

LV dilation or hypertrophy.

What does a parasternal lift suggest in HF?

RV hypertrophy, often from pulmonary hypertension.

What pulmonary findings occur in HF?

Bibasilar crackles/rales and possible wheezing called "cardiac asthma" with pulmonary edema. - bibasilar (b/l at bottom) edema is from pressure gets so high that fluid is literally "pushed" out of the blood vessels and into the alveoli. This is pulmonary edema.

What physical findings indicate systemic congestion in HF?

JVD, positive hepatojugular reflux, hepatomegaly, ascites, and peripheral pitting edema.

What is hepatojugular reflux?

Increased JVD when pressure is applied over the liver.

Can chronic HF have a relatively normal physical examination?

Yes. Many expected signs may be absent in chronic HF.

What initial labs should be obtained in heart failure?

CBC, CMP, urinalysis, lipid profile, TSH, iron studies, BNP or NT-proBNP, and troponin when appropriate.

(urinalysis to check on the kidneys)

What BNP level makes heart failure unlikely according to the lecture?

BNP

What BNP level makes heart failure likely according to the lecture?

BNP >500 pg/mL, interpreted in clinical context.

What does an elevated BNP reflect?

Increased ventricular filling pressures; BNP is expressed primarily in the ventricles.

What conditions can falsely increase BNP?

CKD; BNP may also be less specific in older adults, women, and patients with COPD.

What condition can cause a lower-than-expected BNP?

Obesity…. Fat cells (adipocytes) express high levels of natriuretic peptide clearance receptors (NPR-C).

What does a higher BNP generally indicate about prognosis?

Higher BNP levels correlate with worse prognosis.

Can troponin be elevated in heart failure without ACS?

Yes. Troponin can be elevated in acute and chronic HF, but persistent elevation is associated with worse outcomes and ACS should be evaluated when clinically indicated.

What CXR findings suggest heart failure?

Cardiomegaly, pulmonary vascular congestion/cephalization, Kerley B lines, alveolar pulmonary edema with bat-wing opacities, and pleural effusions.

What are Kerley B lines?

Horizontal peripheral lung lines extending to the pleural surface caused by thickened, edematous interlobular septa, often from pulmonary edema.

What is the "bat-wing" appearance on CXR in severe HF?

Bilateral symmetric central alveolar opacities representing pulmonary edema.

Does a normal CXR exclude heart failure?

No. A normal CXR does not exclude HF, especially in chronic or early disease.

What does cardiomegaly indicate prognostically in HF?

It is a poor prognostic sign.

What should be evaluated on ECG in suspected HF?

Myocardial ischemia/prior infarction, arrhythmias, conduction abnormalities, LVH, and evidence of cardiomyopathy.

What is the most important diagnostic test for heart failure?

Transthoracic echocardiography (TTE).

What information does echocardiography provide in HF?

Confirms HF/type, measures LVEF, differentiates HFrEF from HFpEF, evaluates chamber size, wall motion, ventricular function, valves, and estimated pulmonary pressures.

When is cardiac MRI used in HF?

To evaluate cardiomyopathies, myocarditis, infiltrative disease, or myocardial scar.

When is coronary CT angiography or coronary angiography used in HF?

When CAD is suspected.

When is stress testing used in HF?

To assess for myocardial ischemia when appropriate.

What does right heart catheterization measure in HF?

Filling pressures and cardiac output.

What does pulmonary capillary wedge pressure approximate?

Left atrial pressure.

When is endomyocardial biopsy used in HF?

Rarely; reserved for selected cases such as suspected myocarditis or infiltrative disease.

When should EF be reevaluated according to the lecture?

>40 days after MI, >90 days after revascularization, and >90 days after GDMT.

What two classification systems should be assigned to a HF patient?

ACC/AHA Stage A-D AND NYHA functional class I-IV.

What is ACC/AHA Stage A heart failure?

Risk factors for HF but NO structural heart disease and NO symptoms.

What patients are considered Stage A?

Patients with HTN, DM, obesity/metabolic syndrome, ASCVD, family history of cardiomyopathy, or exposure to cardiotoxins.

What is the goal of Stage A HF management?

Prevent heart failure through risk-factor modification.

How is Stage A managed?

Control BP, treat diabetes, consider SGLT2 inhibitors when appropriate, treat hyperlipidemia/statins when indicated, exercise, healthy diet, weight loss, smoking cessation, and avoid cardiotoxins.

What is ACC/AHA Stage B heart failure?

Structural heart disease without current or previous HF symptoms; "pre-HF."

What are examples of Stage B HF?

Asymptomatic reduced LVEF, prior MI with reduced EF, or significant structural/valvular disease without symptoms.

What is the goal of Stage B management?

Prevent progression to symptomatic HF.

How is Stage B HF managed?

Continue Stage A risk-factor modification; ACEi/ARB in appropriate patients, evidence-based beta-blocker particularly with low EF/post-MI, treat diabetes, statin for ASCVD, and consider ICD or valve intervention in selected patients.

Does every Stage B patient automatically receive all four HFrEF pillars?

No. The lecture's Stage B management lists ACEi/ARB and evidence-based beta-blocker in appropriate patients, SGLT2 consideration for appropriate patients with diabetes, plus risk-factor treatment. The full Four Pillars are specifically listed for Stage C HFrEF.

What is ACC/AHA Stage C heart failure?

Structural heart disease with current or previous symptoms of HF.

What is the goal of Stage C treatment?

Relieve symptoms, improve survival, and prevent hospitalization.

How is Stage C HFrEF treated?

Continue Stage A/B therapies + Four Pillars of GDMT + diuretics for volume overload + lifestyle/cardiac rehab + device therapy when indicated.

What is ACC/AHA Stage D heart failure?

Advanced HF with refractory symptoms at rest despite optimal GDMT.

How is Stage D HF managed?

Advanced HF specialist referral, continue GDMT as tolerated, evaluate IV inotropes, LVAD, cardiac transplantation, palliative care, and hospice when appropriate.

What is the overall approach to treating heart failure?

Classify HF by EF → determine ACC/AHA stage and NYHA class → treat congestion → initiate EF-appropriate GDMT once hemodynamically stable → treat underlying cause.

What are the goals of HFrEF therapy?

Improve symptoms/quality of life, reduce HF hospitalizations, improve survival, and rapidly initiate/up-titrate all Four Pillars.

What are the Four Pillars of HFrEF GDMT?

1. ARNI preferred or ACEi/ARB; 2. Evidence-based beta-blocker; 3. MRA; 4. SGLT2 inhibitor.

Should one HFrEF medication be maximized before another pillar is started?

No. Initiate all four pillars early in eligible patients, then titrate toward target or maximally tolerated doses.

What is Pillar 1 of HFrEF treatment?

ARNI preferred, or ACE inhibitor/ARB when appropriate.

How do ACE inhibitors and ARBs benefit HFrEF?

Inhibit RAAS → ↓ vasoconstriction, ↓ sodium/water retention, ↓ ventricular remodeling/fibrosis → reduce mortality and HF hospitalizations, improve symptoms, and slow progression.

When is an ACE inhibitor used instead of an ARNI in HFrEF?

When ARNI is not feasible.

When is an ARB used instead of an ACE inhibitor?

If an ACE inhibitor is not tolerated, such as due to cough.