9. Heart Failure and Cardiomyopathies

General pathophys of heart failure

Structural OR functional impairment of ventricular filling OR ejection

"Cardinal" S/S of HF

- Dyspnea, fatigue

- Edema, rales

Why is prevalence of HF increasing?

Patients surviving longer

How is HF classified?

LVEF

HF with reduced EF value (HFrEF)

EF ≤ 40%

HF with preserved EF value (HFpEF)

EF ≥ 50%

Borderline/mid-range HF EF value

EF 41-49%

Diastolic HF AKA

HFpEF

Changes of heart that results in HFpEF

Ventricle(s) stiffen → thickened myocardium

- EF can be normal

MCC of HFpEF (3)

- HTN

- Vent hypertrophy

- Restrictive cardiomyopathy

Systolic HF AKA

HFrEF

Changes of heart that results in HFrEF

Structural changes to heart → decreased contractility → decreased emptying during systole

- EF decreased

MCC of HFrEF

- MI w/ scarring

- Severe valve disease

- Dilated cardiomyopathy

High output HF (+ potential causes)

Cardiac output/function is normal BUT HF presentation due to high metabolic demand

- Hyperthyroid

- Anemia

New York association (NYHA) HF classification levels of functional capacity

Class 1: Asymptomatic

Class 2: Symptoms w/ moderate activity

Class 3: Symptoms w/ mild activity

Class 4: Symptoms at rest

Most significant stage of AHA stages of HF (+ why?)

Stage A: HIGH risk, no dysfunction

- Interventions of HTN, CAD, diabetes, etc. can PREVENT HF

Compensatory mechanisms to maintain CO with HF (2)

RAAS → Na and H2O retention

Adrenergic nervous system activation → Increases contractility

LV remodeling & HF

Remodeling is result of HF BUT worsens HF

Issue with kidney activation of RAAS & HF

In HF, the heart cannot handle CURRENT volume → increasing volume WORSENS HF

Preload

Length of muscle at start of contraction

Afterload

Tension/power the muscle must develop during contraction

Review starling mechanism slide 18

Starling force mechanism of HF

Increased capillary hydrostatic pressure

S/S of L-sided HF

- Pulm edema symptoms

- Cough (acute pulm edema → frothy/blood-tinged sputum)

- Paroxysmal nocturnal dyspnea

S/S of R-sided HF

- Peripheral edema

- Anasarca

- Ascites

Vitals findings with acute pulm edema

- Resp distress

- Tachy

Vitals findings with advanced HF

Low BP

Neck findings of HF

JVD w/ hepatojugular reflux

Lung findings of HF

Rales base upward, expiratory wheeze (cardiac asthma), R or bilateral effusion

Heart findings of HF

- Displaced PMI

- Extra heart sounds

Advanced HF → TR and MR murmur

Abdominal findings of HF

Hepatosplenomegaly

Lab workup for HF

- Electrolytes

- Liver enzymes (R-sided HF)

- UA (renal injury)

Diagnostic workup for HF

Echo → EF

EKG → hypertrophy, MI

CXR → pulm edema (L-sided HF)

Most important imaging for HF

Echocardiogram

Biomarkers for HF

BNP or pro-BNP

BNP for HF

- Acute → Obtain at "dry weight"

- Increased levels used for diagnosis and management

Cor pulmonale

RVHF due to chronic lung disease and pulm HTN

Medications for treatment of HFpEF

- SGLT2 inhibitors (dapagliflozin or empagliflozin) &

- Thiazide or loop diuretic

What do SGLT2 inhibitors address w/ HF?

Reduces CV mortality and HF hospitalization

Management of HF with lifestyle modifications

Diet: ≤3 g of Na+/day, fluid restrictions

Medications for treatment of HFrEF (4)

- Diuretics (loop/aldosterone antagonist) &

- ACEI/ARNI (pref for ARNI) &

- BB &

- SGLT2 inhibitors

Methods to monitor efficacy of diuretics

- Intake vs. output

- Renal function

Goal of diuretic use with HFrEF

Euvolemia (normal volume)

Input/output by weight

1L = 1kg

Loop diuretics for HF (+ risk)

- Furosemide, bumetanide, torsemide

- Hypokalemia

Acute mainstay diuretic treatment for HF

Loops

Chronic diuretic treatment for HF

Aldosterone antagonists

Indications for use of ACEI/ARB with HF

EF ≤ 40%

FYI with BP & HF

Chronic HF can tolerate lower BP

Adverse effects of ACEI/ARB (seen on labs)

Increase in creatinine (up to 30% OK)

Medication in angiotensin receptor-neprilysin inhibitor (ARNI)

Sacubitril/Valsartan (Entresto)

Function of Entrestio (ARNI) & HF (+ monitor what)

- Decrease mortality in HF

- Monitor renal function closely

Function of beta-blockers & HF

- Decrease mortality in HF and improve symptoms

- Myocardial relaxation and decrease contractility (decreases stress on heart)

Contraindications for use of BB

DO NOT use with acute HF exacerbation

Type of HF where BB are effective

HFrEF

Medications of BB class used to HF (3)

Metoprolol, carvedilol, bisoprolol

Function of SGLT2 inhibitors in HF

Preservation of kidney health with HF and/or CKD

MOA of SGLT2 inhibitors

Inhibit Na/glucose cotransporter in kidneys

SGLT2 inhibitors for non-diabetics with CKD +/- HF

Dapagliflozin and empagliflozin

Function of digoxin (+ caution)

- Positive inotropic by increasing intracellular Ca

- Caution w/ renal impairment

Digoxin dosing w/ advanced CKD

Decrease dose

Type of HF where digoxin is effective

HFrEF

Function of hydralazine/nitrates

Vasodilation → symptomatic benefit

Type of HF where hydralazine/nitrates are effective

HFrEF

Indications for hydralazine/nitrates with HF

HFrEF with refractory symptoms to meds OR cannot tolerate ACEI/ARB/ARNI

Function of inotropes (+ monitor what)

- Increase contractility and CO

- Hemodynamics, renal function, volume status

Indications of inotropic meds with HF

Used acutely for severe, decompensated HF w/o tolerance for diuresis

FYI with inotropic meds with HF

Improve symptoms BUT increase mortality

Utilization of all 4 HFrEF medications reduce mortality by...

70%!

HF & initiation of pharmacology therapy

FOR ALL 4 THERAPIES, start with low initial dose, titrate upwards to target dose

Indications for automatic implantable cardioverter-defibrillator (AICD)

- LVEF ≤ 35% due to MI / >40 days post-MI OR NYHA class 2/3

- Spontaneous sustained VT

Bi-ventricular ICD (function/lead placement in heart)

- Lead in RA, lead in RV, lead in coronary sinus

- Defibrillator AND pacemaker

Coronary sinus → cardio resynchronization therapy

Indications for bi-ventricular ICD

LBBB with QRS complex ≥ 1.5 sec and EF ≤ 35%

Indications for heart transplant for HF

End-stage HF with refractory medical therapy and cardiac resynchronization

Contraindications of heart transplant

- Irreversible pulm HTN

- Malignancy

- Other end-stage organ disease

Bridges to heart transplant

LV assist device to assists w/ contraction

Common exacerbations of HF

High salt intake, acute illness, new med

Monitoring of acute HF

- Daily weight

- Electrolytes, BUN, creatinine

- Tele until stable VS / electrolytes

- BNP on admin and dc

Inpatient medication management of acute HF

- Supplemental O2

- IV loop: NOT on already → furosemide 40 mg; ON already → 1-2x normal dose as IV

After initiation of IV loop for acute HF, you should see...

Increased UOP within 30-60 mins

With acute HF, avoid BB with...

Cardiogenic shock

With acute HF, avoid which antihypertensives...

ALL to make room for diuresis

With acute HF, avoid SGLT2 inhibitors in...

Fasting diabetics

Post-discharge management of HF

- Readmission COMMON → thorough dc plan

- Home weights

Types of cardiomyopathies (4)

- Dilated

- Hypertrophic

- Restrictive

- Stress induced

Cardiomyopathy

Disease of heart muscle

Cardiomyopathy & HF

ALL cardiomyopathies can cause HF

MCC of dilated cardiomyopathy

Ischemia/MI

Dilated cardiomyopathy

Enlargement of ventricles → unable to contract efficiently

Nonischemic causes of cardiomyopathy

- Postpartum

- Chemo

- Infection

- Idiopathic (genetic)

Diagnostic workup & findings with cardiomyopathy

Echo → reduced LV function

CXR → cardiomegaly

Cardiac cath:

- L ventriculogram → dilation

- Angiogram → ischemia eval

Nonischemic dilated cardiomyopathy

Dilated cardiomyopathy with NO evidence of CAD

Type of HF MC associated with nonischemic dilated cardiomyopathy

HFrEF

Treatment of dilated cardiomyopathy

- Diuretics (loop/aldosterone antagonist) &

- ACEI/ARNI &

- BB &

- SGLT2 inhibitors

**Same as HF

Hypertrophic cardiomyopathy

LV hypertrophy in the absence of causative factors

Hypertrophic cardiomyopathy with obstruction

Thickened septum blocks LV outflow

Leading cause of sudden death in young

Hypertrophic cardiomyopathy

Genertics of hypertrophic cardiomyopathy

Autosomal dominant

Clinical presentation of hypertrophic cardiomyopathy

- Asymptomatic (significance of screening PE)

- Murmur

- Palpable thrill/heave, strong apical pulse

Heart sound associated with hypertrophic cardiomyopathy

Harsh, crescendo-decrescendo that increases with valsalva/standing