Heart Failure¶
Leonie Dupuis
Background¶
ACC/AHA Stages of HF
- Stage A: At risk but without structural heart disease, symptoms, or cardiac biomarkers
- Stage B: no symptoms/signs of HF; presence of structural heart disease, incr filling pressures, or incr cardiac biomarkers
- Stage C: + structural HD, + prior or current symptoms
- Stage D: marked HF, symptoms interfere with daily life and recurrent hospitalizations
NY Heart Association (NYHA) Functional Classes of HF
- Class I: Normal physical activity is not limited
- Class II: Comfortable at rest; normal physical activity results in HF symptoms
- Class III: Comfortable at rest; less than normal activity leads to HF symptoms
- Class IV: Inability to perform any physical activity without symptoms
Etiologies¶
- HFrEF (Clinical diagnosis + LVEF \< 40%)
- Ischemic (approx. ⅔): Obstructive CAD, previous/current myocardial infarction
- Non-ischemic:
- Load: HTN, valvulopathy
- Arrhythmia: tachyarrhythmia, pacemaker induced
- Myocardium
- Toxins (EtOH, drugs, chemo, radiation),
- Inflammatory (infections, autoimmune),
- Metabolic (thyroid, thiamine deficiency),
- Infiltrative (amyloid, sarcoid, hemochromatosis)
- Stress induced/takotsubo CM
- Genetic
- Idiopathic
- HFpEF: HTN, CAD, obesity, DM, infiltrative, hypertrophic cardiomyopathy
Causes of Heart Failure Exacerbations (FAILURES)¶
- Forgetting medications or taking drugs that can worsen HF (e.g. BB, CCB, NSAIDs, TZDs), chemo (anthracyclines, trastuzumab)
- Arrhythmia/Anemia: AF, VT, PVCs; Increased arrhythmia burden on device check?
- Ischemia/Infarction/Infection: myocarditis; Acute vascular dysfunction (e.g. endocarditis), especially mitral or aortic regurgitation.
- Lifestyle choices: Dietary indiscretions - high salt, EtOH, excessive fluid intake. Obesity.
- Upregulation (of CO): pregnancy and hyperthyroidism
- Renal failure: acute, progression of CKD, or insufficient dialysis (Increased preload)
- Embolus (pulmonary) or COPD (leads to increase right-sided afterload)
- Stenosis (worsening AS, RAS) leading to hypertensive crisis high left-sided afterload
Presentation¶
- Volume overload: shortness of breath, dyspnea on exertion, Orthopnea, PND
- Nausea/poor po intake (hepatic and gut congestion)
- Confusion (decreased CO)
- Exam: Edema (legs, sacrum), rales, S3, S4, murmur (AS, MR), elevated JVD, + hepatojugular reflex, ascites
Evaluation¶
- CBC, CMP, Magnesium, Lactate, TSH, iron studies
- Troponin, ECG
- BNP (Pro-BNP if on Entresto) – high negative predictive value for HF (false negative can occur in obese patients)
- CXR – differentiate other causes of dyspnea
- TTE
- Determine hemodynamic and volume profile
- Cold vs warm
- Dry vs wet
Cardiac Index | Euvolemia | Hypervolemia | |
---|---|---|---|
Low | Warm Extremities Adequate UOP Normal PPP |
Warm and Dry Forrester Class I Tx: GDMT as tolerated |
Warm and Wet Forrester Class II Tx: Diuresis, Vasodilators |
Normal | Cardiogenic Shock Cool Extremities Renal Failure Narrow PP |
Cold and Dry Forrester Class III Tx: Inotropes |
Cold and Wet Forrester Class IV Tx: Diuresis +Tailored therapy (+/- vasodilators, inotropes) |
Management of exacerbations¶
- Tele, Daily STANDING weights, 2L fluid restriction, 2g sodium diet, strict I/Os
- Diuresis: Place on 2.5 x home dose of IV diuretic, dose BID-TID (DOSE Trial)
- Goal is to be net negative (generally 1-2 L per day but patient dependent)
- Check BMP BID and Mg QD, keep K>4 and Mg>2
- Low threshold for substantial increase (double) in loop vs transition to drip if not diuresing adequately
- Can also augment with sequential nephron blockade (thiazides, acetazolamide)
- Lasix 40mg PO = Lasix 20mg IV = Torsemeide 20mg PO/IV = Bumex 1mg PO/IV
- Continuation/optimization of GDMT (below)
Guideline-Directed Medical Therapy for HFrEF¶
General Principles¶
- Starting patients on low dose of multiple agents preferred to max dose of single agent
- D/C summary should have discharge weight, GDMT and diuretic regimen, and renal function
- Daily home weights with rescue diuretic plan (pm dose for 3 lbs in 1 day, 5 lbs in 3 days
Drug | Indication | Mechanism/ Benefits | Precautions |
---|---|---|---|
Beta Blockers | |||
Carvedilol Metoprolol succinate Bisoprolol |
HFrEF <40 % Stage C HF (NYHA class I – IV) |
Reduces catecholamine stimulation. Decreased HR, myocardial energy demand, less adverse remodeling. | Avoid if pt is decompensated (cold); “start low and go slow” Can continue during exacerbation if patient compensated |
ARNIs | |||
Sacubitril/ valsartan | HFrEF < 40% NYHA class II – IV Used in place of ACE/ARB |
Prevents vasoactive natriuretic peptide degradation involved in pathogenesis of HF (+ action of ARB) | Need a 36 hr wash-out period if transitioning from ACEi to ARNI Hypotension Risk of angioedema |
ACEIs | |||
Lisinopril Enalapril Captopril Ramipril |
HFrEF <40 % Stage C HF (NYHA class I – IV) |
Blocks harmful effects of RAAS activation and attenuates adverse cardiac and vascular remodeling | Risk of angioedema Monitor renal function and K |
ARBs | |||
Losartan Valsartan Candesartan |
HFrEF <40 % Stage C HF (NYHA class I – IV) |
See ACEIs | See ACEIs Preference for ARB > ACEi if plans to start ARNI |
MRAs | |||
Eplerenone Spironolactone |
NYHA class II-IV and GFR >30 |
Diuretic and blood pressure lowering effects and blocks deleterious effects of aldosterone on the heart (including hypertrophy and fibrosis) | Hyperkalemia – avoid if CrCl <30 or K >5 |
SGLT2i | |||
Dapagliflozin Empagliflozin |
HFrEF <40% with and without DM NYHA class II-IV In conjunction with background GDMT |
Osmotic diuresis and natriuresis, improve myocardial metabolism, inhibit sodium-hydrogen exchange in myocardium, reduce cardiac fibrosis | UTI/ GU infections Risk of ketoacidosis (both DKA and euglycemic) |
Vasodilators | |||
Hydralazine Isosorbide Dinitrate |
Persistently symptomatic black patients despite ARNI/ BB/ MRA/ SGLT2i NYHA class III-IV |
Reduces cardiac afterload and preload and may also enhance nitric oxide bioavailability Reduction in mortality for African American patients |
Hypotension |
Ivabradine | |||
Ivabradine | HFrEF <35%, on maximally tolerated BB, sinus rhythm with HR > 70 NYHA class II or III |
If current inhibitor involved in SA node activity Decr HR associated with improved outcomes |
Need sinus rhythm Caution in sinus node disease and conduction defects |
Iron Repletion (IV) | |||
Iron sucrose Ferric carboxymaltose Iron dextran |
Ferritin <100 µg/L or ferritin 100-299 µg/L AND transferrin saturation <20% | Decreases HF hospitalizations Improves exercise function and QOL |
Risk of anaphylaxis higher in iron dextran |
Device therapies (after optimization of medical GDMT for 3 months)¶
- Cardiac resynchronization therapy (CRT)
- Class I indication: NYHA class II to IV, LVEF ≤35% with QRS ≥150 ms and left bundle branch block (LBBB)
- ICD
- Class I indication: NYHA class II – VI with LVEF \<35% (must have >1yr expected survival and 40+ days from MI)
- Mitra Clip
- Criteria: moderate to severe mitral regurgitation (3-4+), on maximally tolerated GDMT, an ejection fraction >20%, and a left ventricle end-systolic dimension of less than 7 cm
Guideline-Directed Medical Therapy for HFpEF¶
- Medications overlap with HFrEF treatment (above) but outcomes are less
significant
- SGLT2 inhibitors can decrease HF hospitalizations and CV mortality
- MRAs can decrease HF hospitalizations
- ARBs and ARNis can be used to decrease hospitalizations
- Diuretics as needed for congestion (no morbidity or mortality benefit)