Heart Failure

Differential Diagnosis of HF Exacerbation/ Dyspnea

Cardiac

Myocardial HF exacerbation, myocardial infarction

Valvur aortic stenosis, acute aortic regurgitation, mitral regurgitation/stenosis, endocarditis

Pericardial Tamponade

Dysrhythmia

Respiratory

Airway COPD exacerbation, asthma exacerbation, acute bronchitis, bronchiectasis, foreign body obstruction

Parenchyma pneumonia, cryptogenic organizing pneumonia, ARDS, interstitial lung disease exacerbation

Vascular pulmonary embolism, pulmonary hypertension

Pleural pneumothorax, pleural effusion

Systemic sepsis, ARDS, metabolic acidosis, anemia, neuromuscular, psychogenic, anxiety.

Pathophysiology

Anatomic/Physiologic Classification of Cardiomyopathy

Dilated (dilatation and impaired contraction of one or both ventricles) idiopathic, ischemic, valvular, viral, genetic, late manifestation of hypertrophic heart disease, tachycardia induced, alcohol induced, peripartum.

Hhypertrophic (disorder with disproportionate hypertrophy of the left ventricle and occasionally right ventricle) idiopathic (autosomal dominant inheritance with incomplete penetrance), storage disease (Fabry’s disease, Pompe disease, Hurler’s syndrome, Noonan’s syndrome), athlete’s heart, obesity, amyloid.

Restrictive (non dilated ventricles with impaired ventricular filling) idiopathic familial, infiltrative (amyloidosis, hemochromatosis, sarcoidosis), drugs, radiation, endomyocardial fibrosis.

Arrhythomogenic Right Ventricular (replacement of right ventricular free wall with fatty tissue) arrhythmogenic RV dysplasia.

Unclassifiable endocardial fibroelastosis, left ventricular non compaction

Etiologic Classification of Cardiomyopathy

Ischemic Cardiomyopathy (mostly dilated) varying degrees of persistent ischemia, infarction, and left ventricular remodeling.

Valvular Cariomyopathy (mostly dilated) abnormal loading conditions and secondary left ventricular remodeling and dysfunction.

Hypertensive Cardiomyopathy (dilated, restrictive) left ventricular hypertrophy and dysfunction.

Diabetic Cardiomyopathy (dilated) left ventricular dysfunction in the absence of atherosclerosis or hypertension.

Inflammatory Cardiomyoathy (mostly dilated) infectious (diphtheria, rheumatic fever, scarlet fever, typhoid fever, meningococcal, TB, Lyme disease, Leptospirosis, RMSF, poliomyelitis, influenza, mumps, rubella, rubeola, variola, varicella, EBV, Coxsackie virus, echovirus, CMV, hepatitis, rabies, mycoplasma, psittacosis, arboviruses, histoplasmosis, cryptococcosis, Chagas disease), autoimmune, idiopathic myocardial inflammatory diseases.

Metabolic Cardiomyopathy (dilated, restrictive, and/or hypertrophic) endocrine (thyrotoxicosis, hypothyroidism, acromegaly, pheochromocytoma), storage diseases (glycogen storage disease, Fabry’s disease, Gaucher’s disease, Niemann Pick disease), nutritional deficiencies (Beriberi, Kwashiorkor, pellagra), deposition (amyloidosis, hemochromatosis, sarcoidosis).

Muscular Dystrophies (mostly dilated) Duchenne, Becker’s, myotonic dystrophy.

Neuromuscular Friedreich’s ataxia (hyper trophic), Noonan’s syndrome, lentiginosis.

General Systemic Disease (mostly dilated) connective tissue diseases (rheumatoid heart disease, ankylosing spondylitis, SLE, scleroderma, der matomyositis), granulomatous (sarcoidosis, Wegener’s granulomatosis, granulomatous myocarditis), other inflammatory (giant cell myocarditis, hypersensitivity myocarditis), neoplasm (pri mary, secondary, restrictive pattern).

Sensitivity and Toxic Reactions (mostly dilated) alcohol, amphetamine, arsenic, catecholamines, cocaine, anthracyclines, zidovudine, radiation (restrictive as well).

Functional Classification of Heart Failure

Systolic Dysfunction (lower LVEF < 45%) S3 (dilated ventricle with volume overload). Mechanisms include decreased contractility and increased afterload. Causes include MI, cardiomyopathy (dilated, infiltrative), valvular (aortic regurgitation, mitral regurgitation, burn out aor tic stenosis), burn out hypertension and Myocarditis.

Diastolic Dysfunction (normal LVEF) S4 (stiff ventricle), LVH, lower ventricular relaxation, normal LVEF, raised chamber pressures. Mechanisms include decreased active relaxation and passive relaxation (stiff ventricle). Causes include ischemia, hypertension, valvular (aortic stenosis), cardio myopathy (restrictive, hypertrophic), and pericardial disease.

Mixed Dysfunction in many cases, diastolic dys function is present with systolic heart failure.

Precipitants of the HF *Heart Failure*

Forget to take medications (non adherence).

Arrhythmia, anemia.

Infection, ischemia, infarction.

Lifestyle change.

Upregulators (thyroid, pregnancy).

Rheumatic heart disease, acute valvular disease.

Embolism.

Clinical Features

Distinguishing Features Between COPD and HF
	COPD	Heart Failure
History	Previous COPD Medications	Previous HF Medications
Inspect	Nicotine stain, barrel chest Laryngeal height <4cm
Cardiac exam	Subxyphoid cardiac pulse	Elevated JVP, S3, S4
Resp. exam	Hyperresonance Prolonged expiratory time
Investigations	CXR shows hypeinflation ABG shows hypercapnia and hypoxemia	CXR shows redistribution and cardiomegaly ABG shows hypoxemia Elevated BNP

Left Heart Failure left sided S3, rales, wheezes, tachypnea. Causes include previous MI, aortic stenosis, and left sided endocarditis.

Right Heart Failure right sided S3, raised JVP, ascites, hepatomegaly, peripheral edema. Causes include left heart failure, pulmonary hypertension, right ventricular MI, mitral stenosis, and right sided endocarditis.

Grading of Pitting Edema 0= no edema, 1= trace edema, 2= moderate edema disappears in 10 15 s, 3= stretched skin, deep edema disappears in 1 2 min, 4= stretched skin, fluid leaking, very deep edema present after 5 min

Rational clinical examination series: Does this dyspneic patient in emergency department have congestive heart hear failure??
	Sensation	Spc	LR+	LR
History
Initial clinical judgment	61%	80%	4.4	0.45
Hx heart failure	60%	90%	5.8	0.45
Myocardial infarction disease	40%	87%	3.1	0.69
Coronary artery	52%	70%	1.8	0.68
Dyslipidemia	23%	87%	1.7	0.89
Diabetes	28%	83%	1.7	086
Hypertension	60%	56%	1.4	0.71
Smoker	62%	27%	0.84	1.4
COPD	34%	57%	0.81	1.1
PND	41%	83%	2.6	0.70
Orthopnea	50%	77%	2.2	0.65
Edema	51%	76%	2.1	0.64
Dyspnea on exertion	84%	34%	1.3	0.48
Fatigue and weight gain	31%	70%	1.0	0.99
Cough	36%	61%	0.93	1.0
Physical
S3	13%	99%	11	0.88
AJR	24%	96%	6.4	0.79
JVD	39%	92%	5.1	0.66
Rales	60%	78%	2.8	0.51
Any murmur	27%	90%	2.6	0.81
Lower extremity edema	50%	78%	2.3	0.64
Valsalva maneuver	73%	65%	2.1	0.41
SBP < 100 mmHg	6%	97%	2.0	0.97
S4	5%	97%	1.6	0.98
SBP > 150 mmHg	28%	73%	1.0	0.99
Wheezing	22%	58%	0.52	1.3
Ascites	1%	97%	0.33	1.0
CXR
Pulmonary venous         Congestion	54%	96%	12	0.48
Interstitial edema	34%	97%	12	0.68
Alveolar edema	6%	99%	6.0	0.95
Cardiomegaly	74%	78%	3.3	0.33
Pleural effusions	26%	92%	3.2	0.81
Any edema	70%	77%	3.1	0.38
Pneumonia	4%	92%	0.50	1.0
Hyperinflation	3%	92%	0.38	1.1
ECG
Atrial fibrillation	26%	93%	3.8	0.79
New T wave changes	24%	92%	3.0	0.83
Any abnormal finding	50%	78%	2.2	0.64
ST elevation	5%	97%	1.8	0.98
ST depression	11%	94%	1.7	0.95
BNP
BNP > 100 pg/mL			4.1	0.09
For patients with an estimated GFR of 15 60 mL/min/1.73 m2 , a threshold of 201 pg/mL can be used
Approach ‘‘the features evaluated in more than one study with the highest LRs (>3.5) for diagnosing heart failure were the following: the overall clinical judgment, history of heart failure, S3, jugular venous distension, pulmonary venous congestion or interstitial edema on CXR, and atrial fibrillation on ECG. The features evaluated in more than one study with the lowest LRs (<0.60) for diagnosing of heart failure were the following: the overall clinical judgment, no prior history of heart failure, no dyspnea on exertion, the absence of rales, and the absence of radiographic pulmonary venous congestion, or cardiomegaly. The single finding that decreased the likelihood of heart failure the most was a BNP ><100 pg/mL. While the findings of this study are useful when assessing dyspneic patients suspected of having heart failure, no individual feature is sufficiently powerful in isolation to rule heart failure in or out. Therefore, an overall clinical impression based on all available information is best. If the appropriate constellation of findings with high LRs for heart failure are present, that may be sufficient to warrant empirical treatment without further urgent investigations’’><0.60) for diagnosing of heart failure were the following: the overall clinical judgment, no prior history of heart failure, no dyspnea on exertion, the absence of rales, and the absence of radiographic pulmonary venous congestion, or cardiomegaly. The single finding that decreased the likelihood of heart failure the most was a BNP < 100 pg/ml. While the findings of this study are useful when assessing dyspneic patients suspected of having heart failure, no individual feature is sufficiently powerful in isolation to rule heart failure in or out. Therefore, an overall clinical impression based on all available information is best. If the appropriate constellation of findings with high LRs for heart failure are present, that may be sufficient to warrant empirical treatment without further urgent investigations’’
Rational clinical examination series Does this patient have abnormal central venous pressure? JVP vs. Carotid JVP has biphasic waveforms, is non palpable, is occludable, decreases with inspiration, changes with position, and increases with abdominojugular reflux (AJR). To perform the AJR, the blood pressure cuff is pumped 6 x and then pressed against the abdomen at 20 35 mmHg for 15 30 s. Normal = no change in JVP, or transient increase of >4cm 4 cm that returns to baseline before 10 s, or sustained increase <3 cm throughout. Positive AJR occurs when abdominal compression causes a sustained increase in JVP >4cm (sens 24%, spc 96%, LR+ 6.4) Approach ‘‘once the JVP is identified, measure the vertical height. A distance >4 cm above the sternal angle is considered abnormal (i.e. CVP >9cmH2O). An assessment of low JVP has an LR+ for low CVP of 3.4, while an assessment of high JVP has an LR+ for high CVP of 4.1’’
Rational clinical examination series: Can tge clinical examination diagnose left sided heart failure in adults?
Increased filling pressure very helpful findings are radiographic redistribution and jugular venous distension. Somewhat helpful findings are dyspnea, orthopnea, tachycardia, decreased systolic or pulse pressure, S3, rales, and abdominojugular reflux. Edema is helpful only when present. Systolic Dysfunction very helpful findings are radiograph (cardiomegaly, redistribution), anterior Q waves, LBBB, and abnormal apical impulse (especially if sustained). Somewhat help ful findings are tachycardia, decreased blood pres sure or pulse pressure, S3, rales, dyspnea, previous infarction other than anterior, and high peak CK (post infarct). Edema and increased jugular venous pressure are helpful if present Diastolic Dysfunction very helpful finding is elevated blood pressure during the episode of increased filling pressure. Somewhat helpful findings are obesity, lack of tachycardia, older age, and absence of smoking or CAD. Normal radiographic heart size is helpful if present Approach ‘‘in patients without known systolic dysfunction, <1 finding of increased filling pressure can exclude diagnosis >3 findings suggests increased filling pressure. In patients with known systolic dysfunction, absence of finding of increased filling pressure can exclude diagnosis, >1 finding suggests increased filling pressure. For systolic dysfunction, can exclude diagnosis if no abnormal findings, including no sign of increased filling pressure are present (LR 0.1). >3 findings are needed to confirm the diagnosis (LR+ 14)’’

Investigations

Basic

Labs CBCD, electrolytes, urea, Cr, troponin/CK 3, BNP, D dimer, TSH, albumin.

Imaging CXR, echocardiogram (check E/A ratio if diastolic dysfunction)

ECG

Special

Further Imaging MIBI, MUGA

Stress test to assess ischemic heart disease

Cardiac Catherization

ABG if severe dyspnea

Diagnostic and prognostic issue

B Type natriuretic peptide

DIAGNOSIS in addition to heart failure, BNP is also elevated with PE, pulmonary hypertension, LVH, ACS, AF, renal failure, overload, and sepsis

BNP	Heart Failure diagnosis
<100 pg/mL	Unlikely
100 to 250 pg/mL	Compensated LV dysfunction
250 500 pg/mL	HF with both diastolic and systolic dysfunction
500 1000 pg/mL	Decompensate HF
>1000 pg/mL	High risk of substantial HF

Acute Management

Symptom Control wLMNOPw Lasix/furose mide 20 100 mg IV PRN, Morphine 2 5 mg IV PRN, Nitroglycerin 0.4 mg SL PRN, O2, Position (upright)

Long Term Management

Diet low salt (<100 mmol/day, 1.5 2 g/day), fluid restriction (1.5 2 L/day)><100 mmol/day, 1.5 2 g/day), fluid restriction (1.5 2 L/day)

Diuretics furosemide 20 100 IV/PO daily BID with daily adjustments (try to use smallest dose possible to allow ACE inhibitor) + metolazone 2.5 5 mg PO 30 min before furosemide, spironolactone 12.5 50 mg PO daily or eplerenone 25 50 mg PO daily VASODILATORS ACE inhibitor (captopril 6.25 50 mg PO TID, enalapril 2.5 20 mg PO BID, ramipril 2.5 10 mg PO daily, lisinopril 2.5 20 mg PO daily, perindopril 2 8 mg PO daily). ARB (valsartan 40 160 mg PO BID, candesar tan 8 32 mg PO daily). Hydralazine 10 mg PO QID and nitropatch 0.4 mg PO daily. b blockers (metoprolol 50 100 mg PO BID, carvedilol 3.125 25 mg PO BID, bisoprolol 2.5 10 mg PO daily)

Digitalis digoxin 0.125 0.25 mg PO daily

Treatment underlying cause CAD (CABG), aortic stenosis (AV replacement), sleep apnea (CPAP)

Devices if ejection fraction <30 35%, consider cardiac resynchronization therapy (CRT/biventricular pacing) + implantable cardioerter defibrillators (ICD). Ventricular assist devices may also be considered in selected cases of refractory HF

Treatment Issues

ACE Inhibitor hazard ratios for total mortality 0.77 and mortality/hospitalization 0.65 for any patients with LVEF <40%. Target dose = maximum tolerated. Contraindications include SBP <80 mmHg, bilateral renal artery stenosis, severe renal failure, and hyperkalemia.

ARB consider substitution with ARB if ACE inhibitor not tolerated (e.g. cough). May also be used as adjunct to ACE inhibitor if b blocker not tolerated. Contraindications similar to ACE inhibitor.

Hydralazin/Nitrates (VHEFT I and II, A HeFT) less effective than ACE inhibitor. Particularly useful for pregnant patients, African Americans, or those who developed renal insufficiency while on ACE inhibitor, or as add on therapy

β Blockers hazard ratios for total mortality 0.65 and mortality/hospitalization 0.64. May worsen symptoms in first few weeks and may take up to 1 year to see full effect in LVEF. Useful for patients with NYHA II III (and stable IV) and LVEF <40%, also NYHA I, LVEF <40%, and post MI. Contra indications include fluid overload and severe asthma. Start only when patient euvolaemic

Spironolactone hazard ratios for total mortality 0.7 and mortality/ hospitalization 0.65. For patients with NYHA III IV LVEF<35%, and on maximum treatment already. Caution in elderly and renal failure patients as higher risk of hyperkalemia.

Digoxin hazard ratios for total mortal ity 0.99 and mortality/hospitalization 0.92. Particularly useful for patients with both HF and atrial fibril lation, or symptomatic HF despite maximum treatment.

Specific Entities

Causes of Flash Pulmonary Edema cardiac (ischemic heart disease, acute aortic regurgitation, acute mitral regurgitation, mitral stenosis/obstruction, arrhythmia), pulmonary (pulmonary embolism, pneumonia), renal (bilateral renal artery stenosis), systemic (hypertension crisis, fever, sepsis, anemia, thyroid disease)

Hypertrophic Obstructive Cardiomyopathy (HOCM)

Pathophysiology autosomal dominant condition with mutated cardiac sarcomere, leading to massive ventricular hypertrophy (particularly septum). This results in left ventricular outflow tract obstruction, mitral regurgitation, diastolic dysfunction, and subsequently myocardial ischemia and overt heart failure. Cardiac arrhythmias may lead to sudden death (<1%/year). Other complications include atrial fibrillation and infective endocarditis.

Risk Factors for Sudden Death major risk factors include history of cardiac arrest (VF), sustained VT, unexplained syncope, non sustained VT on Holter, abnormal BP response on exercise test, left ventri cular wall thickness >30 mm, and family history of sudden death. Minor risk factors include left ventricular outflow obstruction (gradient >30 mmHg), microvascular obstruction, and high risk genetic defect.

Clinical Features most are asymptomatic although dyspnea, chest pain, syncope, and sudden death may develop. Family history should be obtained. Physical findings include brisk carotid upstroke, bifid carotid pulse, double apical impulse, systolic ejection murmur (LLSB, louder with stand ing and Valsalva) + mitral regurgitation murmur

Diagnosis echocardiogram (septal thickening, systolic anterior motion of mitral valve). Further workup includes 48 h holter monitor and exercise testing annually

Treatments avoidance (dehydration and strenuous exercise), medical (β blockers and non dihydropyridine calcium channel blockers as first line, disopyramide as second line), interventional/surgical (septal myomectomy, alcohol septal ablation, dual chamber pacing), prophylaxis (implantable cardioverter defibrillator for high risk patients to prevent sudden cardiac death, anticoagulation if atrial fibrillation).