Heart Failure (Chronic (Management (CRT ( Screenshot 2018-10-11 at 21.04…
CHF is a syndrome, so always look for an underlying cause!
• Ischemic heart disease 65-75%
• Dilated cardiomyopathy~30%
• valvular heart disease ~ 10 %
• Hypertension ~ 10 %
• Other~5% ( Alcohol and drugs (chemotherapy), Arrhythmias, Pericardial disease, Infections (Chagas’ disease)).
As HF evolves, changes in vascular function, blood volume, and neurohumoral status occur throughout the body.
These changes serve as compensatory mechanisms to help maintain cardiac output (primarily by the Frank-Starling mechanism) and arterial blood pressure (by systemic vasoconstriction).
Cardiac changes during HF include increased end-diastolic volume; ventricular dilatation or hypertrophy; decreased stroke volume and cardiac output; reduced ejection fraction (systolic dysfunction) or impaired filling (diastolic dysfunction).
Compensatory mechanisms during HF
Cardiac: Frank-Starling mechanism, tachycardia, ventricular dilatation, hypertrophy, Ventricular remodeling,
Neuronal: increased sympathetic adrenergic activity, reduced cardiac vagal activity
Hormonal: activation of angiotensin-aldosterone system, vasopressin, catecholamines, and natriuretic peptides
Typical: Dyspnea, Orthopnea, Paroxysmal nocturnal dyspnea, Reduced exercise tolerance, Fatigue, Ankle swelling
Less typical: Nocturnal cough, Wheezing, Depression, Loss of appetite, Palpitation, Dizziness, Syncope, Bloated feeling
More specific: HIGH jugular venous pressure, Hepatojugular reflux, S3 (ventricular gallop), Displaced PMI
Less specific: Weight gain / Weigh loss, Cachexia, Cardiac murmur, pleural effusion, Tachycardia, irregular pulse, tachypnoe, Hepatic enlargement, Ascites, Cold extremities, Oliguria, Cheyne-Stokes respiration
Systolic: Impaired contractility / ejection (EF<40) 2/3 of the patients
diastolic Impaired filling / relaxation (EF>40)
• Plasma natriuretic peptides should be measured to identify those who need echocardiography.
• BNP levels correlate with the severity of HF
Common echocardiographic abnormalities
LV ejection fraction
Left ventricular function global and focal
End diastolic/systolic diameter
Fractional shortening, Left atrial size
Left ventricular thickness, Valvular structure/function
Mitral diastolic flow profile, Tricuspid regurgitation
Pericardium, Inferior Vena cava
E/A waves ratio - restrictive, slowed relaxation, normal
E/Ea -increased, reduced, intermediate
A mitral-A pulm duration
Pulmonary S wave
• ECHO is the method of choice in pts with suspected HF.
• We perform ECHO to establish:
a diagnosis of either HFrEF, HFmrHF or HFpEF
a cause of HF (MI,valvular diseaseetc.)
a severity of HF
pts who would be suitable for pharmacological and device (ICD, CRT), treatment
Laboratory tests (include BNP/NT-pro-BNP)
ECG: ischaemia, arrhythmia
Chest X-ray: Kerley B lines, pulmonary oedema, cardiomegaly
Sometimes: exercise tests, spirometry, CMR, CT, Holter-ECG, invasive coronary angiography, right heart catheterisation, endomiocardial biopsy
preserved (HFpEF), mid-range (HFmrEF) and reduced ejection fraction (HFrEF)
poor prognosis in HF
New York Heart Association classification of heart failure.
Focuses on symptoms
Class I: No limitation of physical activity.
Class II: Slight limitation with ordinary exertion.
Class III: Marked limitation with less than ordinary exertion.
Class IV: Symptoms are present at rest.
ACC/AHA Classification: Emphasizes evolution and progression of heart failure.
Class A: risk of HF, no structural changes
Class B: structural changes, no symptoms
Class C: structural changes, symptoms
Class D: End-stage symptoms
• Exercise training for stable HF patients
• Weight loss in obese patients
• Dietary Na restriction (≤ 2 g/day)
• Fluid and free water restriction (≤ 1.5 L/day)
• Minimize medications like (negative inotrops, NSAIDs)
• Smoking cessation and alcohol intake reduction
ACE inhibitors: (lisinopril, Captopril, ramipril, trandolapril, perindopril, enalapril)
Beta-blockers: (carvedilol, bisoprolol, metoprolol CR, nebivolol)
Aldosterone antagonists: (spironolacton, eplerenon)
Angiotensin II rec. inhibitors: (candesartan, valsartan, losartan)
Ivabradine (HR>70/min., BB intolerance-Iia class indications) Vasodilators
Digoxin Cardiac glycosides
Diuretics: (Furosemide, Metolazone, Bumetanide)
Drugs to avoid in HF patients
NSAIDs: Induce systemic vasoconstriction, counteract ACE inhibitors.
Thiazolidinediones: Contribute to fluid retention. Should be avoided in severe (class III-IV) failure.
Class I antiarrhythmic drugs: Can be proarrhythmic and have inotropic negative effect.
Calcium channel blockers: (avoid Verapamil and Diltiazem).
Other management considerations
• Cardiac resynchronization therapy (CRT)
• Implantable cardioverter-defibrillator (ICD). Significant benefit in NYHA class II -III HF and EF ≤ 35%
• Revascularisation, valvular disease operation, aneurysmectomy
• Mechanical circulatory support.
• Cardiac transplantation.
for HTN pats.
Precipitants and Causes:
de novo,arrhythmia , Acute coronary syndrome (ACS)
pulmonary embolism, Hypertensive crisis, Cardiac tamponade
Aortis dissection, Surgery, Peripartum cardiomyopathy, Infection (include endocarditis)
COPD/asthma, Anaemia, Kidney dysfunction, Hypo/Hyperthyroidism
Alcohol and drug abuse
Blood chemistry, Oxygen saturation
Chest X-ray, ECHO (within 48 hours)
Monitoring of the patient's vital functions:
Systolic blood pressure, Heart rhythm and rate
Saturation of oxygen, Respiratory rate
Monitoring of the patients with AHF:
Intra-arterial line should be considered in pts with hypotension
Pulmonary artery catheter may be considered in pts who, present refractory symptoms (hypotension, hypoperfusion)
Initial management of a patient with AHF
Management of patient with AHF
to treat hypoxaemia (SpO2 <90%, PaO2<60 mmHg)
should not be used routinely in non-hypoxaemic patients
Loop diuretics i.v.
for all pts with signs/symptoms of fluid overload
regularly monitor symptoms, urine output, renal function and electrolytes
the initial dose should be 20-40mg iv furosemide
useful in patients with pulmonary oedema, ischaemic chest pain
reduce sympathetic drive
but depress respiratory drive and nausea may occur
reduce preload and afterload
increase stroke volume
should be considered for symptomatic relief in AHF pts with SBP > 90mmHg
should be used with caution in pts with significant mitral or aortic stenosis
Inotropes (dobutamine, dopamine, levosimendan, PDE III inhibitors)
to increase cardiac output, blood pressure, improve peripheral perfussion and maintain end-organ function
cause sinus tachycardia, may induce myocardial ischaemia and arrhythmias (monitor ECG, SBP)
to raise blood pressure and redistribute cardiac output from extremities to the vital organs
have adverse effect similar to those of inotropes
In pts with atrial fibrillation:
Digoxin and/or beta-blocker should be considered as first line therapy
Amiodarone may be considered
In pts with reduced EF <40%:
ACEi / ARB
Aldosterone rerceptor antagonist
Digoxin – to control ventricular rate in atrial fibrillation
rapid onset or worsening of symptoms and/or signs of HF
Features of Heart Failure on CXR
Heart enlargement, Pleural Effusion, Re-distribution (alveolar edema), Kerley B lines (short lines near periphery of the lung near the costophrenic angles, and indicate pulmonary congestion secondary to dilation of pulmonary lymphatic vessels), Bronchiolar-alveolar cuffing
clinical syndrome characterized by typical symptoms (e.g. breathlessness, ankle swelling and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles and peripheral oedema) caused by a structural and/or functional abnormality, resulting in a reduced cardiac output and/ or elevated intracardiac pressures.
Left ventricular systolic dysfunction (LVSD) is commonly caused by ischaemic heart disease but can also occur with valvular heart disease and hypertension.
features: due to decreased forward perfusion and pulmonary congestion ( dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles)
Right ventricular systolic dysfunction (RVSD) may be sec- ondary to chronic LVSD but can occur with primary and secondary pulmonary hypertension, right ventricular infarc- tion, arrhythmogenic right ventricular cardiomyopathy and adult congenital heart disease.
features: Jugular venous distension, hepatosplenomegaly with characteristic 'nutmeg' liver, pitting edema (due to increased hydrostatic pressure), Ascites
Systolic HF (systolic dysfunction) is due to a loss of con- tractile strength of the myocardium accompanied by ventricular dilatation. This type of HF is also accompanied by a decrease in normal ventricular emptying
Heart failure with preserved ejection fraction (diastolic dysfunction) occurs when the filling of one or both ventricles is impaired while the emptying capacity is normal.