Heart Failure

HEART FAILURE
Randa Mahmoud Al-Harizy
Prof. of Internal Medicine

HEART FAILURE
Clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood

Main causes
Ischemic heart disease, Cardiomyopathy, Hypertension
Other causes: Valvular heart disease, Congenital heart
disease, Alcohol and drugs, Hyperdynamic circulation
(anaemia, thyrotoxicosis, haemochromatosis, Paget's
disease), Right heart failure (RV infarct, pulmonary
hypertension, pulmonary embolism, cor pulmonale
(COPD)), Arrhythmia and Pericardial disease.
Causes of heart failure

Impaired cardiac contractility as in myocardial infarction and cardiomyopathy
Ventricular outflow obstruction (pressure overload) as in hypertension and aortic stenosis
Impaired ventricular fillings as in mitral stenosis and constrictive pericarditis
Volume overload as in mitral regurgitation
Mechanisms leading to heart failure

Infections
Arrhythmias
Physical, Dietary, Fluid, Environmental, and Emotional Excesses.
Myocardial infarction
Pulmonary embolism
Anemia
Thyrotoxicosis and pregnancy
Aggravation of hypertension
Rheumatic, Viral, and Other Forms of Myocarditis
Infective endocarditis
PRECIPITATING FACTORS

The heart depends on a number of adaptive
mechanisms for maintenance of its pumping
function:
1- The Frank Starling mechanism (cardiac dilatation)
2- Myocardial hypertrophy
3- Increased release of catecholamines, activation
of renin-angiotensin-aldosteron system and other
Neurohumoral adjustments
N.B.: These effects are compensatory at first, then they are overwhelmed and become pathophysiological
Adaptive mechanisms

PATHOPHYSIOLOGICAL CHANGES
Ventricular dilatation
Myocyte hypertrophy
Increased collagen synthesis
Altered myosin gene expression
Altered sarcoplasmic Ca2+-ATPase density
Increased ANP secretion
Salt and water retention
Sympathetic stimulation
Peripheral vasoconstriction

Neurohormonal changes

⇩ C.O.P
Cardiac remodeling:
Hypertrophy & Dilatation
↑ E.D.V
⇩
2. ↑Sympathetic activity:
⮥ H.R.
V.C
↑ After-load
↑ Pre-load.
Angiotensine
Aldosterone
Na+ & water retention
?

CLINICAL SYNDROMES OF HEART FAILURE
Left ventricular systolic dysfunction (LVSD) is commonly caused by ischaemic heart disease but can also occur with valvular heart disease and hypertension.
Right ventricular systolic dysfunction (RVSD) may be secondary to chronic LVSD but can occur with primary and secondary pulmonary hypertension, right ventricular infarction.
Diastolic heart failure is a syndrome consisting of symptoms and signs of heart failure with preserved left ventricular ejection fraction above 45–50% and abnormal left ventricular relaxation assessed by echocardiography. Diastolic heart failure is more common in elderly hypertensive patients but may occur with primary cardiomyopathies (hypertrophic, restrictive, infiltrative).

SYMPTOMS & SIGNS OF HEART FAILURE
Left heart failure
Symptoms are predominantly fatigue,
exertional dyspnoea, orthopnoea and PND
Physical signs: Cardiomegaly, gallop,
functional mitral regurgitation and crackles at
the lung bases.

Right heart failure
Symptoms (fatigue, breathlessness, anorexia and nausea) relate to distension and fluid accumulation in areas drained by the systemic veins.
Physical signs are usually more prominent than the symptoms, with:
jugular venous distension (± v waves of tricuspid regurgitation)
tender smooth hepatic enlargement
dependent pitting oedema
development of free abdominal fluid (ascites)
pleural transudates (commonly right-sided).
Dilatation of the right ventricle produces cardiomegaly and may give rise to functional tricuspid regurgitation. Tachycardia and a right ventricular third heart sound are usual.

Major symptoms
&
signs
of heart failure

New York Heart Association (NYHA)
Classification of heart failure
Class I No limitation. Normal physical exercise does not cause fatigue, dyspnoea or palpitations
Class II Mild limitation. Comfortable at rest but normal physical activity produces fatigue, dyspnoea or palpitations
Class III Marked limitation. Comfortable at rest but less gentle physical activity produces marked symptoms of heart failure
Class IV Symptoms of heart failure occur at rest and are exacerbated by any physical activity

Framingham Criteria for Diagnosis of Congestive Heart Failure
MAJOR CRITERIA PND, Neck vein distention, Rales, Cardiomegaly, Acute pulmonary edema, S3 gallop, Increased venous pressure (>16 cmH2O) and Positive hepatojugular reflux.
MINOR CRITERIA Extremity edema, Night cough, Dyspnea on exertion, Hepatomegaly, Pleural effusion, Vital capacity reduced by one-third from normal and Tachycardia (≥120 bpm). Weight loss ≥4.5 kg over 5 days' treatment.
To establish a clinical diagnosis of congestive heart failure by these criteria, at least one major and two minor criteria are required.

Diagnostic Investigations
Blood tests - CBC, liver biochemistry, urea and electrolytes, cardiac enzymes , BNP or N-terminal portion of proBNF (NPproBNP), thyroid function.
Chest X-ray - cardiac size and evidence of pulmonary congestion
Electrocardiogram - evidence of ischaemia, hypertension or arrhythmia.
Echocardiography. To establish the presence of systolic and/or diastolic impairment of the left or right ventricle. They may also reveal the aetiology

BRAIN NATRIURETIC PEPTIDE (BNP)
Pre pro-BNP is formed in the ventricles and, with myocyte stretch, is broken down to N-terminal-pro-BNP (NT-pro-BNP) and BNP.
These hormones are highly accurate for identifying or excluding HF with high sensitivity and specificity.
BNP is particularly valuable in differentiating cardiac from pulmonary causes of dyspnea.
The availability of a bedside assay makes BNP useful in evaluating patients in the Emergency Department.

Stress echocardiography. Exercise or pharmacological stress echocardiography has no radiation hazard and is a reliable technique for detecting ischaemia
Nuclear cardiology. Radionuclide angiography (RNA) provides accurate measurements of left, and to a lesser extent, right ventricular ejection fractions, cardiac volumes and regional wall motion.
Cardiac MRI.
Positron emission tomography (PET). When other tests (e.g. stress echocardiography) cannot provide satisfactory results, PET scanning can be used, especially to identify potentially viable muscle that is hibernating.
Cardiac catheterization
Cardiac biopsy for infiltrative disease, e.g. amyloid.

Treatment of Heart Failure
The treatment of HF may be divided into five
components:
general measures.
Correction of the underlying cause.
Removal of the precipitating cause.
Prevention of deterioration of cardiac function.
Control of the congestive HF state.

Treatment of Heart Failure
General measures:
Rest, salt restriction, stop smoking
Removal of the cause:
This deserves top priority in all cases and includes surgical measures correcting valvular lesions or congenital malformations and medical measures for treating hypertension or infective endocarditis when Present
Removal of precipitating causes of heart failure

⇩ C.O.P
Hypertrophy & Dilatation
↑ E.D.V
⇩
2. ↑Sympathetic activity:
⮥ H.R.
V.C
↑ After-load
↑ Pre-load.
Angiotensine
Aldosterone
Na+ & water retention
?
Positive Inotropics
Diuretics
ACE inhibitors
vasodilators
Treatment of heart failure

Diuretics
• Essential to control symptoms
secondary to fluid retention
• Prevent progression from HT to HF
• Spironolactone improves survival
• New research in progress

Diuretics & ACEI reduces the number of sacks on the wagon

Cortex
Medulla
Thiazides
Inhibit active exchange of Cl-Na
in the cortical diluting segment of the ascending loop of Henle
K-sparing
Inhibit reabsorption of Na in the
distal convoluted and collecting tubule
Loop diuretics
Inhibit exchange of Cl-Na-K in
the thick segment of the ascending
loop of Henle
Loop of Henle
Collecting tubule
Diuretics

Pharmacological Treatment
Diuretics
(loop diuretics, thiazide diuretics and potassium sparing diuretics)
These act by promoting the renal excretion of salt and water by blocking tubular reabsorption of sodium and chloride. The resulting loss of fluid reduces ventricular filling pressures (preload), produces consistent haemodynamic and symptomatic benefits and rapidly improves dyspnoea and peripheral oedema.

Diuretics (continue)
Loop diuretics: such as furosemide and
bumetanide
Have a rapid onset of action (i.v. - 5 min; oral - 1-2 h) and generally short-lived (4-6 h) diuresis as the concentrating power of the kidney is reduced.
These agents also produce potassium loss and promote hyperuricaemia, and renal function should be monitored.

Diuretics (continue)
Thiazide diuretics:
Thiazides are less effective in patients with reduced glomerular filtration rates.
Thiazide diuretics in combination with loop diuretics have a synergistic action and greater diuretic effect. Associated metabolic abnormalities are more likely and close supervision is needed.

Diuretics (continue)
Potassium-sparing diuretics:
Spironolactone is a specific competitive antagonist to aldosterone, producing a weak diuresis but with a potassium-sparing action.
The Randomized Aldactone Evaluation Study (RALES) showed a 30% reduction in all-cause mortality when spironolactone (up to 25 mg) was added to conventional treatment in patients with moderate to severe heart failure.
Risk factors for developing hyperkalaemia include spironolactone dose > 50 mg/day, high-dose angiotensin-converting enzyme inhibitor (ACEI) and renal impairment.

Vasodilator therapy
Angiotensin-converting enzyme inhibitors ACEI:
ACEI lower systemic vascular resistance and venous pressure, and reduce levels of circulating catecholamines, thus improving myocardial performance.
These drugs should be carefully introduced in patients with heart failure because of the risk of first-dose hypotension.
ACEI are contraindicated in patients with bilateral renal artery stenosis.
Between 10% and 15% of patients develop a cough, owing to the inhibition of bradykinin metabolism.

Vasodilator therapy
Angiotensin receptor antagonists:
Angiotensin II receptor antagonists (ARA) (e.g. losartan, ibersartan, candesartan and valsartan) have similar haemodynamic effects to ACEI, but as they do not affect bradykinin metabolism, they do not produce a cough.

Arteriolar vasodilators:
Drugs such as α-adrenergic blockers (e.g. prazosin) and direct smooth-muscle relaxants (e.g. hydralazine) are potent arteriolar vasodilators but are not very effective in heart failure.
Calcium-channel blockers also reduce afterload, but first-generation calcium antagonists (diltiazem, nifedipine) may have a detrimental effect on left ventricular function in patients with heart failure.

Venodilators:
Short- and long-acting nitrates act by reducing preload and lowering venous pressure, with resulting reduction in pulmonary and dependent oedema but tolerance occurs.
Only combination therapy of nitrate with hydralazine has been shown to improve mortality and exercise performance, and may be useful when ACEI are contraindicated.

β-Adrenoceptor blocking agents
There is considerable evidence to support the use of beta-blockers in patients with chronic stable heart failure. The current guidelines recommend that beta-blockers licensed for use (bisoprolol and carvedilol) in heart failure should be initiated in patients with confirmed heart failure due to left ventricular systolic dysfunction after diuretics and ACE inhibitor therapy, regardless of whether or not symptoms persist.
Initial doses should be low, e.g. carvedilol 3.125 mg twice daily and should be titrated slowly.
Nebivolol is used in the treatment of stable mild–moderate heart failure in patients over 70 years old.

ß-Blockers
Limit the donkey’s speed, thus saving energy

Inotropic Agents
Intravenous inotropes are frequently used to support myocardial function in patients with acute left ventricular failure and following cardiac surgery. Epinephrine (adrenaline), dobutamine, dopexamine and dopamine are intravenous adrenergic agonists.

Cardiac Glycosides
Cardiac glycosides in clinical use are:
Digoxin,
Digitoxin
Ouabain.

Digitalis Compounds
Like the carrot placed in front of the donkey

Cardiac Glycosides
Digitalis glycosides have been used for many years in patients with heart failure and atrial fibrillation.
Digoxin acts as a positive inotrope by competitive inhibition of Na+/K+-ATPase, producing high levels of intracellular sodium. This is then exchanged for extracellular calcium. High levels of intracellular calcium result in enhanced actin-myosin interaction and increased contractility. Digoxin also improves baroreceptor responsiveness, and reduces sympathetic activity and circulating renin.

Digitalis
Mechanism of the +ve inotropic action:
ca++
ATPase
ca++
Na+
Normally
Digitalis
In therapeutic dose leads to partial inhibition of Na+/K+ ATPase enzyme
Na+
Na+
Na+
Na+
Na+
Na+
⮉ intracellular Na+ resulting in:
Na + /ca + +
exchange
ca++
Na+
K+
ca++
ca++
ca++
sarcoplasmic reticulum
ca++
ca++
ca++
ca++
ca++
ca++
ca++
ca++
❶
❷
❸
troponin
Actin
Myosin
?? Force Of Contractility

They have narrow safety margin
GIT:
Anorexia, nausea, vomiting (early toxicity)
abdominal discomfort or pain and diarrhea.
Neurological effects:
Headache, malaise, fatigue, drowsiness, confusion, delirium, hallucination or rarely convulsions.
Vision:
Blurred vision, chromatopsia mostly for yellow and green vision, transient amblyopia or diplopia.
Digitalis
- Adverse (toxic) effects:

C.V.S.:
Any type of arrhythmia may be produced including:
Bradycardia,
Heart block,
Ventricular extrasystole
Ventricular fibrillation.
Digitalis
- Adverse (toxic) effects:

Gynecomastia:
May be due to steroidal structure.
Digitalis
- Adverse (toxic) effects:

Treatment Of Digitalis Toxicitiy:
1) Stop the responsible drug.
2) KCl syrup or slow release or I.V. with ECG monitoring if plasma potassium is low or normal.
3) If due to calcium injection give disodium edetate I.V. which is chelating agent for calcium.
4) Cholestyramine binds to digitalis in gut, thus inhibit absorption and decreases the toxicity especially of digitoxin.
5) In acute toxicity give specific digitalis antibodies (Fab fragment).

⮲Partial heart block is treated by atropine.
⮲ Ventricular arrhythmia without A-V block is treated by lidocaine I.V. or beta blockers.
⮲ Ventricular arrhythmia with A-V block & atrial arrhythmia is treated by Diphenylhydantoin (phenytoin)
Treatment Of Digitalis Toxicitiy:
6) Treatment of associated arrhythmia:

OTHER MEDICATIONS
Anticoagulants:
Oral anticoagulants are recommended in patients with atrial fibrillation and in sinus rhythm with a history of thromboembolism, endocardial thrombus or LV aneurysm.

Antiarrhythmic agents:
Precipitating factors should be treated, in particular electrolyte disturbance.
Atrial fibrillation is common in heart failure and leads to a deterioration in symptoms.
Restoration of sinus rhythm, either by electrical cardioversion or drugs, is desirable but less successful in the presence of structural heart disease and decompensated heart failure.
Rate control with digoxin is often preferred.

The administration of synthetic BNP (Nesritide) produces beneficial haemodynamic effects in acute heart failure (reducing pulmonary capillary wedge pressure and peripheral vascular resistance) but has been associated with an increased risk of death.
Neutral endopeptidase (NEP) is a metallo-endopeptidase involved in the degradation of a variety of vasoactive peptides (including ANP, BNP, CNP and bradykinin). In animal studies NEP inhibitors can produce diuresis and natriuresis.
Acute intravenous administration of endothelin antagonists improves haemodynamic abnormalities in patients with congestive cardiac failure, and oral endothelin antagonists are being developed.

NON-PHARMACOLOGICAL TREATMENT OF HEART FAILURE
Revascularization
Biventricular pacemaker or implantable cardioverter–defibrillator
Cardiac transplantation

Cardiac Resynchronization Therapy
Increase the donkey’s (heart) efficiency

Acute Heart FAILURE
Acute heart failure (AHF) occurs with the rapid onset of symptoms and signs of heart failure secondary to abnormal cardiac function, causing elevated cardiac filling pressures.
This causes severe dyspnoea and fluid accumulates in the interstition and alveolar spaces of the lung (pulmonary oedema).

Clinical Syndromes of Heart Failure

Diagnosis
Initial investigations performed in the emergency
room should include:
■ a 12-lead ECG for acute coronary syndromes, left ventricular hypertrophy, atrial fibrillation
■ a chest X-ray (cardiomegaly, pulmonary oedema, pleural effusion, non-cardiac disease)
■ blood investigations (serum creatinine and electrolytes, full blood count, blood glucose, cardiac enzymes and troponin, CRP and D-dimer)
■ plasma BNP or NTproBNP (BNP > 100 pg/ml or NTproBNP > 300 pg/ml) indicates heart failure
■ transthoracic echocardiography should be performed without delay to confirm the diagnosis of heart failure and possibly identify the cause.

Management of Acute Heart Failure

Pulmonary Oedema
PULMONARY OEDEMA
This is a very frightening, life threatening emergency characterized by
Extreme breathlessness.
Clinical features
Patients with alveolar oedema are acutely breathless, wheezing, anxious and perspiring profusely.
Cough productive of frothy, blood-tinged (pink) sputum, which can be copious with tachypnea and peripheral circulatory shutdown.
Tachycardia, a raised venous pressure and a gallop rhythm.
Crackles and wheezes are heard throughout the chest.
The arterial Po2 falls and initially the Paco2 also falls, owing to overbreathing. Later, the Paco2 increases because of impaired gas exchange.
The chest X-ray shows diffuse haziness, owing to alveolar fluid, and the Kerley B lines of interstitial oedema.

TREATMENT
- The patient must be placed in a sitting position. High-concentration oxygen is given. In severe cases, ventilation is
necessary.
Intravenous diuretic treatment with furosemide or bumetanide is
given. These diuretics induce an acute venodilatory response with a reduction in preload that helps to relieve pulmonary congestion in addition to the more delayed diuretic response.
- Morphine (10-20 mg i.v.) together with an antiemetic such as metoclopramide (10 mg i.v.) is given.
- Venous vasodilators, such as glyceryl trinitrate, may produce prompt relief by reducing the preload.
- Aminophylline (250-500mg or 5mg/kg IV) is infused over 10 minutes
Pulmonary Oedema

Cardiogenic Shock
SHOCK is a severe failure of tissue perfusion, characterized by hypotension, a low cardiac output and signs of poor tissue perfusion such as oliguria, cold extremities and poor cerebral function. Cardiogenic shock is commonly due to myocardial infarction, acute massive pulmonary embolus, pericardial tamponade & sudden-onset valvular regurgitation.
TREEATMENT: Patients require intensive care
General measures such as complete rest, continuous 60% oxygen administration and pain and anxiety relief are essential.
The infusion of fluid is necessary if the pulmonary capillary wedge pressure is below 18 mmHg.
Short-acting venous dilators such as glyceryl trinitrate or sodium nitroprusside should be administered intravenously if the wedge pressure is 25 mmHg or more.
Cardiac inotropes to increase aortic diastolic pressure.
Emergency revascularization of occluded arteries