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					CONGESTIVE HEART FAILURE
BY MAHMOUD HASSANEIN,MD Professor Of Cardiology Alexandria university

Definition of Heart Failure

HF is a complex 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.

HYPOTHESES OF HEART FAILURE

BACKWARD VS FORWARD HEART FAILUREE HYPOTHESIS

Backward failure Ventricle fails Blood accumulates

Atrial pressure rises
Venous pressure rises Systemic venous congestion pulmonary venous congestion

FORWARD FAILURE
Low cardiac output

Diminished perfusion of vital organs

Kidney

Skin

Skeletal muscle

GIT

Left-sided vs Right-sided Congestive Heart failure

Left-sided heart failure Congestive symptoms
• • • • • Exertional dyspnea Orthopnea Paroxysmal nocturnal dyspnea Cough Cardiac asthma Low output symptoms • Fatigue • Diminished exercise tolerance

Left-sided heart failure Congestive signs
• Inspiratory rales

• S3 gallop [ LV ]
• • • • Tachypnea Cardiomegaly Pulsus alternans Pulmonary venous congestion [CXR ]

Left-sided heart failure Low-output signs
• Altered mentation
• Cool clammy skin • Oliguria

Right-sided heart failureCongestive Symptoms
• Ankle edema • Abdominal distension {ascitis } • Nausea and/or vomiting

• Nocturia

Right-sided heart failure Congestive signs
• • • • • Distended jugular veins Congestive hepatomegaly Ascitis Peripheral edema S3 gallop [ RV ]

LOW OUTPUT VS HIGH OUTPUT HEART FAILURE

Low-output Heart Failure
• Occurs in most forms of heart diseases • Clinical evidence of impairment of the peripheral circulation: Pale and clammy skin Cyanotic extremities Oliguria Altered mentation

High-Output Heart Failure
• Occurs in high-output states • Extremities are usually flushed and warm • Arterio/venous Oxygen difference is minimal • Pulse pressure is widened

High Cardiac Output States
• • • • • • Thyrotoxicosis Severe anemia Arteriovenous fistula Beri Beri Paget’s disease of bone Pregnancy

SYSTOLIC VS DIASTOLIC HEART FAILURE

Systolic Heart Failure
• Definition: inability to pump an adequate
volume of blood to the tissues

• Pathophysiology: inadequate forward
cardiac output

• Examples: Dilated cardiomyopathy

Diastolic Heart Failure
Definition: defect in ventricular filling, thus the ability of the ventricle to accept blood is impaired Pathophysiology Stiff ventricle Elevation of ventricular filling pressure Elevation of venous pressure upstream to the ventricle Pulmonary and/or systemic venous congestion

• • • •

Diastolic Heart Failure Pathophysiology
Stiff ventricle
Elevation of ventricular filling pressure

Elevation of venous pressure upstream to the ventricle
Pulmonary and/or systemic venous congestion

Diastolic Heart Failure Examples
• Transient: acute myocardial ischemia • Sustained: Left ventricular hypertrophy Hypertrophic cardiomyopathy Restrictive heart disease endomyocardial fibrosis amyloidosis,etc…..

Acute vs Chronic heart failure
• Time factor: How rapid the syndrome develops • Compensatory mechanisms: need sufficient time to take effect

Mechanisms Of Cardiovascular Reserve In Heart Failure Major Mechanisms
• • • • Increased heart rate [ tachycardia ] Increased contractile mass [ hypertrophy ] Cardiac dilatation [ Starling’s law ] Increased myocardial contractility [sympathetic adrenergic hyperactivity]

Mechanisms Of Cardiovascular Reserve In Heart Failure MINOR Mechanisms A- Vascular

• Redistribution of cardiac output [resistance regulation ] • Redistribution of blood volume [capacitance regulation] • Increased myocardial perfusion[collaterals]

Mechanisms Of Cardiovascular Reserve In Heart Failure MINOR Mechanisms B- Volume regulation

• Increased plasma volume[ hypervolemia] • Increased red cell mass

Mechanisms Of Cardiovascular Reserve In Heart Failure MINOR Mechanisms C- Widened arterial-mixed venous oxygen difference

ETIOLOGY OF HEART FAILURE

Mechanisms Of Heart Failure

Primary myocardial abnormality or insult

Increase in the workload of the heart

Decease in the work capacity of the heart

Exhaustion of compensatory cardiovascular reserve mechanisms

Pressure Overload
• Left Ventricle: Aortic stenosis Hypertension • Right ventricle Pulmonary stenosis Pulmonary hypertension

Volume Overload
Left ventricle

• Aortic regurgitation • Mitral regurgitation • Arteriovenous fistula
Right ventricle

• Atrial septal defect • Pulmonary regurgitation • Tricuspid regurgitation

Myocardial Disease
• • • • Idiopathic dilated cardiomyopathy Secondary cardiomyopathy Myocarditis Coronary artery disease

For a substantial proportion of patients, causes are:
1. 2. 3. Coronary artery disease Hypertension Valvular heart disease

4.

Dilated cardiomyopathy

Pathophysiology Of Heart Failure

Neuroendocrine Derangements in Congestive Heart Failure

I-Excessive Sympathetic Nervous System Activation In Heart Failure
• Increased plasma norepinephrine toxic to myocardial cells • Increased myocardial NEP spillover decreased myocardial NEP stores • Downregulation of B1 receptors lack of response to sympathetic stimulation • Increased activation of renin angiotensin aldosterone system[RAAS] increased plasma angiotensin levels

II-Activation of the ReninAngiotensin-Aldosterone system

Hemodynamic Alterations in Congestive Heart Failure

Abnormal Baroreflex Responses in Heart Failure

Background on Remodelling
Acute infarction (hours)
Infarct expansion (hours to days)

Global remodelling (days to months)

Improvement of LV remodelling has been associated with improvement in mortality and morbidity outcomes in CHF

NewYork Heart Association classification of functional capacity of patients with chronic heart failure

• Class I: No limitation of ordinary physical activity • Class II: Symptoms occur with ordinary physical activity • Class III: Symptoms occur with minimal physical activity • Class IV: Symptoms occur at rest

Aggravating (or precipitating ) factors for heart failure
1. 2. 3. 4. 5. Arrhythmias……atrial fibrillation Pulmonary thromboembolism Systemic infection… pneumonia Infective endocarditis Myocarditis….recurrence of rheumatic activity

Aggravating (or precipitating ) factors for heart failure-cont.
High cardiac output states Anemia Thyrotoxicosis Pregnancy 7- Development of another form of heart disease……myocardial infarction 8- Development of another systemic illness Renal failure Parenchymal liver disease 6-

Aggravating (or precipitating ) factors for heart failure-cont.
9-Overtransfusion of fluids…postop. State 10-Drugs a) Cardiodepressnat ….betablockers, calcium channel blockers, antiarrhytmic agents, antineoplastic, alcohol b)Salt-retaining…..glucocorticoids, nonsteroidal antiinflammatory, estrogens

Aggravating (or precipitating ) factors for heart failure-cont.
11-Physical, environmental and emotional excesses 12-Negligence of treatment 13-Natural progression of the underlying disease

Investigation in Heart Failure
• Electrocardiogram • CXR • Lab. Work-up…CBC, urinalysis, kidney function tests, serum albumin, serum electrolytes • Echocardiography and Doppler study • Cardiac catheterization and coronary angiography

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Treatment Of Heart Failure
1. Removal of the underlying cause 2. Removal of precipitating or aggravating factors 3. Control of the congestive heart failure state

Control of the congestive heart failure state
1. Improvement of the heart’s pumping performance…..positive inotropic agents 2. Reduction of cardiac workload…. physical and environmental rest vasodilators betablockers 3. Control of excessive salt and water retention…salt restriction and diuretics

Positive Inotropic Agents
• Digitalis • Sympathomimetic agents…. Cyclic AMP agonists…dopamine and dobutamine • Phoshodiesterase inhibitors….amrinone and milrinone

Vasodilators
• Venodilators…..nitrates • Arteriolar dilators…hydralazine • Mixed venous/arteriolar…sodium nitroprusside and prazosin

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Angiotensin converting enzyme inhibitors (ACE-I)
• Block enzymatic conversion of Angio I into Angio II and thus minimise endocrine activation in heart failure • Interfere with the breakdown of bradykinin • Balanced vasodilator action on venous bed and arterioles • Improve morbidity and mortality in heart failure

Angiotensin converting enzyme inhibitors (ACE-I)
• May prevent development of heart failure in asymptomatic patients with left ventricular dysfunction…after myocardial infarction • Considered cornerstone therapy in all patients with heart failure • Examples: captopril 6.25-25 mg tds enalapril 5- 20 mg qd ramipril 1.25- 10 mg qd

Aldosterone Antagonists
Addition of an aldosterone antagonist ( spironolactone 12.5-25 mg qd) is recommended in selected patients with moderately severe to severe symptoms of HF and reduced LVEF who can be carefully monitored for preserved renal function and normal potassium concentration.

Beta Blockers in Heart Failure
• Recently proved to improve morbidity and mortality in patients with heart failure • Suppress sympathetic overactivity incriminated in initiation and progression of heart failure • Three B-blockers are approved for use in heart failure…carvedilol, metoprolol and bisoprolol

Beta-Blockers
I IIa IIb III

Beta-blockers (using 1 of the 3 proven to reduce mortality, i.e., bisoprolol, carvedilol, and sustained release metoprolol succinate) are recommended for all stable patients with current or prior symptoms of HF and reduced LVEF, unless contraindicated.

Beta Blockers in Heart Failure
• Start with very low dose and titrate slowly upwards “start low and go slow” • Prohibited during acute phase of cardiac decompensation

Refractory Heart Failure
Definition: heart failure is termed
refractory when it persists or the patient’s condition deteriorates despite intensive therapy

Management of Refractory Heart Failure
1. Hospitalization 2. Revise diagnosis…… • Exclude any underlying disease that maybe reversible or surgically correctible • Look out for diseases that are not common and not easily recognizable on clinical exam…. Cardiac tumours, constricitive pericarditis and restrictive cardiomyopathies

Management of Refractory Heart Failure
3.Exclude aggravating factors for heart failure 4.Revise every aspect of therapy…suboptimal doses of drugs, patient’ s noncompliance, excessive diuresis, 5.Large volumes of fluids in serous cavities should be removed mechanically

6.Ultracentrifugation to overcome diuretic resistance 7. Intravenous therapy with a vasodilator or a sympathomimetic agent or both for 57 days

Management Of End-Stage Heart Failure

Cardiac Resynchronization Therapy
Patients with LVEF less than or equal to 35%, sinus rhythm, and NYHA functional class III or ambulatory class IV symptoms despite recommended, optimal medical therapy and who have cardiac dyssynchrony, which is currently defined as a QRS duration greater than 120 ms, should receive cardiac resynchronization therapy unless contraindicated.

Device Use
Consideration of an LV assist device as Permanent or “destination” therapy is reasonable in highly selected patients with refractory end-stage HF and an estimated 1-year mortality over 50% with medical therapy.

Implantable CardioverterDefibrillators (ICDs)
An ICD is recommended as secondary prevention to prolong survival in patients with current or prior symptoms of HF and reduced LVEF who have a history of cardiac arrest, ventricular fibrillation, or hemodynamically destabilizing ventricular tachycardia.

Surgical Therapy
Coronary Revascularization

Coronary revascularization is reasonable in patients with HF and coronary artery disease in whom symptomatic or demonstrable myocardial ischemia is judged to be having an adverse effect on cardiac function.

Surgical Therapy
Referral for cardiac transplantation in potentially eligible patients is recommended for patients with refractory end-stage HF.

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THANK YOU

Acute Heart Failure

Major Causes of Acute Heart Failure
• • • • • • • • Extensive myocardial infarction Acute valvular catastrophe (mitral or aortic) Severe poorly controlled hypertension Myocarditis Sustained cardiac arrhythmia Acute pulmonary embolism Decompensation of chronic heart failure Cardiac tamponade

Classification of Acute Heart Failure
• Acute cardiogenic pulmonary edema • Cardiogenic shock • Acute decompensation of chronic heart failure

Management of acute pulmonary edema
• Sublingual nitroglycerin(0.4 mg every 5 min.) • Intravenous nitroglycerin(0.2-0.4 mcg/min.) • Intravenous furosemide(20-40 mg) • Nitroprusside if further afterload reduction is needed • Intravenous morphine(2-6 mg)

Management of acute pulmonary edema
• Supplemental oxygen/mechanical ventilation as guided by arterial blood gases • Reperfusion therapy in case of acute myocardial infarction

Acute Cardiogenic Shock
• • • • • Severe hypotension Diminished pulse pressure Tachycardia Low cardiac output Signs and symptoms of reduced tissue perfusion..oliguria, cool and clammy skin, confusion due to cerebral hypoperfusion and metabolic acidosis

Positive Inotropic therapy
• Synthetic catecholamines: Dobutamine • Phosphodiesterase inhibitors: Milrinone

Vasopressor therapy
• Dopamine • Norepinephrine

Circulatory Support Devices
• Implantable ventricular assist devices • Intraaortic balloon counterpulsation pump


				
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