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Heart Failure
Hilal Al Saffar CABM FRCP FACC
College of Medicine ,Baghdad University
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Objectives At the end of this lecture ,the student will be able to : • To define heart failure , describe the basic
pathogenetic mechanisms and list the causes . • To list the types of heart failure . • To state the main presenting scenarios , ECG
,Echocardiographic and other investigations in patients with heart failure
• To list the main modes of therapy and prognosis.
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What is Heart Failure?
o The heart can not meet the functional need of the body
o It elicit a number of neural, hormonal &
renal responses.
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Incidence of Heart Failure and its Prognosis
• Heart failure is the leading cause of hospitalization of patients over 65 years in age.
• > 15million new cases of Heart failure estimated each year worldwide.
• Rapidly increasing number because of the aging population.
• Despite many new advances in drug therapy and cardiac assist devices, the prognosis for chronic heart failure remains very poor.
• .
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One year mortality figures are
o50-60% for patients diagnosed with severe failure,
o15-30% in mild to moderate failure, and
o about 10% in mild or asymptomatic failure
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:
The disease causes HF can classify into two main groups:
oCardiac (inherited heart disease) o Extra cardiac : o Pressure over load ( hypertension) oVolume over load ( hypervolemia due to
water & sodium retention
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Cardiac Physiology (remember this?)
• CO = SV x HR
• HR: parasympathetic and sympathetic tone
• SV: preload, afterload, contractility
Preload Contractility Afterload
Stroke Volume Heart Rate
Cardiac Output
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Frank-starling Mechanism
•The Frank-Starling law of the heart states that as the ventricular volume increases and stretches the myocardial muscle fibers, the stroke volume increases, up to its maximum capacity. After that point, increasing volume increases pulmonary capillary pressure (and pulmonary congestion), without increasing the stroke volume or cardiac output..
Stro
ke v
olum
e End-Diastolic volume
Maximum capacity to produce stroke volume
Normal range: stroke volume increases with end-diastolic volume
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In the mildest forms of heart failure, cardiac output is adequate at rest and becomes inadequate only when the metabolic demand increases during exercise or some other form of stress. Almost all forms of heart disease can lead to heart failure and it is important to appreciate that, like anemia, the term refers to a clinical syndrome rather than a specific diagnosis
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Class % of patients
Symptoms
FC I 35% No symptoms or limitations in ordinary physical activity
FC II 35% Mild symptoms and slight limitation during ordinary activity
FC III 25% Marked limitation in activity even during minimal activity. Comfortable only at rest
FC IV 5% Severe limitation. Experiences symptoms even at rest
Functional classification of Heart Failure by
New York Heart Association
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Types of heart failure • Left-sided heart failure. There is a reduction in the left ventricular output and/or an increase in the left atrial or pulmonary venous pressure • Right-sided heart failure. There is a reduction in right ventricular output for any given right atrial pressure • Biventricular heart failure. Failure of the left and right heart (congestive)
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Left versus Right Failure
Left Heart Failure Dyspnea Decrease exercise
tolerance Cough Orthopnea Pink, frothy sputum
Right Heart Failure Decrease exercise
tolerance Edema Hepatomegaly Ascites
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Types of Heart failure cont. • Forward and backward heart failure • Diastolic and systolic dysfunction • High-output failure( Anemia, pregnancy,
thyrotoxicosis). • Acute and chronic heart failure. • Compensated heart failure. • Acute-on-chronic heart failure
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Cardiac compensation • Compensatory mechanisms maintain
adequate CO & tissue perfusion • Mechanisms:
o sympathetic stimulation o fluid retention of kidney o varying degrees of recovery of the heart
itself
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FACTORS THAT MAY PRECIPITATE OR AGGRAVATE HEART
FAILURE IN PATIENTS WITH PRE-EXISTING HEART DISEASE
Myocardial ischaemia or infarction. Arrhythmia, e.g. atrial fibrillation. Pulmonary embolism. Administration of a drug with negative inotropic
properties (e.g. β-blocker) or fluid-retaining properties (e.g. non-steroidal anti-inflammatory drugs, corticosteroids.
Intercurrent illness, e.g. infection. Inappropriate reduction of therapy Conditions associated with increased metabolic
demand, e.g. pregnancy, thyrotoxicosis, anaemia Intravenous fluid overload, e.g. post-operative i.v.
infusion
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Mechanisms Reduced myocardial contractility (Myocardial
infarction, CMP, myocarditis) Ventricular outflow obstruction ( pressure overload)
Hypertension , AS, Pulmonary hypertension , PS. Ventricular inflow obstruction ( MS TS) Ventricular volume overload ,( MR AR VSD, ASD ) Dysrrhythmia,( Atrial fibrillation, heart block). Diastolic dysfunction ,(Constrictive
Pericarditis,Restrictive cardiomyopathy , LVH and fibrosis, Cardiac tamponade)
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Neuro hormonal activation • The primary abnormality in heart failure is
impairment of ventricular function leading to a fall in cardiac output.
• This activates counter-regulatory neuro-hormonal mechanisms that in normal physiological circumstances would support cardiac function, but in the setting of impaired ventricular function can lead to a deleterious increase in both afterload and preload
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• Activation of the sympathetic nervous system may initially maintain cardiac output through an increase in myocardial contractility, heart rate and peripheral vasoconstriction.
• However, prolonged sympathetic stimulation leads to cardiac myocyte apoptosis, hypertrophy and focal myocardial necrosis
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Neurohormonal Activation • Angiotensin II. • Caticolamines. • Aldosterone, • Endothelin • Antidiuretic hormone (ADH) • Natriuretic peptides are released from the atria
(BNP).
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Fluid retention by the kidneys • Occurs over hours to days • Occurs due to
o activation of renin- angiotensin-aldosterone system
o Decrease in renal blood flow causes decrease in GFR
o Increased aldosterone secretion o Increased ADH secretion
• Effects: o Increase in mean systemic filling pressure ( increase blood that go back to the Rt heart)
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o Shortness of Breath (Dyspnea) • WHY?
oBlood “backs up” in the pulmonary veins because the heart can’t keep up with the supply an fluid leaks into the lungs
• SYMPTOMS oDyspnea on exertion or at rest oDifficulty breathing when lying flat
(Orthopnea) oWaking up short of breath (PND)
Signs and Symptoms of Heart Failure
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oPersistent Cough or Wheezing( cardiac asthma) • WHY? oFluid “backs up” in the lungs
• SYMPTOMS oCoughing that produces white
or pink blood-tinged sputum
Signs and Symptoms of Heart Failure
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o Edema • WHY?
oDecreased blood flow out of the weak heart
oBlood returning to the heart from the veins “backs up” causing fluid to build up in tissues
• SYMPTOMS oSwelling in feet, ankles, legs or abdomen oWeight gain
Signs and Symptoms of Heart Failure
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o Tiredness, fatigue • WHY?
oHeart can’t pump enough blood to meet needs of bodies tissues
oBody diverts blood away from less vital organs (muscles in limbs) and sends it to the heart and brain
• SYMPTOMS oConstant tired feeling oDifficulty with everyday activities
Signs and Symptoms of Heart Failure
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o Lack of appetite/ Nausea • WHY?
oThe digestive system receives less blood causing problems with digestion
• SYMPTOMS oFeeling of being full or sick to your
stomach
Signs and Symptoms of Heart Failure
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oConfusion/ Impaired thinking • WHY?
oChanging levels of substances in the blood ( sodium) can cause confusion
• SYMPTOMS oMemory loss or feeling of
disorientation oRelative may notice this first
Signs and Symptoms of Heart Failure
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o Increased heart rate • WHY?
o The heart beats faster to “make up for” the loss in pumping function
• SYMPTOMS oHeart palpitations oMay feel like the heart is racing or throbbing
Signs and Symptoms of Heart Failure
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Signs of heart failure
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Investigations
Designed to discover the underlining cause ,severity and complications.
ECG chest X-ray Urea, creatinine, electrolytes( Na , K, Mg). Haemoglobin , PCV. Thyroid function, Brain natriuretic peptide (BNP) is elevated in heart
failure and can be used as a screening test in breathless patients and those with edema
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Chest X-Ray Abnormal distension of the pulmonary veins( start
with lower veins ,then upper lobe diversion). Right and left pulmonary arteries dilate. Interstitial oedema(thickened interlobular septa
and dilated lymphatics), horizontal lines in the costophrenic angles (septal or 'Kerley B' lines).
Alveolar oedema cause a hazy opacification spreading from the hilar regions
pleural effusions
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Bat wing appearance of pulmonary edema
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Lt sided pleural effusion
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Acute pulmonary edema in heart failure
• Acute Left heart failure or de compensation due to any cause ---- pulmonary congestion and edema
• Pulmonary edema→ fluid filled alveoli ---
decreased oxygenation of blood→ further weakening of heart .
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Clinical Presentation Acute Heart failure symptoms Sudden onset of dyspnoea at rest. Orthopnoea and prostration Agitated, pale and clammy
Signs Peripheries are cool Rapid pulse ,small volume. Excessive tachycardia or Inappropriate bradycardia Blood pressure is usually high because of sympathetic
nervous system activation, but may be normal or low if the patient is in cardiogenic shock.
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Signs cont. • jugular venous pressure (JVP) is usually elevated. • Auscultation: • Gallop • Crepitation are heard at the lung bases.
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Management Acute pulmonary oedema
Sit the patient up in order to reduce pulmonary
congestion. Give oxygen (high flow, high concentration). Non-
invasive positive pressure ventilation (continuous positive airways pressure, CPAP, of 5-10 mmHg) by a tight-fitting face mask results in a more rapid improvement in the patient's clinical state.
Continuous monitoring, including cardiac rhythm, blood pressure and pulse oximetry
Administer a loop diuretic such as furosemide 50-100 mg i.v.
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Management of Pulmonary Edema
cont. • Intravenous opiates, reduce sympathetically mediated
peripheral vasoconstriction, risk of respiratory depression and exacerbation of hypoxia and hypercapnia
• Administer nitrates (e.g. i.v. glyceryl trinitrate 10-200 μg/min or buccal glyceryl trinitrate 2-5 mg) titrated upwards every 10 minutes, until clinical improvement occurs or systolic blood pressure falls to < 110 mmHg.
• Inotropic agents may be required to augment cardiac output (Dopamine , Doputamine)
• Insertion of an intra-aortic balloon pump
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DIFFERENTIAL DIAGNOSIS OF PERIPHERAL
OEDEMA Cardiac failure: right or combined left and right heart
failure, pericardial constriction, cardiomyopathy Chronic venous insufficiency: varicose veins Hypoalbuminaemia: nephrotic syndrome, liver disease,
protein-losing enteropathy; often widespread, can affect arms and face
Drugs Sodium retention: fludrocortisone, non-steroidal anti-inflammatory agents , calcium channel blockers) Increasing capillary permeability: nifedipine, amlodipine
Idiopathic: women > men Chronic lymphatic obstruction
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Chronic heart failure Relapsing and remitting course. A low cardiac output causes fatigue, poor effort
tolerance. Peripheries are cold and the blood pressure is
low. To maintain perfusion of vital organs, blood flow
may be diverted away from skeletal muscle and this may contribute to fatigue and weakness.
Poor renal perfusion may lead to oliguria and uraemia
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Cardiac cachexia • Chronic heart failure is sometimes associated with
marked weight loss. • Anorexia and impaired absorption due to
gastrointestinal congestion • Poor tissue perfusion due to a low cardiac output • Skeletal muscle atrophy due to immobility
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Complications of Heart failure
Renal failure. Hypokalaemia. Hyperkalaemia. Hyponatraemia- It is a poor prognostic sign. Impaired liver function. Thromboembolism ( DVT ) Atrial and ventricular arrhythmias, electrolyte
changes (e.g. hypokalaemia, hypomagnesaemia), underlying structural heart disease, pro-arrhythmic effects of increased circulating catecholamines , drugs (e.g. digoxin
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Dysrrhythmia in Heart Failure • Frequent Atrial and ventricular ectopics. • SVT , atrial fibrillation • Frequent ventricular ectopic beats and runs of non-
sustained ventricular tachycardia(VT) • Sudden death occurs in up to 50% of patients with
symptomatic heart failure and is often due to a ventricular arrhythmia( VT ,VF)
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Echocardiography • Determine the etiology( IHD, Valvular heart disease,
CMP). • Assess the severity( measuring the ejection fraction
EF >55%) • Follow up response to treatment.