Heart Failure

Hilal Al Saffar CABM FRCP FACC

College of Medicine ,Baghdad University

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.

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.

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.

• .

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

:

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

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

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)

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

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

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

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)

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

• 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

Neurohormonal Activation • Angiotensin II. • Caticolamines. • Aldosterone, • Endothelin • Antidiuretic hormone (ADH) • Natriuretic peptides are released from the atria

(BNP).

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)

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

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

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

Bat wing appearance of pulmonary edema

Lt sided pleural effusion

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 .

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.

Signs cont. • jugular venous pressure (JVP) is usually elevated. • Auscultation: • Gallop • Crepitation are heard at the lung bases.

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.

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

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

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

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

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

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)

Echocardiography • Determine the etiology( IHD, Valvular heart disease,

CMP). • Assess the severity( measuring the ejection fraction

EF >55%) • Follow up response to treatment.