Heart Failure. Hilal Al Saffar CABM FRCP FACC College of Medicine,Baghdad University

Transcription

1 Heart Failure Hilal Al Saffar CABM FRCP FACC College of Medicine,Baghdad University

2 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.

3 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.

4 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..

5 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

6 : The disease causes HF can classify into two main groups: o Cardiac (inherited heart disease) o Extra cardiac : o Pressure over load ( hypertension) o Volume over load ( hypervolemia due to water & sodium retention

7 Cardiac Physiology (remember this?) CO = SV x HR Preload Contractility Afterload HR: parasympathetic and sympathetic tone SV: preload, afterload, contractility Stroke Volume Heart Rate Cardiac Output 11/26/2013 7

8 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.. Stroke volume Maximum capacity to produce stroke volume Normal range: stroke volume increases with end-diastolic volume End-Diastolic volume 11/26/2013 8

9 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

10 Functional classification of Heart Failure by Class New York Heart Association % 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 11/26/

11 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)

12 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 11/26/

13 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

14 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

15 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

16 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)

17 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

18 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

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

20 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)

21 Signs and Symptoms of Heart Failure 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) 11/26/

22 Signs and Symptoms of Heart Failure opersistent Cough or Wheezing( cardiac asthma) WHY? ofluid backs up in the lungs SYMPTOMS ocoughing that produces white or pink blood-tinged sputum 11/26/

23 Signs and Symptoms of Heart Failure o Edema WHY? o Decreased blood flow out of the weak heart o Blood returning to the heart from the veins backs up causing fluid to build up in tissues SYMPTOMS o Swelling in feet, ankles, legs or abdomen o Weight gain 11/26/

24 Signs and Symptoms of Heart Failure o Tiredness, fatigue WHY? o Heart can t pump enough blood to meet needs of bodies tissues o Body diverts blood away from less vital organs (muscles in limbs) and sends it to the heart and brain SYMPTOMS o Constant tired feeling o Difficulty with everyday activities 11/26/

25 Signs and Symptoms of Heart Failure 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 11/26/

26 Signs and Symptoms of Heart Failure o Confusion/ 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 11/26/

27 Signs and Symptoms of Heart Failure o Increased heart rate WHY? o The heart beats faster to make up for the loss in pumping function SYMPTOMS o Heart palpitations o May feel like the heart is racing or throbbing 11/26/

28 Signs of heart failure

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30 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

31 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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33 Bat wing appearance of pulmonary edema

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35 Lt sided pleural effusion

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37 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.

38 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.

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

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41 Management Acute pulmonary oedema Sit the patient up in order to reduce pulmonary congestion. Give oxygen (high flow, high concentration). Noninvasive 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 mg i.v.

42 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 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

43 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 antiinflammatory agents, calcium channel blockers) Increasing capillary permeability: nifedipine, amlodipine Idiopathic: women > men Chronic lymphatic obstruction

44 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

45 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

46 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

47 Dysrrhythmia in Heart Failure Frequent Atrial and ventricular ectopics. SVT, atrial fibrillation Frequent ventricular ectopic beats and runs of nonsustained 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)

48 Echocardiography Determine the etiology( IHD, Valvular heart disease, CMP). Assess the severity( measuring the ejection fraction EF >55%) Follow up response to treatment.