مواضيع المحاضرة: Heart failure revised
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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.

Case scenario

A 55 year old male patient presented to you at the out patient department complains from ankle edema of 2 weeks duration. He is known to be hypertensive for the last 15 years on Atenolol 100 mg/day taken irregularly , heavy smoker for the last 20 years , diabetic for the last 4 yeas on Glibenclimide 5 mg /day . He recall that his exercise ability was progressively decreased over the last 6/12 so as he could not go upstairs as he used to and he has to use 3 pillows under during sleep at night.


On clinical exam : BP 180/105 mm Hg , pulse 105 beat/min with some irregularity , JVP 8 cm above sternal angle . Apex beat was at 6th intercostal space anterior axillary line ,cardiac auscultation reviled S3 gallop and II/VI ESM over cardiac apex . There was basal crepitation at lung bases and ++ lower limb pitting edema. Q1. What do you think this patient had? Q2. List 3 possible causes for your possible diagnosis. Q3. List 3 symptoms and 3 physical signs which in favor your diagnosis . Q4. what investigation we will request to prove your diagnosis ?

What is Heart Failure?

The heart can not meet the functional need of the body 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

50-60% for patients diagnosed with severe failure, 15-30% in mild to moderate failure, and about 10% in mild or asymptomatic failure

: The disease causes HF can classify into two main groups:

Cardiac (inherited heart disease) Extra cardiac : Pressure over load ( hypertension) Volume 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
* *

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
End-Diastolic volume
Maximum capacity to produce stroke volume
Normal range: stroke volume increases with end-diastolic volume
* *


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
* *

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
* *

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: sympathetic stimulation fluid retention of kidney 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 activation of renin- angiotensin-aldosterone system Decrease in renal blood flow causes decrease in GFR Increased aldosterone secretion Increased ADH secretion Effects: Increase in mean systemic filling pressure ( increase blood that go back to the Rt heart)

Shortness of Breath (Dyspnea)WHY? Blood “backs up” in the pulmonary veins because the heart can’t keep up with the supply an fluid leaks into the lungsSYMPTOMSDyspnea on exertion or at restDifficulty breathing when lying flat (Orthopnea)Waking up short of breath (PND) Signs and Symptoms of Heart Failure
* *

Persistent Cough or Wheezing( cardiac asthma)WHY? Fluid “backs up” in the lungsSYMPTOMSCoughing that produces white or pink blood-tinged sputum
Signs and Symptoms of Heart Failure
* *

EdemaWHY? Decreased blood flow out of the weak heartBlood returning to the heart from the veins “backs up” causing fluid to build up in tissuesSYMPTOMSSwelling in feet, ankles, legs or abdomenWeight gain
Signs and Symptoms of Heart Failure
* *


Tiredness, fatigueWHY? Heart can’t pump enough blood to meet needs of bodies tissuesBody diverts blood away from less vital organs (muscles in limbs) and sends it to the heart and brainSYMPTOMSConstant tired feelingDifficulty with everyday activities Signs and Symptoms of Heart Failure
* *

Lack of appetite/ Nausea WHY? The digestive system receives less blood causing problems with digestion SYMPTOMS Feeling of being full or sick to your stomach

Signs and Symptoms of Heart Failure

* *

Confusion/ Impaired thinking WHY? Changing levels of substances in the blood ( sodium) can cause confusion SYMPTOMS Memory loss or feeling of disorientation Relative may notice this first

Signs and Symptoms of Heart Failure

* *

Increased heart rateWHY? The heart beats faster to “make up for” the loss in pumping functionSYMPTOMSHeart palpitationsMay feel like the heart is racing or throbbing
Signs and Symptoms of Heart Failure
* *

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 hypercapniaAdminister 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.





رفعت المحاضرة من قبل: Abdalmalik Abdullateef
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