Heart failure 6/20/2018 cardiac Failure

Definition Inability of the heart to pump blood at a sufficient rate to meet the body’s metabolic needs (forward failure) or the ability to do so only if the cardiac filling pressure are abnormally high (backward failure) or both. HF may be the principal manifestation of nearly every form of cardiac disease. 6/20/2018 cardiac Failure

Causes of HF Pressure overload Impaired contractility Volume overload Aortic stenosis, uncontrolled hypertension. Pulmonary stenosis, Pulmonary HT Impaired contractility MI, Dilated CMP, transient myocardial ischemia Volume overload Aortic regurgitation, Mitral regurgitation Pulmonary regurgitation, Tricuspid regurgitation 6/20/2018 cardiac Failure

Causes of HF Ventricular diastolic dysfunction ventricular hypertrophy, Hypertrophic CMP Transient myocardial ischemia Obstruction of ventricular filling Mitral stenosis,Tricuspid stenosis Pericardial constriction or tamponade. 6/20/2018 cardiac Failure

Features of Heart failure One possible consequence of HF is that Blood may back up on the atrial/venous side of the failing ventricle Leading to engorgement and distension of veins (and the organs they drain) as the venous pressure rises. Another consequence poor tissue perfusion Reduced CO 6/20/2018 cardiac Failure

Features of Heart failure This can be limited to a single ventricle Lt sided HF Rt sided HF. Commonly biventricular Congestive cardiac failure (CCF) Rt ventricle commonly fails secondary to Lt VF 6/20/2018 cardiac Failure

Features of Lt sided HF Dyspnoea on exertion Orthopnea ? pulmonary venous congestion or decreased CO. Orthopnea sensation of laboured breathing on lying flat Paroxysmal Nocturnal Dyspnoea (PND) Cough Hemoptysis Fatigue and weakness reduced skeletal muscle perfusion 6/20/2018 cardiac Failure

Features of Lt sided HF Signs Cold extremities, tachycardia, tachypnea Rales , wheezes, Gallop rhythm. 6/20/2018 cardiac Failure

Features of Rt sided HF Peripheral edema Rt upper quadrant abdominal discomfort Anorexia and nausea edema GIT. Signs Ascitis Hepatomegally Jugular venous distension 6/20/2018 cardiac Failure

Features of CCF Features of Lt sided & Rt sided HF 6/20/2018 cardiac Failure

Compensatory Mechanisms Frank- starling mechanisms Neurohomornal activation Myocardial hypertrophy 6/20/2018 cardiac Failure

Frank – Starling Mechanisms Reduced SV results in incomplete ventricular emptying during systole Volume of blood accumulating during diastole is higher than normal Increased EDV/EDFL/preload greater SV on subsequent contraction Which helps to empty the enlarged ventricle 6/20/2018 cardiac Failure

Frank – Starling Mechanisms There are limits for this beneficial compensatory mechanisms In severe CF and marked depression of contractility marked elevation of EDV&P transmitted retrograde to the atrium,veins &capillaries Resulting in edema/pulmonary congestion 6/20/2018 cardiac Failure

Neurohormonal activation In response to fall in CO Sympathetic reflexes Fluid retention by the kidneys 6/20/2018 cardiac Failure

Sympathetic reflexes In acute stage of cardiac failure Sympathetic become strongly stimulated within a few seconds (30seconds) parasympathetic become reciprocally inhibited at the same time. 6/20/2018 cardiac Failure

Sympathetic reflexes Baroreceptor reflex Chemoreceptor reflexes operates when arterial pressure is diminished. Chemoreceptor reflexes CNS ischaemic response All these activate the SNS 6/20/2018 cardiac Failure

Sympathetic reflexes Sympathetic stimulation Increases heart rate Increases force of contraction Increase the tone of most of the blood vessels. Especially the veins raising the Mean systemic filling pressure and VR increasing cardiac output. 6/20/2018 cardiac Failure

Fluid retention by the kidneys In Chronic stage of cardiac failure Increase blood volume for hours to days Mechanisms RAS Renal body fluid system 6/20/2018 cardiac Failure

Renin Angiotensin system Effects of Angiotensin II vasoconstriction Increase sodium reabsorption (directly) Activate aldosterone secretion Acts on brain to increase secretion of ADH 6/20/2018 cardiac Failure

Renal body fluid system Decreased GFR in cardiac failure Because of reduced renal blood flow intense sympathetic constriction of afferent arterioles of the kidneys Reduced urine output when cardiac output and arterial pressure are significantly less than normal Sometimes anuria when CO falls to ½ - 1/3 normal 6/20/2018 cardiac Failure

Fluid retention by the kidneys Fluid retention leads to: Increased blood volume Increases venous return by Increasing mean systemic filling pressure Distending the veins which reduces venous resistance. 6/20/2018 cardiac Failure

Fluid retention by the kidneys But excess fluid retention in severe stage of HF Overstretch the heart causing ventricular dilatation thus weakening the heart still more Leads to filtration of fluid into the lungs pulmonary edema Development of extensive edema all the peripheral tissues of the body 6/20/2018 cardiac Failure

Fluid retention by the kidneys Note Stretched atrial walls raises ANP level. ANP has a direct effect on the kidneys to increase greatly their excretion of salt and water. 6/20/2018 cardiac Failure

Decreased CO SNS RAS ADH contractility HR vasoconstriction circulating volume arteriolar venous VR to the heart (preload) Maintain BP CO Peripheral edema &Pul. congestion SV 6/20/2018 cardiac Failure

Ventricular hypertrophy Due to sustained ventricular wall stress Either due to volume overload or high afterload. Increased mass of muscle fibers helps to maintain ventricular contractile force. 6/20/2018 cardiac Failure

Ventricular hypertrophy However this compensation may be at the expense of higher than normal diastolic ventricular pressure and therefore atrial pressures, because of increased stiffness of the hypertrophied wall. 6/20/2018 cardiac Failure

Recovery from cardiac failure There may be progressive recovery of the heart itself over a period of several weeks to month. 6/20/2018 cardiac Failure

Recovery from cardiac failure eg HF caused by MI New collateral blood supply begins to penetrate the peripheral portions of the infracted area of the heart. Hypertrophy of undamaged portion of the heart musculature 6/20/2018 cardiac Failure

Recovery from cardiac failure A - Normal state of circulation normal heart B - acutely damaged heart Few seconds after heart attack but before sympathetic reflexes have occurred 10 5 CO L/min A D C B –2 +2 +6 +10 Rt atrial pressure (mmHg) 6/20/2018 cardiac Failure

Recovery from cardiac failure C - damaged heart & sympathetic stimulation Raise in CO towards normal caused by sympathetic reflexes 10 5 CO L/min A D C B –2 +2 +6 +10 Rt atrial pressure (mmHg) 6/20/2018 cardiac Failure

Recovery from cardiac failure D - Final return of CO to normal after several days to weeks of cardiac recovery and fluid retention. partially recovered heart 10 5 CO L/min A D C B –2 +2 +6 +10 Rt atrial pressure (mmHg) 6/20/2018 cardiac Failure

Recovery from cardiac failure This final state is called compensated heart failure The maximum pumping ability of the heart is still depressed to less than a half normal 10 5 CO L/min A D C B –2 +2 +6 +10 Rt atrial pressure (mmHg) 6/20/2018 cardiac Failure

Recovery from cardiac failure However one of the results of chronic cardiac weakness is a chronic increase in Rt atrial pressure ( 6mmHg) 10 5 CO L/min A D C B –2 +2 +6 +10 Rt atrial pressure (mmHg) 6/20/2018 cardiac Failure

Recovery from cardiac failure A patient with compensated heart failure has a reduced cardiac reserve. 10 5 CO L/min A D C B –2 +2 +6 +10 Rt atrial pressure (mmHg) 6/20/2018 cardiac Failure

Recovery from cardiac failure Has normal CO at rest, but heavy exercises causes immediate return of the symptoms of Acute failure because the heart is unable to increase its pumping capacity to the level required to sustain the exercise 10 5 CO L/min A D C B –2 +2 +6 +10 Rt atrial pressure (mmHg) 6/20/2018 cardiac Failure

Cardiac reserve. It is the maximum percentage that the CO can increase above the normal level. In a heavy young adult the cardiac reserve is 300 – 400% Athletically trained person occasionally up to 500 – 600% In heart failure, no reserve 6/20/2018 cardiac Failure

Cardiac reserve Any factor that prevent the heart From pumping blood satisfactorily decreases cardiac reserve 6/20/2018 cardiac Failure

Precipitating factors: Many patients with chronic HF remain asymptomatic for extended periods, either because impairment is mild or because of compensatory mechanisms. Often clinical manifestation occur only in presence of precipitating factors that increase the cardiac workload. 6/20/2018 cardiac Failure

Precipitating factors Common precipitating factors are; Increased metabolic demands Fever, infection, anemia, tachycardia, hyperthyroidism, pregnancy. Increased circulatory volume (preload) Excessive sodium in diet Excessive fluid administration Renal failure. 6/20/2018 cardiac Failure

Precipitating factors Conditions that increase afterload Uncontrolled HT Pulmonary emboli ↑Rt ventricular afterload Conditions that impair contractility Negatively inotropic drugs Excessively slow HR 6/20/2018 cardiac Failure

Principles of Treatment in HF Identification and correction of the underlying condition causing HF Elimination of the acute precipitating cause of CCF symptoms MEDICATIONS Diuretics Inotropic drugs Vasodilators. 6/20/2018 cardiac Failure

Principles of Treatment in HF Diuretics reduce the venous fluid overload. Inotropic drugs (eg. Digoxin) improve myocardial contractility. Afterload reducing agents (i.e arterial vasodilators) reduce the load against which the ventricle must contract. 6/20/2018 cardiac Failure

NOTE: Cardiac failure can lead to shock. 6/20/2018 cardiac Failure