Heart Failure - Pathophysiology, Clinical Characteristics, and Management (PDF)

Heart failure DR Amir Al-mumin Learning outcomes: By the end of this session and with appropriate self study you should be able to: explain the pathophysiology of heart failure describe the clinical characteristics of the principal types of heart failure, and the circumstances which lead to its...

Heart failure DR Amir Al-mumin Learning outcomes: By the end of this session and with appropriate self study you should be able to: explain the pathophysiology of heart failure describe the clinical characteristics of the principal types of heart failure, and the circumstances which lead to its development identify targets for drug action for the manipulation of cardiac output describe the principles involved in the general management of heart failure, and the categories of drugs used in its therapy In mild to moderate forms of heart failure, cardiac output is normal at rest and only becomes impaired when the metabolic demand increases during exercise or some other form of stress.  HEART FAILURE Heart failure (HF) is a clinical syndrome that occurs in patients who, because of an inherited or acquired abnormality of cardiac structure and/or function, develop a constellation of clinical symptoms (dyspnea and fatigue) and signs (edema and rales) that lead to frequent hospitalizations, a poor quality of life, and a shortened life expectancy Pulmonary vien 4-odema 1-Failure In lung Lead LEFT HEART FAILURE epidemiology HEART FAILURE EJECTION FRACTION FILLING PRESSURE DIASTOLIC FUNCTION ANOTHER DEFINITION  Etiology coronary artery disease (CAD) has become the predominant cause in men and women and is responsible for 60–75% of cases of HF. Hypertension contributes to the development of HF in 75% of patients, including most patients with CAD. Both CAD and hypertension interact to augment the risk of HF, as does diabetes mellitus  Etiology 20-30% unknown ( dilated cardiomyopathy) Viral Alcoholic & toxic Genetic Autosomal dominant Anaemia & arteriovenous fistula Neurohormonal activation of HF  Pathogenesis of heart failure with a depressed ejection fraction However, with time the sustained activation of these systems can lead to secondary end-organ damage within the ventricle, with worsening left ventricular remodeling and subsequent cardiac decompensation there is activation of a family of countervailing vasodilatory molecules, including the atrial and brain natriuretic peptides (ANP and BNP), prostaglandins (PGE2 and PGI2), and nitric oxide (NO), that offsets the excessive peripheral vascular vasoconstriction  The decreased cardiac output in HF patients results in an "unloading" of high-pressure baroceptors in the left ventricle, carotid sinus, and aortic arch. loss of inhibitory parasympathetic tone to the (CNS) with a resultant generalized increase in efferent sympathetic tone, and non-osmotic release of arginine vasopressin (AVP) from the pituitary. AVP [or antidiuretic hormone (ADH)] is a powerful vasoconstrictor that increases the permeability of the renal collecting ducts, leading to the reabsorption of free water. These afferent signals to the CNS also activate efferent sympathetic nervous system pathways that innervate the heart, kidney, peripheral vasculature, and skeletal muscles.  Sympathetic stimulation of the kidney leads to the release of renin, with a resultant increase in the circulating levels of angiotensin II and aldosterone that leads to vasoconstriction of the peripheral vasculature, myocyte hypertrophy, myocyte cell death, and myocardial fibrosis. by maintaining blood pressure, and hence perfusion to vital organs, the same neurohormonal mechanisms are believed to contribute to end-organ changes in the heart and the circulation and to the excessive salt and water retention in advanced HF  Acute HF Chronic HF clinical manifestation Dyspnoea Shortness of breath Exertional Rest Orthopnea Shortness of breath , relived by upright position Paroxysmal nocturnal dyspnea Fatigue cough  signs Sit upright Increased pulse rate Blood pressure Change Jugular venous pulse (Central venous pressure = jagular venous pressure+ 5) >8 cm Abdominojugular reflux Cardiomegaly  chest examination rales are specific for HF if no pulmonary disease. rales are frequently absent in patients with chronic HF, even when LV filling pressures are elevated, because of increased lymphatic drainage of alveolar fluid. Pleural effusions result from the elevation of pleural capillary pressure and the resulting transudation of fluid into the pleural cavities..  chest examination Since the pleural veins drain into both the systemic and the pulmonary veins, pleural effusions occur most commonly with biventricular failure. Although pleural effusions are often bilateral in HF, when they are unilateral, they occur more frequently in the right pleural space  Cardiac examination Apex beat Displaced in cardiomegaly Downward & outward Where is the normal Left parasternal lift Third heart sound S3 (or protodiastolic gallop) is most commonly present in patients with volume overload who have tachycardia and tachypnea, and it often signifies severe hemodynamic compromise. A fourth heart sound (S4) is not a specific indicator of HF but is usually present in patients with diastolic dysfunction.  Abdomen & extremities Hepatomegaly Tender jaundice Due to congestion Ascites Abdominal accumulation of fluid in peritoneal cavity, abdomen swelling Bilateral leg edema Sacral edema  ECG A normal ECG virtually excludes LV systolic dysfunction LVH Old myocardial infarction  chest x-ray acute HF have evidence of pulmonary hypertension, interstitial edema, and/or pulmonary edema. the majority of patients with chronic HF do not. The absence of these findings in patients with chronic HF reflects the increased capacity of the lymphatics to remove interstitial and/or pulmonary fluid.  Echocardiography Assess the size of the ventricles & atria Assess LV function Global Regional EF diastolic Assess the valves Severity of stenosis or regurgitation  Biomarkers Both B-type natriuretic peptide (BNP) and N-terminal pro-BNP, which are released from the failing heart, are relatively sensitive markers for the presence of HF with depressed EF; they also are elevated in HF patients with a preserved EF, albeit to a lesser degree. natriuretic peptide levels increase with age and renal impairment are more elevated in women, and can be elevated in right HF from any cause  Differential diagnosis adult respiratory distress syndrome Renal failure Respiratory disease Both are present Other causes of leg edema Differential diagnosis of peripheral oedema  Treatment HF should be viewed as a continuum Stage A includes patients who are at high risk for developing HF but do not have structural heart disease or symptoms of HF (e.g., patients with diabetes mellitus or hypertension). Stage B includes patients who have structural heart disease but do not have symptoms of HF (e.g., patients with a previous MI and asymptomatic LV dysfunction).  Stage C includes patients who have structural heart disease and have developed symptoms of HF (e.g., patients with a previous MI with dyspnea and fatigue). Stage D includes patients with refractory HF requiring special interventions (e.g., patients with refractory HF who are awaiting cardiac transplantation). In this continuum, every effort should be made to prevent HF not only by treating the preventable causes of HF (e.g., hypertension) but also by treating the patient in stages B and C with drugs that prevent disease progression (e.g., ACE inhibitors and beta blockers) and by symptomatic management of patients in stage D.  For patients who have developed LV systolic dysfunction but remain asymptomatic (class I), the goal should be to slow disease progression by blocking neurohormonal systems that lead to cardiac remodeling For patients who have developed symptoms (class II–IV), the primary goal should be to alleviate fluid retention, lessen disability, and reduce the risk of further disease progression and death Factor ppt HF Management of chronic heart failure General measures Drug therapy  Diuretic therapy furosemide In heart failure, diuretics produce an increase in urinary sodium and water excretion, leading to reduction in blood and plasm volume  Diuretic therapy reduces preload and improves pulmonary and systemic venous congestion. It may also reduce afterload and ventricular volume, leading to a fall in ventricular wall.tension and increased cardiac efficiency  Vasodilator therapy Angiotensin-converting enzyme inhibition therapy Angiotensin receptor blocker therapy  Beta-adrenoceptor blocker therapy Beta-blockade helps to counteract the deleterious effects of enhanced sympathetic stimulation and reduces the risk of arrhythmias and sudden death.e.g bisoprolol started at a dose of 1.25 mg daily, and increased gradually over a 12-week period to a target maintenance dose of 10 mg daily  Ivabradine Ivabradine acts on the If inward current in the SA node, resulting in reduction of heart rate. It reduces hospital admission and mortality rates in patients with heart failure due to moderate or severe left ventricular systolic impairment. In trials, its effects were most marked in patients with a relatively high heart rate (over 77/min) so ivabradine is best suited to patients who cannot take β-blockers or in whom the heart rate remains high despite β- blockade.  Digoxin Digoxin can be used to provide rate control in patients with heart failure and atrial fibrillation. In patients with severe heart failure (NYHA class III–IV), digoxin reduces the likelihood of hospitalisation for heart failure, although it has no effect on long-term survival.  Amiodarone This is a potent anti-arrhythmic drug that has little negative inotropic effect and may be valuable in patients with poor left ventricular function  Implantable cardiac defibrillators and resynchronisation therapy Patients with symptomatic ventricular arrhythmias and heart failure have a very poor prognosis. Irrespective of their response to anti-arrhythmic drug therapy, all should be considered for implantation of a cardiac defibrillator because it improves survival  Coronary revascularisation Coronary artery bypass surgery or percutaneous coronary intervention may improve function in areas of the myocardium that are ‘hibernating’ because of inadequate blood supply, and can be used to treat carefully selected patients with heart failure and coronary artery disease  Heart transplantation Cardiac transplantation is an established and successful treatment for patients with intractable heart failure. Coronary artery disease and dilated cardiomyopathy are the.most common indications  Ventricular assist devices Because of the limited supply of donor organs, ventricular assist devices (VADs) have been :employed as a bridge to cardiac transplantation potential long-term therapy short-term restoration therapy following a potentially reversible insult, e.g. viral myocarditis