Pathophysiology Of Heart Failure PDF

Pathophysiology of Heart Failure Dr Alun Hughes Lecture Overview Systolic vs. diastolic dysfunction Right vs. left ventricular dysfunction Causes of dysfunction Compensatory mechanisms (and their problems) Reminders! Cardiac output = HR x SV Pre-load: determined by venous return; EDV Afterload:...

Pathophysiology of Heart Failure Dr Alun Hughes Lecture Overview Systolic vs. diastolic dysfunction Right vs. left ventricular dysfunction Causes of dysfunction Compensatory mechanisms (and their problems) Reminders! Cardiac output = HR x SV Pre-load: determined by venous return; EDV Afterload: force the contracting heart must generate to eject blood from the heart – Main components: vascular resistance; ventricular wall tension – Excessive afterload may impair ventricular ejection and increase wall tension Lilly, figure 9.2 More reminders! Myocardial contractility (inotropy) Increased contractility increases cardiac output independent of preload and afterload Influenced by Ca2+ – L-type channels • opening facilitated by cAMP – Na+/Ca2+ exchange • inhibited indirectly by cardiac glycosides New York Heart Association Classification of Heart Failure (NYHA) Class Patient Symptoms I No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath). II Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath). III Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, or dyspnea. IV Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest. If any physical activity is undertaken, discomfort increases. Systolic vs. Diastolic Dysfunction Classification based on ejection fraction (%) Systolic ventricular dysfunction – impaired cardiac contractility  ↓ ejec9on frac9on – (<40%; normal ~50-65%) Diastolic ventricular dysfunction – normal ejection fraction but impaired diastolic ventricular relaxation and decreased filling –  ↓ in SV and CO Division somewhat artificial Systolic Dysfunction Commonly results from conditions that affect: 1. contractility – e.g. IHD, cardiomyopathy 2. volume overload 3. pressure overload – valvular stenosis; hypertension Results in ↑EDV (preload), ventricular dila9on, ↑ventricular wall tension Diastolic Dysfunction Less common than systolic dysfunction Normal contraction; impaired relaxation Causes: 1. impedance of ventricular expansion – constrictive pericarditis etc. 2. increased wall thickness – hypertrophy etc. 3. delayed diastolic relaxation – aging; ischaemia 4. ↑heart rate Causes of Systolic and Diastolic Dysfunction Lilly, figure 9.6 Right vs. Left Ventricular Dysfunction Classification according to the side of the heart that is primarily affected Long-term heart failure usually involves both sides Right heart failure Left heart failure Congestion of peripheral tissues Oedema and ascites Liver congestion Impaired liver function GI tract congestion Anorexia, GI distress, weight loss Decreased cardiac output Activity intolerance Signs of decreased tissue perfusion Cyanosis and signs of hypoxia Cough with frothy sputum Pulmonary congestion orthopnea Paroxysmal nocturnal dyspnea Right Ventricular Dysfunction: Causes Conditions impeding flow into the lungs – Pulmonary hypertension – Valve damage/stenosis/incompetence Pumping ability of right ventricle – Cardiomyopathy – Infarction Left ventricular failure Congenital heart defects Pathophysiology of RV failure Leo G. Kevin, and Matthew Barnard Contin Educ Anaesth Crit Care Pain 2007;7:89-94 Left Ventricular Dysfunction: Causes Hypertension (↑TPR) Acute myocardial infarction Aortic or mitral valve stenosis or regurgitation Increase in pulmonary pressure can lead to right ventricular failure Compensatory Mechanisms In the early stages of heart failure, compensatory mechanisms (i.e. those involved in hypovolemia) maintain cardiac output Longer-term, they contribute to the worsening of the condition Reminders! Sympathetic nerve activity Renin-angiotensin-aldosterone Frank-Starling (length-tension) mechanism Fluid movements (see oedema tutorial) Compensatory Mechanisms ↑vascular resistance (afterload) ↑contrac-lity Frank-Starling mechanism ↑heart rate Myocardial hypertrophy and remodelling ↑venous return (preload) ↓cardiac output ↑sympathe-c activity ↓renal blood flow renin aldosterone ↑vascular volume ↑sodium and water reten-on vascular tone Angiotensin II adrenal gland Problems with the Compensatory Mechanisms: 1. Frank-Starling ↑ in vascular volume leads to ↑EDV ↑ in muscle stretch and O2 consumption Problems with the Compensatory Mechanisms: 1. Frank-Starling in Systolic Dysfunction Lilly, figure 9.3 Problems with Compensatory Mechanisms: 2. Sympathetic activity Initially, sympathetic activity can be helpful; long-term it is not: – Tachycardia, vasoconstric9on, ↓ perfusion of tissues, cardiac arrhythmias, renin release – ↑ the workload of the heart • ischaemia, damage to myocytes, ↓ contrac9lity – Desensitisation of b but not a receptors Problems with Compensatory Mechanisms: Summary so far Lilly, figure 9.8 Problems with Compensatory Mechanisms: 3. Renin-Angiotensin ↓ in renal blood flow s9mulates release of renin ↑ renin release  ↑ angiotensin II formation – Vasoconstrictor, plus stimulates aldosterone release  sodium and water reabsorp9on is ↑ both directly (decreased flow rate through the kidney) and indirectly (via aldosterone) Problems with Compensatory Mechanisms Lilly, figure 9.9 Problems with Compensatory Mechanisms: 3. Renin-Angiotensin Angiotensin II and aldosterone are also involved inflammatory responses leading to deposition of fibroblasts and collagen in the ventricles  ↑ the s9ffness and ↓ the contrac9lity of the heart, leading to myocardial remodelling and progressing dysfunction Strategies for treatment ↑ cardiac contrac9lity ↓ preload and/or aGerload to ↓ cardiac work demand – By relaxing vascular smooth muscle – By reducing blood volume Inhibit the RAAS Prevent inappropriate ↑ in heart rate Learning Outcomes To define heart failure in terms of systolic/diastolic function and severity. To describe the pathological impact of heart failure on the systemic and pulmonary circulations. To explain the issues with the compensatory mechanisms that are initiated to deal with low cardiac output and predict how these may worsen the underlying issue in heart failure.