Chapter 19 Heart Failure and Dysrhythmias PDF

Chapter 19 Heart Failure and Dysrhythmias Dr. Tashea S. Hillard, Associate Professor  Inability of heart to maintain sufficient cardiac output to meet metabolic demands of tissues and organs Results in congestion of blood flow in the systemic or pulmonary venous circulation, inability to increa...

Chapter 19 Heart Failure and Dysrhythmias Dr. Tashea S. Hillard, Associate Professor  Inability of heart to maintain sufficient cardiac output to meet metabolic demands of tissues and organs Results in congestion of blood flow in the systemic or pulmonary venous circulation, inability to increase cardiac Heart output to meet the demands of activity or increased tissue metabolism Failure Increasing incidence; most common reason for hospitalization in those >65 years of age Copyright © 2019, Elsevier Inc. All rights reserved. 2 Pathogenesis and Diagnosis Heart failure (HF) is a potential consequence of most cardiac disorders. Most common cause is myocardial Heart ischemia followed by hypertension and dilated cardiomyopathy. Failure Common manifestations: dyspnea, (Cont.) pulmonary rales, cardiomegaly, pulmonary edema, S3 heart sound, and tachycardia Results from impaired ability of myocardial fibers to contract, relax, or both Copyright © 2019, Elsevier Inc. All rights reserved. 3 Systolic Dysfunction MI is a common etiology. Heart Failure Reduced contractility evidenced by low ejection fraction and reduced inotropy (Cont.) during ventricular systole Impaired contractility involves loss of cardiac muscle cells, β-receptor down-regulation, and reduced ATP production. Copyright © 2019, Elsevier Inc. All rights reserved. 4 Diastolic Dysfunction Coronary artery disease and hypertension are two main causes. More likely to develop in elderly, in Heart women, and in those without history of MI Failure Disorder of myocardial relaxation such that the ventricle is excessively (Cont.) noncompliant and does not fill effectively Low cardiac output, congestion, and edema formation with normal ejection fraction Copyright © 2019, Elsevier Inc. All rights reserved. 5 Heart Failure Compensato Remodeling Helpful in Over the long Current ry restoring term are management cardiac output detrimental to of HF directed Mechanisms toward normal the heart toward and reducing the harmful consequences of these compensatory SNS activation responses: Increased preload Myocardial hypertrophy Copyright © 2019, Elsevier Inc. All rights reserved. 6  Sympathetic Nervous System Activation Primarily a result of baroreceptor reflex stimulation, which detects fall in pressure Heart CNS increases activity in the sympathetic nerves to the heart resulting in venoconstriction. Failure (Cont.) Juxtaglomerular cells release renin, activating the RAAS cascade, resulting in increased sodium and water retention. Remodeling: process of myocyte loss, hypertrophy of remaining cells, interstitial fibrosis Copyright © 2019, Elsevier Inc. All rights reserved. 7  INCREASED INITIALLY A PRELOAD CONSEQUENCE OF REDUCED EF WITH RESULTANT INCREASE IN RESIDUAL ESV Heart DECREASED CO TO RAAS CASCADE Failure THE KIDNEY REDUCED GLOMERULAR FILTRATION = FLUID ACTIVATED = ELEVATED BLOOD VOLUME (Cont.) CONSERVATION FRANK–STARLING CAUSES DAMAGE MECHANISM IN HF Copyright © 2019, Elsevier Inc. All rights reserved. 8 Myocardial Hypertrophy and Remodeling Results from a chronic elevation of myocardial wall tension (law of Laplace) High systolic pressure in the Heart ventricle needed to overcome a high afterload leading to hypertrophy Failure (Cont.) Neurohormonal factors have hypertrophic effect on the heart. Angiotensin II involved in remodeling Copyright © 2019, Elsevier Inc. All rights reserved. 9 Clinical Manifestations Left ventricular failure most common Often leads to right ventricular Heart failure Forward failure = insufficient Failure cardiac pumping manifested by poor CO (Cont.) Insufficient cardiac output may be manifested as confusion, fatigue, tachycardia, reduced urine output, and poor peripheral circulation Backward failure = congestion of blood behind the pumping chamber Copyright © 2019, Elsevier Inc. All rights reserved. 10 Left-Sided Heart Failure Most often associated with: Backward effects, which result in accumulation of blood within the pulmonary circulation, pulmonary Heart congestion, and edema Dyspnea, dyspnea on exertion, orthopnea and paroxysmal nocturnal Failure dyspnea Cough, respiratory crackles (rales), (Cont.) hypoxemia, and high left-atrial pressure, cyanosis Forward effects, which result in insufficient CO with diminished delivery of oxygen and nutrients to peripheral tissues Acute cardiogenic pulmonary and organs edema: life-threatening condition Copyright © 2019, Elsevier Inc. All rights reserved. 11  Right-Sided Heart Failure Pulmonary disorders—increased pulmonary vascular resistance—high afterload—right ventricular hypertrophy (cor pulmonale)—right ventricular failure Heart Failure Backward effects caused by congestion in the systemic venous system Edema, ascites, jugular veins distended, impaired mental functioning, hepatomegaly, splenomegaly Hepatojugular reflux test Forward effects cause low output to left ventricle leading to low CO. Copyright © 2019, Elsevier Inc. All rights reserved. 14  Biventricular Heart Failure Most often result of primary left-sided HF progressing to right-sided HF Heart Failure Reduced CO (Cont.) Pulmonary congestion caused by left-sided HF Systemic venous congestion caused by right-sided HF Copyright © 2019, Elsevier Inc. All rights reserved. 17  Class and Stage of Heart Failure FACES (fatigue, activity limitation, congestion, edema, shortness of breath) Heart Failure Diagnostic assessment includes x-ray and echocardiography. (Cont.) B-type natriuretic peptide level Severity of symptoms used to Determine prognosis, identify the 4 therapy, monitoring classes/stages of HF Copyright © 2019, Elsevier Inc. All rights reserved. 18  Treatment Aimed at improving CO while minimizing congestive symptoms Heart and cardiac workload Failure (Cont.) Obtained by manipulating preload, afterload, and contractility Reduce preload—reduces intravascular volume with diuretics and ACE inhibitors, modify fluid and salt intake Copyright © 2019, Elsevier Inc. All rights reserved. 19  Treatment Improve CO—digitalis Heart Inhibit SNS effects—β-blockers Failure Improve contractility—digitalis or other (Cont.) cardiac glycoside, β agonists (not for long-term use) Reduce effects of Ang II—ACE inhibitors and ARBs Pacemakers: synchronize ventricular contraction Copyright © 2019, Elsevier Inc. All rights reserved. 20  Also called arrhythmias Abnormality of the cardiac rhythm of impulse generation or conduction Cardiac Dysrhythmias Three major types Abnormal sites Abnormal rates of Disturbances in (ectopic) of impulse sinus rhythm conduction pathways initiation Dysrhythmias are significant for two reasons: For indicating an underlying For impairing normal CO pathophysiologic disorder Copyright © 2019, Elsevier Inc. All rights reserved. 21  Dysrhythmia Mechanisms Cardiac Impulse generation: abnormalities in rate of impulse generation from a normal pacemaker Dysrhythmias or from impulse generation from an abnormal (Cont.) (ectopic) site Dysrhythmias initiated by three types of depolarizing mechanisms Triggered Abnormal Reentrant activity from automaticity circuits depolarization Copyright © 2019, Elsevier Inc. All rights reserved. 22  Automaticity Cardiac Spontaneous generation Dysrhythmias of an action potential (Cont.) Major causes Plasma membrane Failure to repolarize leakiness to sodium to normal resting Hypokalemia or calcium ions at membrane potential rest Copyright © 2019, Elsevier Inc. All rights reserved. 23 Triggered Activity Occurs when an impulse is generated during or just after repolarization Results from depolarizing oscillation of the membrane potential Cardiac Early occurs in phase 3 Dysrhythmias (Cont.) Allows some of the voltage-gated calcium channels to reopen and trigger another impulse Late/delayed occurs in phase 4 Calcium ions spontaneously released from the sarcoplasmic reticulum after repolarization, resulting in an action potential Copyright © 2019, Elsevier Inc. All rights reserved. 24 Cardiac Dysrhythmias (Cont.) Reentry Associated with most tachydysrhythmias Cardiac impulse continues to depolarize in a part of the heart after the main impulse has finished its path and the majority of the fibers have repolarized. Myocardial ischemia and electrolyte abnormalities predispose to reentry. Can have wavelets or chase its tail Copyright © 2019, Elsevier Inc. All rights reserved. 25 Dysrhythmia Analysis Cardiac Dysrhythmias ECG recordings allow (Cont.) measurement of waveform amplitude, duration, and heart rate. Copyright © 2019, Elsevier Inc. All rights reserved. 26 Normal Sinus Rhythm Impulse rate between 60 and 100 beats/min Regular rhythm Cardiac Dysrhythmias Starts in the SA node and (Cont.) follows the normal pathway P wave precedes every QRS complex. PR, QRS, QT intervals are of normal duration. Copyright © 2019, Elsevier Inc. All rights reserved. 27 Sinus Tachycardia Abnormally fast heart rate of greater than 100 beats/min Often a compensatory response to Cardiac increased demand for CO or reduced SV Dysrhythmias (Cont.) Usually occurs from SNS activation Treatment aimed at correcting underlying cause; sympatholytic agents or calcium channel blocking agents may be indicated Copyright © 2019, Elsevier Inc. All rights reserved. 28  Sinus Bradycardia Heart rate lower than 60 beats/min Cardiac May be normal in physically trained individuals with large resting SVs Dysrhythmias (Cont.) Usually from parasympathetic activation If slow HR precipitates low CO, treatment includes sympathomimetic or parasympatholytic drugs. Copyright © 2019, Elsevier Inc. All rights reserved. 29  Sinus Arrhythmia Associated with fluctuations in autonomic influences and respiratory dynamics Cardiac May be particularly pronounced in Dysrhythmias children (Cont.) Must be differentiated from May need a pacemaker sick sinus syndrome Sinus arrhythmia is normal and needs no treatment. Copyright © 2019, Elsevier Inc. All rights reserved. 30  Sinus Arrest Absence of impulse initiation in the heart results in electrical asystole. Cardiac Dysrhythmias (Cont.) Escape rhythm: a slower pacemaker will generally begin to fire after several seconds of sinus arrest Pacemaker may be required. Copyright © 2019, Elsevier Inc. All rights reserved. 31  Abnormal Site of Impulse Initiation Initiation of cardiac impulse at a site other than the SA node can Cardiac occur with: ○ SA node failure: allows a Dysrhythmias slower pacemaker to take over (escape rhythm) (Cont.) ○ Enhanced excitability, triggered activity or reentrant circuits may cause a premature depolarization and override the SA node Copyright © 2019, Elsevier Inc. All rights reserved. 32  Escape Rhythms Originate in the AV nodal region or ventricular Purkinje fibers Cardiac Junctional escape rhythm originates Dysrhythmias in the AV node (rate of 40 to 60 beats/min with normal QRS). (Cont.) Ventricular escape rhythm originates in Purkinje fibers (rate of 15 to 40 beats/min with abnormally wide QRS). P wave: abnormal or absent Copyright © 2019, Elsevier Inc. All rights reserved. 33  Atrial Dysrhythmias Premature atrial complexes (PACs) ○ Originate in the atria but not the SA node ○ PACs occur earlier than Cardiac normal, preceded by a P wave, and have a normal Dysrhythmias QRS complex configuration. ○ Frequent PACs may indicate (Cont.) underlying pathophysiologic process and be precursors to more serious dysrhythmias. ○ Paroxysmal focal atrial tachycardia: burst of atrial complexes resembling several PACs in a row Copyright © 2019, Elsevier Inc. All rights reserved. 34  Atrial Flutter and Fibrillation Flutter is typically manifested by a rapid atrial rate of 240 to 350 beats/min with sawtooth pattern. Cardiac ○ Type I—240 to 350 beats/min Dysrhythmias ○ Type II—over 350 beats/min (Cont.) Fibrillation is a completely disorganized and irregular atrial rhythm accompanied by an irregular ventricular rhythm. ○ Can cause thrombi Copyright © 2019, Elsevier Inc. All rights reserved. 35  Junctional Dysrhythmias May be initiated by two junctional zones ○ Area just proximal to the AV node ○ Area just distal to the AV Cardiac node Junctional tachycardia is a rapid Dysrhythmias junctional discharge (70 to 140 beats/min). (Cont.) ○ Resembles a series of junctional premature beats with P waves preceding, following, or buried in the QRS complexes Supraventricular tachycardia: may refer to junctional or atrial tachycardia Copyright © 2019, Elsevier Inc. All rights reserved. 36  Ventricular Dysrhythmias Premature ventricular complexes (PVCs) ○ Arise from the ventricular myocardium Cardiac ○ Do not activate the atria or depolarize the sinus node Dysrhythmias ○ Bizarre QRS ○ Compensatory pause is (Cont.) common. ○ Bigeminy (every other beat) or trigeminy (every third beat) ○ With high frequency, CO may be compromised. Copyright © 2019, Elsevier Inc. All rights reserved. 37  Ventricular Tachycardia Three or more consecutive ventricular complexes at a rate greater than 100 beats/minute Cardiac ECG depicts a series of large, Dysrhythmias wide, undulating waves. (Cont.) P waves are not associated with the QRS complexes. Antiarrhythmia drugs May be fatal if not CPR rapidly managed Electrical cardioversion Copyright © 2019, Elsevier Inc. All rights reserved. 38  Ventricular Fibrillation Rapid, uncoordinated cardiac rhythm resulting in ventricular quivering and lack of effective contraction Cardiac Dysrhythmias (Cont.) ECG is rapid and erratic, with no identifiable QRS complexes. Results in death if not reversed within minutes Antiarrhythmia Defibrillation CPR drugs Copyright © 2019, Elsevier Inc. All rights reserved. 39  Conduction Pathway Disturbances Include delays, blocks, and abnormal pathways Cardiac Conduction blocks and delays: associated with cardiac ischemia Dysrhythmias and infarction Abnormal pathways: usually congenital Copyright © 2019, Elsevier Inc. All rights reserved. 40  Disturbances of Atrioventricular Conduction Atrioventricular block: problem between the sinus impulse and ventricular response ○ Slowed or completely Cardiac blocked ○ Defect in the AV node, Dysrhythmias bundle of His, or bundle branches (Cont.) Three types ○ First-degree block (usually no treatment required) ○ Second-degree block (types I and II) ○ Third-degree block (complete) Copyright © 2019, Elsevier Inc. All rights reserved. 41  Disturbances of Atrioventricular Conduction Types of second-degree block ○ Type I (Wenckebach, Mobitz type I): characterized by progressive prolongation of the PR interval until one P Cardiac wave is not conducted; associated with AV nodal Dysrhythmias ○ ischemia Type II second-degree (Cont.) block: identified by a rhythm showing consistent PR interval with some nonconducted P waves; more serious because has a tendency to progress to complete AV (third-degree) block Copyright © 2019, Elsevier Inc. All rights reserved. 42 Disturbances of Atrioventricular Conduction Cardiac Dysrhythmias (Cont.) Third-degree or complete heart block: diagnosed when there is no apparent association between atrial and ventricular conduction; is serious, as it can lead to slow ventricular rhythm and poor CO Copyright © 2019, Elsevier Inc. All rights reserved. 43  Abnormal Conduction Pathways Accessory pathways—congenital Cardiac abnormalities of the cardiac conduction system; have extra conduction paths Dysrhythmias Alternative pathways for depolarization result in abnormally (Cont.) early ventricular depolarization following atrial depolarizations. Wolff-Parkinson-White syndrome Copyright © 2019, Elsevier Inc. All rights reserved. 44 Intraventricular Conduction Defects Bundle branch block—abnormal conduction of impulses through the intraventricular bundle branches Cardiac Dysrhythmias (Cont.) Right bundle branch supplies right ventricle. Left bundle branch supplies left ventricle (further divided into anterior, posterior, and septal). Copyright © 2019, Elsevier Inc. All rights reserved. 45  Treatment Indicated when dysrhythmias produce significant symptoms or are expected to progress to a more serious level Cardiac Antiarrhythmic drugs used (may be Dysrhythmias proarrhythmic) (Cont.) Measures to improve CO (pacemakers and drugs to increase contractility) Ablation procedures Copyright © 2019, Elsevier Inc. All rights reserved. 46