PathoPhysiology Chapter 19

Chapter 19Chapter 19

Heart Failure and Dysrhythmias: Heart Failure and Dysrhythmias: Common Sequelae of Cardiac Common Sequelae of Cardiac

DiseasesDiseases

Elsevier items and derived items © 2010, 2005 by Saunders, an imprint of Elsevier Inc.

HEART FAILURE

• Inability of the 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 output to meet the demands of activity or increased tissue metabolism

• Increasing incidence; the most common reason for hospitalization in those >65 years of age


HEART FAILURE (CONT.)

Etiology and Pathogenesis• HF is a potential consequence of most cardiac

disorders• Most common cause is myocardial ischemia

followed by hypertension and dilated cardiomyopathy

• Results from impaired ability of myocardial fibers to contract, relax, or both



Systolic Dysfunction• MI is a common etiology• Reduced contractility evidenced by low ejection

fraction and reduced inotropy during ventricular systole

• Impaired contractility involves loss of cardiac muscle cells, β-receptor down-regulation, and reduced ATP production


HEART FAILURE (CONT.)Diastolic Dysfunction• Ischemic heart disease and hypertension are

two main causes• More likely to develop in elderly, in women,

and in those without history of MI• Disorder of myocardial relaxation such that

the ventricle is excessively noncompliant and does not fill effectively

• Low cardiac output, congestion, and edema formation with normal ejection fraction



Compensatory Mechanisms and Remodeling• Helpful in restoring cardiac output toward normal• Over the long term are detrimental to the heart• Current management of HF directed toward

reducing the harmful consequences of these compensatory responses:• SNS activation• Increased preload• Myocardial hypertrophy



Sympathetic Nervous System Activation• Primarily a result of baroreceptor reflex

stimulation, which detects fall in pressure• CNS increases activity in the sympathetic nerves

to the heart resulting in venoconstriction• Juxtaglomerular cells release renin, activating the

RAAS cascade, resulting in increased sodium and water retention





Increased Preload• Initially a consequence of reduced EF with

resultant increase in residual ESV• Decreased CO to the kidney reduced glomerular

filtration = fluid conservation• RAAS cascade activated = elevated blood volume• Frank-Starling mechanism





Myocardial Hypertrophy and Remodeling• Results from a chronic elevation of myocardial

wall tension (law of Laplace)• High systolic pressure in the ventricle needed to

overcome a high afterload leading to hypertrophy• Neurohormonal factors have hypertrophic effect

on the heart• Angiotensin II involved in remodeling





Clinical Manifestations• Left ventricular failure most common• Often leads to right ventricular failure • Forward failure = insufficient cardiac pumping

manifested by poor CO• Backward failure = congestion of blood behind

the pumping chamber





Left-Sided Heart Failure• Most often associated with:

• Backward effects, which result in accumulation of blood within the pulmonary circulation, pulmonary congestion, and edema

• Forward effects, which results in insufficient CO with diminished delivery of oxygen and nutrients to peripheral tissues and organs







Right-Sided Heart Failure• Pulmonary disorders—increased pulmonary

vascular resistance—high afterload—right ventricular hypertrophy (cor pulmonale)—right ventricular failure

• Backward effects due to congestion in the systemic venous system

• Forward effects cause low output to left ventricle leading to low CO







Biventricular Heart Failure• Most often result of primary left-sided HF

progressing to right-sided HF• Reduced CO• Pulmonary congestion due to left-sided HF• Systemic venous congestion due to right-sided HF



Class and Stage of Heart Failure• FACES (fatigue, activity limitation, congestion,

edema, shortness of breath)• Diagnostic assessment includes x-ray and

echocardiography• B-type natriuretic peptide level• Severity of symptoms used to identify class/stage

of HF





Treatment• Aimed at improving CO while minimizing

congestive symptoms and cardiac workload• Obtained by manipulating preload, afterload, and

contractility



• Preload—reduces intravascular volume with diuretics and ACE inhibitors

• Afterload—β-blockers• Contractility—digitalis or other cardiac glycoside• Pacemakers may be used to help synchronize

ventricular contraction


CARDIAC DYSRHYTHMIAS

• Abnormality of the cardiac rhythm of impulse generation or conduction

• Three major types• Abnormal rates of sinus rhythm• Abnormal sites (ectopic) of impulse initiation• Disturbances in conduction pathways

• Dysrhythmias are significant for two reasons:• Indicate an underlying pathophysiologic disorder• May impair normal CO


CARDIAC DYSRHYTHMIAS (CONT.)

Dysrhythmia Mechanisms • Dysrhythmias initiated by three types of

depolarizing mechanisms• Abnormal automaticity• Triggered activity from depolarization• Reentrant circuits



Automaticity• Spontaneous generation of an action potential• Major causes

• Failure to repolarize to normal resting membrane potential

• Plasma membrane leakiness to sodium or calcium ions at rest



Triggered Activity• Occurs when an impulse is generated during or

just after repolarization • Due to depolarizing oscillation of the membrane

potential


TRIGGERED ACTIVITY


CARDIAC DYSRHYTHMIAS

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



Dysrhythmia Analysis• ECG recordings allow measurement of waveform

amplitude, duration, and heart rate



Normal Sinus Rhythm• Impulse rate between 60 and 100 beats/minute• Regular rhythm• P wave precedes every QRS complex• PR, QRS, QT intervals are of normal duration





Sinus Tachycardia• Abnormally fast heart rate of greater than 100

beats/minute• Often a compensatory response to increased

demand for CO or reduced SV• Treatment aimed at correcting underlying cause;

sympatholytic agents or calcium-channel blocking agents may be indicated



Sinus Bradycardia• Heart rate lower than 60 beats/minute• May be normal in physically trained individuals

with large resting SVs• If slow HR precipitates low CO, treatment includes

sympathomimetic or parasympatholytic drugs



Sinus Arrhythmia• Associated with fluctuations in autonomic

influences and respiratory dynamics• May be particularly pronounced in children• Must be differentiated from sick sinus syndrome



Sinus Arrest• Absence of impulse initiation in the heart results

in electrical asystole• May lead to prolonged intervals of electrical

asystole and no SV until another pacemaker begins to fire

• Pacemaker may be required



Abnormal Site of Impulse Initiation• Initiation of cardiac impulse at a site other than

the SA node can occur with:• SA node failure: allows a slower pacemaker to take over

(escape rhythm)• Enhanced excitability: triggered activity or reentrant

circuits may cause a premature depolarization and override the SA node



Escape Rhythms• Originate in the AV nodal region or ventricular

Purkinje fibers• Junctional escape rhythm originates in the AV

node (rate of 40-60 beats/minute)• Ventricular escape rhythm originates in Purkinje

fibers (rate of 15-40 beats/minute with abnormally wide QRS)



Atrial Dysrhythmias• Originate in the atria but not the SA node• PACs occur earlier than normal, preceded by a P

wave, and have a normal QRS complex configuration

• Frequent PACs may indicate underlying pathophysiologic process and be precursors to more serious dysrhythmias



Atrial Flutter and Fibrillation• Flutter is typically manifested by a rapid atrial

rate of 240-350 beats/minute with sawtooth pattern

• Fibrillation is a completely disorganized and irregular atrial rhythm accompanied by an irregular ventricular rhythm



Junctional Dysrhythmias• May be initiated by two junctional zones

• Area just proximal to the AV node• Area just distal to the AV node

• Junctional tachycardia is a rapid junctional discharge (70-140 beats/minute)

• Resembles a series of junctional premature beats with P waves preceding, following, or buried in the QRS complexes



Ventricular Dysrhythmias• Premature ventricular complexes

• Arise from the ventricular myocardium• Do not activate the atria or depolarize the sinus node• Compensatory pause is common• With high frequency, CO may be compromised



Ventricular Tachycardia• Three or more consecutive ventricular complexes

at a rate greater than 100 beats/minute• ECG depicts a series of large, wide, undulating

waves• P waves are not associated with the QRS

complexes• May be fatal if not rapidly managed



Ventricular Fibrillation• Rapid, uncoordinated cardiac rhythm resulting in

ventricular quivering and lack of effective contraction

• ECG is rapid and erratic, with no identifiable QRS complexes

• Results in death if not reversed within minutes



Conduction Pathway Disturbances• Include delays, blocks, and abnormal pathways• Conduction blocks and delays commonly

associated with cardiac ischemia and infarction• Abnormal pathways are usually congenital



Atrioventricular Conduction Disturbances• Disturbance in conduction between sinus impulse

and associated ventricular response• First-degree block• Second-degree block (types I and II)• Third-degree block



Abnormal Conduction Pathways• Accessory pathways—congenital abnormalities of

the cardiac conduction system• Alternative pathways for depolarization result in

abnormally early ventricular depolarization following atrial depolarizations

• Wolff-Parkinson-White syndrome



Intraventricular Conduction Defects• Bundle branch block—abnormal conduction of

impulses through the intraventricular bundle branches

• Right bundle branch supplies right ventricle• Left bundle branch supplies left ventricle (further

divided into anterior, posterior, and septal)



Treatment• Indicated when they produce significant

symptoms or are expected to progress to a more serious level

• Antiarrhythmic drugs used (may be proarrhythmic)

• Measures to improve CO (pacemakers and drugs to increase contractility)

• Ablation procedures

Education

PathoPhysiology Chapter 19