PathoPhysiology Chapter 19

1. Chapter 19Chapter 19
Heart Failure and Dysrhythmias:Heart Failure and Dysrhythmias:
Common Sequelae of CardiacCommon Sequelae of Cardiac
DiseasesDiseases

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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

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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

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HEART FAILURE (CONT.)
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

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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

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HEART FAILURE (CONT.)
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

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HEART FAILURE (CONT.)
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

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HEART FAILURE (CONT.)

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HEART FAILURE (CONT.)
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

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HEART FAILURE (CONT.)

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HEART FAILURE (CONT.)
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

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HEART FAILURE (CONT.)

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HEART FAILURE (CONT.)
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

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HEART FAILURE (CONT.)

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HEART FAILURE (CONT.)
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

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HEART FAILURE (CONT.)

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HEART FAILURE (CONT.)

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HEART FAILURE (CONT.)
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

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HEART FAILURE (CONT.)

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HEART FAILURE (CONT.)

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HEART FAILURE (CONT.)
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

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HEART FAILURE (CONT.)
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

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HEART FAILURE (CONT.)

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HEART FAILURE (CONT.)
Treatment
• Aimed at improving CO while minimizing congestive
symptoms and cardiac workload
• Obtained by manipulating preload, afterload, and
contractility

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HEART FAILURE (CONT.)
• 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

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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

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CARDIAC DYSRHYTHMIAS (CONT.)
Dysrhythmia Mechanisms
• Dysrhythmias initiated by three types of depolarizing
mechanisms
• Abnormal automaticity
• Triggered activity from depolarization
• Reentrant circuits

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
Triggered Activity
• Occurs when an impulse is generated during or just
after repolarization
• Due to depolarizing oscillation of the membrane
potential

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TRIGGERED ACTIVITY

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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

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CARDIAC DYSRHYTHMIAS (CONT.)
Dysrhythmia Analysis
• ECG recordings allow measurement of waveform
amplitude, duration, and heart rate

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
Sinus Arrhythmia
• Associated with fluctuations in autonomic
influences and respiratory dynamics
• May be particularly pronounced in children
• Must be differentiated from sick sinus syndrome

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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)

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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

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CARDIAC DYSRHYTHMIAS (CONT.)
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)

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CARDIAC DYSRHYTHMIAS (CONT.)
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