Phys Chapter 13
Saturday, November 17, 2012
4:34 PM
Cardiac Arrhythmias and Their Electrocardiographic Interpretation
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Causes of cardiac arrhythmias
o Abnormal rhythm of pacemaker
o Pacemaker shift from SA node
o Impulse blocks
o Abnormal pathways of impulse transmission
o Spontaneous generation of spurious impulses
Abnormal Sinus Rhythms
o Tachycardia - fast heart rate (usually faster than 100 beats/min)
 Causes
 Increased body temp (HR increases ~10 beats/min for each degree of F up to
105. Past that HR may decrease as a result of fever
 Increased temp increase rate of metabolism of SA node, increases it's
excitability and rhythm rate
 Stimulation of heart by sympathetics
 i.e. losing blood and going into shock, HR often increased to 150-180
beats/min
 Toxic conditions of the heart
o Bradycardia - slow heart rate (fewer than 60 beats/min)
 Athletes
 Larger/stronger than normal, allowing heart to pump large stroke volume
output
 Vagal Stimulus releases acetylcholine giving parasympathetic effect
 Carotid Sinus Syndrome
 Baroreceptors in carotid sinus region of artery walls are extra sensitive
 Mild external pressure on neck elicits strong reflex -> intense vagal-Ach
effects
 Can actually stop heart for 5-10 sec
o Sinus Arrhythmia
 Cardiotachometer - records by the height of successive spikes b/w successive QRS
complexes
 Can result from anything that alters strengths of sym/parsym nerve signals to sinus
node
 Respiratory type
 Spillover signals from medullary respiratory center to vasomotor center
 Can cause alternate increase/decrease in number of impulses thru sym/vagal
nerves
o Sinoatrial Block
 Impulse from sinus node is blocked before entering atrial muscle
 Sudden cessation of P waves - standstill of atria
 Ventricles - spontaneous AV node stimulation (QRS and T waves slowed but
unaltered)
o Atrioventricular Block
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Conditions that decrease or block impulse thru AV bundle (bundle of His)
 Ischemia of AV node/AV bundle fibers
 Delays/blocks atria to ventricle conduction (i.e. coronary insufficiency)
 Compression of the AV bundle
 i.e. scar tissue or calcified portions of heart depress/blocks atria to vent
conduction
 Inflammation of AV node or AV bundle
 Depress conductivity from atria to ventricles (i.e. inflammation)
 Extreme stimulation of heart by vagus nerves
 Strong stimulation of baroreceptors (see carotid sinus syndrome above)
Incomplete AV Heart Block
 First-Degree Block (prolonged PR or PQ interval)
 Beginning P wave to beginning QRS complex (PR interval) usually ~0.16 s
(HR=normal)
 PR interval decreases in length when HR increases, and vice versa
 PR prolonged when > 0.20 s
 Defined as a delay of conduction but not actual blockage
 Can measure severity of some heart dz's (i.e. acute rheumatic heart dz) by
measuring PR interval
 Second-Degree Block
 Conduction thru AV bundle increases PR interval to 0.25-0.45 s
 Atrial P wave but no QRS-T waves, "dropped beats" of the ventricles
 Can have every of vent beat dropped, 2:1 rhythm develops (2 atrial beats
for every 1 ventricular beat). Can also develop 3:2 or 3:1 rhythm.
 Third-Degree Block (Complete AV Block)
 Ventricles spontaneously establish own signal (usually from AV
node/bundle)
 P waves become dissociated from QRS-T complexes
 No relation b/w atrial/vent beats b/c ventricles have escaped from atrial
control
 Stokes-Adams Syndrome - Ventricular Escape
 Total block comes and goes
 Duration of block may be a few seconds to a few weeks or longer
 Occurs in hearts w/borderline ischemia of conductive system
 Overdrive suppression resulting in ventricular escape
 When AV conduction ceases, vent don't start own beating until 530s delay
 Part of heart beyond the block begins discharging rhythmically
acting as own pacemaker after atria conduction is blocked.
 Brain can't remain active for more than 4-7 s w/o blood supply -> pt
faints
 After escape pt's blood flow to brain can be sustained
 Periodic fainting spells are the syndrome
 Tx: artificial pacemaker
 Incomplete Intraventricular Block - Electrical Alternans
 Caused by similar factors as AV block
 Results from partial intraveventricular block every other heartbeat
 Conditions that depress the heart can result in this
o
 i.e. ishcemia, myocarditis, or digitalis toxicity
Premature Contractions (also called extrasystole, premature beat, or ectopic beat)
 Most caused by ectopic foci in the heart
 Emit abnormal impulses at odd times caused by:
 Local areas of ischemia
 Small calcified plaques - press against adjacent cardiac muscle irritating
fibers
 Toxic irritation of the AV node, Purkinje system or myocaridum
 Drugs, nicotine, or caffeine
 Mechanical due to cardiac catheterization
 Premature Atrial Contractions
 P wave occurs too soon
 PR interval is shortened - ectopic origin of the beat in atria near AV node
 Interval b/w premature contraction and succeeding contraction is prolonged compensatory pause
 Occur frequently in healthy hearts
 Smoking, lack of sleep, too much coffee, alcoholism, and various drugs.
 Pulse Deficit - premature contraction, decreased stoke output, may not be felt
in radial artery
 AV nodal or AV bundle Premature Contractions
 P wave missing, superimposed onto QRS-T complex distorting it slightly
 b/c impulse traveled backward into atria when it moved forward into the
ventricles.
 Same significance and causes as atrial premature contractions
 Premature Ventricular Contractions
 QRS complex very prolonged
 b/c impulse is conducted thru muscle of ventricles rather than purkinje
system
 QRS complex has high voltage
 Impulse travels in one direction and depolarizes one side/end of vent
before the other (instead of at the same time) causing large electrical
potentials
 T wave has an electrical potential polarity opposite of QRS complex b/c slow
conduction of the impulse
 Can be benign in effects resulting from caffeine, nicotine, lack of sleep or
irritability
 May result from stray impulses or re-entrant signals originate near borders of
 infarcted/ischemic areas
 Pt's w/significant numbers of PVCs are at higher risk of spontaneous lethal
ventricular fibrillation
 Vulnerable period for V-fib is the end of T wave
 Vector Analysis of Ectopic Origin for PVC
 Leads II and II strongly positive
 Disorders of Cardiac Repolarization - Long QT Syndromes
 Delay the repolarization of ventricular muscle following the AP cause prolonged
vent APs->excessively long QT intervals --> Long QT Syndrome (LQTS)
 Increases susceptibility to develop ventricular arrhythmias "torsades de pointes"
 May trigger arrhythmias, tachycardia, and sometime V-fib
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Disorders may be inherited or acquired
 Congenital forms are rare caused by mutations of Na+ or K+ channel
genes
 Acquired more common assoc. w/plasma electrolyte disturbances
 i.e. hypomagnesemia, hypokalemia, or hypocalcemia
 Admin of excess antiarrhythmic drugs (i.e. quinidine) or some
antibiotics (i.e. fluoroquinolones or erythromycin) that prolong QT
interval
 Pt may exhibit fainting and vent arrythmias
 Tx: magnesium sulfate for acute LQTS, Long-term LQTS antiarrhythmia
meds (i.e. beta-adrenergic blockers) or surgical implantation of cardiac
defibrillator
Paroxysmal Tachycardia
 Rapid rhythmical discharge of impulses that spread in all directions thru the heart
 Caused most frequently by re-entrant circus movement feedback pathways local repeated self-re-excitation
 Paroxysmal - HR becomes rapid in paroxysms, begins and ends suddenly
 Often can be stopped by vagal reflex - press on the neck in carotid sinus regions
or use drugs (i.e. quinidine and lidocaine which depress normal increase in Na+
permeability of cardiac muscle membrane during generation of AP blocking
discharge of the focal point causing the attack
 Atrial Paroxysmal Tachycardia
 Inverted P wave, partially superimposed onto normal T wave
 AV Nodal Paroxysmal Tachycardia
 Often results from aberrant thythm involving AV node
 Abnormal QRS-T complexes, missing or obscured P waves
 Both Atrial and AV PT usually occur in young, healthy people and is usually
grown out of. Attacks seldom cause permanent damage
 Ventricular Paroxysmal Tachycardia
 Series of ventricular premature beats, no normal beats interspersed
 Serious condition:
 Usually considerable ischemic damage is present in ventricles
 Frequently initiates the lethal condition of V-fib
 Sometimes caused by Digitalis
 Quinidine increases refractory period and threshold for excitationof
cardiac muscle - used to block irritable foci
Ventricular Fibrillation
 Most serious of all, Fatal is not stopped w/in 1-3min
 Cardiac impulses that have gone berserk w/in ventricular muscle mass, feedsback to
re-excited the same vent muscle over and over (many small portions of muscle
contracting at the same time w/equal number relaxing)
 Vent chambers neither enlarge nor contract (no or negligible amounts blood pumped)
 Unconsciousness occurs w/in 3-5 seconds, irretrievable death of tissues begins
thruout the body w/in a few min
 Likely initiated by:
 Sudden electrical shock of the heart
 Ischemia of heart muscle, conducting system or both
 Phenomenon of Re-entry "Circus Movements" as the Basis of V-fib
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Instead of the impulse stopping b/c refractory muscle cannot transmit a 2nd
impulse, the impulse can continue to travel around to those fibers causing a reentry of the impulse into already excited muscle - Circus Movement
 Three different conditions can cause this:
 Pathway around the circle is too long
 Original stim muscle will no longer be refractory by the time the
impulse gets back to it
 Occurs in dilated hearts
 Velocity of conduction becomes decreased (circle length is the same)
 Increased time interval elapses before impulse reaches original stim
muscle, which might no longer be refractory
 Occurs from blockage of purkinje system, ishcemia of muscle, high
blood K+ levels, or many other factors
 Refractory period of muscle becomes shortened
 Impulse continues around and around
 Occurs in response to various drugs (epinephrine) or after repetitive
electrical stimulation
 Chain Rxn Mechanism of Fibrillation
 Fibrillation caused by 60-Cycle alternating current
 60-cycle stimulus applied thru electode to central point in ventricles
 First cycle of stimulus caused depol wave to spread in all directions
 After 0.25s only part of muscle comes out of refractory state
 Now stimulus can only travel is certain directions (thru muscle not in
refrac state)
 Causes:
 block of impulses in some directions but transmission in others
 Changes in cardiac muscle
 Velocity of conduction thru heart muscle decreases
 Refractory period of muscle is shortened
 Division of impulses (impulse hits portion in refrac and splits into
two)
 Progressive chain rxns - sustain fibrillation
 Electroshock Defibrillation of Ventricles
 Strong high-voltage alternating electrical current passed thru ventricles for
fraction of a second can stop fibrillation - putting all vent muscle into
refractoriness simultaneously
 All AP's stop and heart remains quiescent for 3-5seconds
 Usually stopped w/ 110V of 60-cycle alternating current applied for 0.1s or
1000V of direct current applied for a few thousandths of a second
 Hand Pumping of the Heart
 If heart isn't defibrillated w/in 1 min after beginning of fibrillation, heart no
longer has the nutrients available to be revived
 w/hand pumping small quantities of blood renew coronary blood supply and
defibrillation becomes an option again
 Lack of blood flow to the brain for more than 5-8min - permanent brain
damage/impairment
Atrial Fibrillation
 Mechanism identical to ventricular fibrillation
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Frequent cause is atrial enlargement resulting from heart valve lesions that prevent
atria from emptying adequately into ventricles or ventricular failure w/excess
damming of blood in atria
 Atria become useless primer pumps, blood flows passively, ventricular pumping is
decreased only 20-30% (person can live months to years w/A-fib, even w/reduced
efficiency)
 Either no P waves or only fine, high freq, very low voltage wavy record; QRS-T
complexes are normal but timing is irregular
 Timing:
 Impulses from atria to AV node are rapid and irregular
 AV node delays ~0.35s
 Additional 0-0.6s before next impulse to AV node
 Total delay 0.35-0.95s = very irregular
 Ventricles driven usually b/w 125 and 150 beats/min
 Converted by electroshock w/normal rhythm following if hearts is capable
Atrial Flutter
 Caused by a circus movement in the atria
 Electrical signal travels as a single large wave in one direction around atrial mass
 Rapid rate of contraction, 200-350 beats/min
 Usually 2-3 atrial beat for every 1 ventricular beat (2:1 or 3:1 rhythm)
 P waves are strong, QRS-T complex follows every 2 or 3
Cardiac Arrest
 Cessation of all electrical control signals in the heart, no spontaneous rhythm
 May occur during deep anesthesia - develop severe hypoxia
 Do CPR silly!!