Cardia Arrhythmias and Their Electrocardigraphic Interpretation.

1. Abnormal rythmicity of the pacemaker

2. Shift od the pacemaker from the sinus node to another place in the heart
3. Blocks at different points in the spread of the impulse through the heart
4. Abnormal pathways of impulse transmission through the heart
5. Spontaneous generation of spurious impulses in almost any part of the heart

Tachycardia “fast heart rate”- faster than 100 beats per minute; time intervals between QRS complexs 150
beats per minute- caused by increased body temperature, stimulation of the heart by sympathetic nerves, or
toxic conditions of the heart. 10beats/degree F Fever=tachycardia

Bradycardia “slow heart rate”- fewer than 60 beats per minute. Common in athletes stronger, larger heart,
large stroke volume.Vagal stimulationAchparasympathetic effect (carotid sinus syndrome-bar
receptors are excessively sensitive)

Sinus Arrhythmia- heart rate increases and decreases during deep respiration
(sympathetic/parasympathetic innervation)

Abnormal Ryhthms that Result from Block of Heart Signals w/In the Intracardiac Conduction
Pathways

Sinoatrial Block- EKG shows cessation of P waves, standstill of Atria- Ventricles pick up new rhythm from
AV node QRST complex is slowed but otherwise not altered

Atrioventricular Block- only means impulses can pass from atria to ventricles is though the AV bundle (aka
bundle of His) Prolonged P-R interval
1. Ischemia of the AV node or AV bundle fibers (coronary insufficiency)
2. Compression of the AV bundle (scar tissue/ calcified portions of the beart)
3. Inflammation of the AV node or AV bundle ( depress conductivity from AV)
4. Extreme Stimulation of the heart by the vagus nerves (Carotid Sinus Syndrome)

Incomplete Atrioventricular Heart Block

Prolonged P-R (or P-Q) Interval -- First Degree Block (usual lapse between beginning of P wave and
beginning of QRS is 0.16 seconds) Increases in slower HR and Decreases in Faster HR (Greater than 0.20
second - first degree incomplete heart block) delay of conduction

Second Degree Block- P-R Interval is 0.25-->0.45 sec; There will be a P wave but no QRS-T because AP
is not strong enough pass through the bundle to ventricles

Complete A-V Block (Third degree Block); Ventricles establish their own signal originating in AV node; P
waves dissociated from the QRS-t complexes, rates of Atria and Ventricles will be different no relation

Stokes-Adams Syndrome- Ventricular Escape- Pts with AV block total block comes and goes, this
condition occurs in hearts with borderline ischemia of the conductive system. Overdrive Suppression- AV
node begins its own beating 5-30 seconds after block. Ventricular Escape- AV bundle actas as pacemaker.
No blood to brain during time lapse causes faint spells “Stokes-Adams syndrome” (Artificial Pacemaker
can be installed if detrimental to health)

Incomplete Intraventricular Block - Electrical Alternans

-Electrical Alternans- partial intraventricular block on every other heartbeat, also associated w/ tachycardia
it may be impossible for some portions of Purkinje system to recover from previous refractory period.

Premature Contraction- premature contraction of the heart before the taim that normal contraction would
have been expected. (Extrasystole, premature beat, ectopic beat) Result from ectopic foci in the heart
which emit abnormal impulses at odd times during cardia rhythm. (areas of ischemia, small calcified
plaques which press against adjacent cardiac muscle so fibers are irritated, toxic irritation of AV node,
Purkinje system, or myocardium by drugs, nicotine, caffeine.
Premature Atrial Contractions- P wave occurred too soon in the heart cycle; P-R interval is shortened
indicating that the ectopic origin of the beat is in the artria near the A-V node. Compensatory pause
(interval between premature contraction and next contraction is prolonged) Causes: Smoking, lack of sleep,
Caffeine, Alcoholism, Drugs

AV Nodal or AV Bundle Premature Contractions- P wave is missing from the EKG. P wave is super
imposed on QRST complex because the cardia impulse traveled backward into atria at the same time it
traveled forward in the ventricles.

Premature Ventricular Contractions- QRS complex is prolonged, QRS has a high voltage (one ventricle
contracted before the other, causing large electrical potentials; T wave has opposite electrical potential
polarity (slow conduction impulse causes the muscle fibers that depolarize first to repolarize first)

Paroxymal Tachycardia- abnormalities in other portions of the hears, can cause rapid rhythmical
discharge of impulses that spread in all directions thoughout the heart. heart rate becomes rapid in
paroxyms. Stoped by Vagal Reflex, pressing on Carotid sinuses, Drugs (guanidine, lido cane depress Na
permeability)

Atrial Paroxymal Tachycardia- inverted P wave origin in atrium yet due to inverted P wave, it is not in
sinus node.

Ventricular Paroxymal Tachycardia- series of ventricular premature beats occurring one after another
without any normal beats dispursedfrequently initiates the lethal condition of ventricular fibrillation
(digitalis cause)

Ventricular Fibrillation- MOST SERIOUS - must be stopped in 1-3 minutes, cardiac impulses have gone
berserk w/in the ventricular muscle mass (stimulates one portion then the next and feeding back into itself,
never stopping). Never a coordination of control all at once. Heart pumps NO blood. Unconscious in 4-5
sec. Caused by: Electrical shock to the heart, ischemia of heart muscle or its specialized conducting
system.

Circus MovementsVentricular Fibrillation (caused by pathway being too long (dilated heart), allowing
for relative refractory period and new muscle contraction to continue, or if the velocity of conduction
becomes decreased (blockage in purkinje system, ischemia of muscle, high K levels), enough time has
passed to allow muscle to be contracted again, or refractory period of the muscle might be
shortened(epinephrine,other drugs,))

Electroshock Defibrillation of the Ventricles

Current passed through ventricles for a second throws the entire muscle into refractory simultaneously.
“Restart the Heart”

Hand Pumping of the Heart (Cardiopulmonary Resuscitation) CPR- pump the heart by squeezing (to
supply nutrients to heart)- the defibrillate

Atrial Fibrillation- Caused by atrial enlargement, resulting from heart valve lesions that prevent atria from
empting into ventricules or ventricular failure with excess blood damming in the atria. Dilated walls (long
pathway) and slow conduction Atrial Fibrillation; Atria useless as primer pumps for ventricles (ventricles
decrease by 20-30%) People can live for months or years EKG- NO P WAVES, QRST complexes are
normal except for irregular spacing

Electroshock Treatment of Atrial Fibrillation

Atrial Flutter- circus movement in the atria- rapid rate of contraction of the atria (200-350 beats per
minute), one side is contracting of atria while the other side is relaxing, little blood is pumped. Signals
reach AV node too rapidly to passed on. 2-3 beats Atria for one beat of Ventricles. 3P waves: 1 QRST
Complex
Cardiac Arrest- Cessation of all electrical control signals in the heart. Occurs during deep anesthesia (pts
develop severe hypoxia because of inadequate respiration. Hypoxia prevents muscle fibers and
conductive fibers from maintaining notmal electrolyte concentration differentials across their membranes,
excitability affected that the automatic rhythm city disappears.