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.

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