Physio Ch 13; Cardiac Arrhythmias & Ekg

Front 1

Tachycardia

Back 1

faster than 100 beats per minute

Front 2

General causes of tachycardia include

Back 2

increased body temperature (inc 10 beats per minute for each degree farenheit - 18 beats per min per degree celsius); stimulation by sympathetics; toxic conditions of the heart

Front 3

After body temp of 105oF, the heart rate

Back 3

may decrease because of progressive debility of the heart muscle as a result of the fever

Front 4

Fever causes tachycardia because increased temp increases

Back 4

the rate of metabolism of the SA node which in turn directly increases its excitability and rate of rhythm

Front 5

When a patient loses blood and passes into a state of shock or semishock, sympathetic reflex stimulation

Back 5

often increases the heart rate to 150 to 180 bpm

Front 6

Simple weakening of the mycardium usually increases heart rate

Back 6

because the weakened heart does not pump blood into the arterial tree to a normal extent & this causes sympathetics to increase heart rate

Front 7

Bradycardia

Back 7

fewer than 60 bpm

Front 8

The athlete's heart is larger and considerably stronger which allows the heart to pump

Back 8

a large stroke volume output per beat even during periods of rest. Slower heart.

Front 9

Carotid sinus syndrome

Back 9

The baroreceptors in the carotid sinus region of the carotid artery walls are excessively sensitive. So even mild external pressure on the neck elicits a strong baroreceptor reflex causing intense vagal-acetylcholine effects on the heart, including extreme bradycardia. This can even stop the heart for 5 to 10 seconds.

Front 10

Sinus arrhythmia can result from any one of many circulatory conditions that alter the strengths of the

Back 10

sympathetic and parasympathetic nerve signals to the SA node.

Front 11

respiratory type of sinus arrhythmia,

Back 11

this results mainly from spillover of signals from the medullary respiratory center into the adjacent vasomotor center during inspiratory and expiratory cycles of respiration. The spillover signals cause alternate increase and decrease in the number of impulses transmitted through the sympathetic and vagus nerves to the heart.

Front 12

SA block

Back 12

The impulse from the SA node is blocked before it enters the atrial muscle. EKG shows sudden cessation of P waves with standstill of the atria. The ventricles then pick up a new rhythm, the impulse usually originating spontaneously in the AV node so that the rate of the ventricular QRS-T complex is slowed but not otherwise altered.

Front 13

AV (bundle of HIS) block. conditions that can either decrease the rate or block the impulse entirely are:

Back 13

1) ischemia of the AV node or AV bundle fibers
2) compression of the AV bundle
3) inflammation of the AV node or AV bundle
4) extreme stimulation of the heart by the vagus nerves

Front 14

Ischemia of the AV node or AV bundle fibers can cause AV block -

Back 14

delays or blocks conduction from the atria to the ventricles. Coronary insufficiency can cause ischemia of the AV node and bundle in the same way that it can cause ischemia of the myocardium

Front 15

compression of the AV bundle can cause AV block -

Back 15

compression by scar tissue or by calcified portions of the heart can depress or block conduction from the atria to the ventricles

Front 16

Inflammation of the AV node or AV bundle can cause AV block -

Back 16

inflammation can depress conductivity from the atria to the ventricles. Inflammation results frequently from different types of myocarditis, caused, for example, by diphtheria or rheumatic fever

Front 17

extreme stimulation of the heart by the vagus nerves can cause AV block-

Back 17

extreme stimulation of the heart by the vagus nerves in rare instances blocks impulse conduction through the AV node. Such vagal excitation occasionally results from strong stimulation of the baroreceptors in people with carotid sinus syndrome

Front 18

Incomplete atrioventricular heart block (1st degree)

Back 18

Prolonged P-R (or P-Q) interval. It is a delay of conduction (increasing greater than 0.20 second) from the atria to the ventricles but not actual blockage of conduction. The P-R interval seldom increases above 0.35 to 0.45 second because, by that time, conduction through the AV bundle is depressed so much that conduction stops entirely.

Front 19

Time between beginning of the P wave and beginning of the QRS complex

Back 19

about 0.16 second at a normal rate. This P-R interval usually decreases in length with faster heartbeat and increases with slower heartbeat.

Front 20

The P-R interval is prolonged when the PR interval is greater than

Back 20

0.20 second. 1st degree heart block

Front 21

One means for determining the severity of some heart diseases -- acute rheumatic heart disease, is to measure the

Back 21

P-R interval

Front 22

2nd degree block

Back 22

When conduction through the AV bundle is slowed enough to increase the PR interval to 0.25 to 0.45 second, the action potential sometimes is strong enough to pass through the bundle into the ventricles and sometimes is not strong enough. So will be P wave, but not QRS-T wave and there are "dropped beats" of the ventricles

Front 23

Complete AV block (3rd degree block)

Back 23

The ventricles spontaneously establish their own signal, usually originating in the AV node of AV bundle. Therefore the P waves become dissociated from the QRS-T complexes

Front 24

Stokes-Adams Syndrome - ventricular escape

Back 24

When the total AV block comes and goes. Each times the AV conduction ceases, the ventricles often do not start their own beating until after a delay of 5 to 30 seconds from the phenomenon called overdrive suppression. Because the brain cannot remain active for more than 4 to 7 seconds without blood supply, most patients faint a few seconds after complete block occurs. Pacemakers are usually put in people like this.

Front 25

Electrical alternans

Back 25

results from partial intraventricular block every other heartbeat. Can be from tachycardia when the ventricles can't recover fast enough. Can be from ischemia, myocarditis or digitalis toxicity.

Front 26

Premature contraction

Back 26

aka extrasystole, premature beat or ectopic beat.

Front 27

Causes of premature contractions.

Back 27

most result from ectopic foci in the heart, which emit abnormal impulses at odd times during the cardiac rhythm. Possible causes are 1) local areas of ischemia; 2) small calcified plaques at different points in the heart which press against the adjacent cardiac muscle so that some of the fibers are irritated; and 3) toxic irritation of the AV node, Purkinje system or myocardium caused by drugs, nicotine or caffeine.

Front 28

Mechanical initiation of premature contractions is also frequent during

Back 28

cardiac catheterization; large numbers of premature contractions often occur when the catheter enters the right ventricle and presses against the endocardium

Front 29

Premature atrial contractions

Back 29

Then there's a compensatory pause. They occur frequently in otherwise healthy people. Even in athletes. Mild toxic conditions resulting from such factors as smoking, lack of sleep, ingestion of too much coffee, alcoholism and use of various drugs can also initiate such contractions.

Front 30

The pulse wave passing to the peripheral arteries after a premature contraction

Back 30

may be so weak that it cannot be felt in the radial artery. (Because the ventricles hadn't filled with blood yet)

Front 31

AV nodal or AV bundle premature contractions

Back 31

P wave cannot be discerned

Front 32

Premature ventricular contractions on EKG

Back 32

1) QRS complex is usually considerably prolonged 'cause impulse is conducted mainly through slowly conducting muscle of the ventricles rather than through the Purkinje system. 2) QRS has high voltage 'cause impulse travels in one direction rather than 2 directions that neutralize one another. 3) Usually after PVCs the T wave has an electrical potential polarity exactly opposite to that of the QRS complex because the slow conduction of the impulse through the cardiac muscle causes muscle fibers that depolarize first also to repolarize first.

Front 33

Some PVCs (premature ventricular contractions) are relatively benign in their effects on overall pumping by the heart. They can result from such factors as

Back 33

cigarettes, coffee, lack of sleep, various mild toxic states and even emotional irritability.

Front 34

Some PVCs result from stray impulses or re-entrant signals that originate around the borders of infarcted or ischemic areas of the heart.

Back 34

Do not take this lightly! Statistics show that people with significant numbers of PVCs have a much higher than normal chance of developing spontaneous lethal ventricular fibrillation, presumably initiated by one of the PVCs.

Front 35

Paroxysmal tachycardia

Back 35

Some abnormalities in different portions of the heart, including the atria, the Purkinje system, or the ventricles, can occasionally cause rapid rhythmical discharge of impulses that spread in all directions throughout the heart. Believed to be caused usually by re-entrant circus movement feedback pathways that set up local repeated self-re-excitation. Because of the rapid rhythm in the irritable focus, this focus becomes the pacemaker of the heart.

Front 36

Paroxysmal tachcardia often can be stopped by eliciting a

Back 36

vagal reflex. A type of vagal reflex sometimes elicited for this purpose is to press on the neck in the regions of the carotid sinuses which may cause enough of a vagal reflex to stop the paroxysm. Drugs may also be used like quinidine and lidocaine, either of which depresses the normal increase in sodium permeability of the cardiac muscle membrane during generation of the action potential thereby often blocking the rhythmical discharge of the focal point that is causing the proxysmal attack.

Front 37

Atrial paroxysmal tachycardia

Back 37

An inverted P wave before the QRS-T complex indicates that the origin is in the atrium, but if the P wave is abnormal in shape, the origin is not near the sinus node.

Front 38

AV nodal paroxysmal tachycardia.

Back 38

both called supraventricular tachycardias, usually occurs in young, otherwise healthy people and they generally grow out of the predisposition to tachycardia after adolescence. Frightening, but seldom harmful.

Front 39

Ventricular paroxysmal tachycardia

Back 39

The EKG looks like a series of ventricular premature beats occurring one after another without any normal beats interspersed. Usually serious condition because 1) this type of tachycardia usually does not occur unless considerable ischemic damage is present in the ventricles. 2) ventricular tachycardia frequently initiates the lethal condition of ventricular fibrillation because of rapid repeated stimulation of the ventricular muscle.

Front 40

Sometimes intoxication from the heart treatment drug digitalis causes

Back 40

irritable foci that lead to ventricular tachycardia.

Front 41

Quinidine, which increases the refractory period and threshold for excitation of cardiac muscle may be

Back 41

used to block irritable foci causing ventricular tachycardia.

Front 42

Ventricular fibrillation

Back 42

The most serious of all cardiac arrhythmias. If not stopped within 1 to 3 minutes is almost invariably fatal.

Front 43

Ventricular fibrillation results

Back 43

from cardiac impulses that have gone berserk within the ventricular muscle mass, stimulating first one portion of the ventricular muscle, then another portion, then another, and eventually feeding back onto itself to re-excite the same ventricular muscle over and over - never stopping. there is never coordination.

Front 44

After ventricular fibrillation begins, unconsciousness occurs within

Back 44

4 to 5 seconds for lack of blood flow to the brain and irretrievable death of tissues begins to occur throughout the body within a few minutes.

Front 45

Especially likely to initiate V fib are

Back 45

1) sudden electrical shock of the heart, or 2) ischemia of the heart muscle, of its specialized conducting system, or both

Front 46

Phenomenon of re-entry - "circus movements" as the basis for

Back 46

ventricular fibrillation

Front 47

Re-entry of the impulse - "circus movement"

Back 47

Usually impulse dies out because muscle is all refractory and cannot transmit a second impulse. But if 1) the pathway around the circle is too long, by the time the impulse returns to the original position, the originally stimulated muscle will no longer be refractory and the impulse will continue again. 2) if length of the pathway remains constant but the velocity of conduction becomes decreased enough, an increased interval of time will elapse before the impulse returns to the start. By this time, the originally stimulated muscle might be out of the refractory state and the impulse can continue around again. 3) The refractory period of the muscle might become greatly shortened. In this case, the impulse could also continue again.

Front 48

Re-entry of the impulse - "circus movement" (long pathway, velocity is decreased, refractory period is shortened) occur in different pathological states as follows:

Back 48

1) a long pathway in dilated hearts. 2) decreased rate of conduction frequently results from a blockage of the Purkinje system, ischemia of the muscle, high blood potassium levels, or other factors. 3) a shortened refractory period commonly occurs in response to various drugs, such as epinephrine or after repetitive electrical stimulation.

Front 49

Condition necessary for re-entrant signal to develop

Back 49

transmission of some of the depolarization waves around the heart in only some directions but not other directions

Front 50

Another condition for re-entrant signal to develop

Back 50

rapid stimulation of the heart causes 2 changes in the cardiac muscle itself, both of which predispose to circus movement: 1) the velocity of conduction through the heart muscle decreases, which allows a longer time interval for the impulses to travel around the heart 2) the refractory period of the muscle is shortened, allowing re-entry of the impulse into previously excited heart muscle within a much shorter time than normally

Front 51

One of the most important features of fibrillation is

Back 51

the division of impulses. When a depolarization wave reaches a refractory area in the heart, it travels to both sides around the area. It's a division of chain reactions. This irregular pattern of impulse travel causes many circuitous routes for the impulses to travel, greatly lengthening the conductive pathway, which is one of the conditions that sustains the fibrillation.

Front 52

A strong, high-voltage alternating electrical current passed through the ventricles for a fraction of a second can stop fibrillation by

Back 52

throwing all the ventricular muscle into refracotiness simultaneously.

Front 53

electroshock defibrillation of the ventricles

Back 53

All action potentials stop, the heart remains quiescent for 3 to 5 seconds, after which it begins to beat again. Fibrillation may begin again immediately because of the re-entrant focus that is still there.

Front 54

Electroshock defib

Back 54

When applied through two electrodes on the chest wall, the usual procedure is to charge a large electrical capacitor up to several thousand volts and then to cause the capacitor to discharge for a few thousandths of a second through the electrodes and through the heart.

Front 55

Unless defibrillated within 1 minute after fibrillation begins, the heart

Back 55

is usually too weak to be revived by defibrillation because of the lack of nutrition from coronary blood flow. Revive the heart by preliminarily pumping the heart by hand and then defibrillate. (CPR first)

Front 56

Atrial fibrillation

Back 56

A frequent cause of atrial fibrillation is atrial enlargement resulting from heart valve lesions that prevent the atria from emptying adequately into the ventricles or from ventricular failure with excess damming of blood in the atria. The dilated atrial walls provide ideal conditions of a long conductive pathway as well as slow conduction, both of which predispose to atrial fibrillation.

Front 57

During A fib, the atria

Back 57

become useless as primer pumps for the ventricles. Which decreases the efficiency of ventricular pumping only 20 to 30 percent. So a person can live for months or years with atrial fibrillation.

Front 58

EKG and A fib

Back 58

The P waves from the atria are either absent or fine,high-frequency, very low voltage wavy record. The QRS-T complexes are normal unless there is some pathology of the ventricles, but their timing is irregular.

Front 59

Irregularity of ventricular rhythm (QRS-T) during A fib

Back 59

When the atria are fibrillating, impulses arrive from the atrial muscle at the AV node rapidly but also irregularly. Because the AV node will not pass a second impulse for about 0.35 second after a previous one, at least 0.35 second must elapse between one ventricular contraction and the next. Then a variable interval of 0 to 0.6 second occurs before one of the irregular atrial fibrillatory impulses happens to arrive at the AV node. Thus the interval between successive ventricular contractions varies from a minimum of 0.35 second to a maximum of 0.95 second causing a very irregular heartbeat. This is one of the clinical findings used to diagnose the condition.The ventricle is driven at a fast heart rate, usually 125 and 150 beats per minute

Front 60

Atrial flutter

Back 60

caused by a circus movement in the atria. It is different from atrial fibrillation in that the electrical signal travels as a single large wave always in one direction around and around the atrial muscle mass. Rapid. 200 and 350 beats of atria per minute.

Front 61

Atrial flutter

Back 61

even though beating fast (200-350 bpm), the amount of blood pumped is slight. Furthermore, the signals reach the AV node too rapidly for all of them to be passed into the ventricles, because the refractory periods of the AV node and AV bundle are too long to pass more than a fraction of the atrial signals.

Front 62

Cardiac arrest

Back 62

A final serious abnormality of the cardiac rhythmicity conduction system is cardiac arrest. This results from cessation of all electrical control signals in the heart.

Front 63

Cardiac arrest is especially likely to occur

Back 63

during deep anesthesia, when many patients develop severe hypoxia because of inadequate respiration. The hypoxia prevents the muscle fibers and conductive fibers from maintaining normal electrolyte concentration differentials across their membranes, and their excitability may be so affected that the automatic rhythmicity disappears.