Chapter 13 - Guyton Flashcards

1
Q

Tachycardia

A

defined as heart rate >100bpm; caused by increased body temperature, stimulation of the heart by sympathetic nerves, or toxic conditions of the heart

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2
Q

Bradycardia

A

defined as parasympathetic on heart

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3
Q

What is carotid sinus syndrome?

A

patients with this have pressure receptors (baroreceptors) in the carotid sinus region of the carotid artery walls that are excessively sensitive, even mild external pressure on the neck elicits a strong baroreceptor reflex, causing intense vagal acetylcholine effects on the heart, including extreme bradycardia

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4
Q

SA Block

A

impulse from the sinus node is blocked before it enters the atrial muscle, ventricles pick up a new rhythm (AV node) so that the rate of the ventricular QRS-T complex is slowed but not otherwise altered

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5
Q

Bundle of His

A

means by which impulses ordinarily can pass from the atria into the ventricles

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6
Q

AV Block

A

ischemia (coronary insufficiency), compression (scar tissue or calcified portions of heart), inflammation (myocarditis), extreme stimulation by vagus nerves (carotid sinus syndrome)

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7
Q

First Degree (Incomplete) AV Block

A

PR interval > 0.20 sec, delay of conduction from
the atria to the ventricles but not actual blockage of conduction (could be caused by some heart diseases such as acute rheumatic heart disease)

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8
Q

Second Degree AV Block

A

PR interval increased to 0.25 - 0.45 sec, sometimes the action potential is not strong enough to pass through the bundle so will see dropped beats

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9
Q

Third Degree (Complete) AV Block

A

complete block of the signal from the atria to ventricles occur and ventricles establish their own rhythm originating in the A-V node or A-V bundle, P waves become dissociated from the
QRS-T complexes (separate rates for atria and ventricles)

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10
Q

Stokes-Adams Syndrome - Ventricular Escape

A

in some patients with A-V block, the total block comes and goes; each time A-V conduction ceases, the ventricles often do not start their own beating until after a delay of 5 to 30 seconds (overdrive suppression); some part of the Purkinje system beyond the block begins discharging rhythmically at a rate of 15 to 40 times per minute and acting as the pacemaker of the ventricles (ventricular escape)

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11
Q

Why would a person with Stokes-Adams syndrome faint?

A

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 because the heart does not pump any blood for 5 to 30 seconds, until the ventricles “escape.”

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12
Q

Incomplete Intraventricular Block—Electrical Alternans

A

blocked impulse conduction in the peripheral ventricular Purkinje system; partial intraventricular block every other heartbeat

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13
Q

What is a premature contraction?

A

also known as ectopic beat or extrasystole, most premature contractions result from ectopic foci in the heart, which emit abnormal impulses at odd times during the cardiac rhythm

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14
Q

Premature Atrial Contractions

A

P-R interval is shortened, indicating that the ectopic origin of the beat is in the atria near the A-V node. Also, the interval between the premature contraction and the next succeeding contraction is slightly prolonged (compensatory pause); these are not as serious and can occur in athletes, smoking, lack of sleep, too much coffee, alcoholism

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15
Q

What is pulse deficit?

A

pulse wave passing to the peripheral arteries after a premature contraction may be so weak that it cannot be felt in the radial artery (decreased stroke volume)

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16
Q

AV Node or Bundle Premature Contractions

A

P wave is superimposed onto the QRS-T complex because the cardiac impulse traveled backward into the atria at the same time that it traveled forward into the ventricles (this condition is usually not as serious like premature atrial contractions)

17
Q

Premature Ventricular Contractions (PVCs) result in what on the electrocardiogram?

A

QRS complex is usually considerably prolonged, QRS complex has a high voltage (uneven depolarization of ventricles), T wave has an electrical potential polarity exactly opposite to that of the QRS complex (slow conduction of the impulse)

18
Q

Paroxysmal Tachycardia

A

Some abnormalities in different portions of the heart, including the atria, Purkinje system, or ventricles, can occasionally cause rapid rhythmical discharge of impulses that spread in all directions throughout the heart (can be stopped by vagal reflex).

19
Q

Atrial Paroxysmal Tachycardia

A

inverted P wave is seen before each QRS-T complex, and this P wave is partially superimposed onto the normal T wave of the preceding beat; this indicates that the origin of this paroxysmal tachycardia is in the atrium

20
Q

AV Nodal Paroxysmal Tachycardia

A

usually causes almost normal QRS-T complexes but totally missing or obscured P waves

21
Q

Supraventricular Tachycardias

A

atrial or AV nodal paroxysmal tachycardia, usually
occurs in young, otherwise healthy people, and they generally grow out of the predisposition to tachycardia after adolescence

22
Q

Ventricular Paroxysmal Tachycardia

A

usually a serious condition, usually does not occur unless considerable ischemic damage is present in the ventricles, frequently initiates the lethal
condition of ventricular fibrillation

23
Q

Ventricular Fibrillation

A

results from cardiac impulses stimulating
first one portion of the ventricular muscle, then another portion, and eventually feeding back onto itself to re-excite the same ventricular muscle repeatedly (usually fatal within minutes)

24
Q

Causes of ventricular fibrillation?

A

sudden electrical shock of the heart, or ischemia of

the heart muscle, of its specialized conducting system, or both

25
Q

What could cause circus movement (re-entry of impulse into muscle that has already been excited)?

A

pathway is too long (dilated hearts), velocity of conduction becomes decreased (blockage of Purkinje, ischemia, high potassium), refractory period of muscle becomes shortened (drugs such as epinephrine)

26
Q

If electroshock can cause ventricular fibrillation, how does it cause defibrillation?

A

Although a moderate alternating-current voltage
applied directly to the ventricles almost invariably
throws the ventricles into fibrillation, a strong high voltage alternating electrical current passed through the ventricles for a fraction of a second can stop fibrillation by throwing all the ventricular muscle into refractoriness simultaneously.

27
Q

Atrial Fibrillation

A

same as ventricular fibrillation except in atria, frequent cause 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 (no P waves, will cause a fast, irregular heartbeat but person can live and efficiency of ventricles is only reduced 20-30%).

28
Q

Atrial Flutter

A

circus movement in the atria, rapid rate usually 25-300 bpm, signals reach the A-V node too rapidly for all of them to be passed into the ventricles, refractory periods of the A-V node and A-V bundle are too long to pass more than a fraction of the atrial signals. Therefore, there are usually two to three beats of the atria for every single beat of the ventricles (P waves without QRS complexes).

29
Q

Cardiac Arrest

A

buh-bye! hypoxia can prevent 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