Lecture 9: Cardiac arrhythmias Flashcards

1
Q

Endogenously mediated tachycardia

A

Heart rate increases
Cardiac output increases
Filling time is reduced by stroke volume does not fall
Sympathetic stimulation contracts veins and increases venous return to help maintain ventricular filling

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2
Q

First-degree incomplete AV block

A

Normal P-R time interval is 0.16 sec

When P-R interval increases to greater than 0.20 seconds, the patient has a first degree incomplete heart block

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3
Q

Fibrillation occurs a result of

A

Circus movements

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4
Q

Pathologically mediated tachycardia

A

Heart rate increases
Cardiac output decrease
Mean atrial pressure decreases and activates sympathetic nervous system, which occurs after the fact and is unable to compensate

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5
Q

Spillover signals

A

Related to respiratory sinus arrhythmia
These signals alternately increase and decrease number of impulses transmitted through sympathetic and vagus nerves to the heart

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6
Q

Causes of Atrial fibrillation

A

Enlargement of the atria (due to valve lesions)

Inadequate emptying of the ventricles, causing blood to back up into the atria

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7
Q

What causes conduction velocity to be slowed down

A

Blockage of the Purkinje system
Ischemia
High potassium levels

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8
Q

Sinoatrial block characteristics

A

Sudden cessation of P waves
Resultant standstill of atria
Ventricles pick up a new rhythm, usually originating in AV node
Rate of QRS is slowed

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9
Q

What can shorten the refractory period

A

Response to drugs such as epinephrine

Repepitive electrical stimulation

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10
Q

Paroxysmal tachycardia

A

Heart becomes rapid in paroxysms
Paroxysm begins suddenly and last for variable amounts of time, then ends suddenly
Pacemaker of heart shifts back to sinus node

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11
Q

Premature contraction causes

A

Most are result of ectopic foci:

  • Local ischemic areas
  • Calcified plaques
  • Irritation of the conduction system or nodes
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12
Q

Causes of Tachycardia

A

Increased body temperature
Stimulation of heart by sympathetic nerves (due to loss of blood/state of shock)
Toxic conditions of heart (results in weakening of myocardium)

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13
Q

Complete AV block

A

Ventricles establish their own signal (usually AV node)

No relation between rate of P waves and QRS-T complex

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14
Q

Fibrillation

A

Twitching of individual muscle fibers in the atria or ventricles and also in recently denervated skeletal muscle fibers

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15
Q

Stokes-adams syndrome

A

Periodic fainting spells due to complete AV block

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16
Q

Partial intraventricular block

A

Referred to as “electrical alternans”

Term refers to an alternation in the amplitude of P waves, QRS complexes or T waves

17
Q

Causes of AV block

A

Ischemia of AV node or AV bundle fibers
Compression of AV bundle by scar tissue
Inflammation of AV node/bundle
Extreme stimulation of the heart by vagus nerves

18
Q

Second-degree incomplete AV block

A

When P-R time interval increases to 0.25–>0.45 seconds
Atrial P wave is present but QRS-T wave may be missing, resulting in dropped beats of the ventricle
2:1 rhythm or other variations may develop

19
Q

Tachycardia

A

Fast heart rate (>100 beats/min)

20
Q

Causes of Bradycardia

A

Athletic heart
Vagal stimulation
Extremely sensitive carotid baroreceptors in carotid sinus syndrome

21
Q

Three conditions that cause the impulse to travel around the circle (circus movements)

A

The pathway around the circle is too long
The length of the pathway remains constant but the velocity of conduction slows down
The refractory period of the muscle might become greatly shortened

22
Q

What happens when pathway is too long

A

If the heart is dilated (making pathway too long) impulse takes longer to get back to starting point and the muscle is no longer in its refractory period, allowing for another depolarization

23
Q

Ventricular escape

A

Resumption of ventricular beat in complete AV block-may be due to parts of purkinje system acting as ectopic pacemaker

24
Q

Bradycardia

A

Slow heart rate (<60 beats/min)