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A&P 1 > Exam 4 - Lecture 7 > Flashcards

Exam 4 - Lecture 7 Flashcards

1
Q

If the APs are generating faster than normal, this means we have a

A

abnormal pacemaker

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1
Q

Definition of arrhythmias

A

problems with conduction system of the heart or how the APs travel through the heart

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2
Q

5 causes of cardiac arrythmias

A

Abnormal rhythmicity of pacemaker
Shift of pacemaker from sinus node
Blocks at different points in transmission of cardiac impulse
Abnormal pathways for transmission
Spontaneous generation of abnormal impulses from any part of the heart

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2
Q

ectopic pacemaker

A

site within heart other than SA node that is generating heartbeats

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3
Q

Moving the VRm closer to threshold potential in pacemaker cell can

A

fire an early AP

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4
Q

Generally speaking, increase VRm causes

A

the heart to not completely reset itself

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5
Q

If VRm increaes at AV node, it may

A

fire an AP early before the SA node does, causing an arrythmia

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5
Q

Anything that increases VRm, will

A

increase risk of arrythmia

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6
Q

Tachycardia is due to a

A

abnormal SA node

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7
Q

Sinus tachycardias will have _____ in the normal orientation with a ____ PR interval.

A

P-wave; short

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8
Q

NSR officially becomes sinus tach at

A

101bpm

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9
Q

Why does increased body temp cause a abnormal rhythm?

A

sinus tach, due to increased energy demands

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10
Q

Causes of sinus tach in relation to nervous system?

A

overactive SNS, underactive PNS

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11
Q

If you have co-arrythmias, what can you do to combat the sinus tach associated with them?

A

d/t decreased stroke volume from arrythmia, heart may try to speed up to compensate. Need a beta blocker to combat that as long as a med to help with arrythmia.

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12
Q

Toxic conditions of heart leading to sinus tach (SA node)

A

Acidosis, nicotine, alcohol

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13
Q

Why do athletes have bradycardia?

A

Large stroke volume

physiologically large heart d/t athletic training

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14
Q

3 Causes of bradycardia

A

athletes
vagal stim
nerual reflex to drugs

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15
Q

Generally speaking, the higher your resting heart rate, the

A

worse off your heart bc it probably has a lower stroke volume

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16
Q

High heart rate is usually d/t

A

hyperthyroidism

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17
Q

What usually accomplishes bradycardia? vagaling or decreasing SNS?

A

increasing vagal stimulation

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18
Q

If you pump someone full of phenylephrine to drive the BP up, the baroreceptors detect that and will

A

slow heart rate down, reflex bradycardia.

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19
Q

Paroxysmal atrial tachycardia characteristics

A

Abnormal atrial excitation, SA nodes are firing irregularly, P and T waves overlap d/t timing, morph into eachother.

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20
Q

What are drug tx for paroxysmal atrial tachycardia?

A

Vagal reflex, beta blocker, digoxin

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21
Q

Sinoatrial block

A

impulses from SA node are blocked, may be from ischemia and cant reset its VG ion channels.
Causes cessation of P-waves, or inverted p-wave
usually results in AV node controlling heart rate.

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22
Q

What determines whether P-wave is inverted or absent?

A

Where it comes from in the AV node.
Early part of AV node: inverted
Late part of AV node: absent

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23
Q

Why is the p-wave absent if it comes from later part of AV node?

A

takes so long for the retrograde current to reach the rest of the tissue, it gets masked by ventricular current.

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24
Q

Main issues that arrythmias cause physiologically with the heart

A

reduces stroke volume from abnormal beats

AV valves aren’t in correct timing, so they may be closed, causes turbulence, may damage/calcify the valves, cause blood clots.

25
Q

Atrioventricular block

A

AV node and AV bundles of his are slowed or blocked.

26
Q

normal PR interval

A

0.16

27
Q

Causes of atrioventricular block (5 things)

A

-Ischemia of AV node or AV bundle (raises VRm, less VG ion channels participating in AP)
-Compression of AV bundle by scar tissue or calcified tissue, maybe from CHF or an MI from fiberblasts laying down scar tissue, also creates a smaller inner diameter, causing slower APs
-AV nodal or AV bundle inflammation
-Excessive vagal stimulation (such as five and dien)
-Excess digitalis/beta blockers

28
Q

How does digitalis work

A

Sodium/K ATPase inhibitor, causing excess sodium in heart cell, decreasing the sodium gradient, increased VRm

29
Q

Last HF drug you get put on is

A

digitalis, because it affects such an important mechanism of the heart, and it affects other systems.

30
Q

1st degree heart block

A

Increases PR interval to > 0.20 seconds.
- just a delay, not losing any QRS complexes or anything like that.

31
Q

2nd degree heart block

A

PR interval increases to 0.25 - 0.45 seconds
- some impulses pass through AV node, some dont.
- Dropped beats.
- Atria has a faster rate than Ventricles.
- wenkebach, mobitz type I

32
Q

Mobitz type I/wenkebach

A

type of 2nd degree heart block, irregular PR interval,
1st PR interval after dropped beat is normal

33
Q

2nd degree heart block

A
  • mobitz type II, fixed P-wave to QRS complex ratio, fixed PR interval on the the QRS complexes we do have. (may be 2:1, 3;2, 3:1, etc.)
  • 0.25 - .45 seconds
  • dropped beats
  • need a pacemaker
33
Q

Which of the heart blocks is more dangerous?

A

2nd degree

33
Q

How do you treat 2nd degree heart block?

A

Pacemaker

33
Q

Complete heart block: 3rd degree

A

Total AV nodal or bundle of his block
-complete dissociation of QRS from P waves
- Ventricular escape @ 15-40bpm
- Atrial rate elevated

34
Q

why is the atrial rate elevated in complete heart block?

A

Body senses decreased cardiac output from low heart rate, speeds up the atrial rate in response.

35
Q
A
36
Q

Atrial flutter

A

Circular reentry in atria that is completely separate from SA node
- really slow conduction rate in atria with circular movements, and the AP are going around in a slow circle and not waiting around for SA node to fire AP.

  • it’s a slower conduction rate, cause if it was faster, the AP would run into tissue that’s in refractory period, and if it’s in complete refractory period it wouldn’t allow circular movement.
37
Q

What increase likelihood of a-flutter?

A

When the conduction is slow, and When the atria is all stretched out, the electricity has a longer pathway to take, and less likely to hit refractory period/makes it a slower conduction rate.

38
Q

The net result of a-flutter is

A

High atrial and high ventricular heart rates

39
Q

Does A-flutter have a P wave?

A

No, there’s no normal pathway for the P-wave to exist.

40
Q

Atrial fibrillation

A

Stretched out atria, No defined pathway for electrical current, bunch of ectopic pacemakers, and all firing on their own. It’s uncoordinated and irregular. Causes lots of turbulence in atria, causing blood clots in the atria.

41
Q

What can cause a PE?

A

Blood clot in right atria, dislodging and being sent into right ventricle, into pulmonary circulation.

42
Q

Factors to cause A-fib

A

Usually age, stretching out the atrias

43
Q

Treatments for A-fib

A

Ablation, blood thinners for blood clots, anti-arrhythmics

44
Q

What are circus movements?

A

During a-fib, got action potentials running in all different directions

45
Q

Stokes-Adams syndrome

A

HEREDITARY, causing fainting/syncope d/t low BP/stroke volume.
-irregular complete AV block at random times. Ventricular pacing has to take over, takes 5-30 seconds for that to kick in and help you regain consciousness.

Takes 7-8 seconds to pass out

46
Q

What does your heart rate return to after stokes-adams syncope episode?

A

15-40 as the ventricles are taking over pacing.

47
Q

Incomplete intraventricular block

A

Called Alternans.
- slowed conduction in purkinje system.
- occurs every other heart beat, the abnormal beats are smaller and wider QRS complexes
- more likely during ventricular tachycardia
- tissue is not fully repolarizing itself as fast as it normally would, so that’s why they’re smaller.
- ischemia and digitalis prevent full resetting of purkinje system
- p-wave being hidden in T-wave

48
Q

Premature contractions: atrial source

A

Ectopic tissue in atria firing early APs
-result from ischemia, irritation, or calcified plaques
-radial pulse deficits, early depolarizations result in less filling time, lower SV

49
Q

Premature contractions: AV nodal/bundle source

A

Missing P wave during premature beat cause it’s coming from AV mode, originates from middle AV junction and P-wave gets obscured by QRS complex

50
Q

For premature contractions from AV node/bundle source, p-wave early and inverted means it came from ______. Late and inverted came from ______.

A

High AV junction; Low AV junction (but should be hidden in QRS)

51
Q

PVCs

A

Prolonged QRS due to slower conduction speed of ventricular muscle
Taller QRS due to ventricles pumping at separate times, causing an additive affect on the current reading.
T-wave is usually inverted after PVC QRS
caused by caffeine, nicotine, stress, lack of sleep

52
Q

Ventricular tachycardia: paroxysmal

A

QRS originating within ventricles, high voltage prolonged QRS, No normal QRS interspersed, dangerous and usually requires infarction, initiates V-fib. P-waves are not visible or inverted.

53
Q

Ventricular premature depolarization

A

EAD, DAD, early AP initiation, very inefficient pumping, looks like a long QT interval.

54
Q

What predisposes ventricular premature depolarization?

A

Beta adrenergic agonists, mACh-r antagonists

55
Q

Taking too much Benadryl will cause

A

Long QT prolongation

56
Q

What looks like mACh-r?

A

Histamine receptors, so the anti/histamine Benadryl binds to mACh-r

57
Q

Repetitive ventricular premature depolarization can lead to

A

Torsades de pointes

58
Q

Torsades de pointes is a precursor to

A

V-fib

59
Q

If the stroke volume is low enough, what happens to coronary arteries?

A

Coronary blood flow comes from the aorta, so if that blood pressure is low from low ventricular output, then none of the tissues repolarize and are ischemic

60
Q

Re-entry sources

A

Accessory pathways, bundles of Kent (extra tissue that connects ventricles to atria, is in 0.2% of the population).

A&P 1 (39 decks)

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