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Spring '20/ L. A&P > A&P CV 2 Rhythmical Excitation of Heart > Flashcards

A&P CV 2 Rhythmical Excitation of Heart Flashcards

1
Q

Sinoatrial (SA) node is known as the

A

pacemaker

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2
Q

SA node —>

A

Internodal tracts

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3
Q

Internodal tracts –>

A

Atrioventricular (AV) node

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4
Q

Atrioventricular (AV) node —->

A

Bundle of His

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5
Q

Bundle of His —>

A

Bundle branches

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6
Q

Bundle branches —>

A

Purkinje fibers

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7
Q

Purkinje fibers —>

A

Ventricular muscle

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8
Q

Depolarization slows down within

A

the AV Node

think of it as the speeding zone

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9
Q

Speed of conduction (secs) to AV node

A

0.03

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10
Q

Speed of conduction (secs) to AV bundle

A

0.12

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11
Q

Speed of conduction (secs) to bundle branches/ Ventricular septum

A

0.16

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12
Q

Speed of conduction (secs) at the SA node

A

0.00

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13
Q

Why is the conduction velocity through the AV node so slow?

A

so that depolarization is delayed within the AV node; allowing for a pause.

This pause allows blood from Atria to pass through AV Valves into ventricles with enhanced ventricular filling

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14
Q

How long is the brief delay at the AV node?

A

~ 100-150 msec

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15
Q

The atrial pause enhances:

A

ventricular filing.

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16
Q

This extremely slow conduction through the AV node is due to decreased

A

number of gap junctions

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17
Q

A decreased number of gap junctions results in

A

Great Ion resistance ( increased resistance = increased delay)

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18
Q

The fastest conduction is in:

A

Purkinje fibers

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19
Q

The slowest conduction is in:

A

AV Node

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20
Q

P -Wave

A
  • atrial depolarization

- does not include atrial repoloarization; which is ‘buried” in the QRS

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21
Q

P-R Interval

A

-conduction through AV Node (<200msec)

  • decreased AV Conduction (Heart block) Increased PR Interval
  • decreased in sympathetic stimulation
  • increased in parasympathetic stimulation
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22
Q

QRS complex =

A

ventricular depolarization (<120msec)

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23
Q

QT Interval -

A

represents the entire period of DE and REpoloarization of ventricles

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24
Q

ST segment-

A

Isoelectric

ventricles are depolarized

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25
Q

T Wave

A

Ventricular Repolarziation

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26
Q

Causes of Cardiac Arrhythmia’s:

A
  • abn rhythmicity of pacemaker
  • shift of pacemaker from SA node
  • blocks at different point in the transmission of the cardiac impulse
  • abn pathways of transmission in the heart
  • spontaneous generation of abn impulses from any part of the heart
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27
Q

Sinus Tach =

A

HR > 100bmp

Normal P wave & QRS

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28
Q

Causes of Sinus Tach?

A 
Fever
SNS - blood loss; reflex stimulation of heart
Stress
Ischemia
Reduced SV (HF)
Infection
Dehydration
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29
Q

Tx for Sinus Tach

A

Tx underlying cause

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30
Q

Bradycardia =

A

slow HR < 60bpm

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31
Q

Causes for Bradycardia

A 
athletes who have a large SV
Vagal stimulation (carotid Sinus Syndrome)
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32
Q

carotid Sinus Syndrome can cause what arrhythmia?

A

Brady

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33
Q

TX for bradycardia

A

atropine

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34
Q

SVT (proxysmal atrial tachycardia)

A

HR 150-250 - rapid HR; transient or continuous
Narrow QRS
P waves buried in QRS or T wave
Occurs by re-entrant pathways

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35
Q

TV of SVT

A 
-Increase Vagal stimulation
carotid massage
valsalva maneuver
-Drugs 
verapamil
beta blockers (esmolol)
digoxin or adenosine
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36
Q

You’d use beta blockers (esmolol) to tx:

A

SVT

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37
Q

what would you be treating with digoxin or adenosine?

A

SVT

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38
Q

verapamil is an option to tx what?

39
Q

Atrial Flutter =

A

Atria contracts at 200-350bmp

  • usually w/some degree of AV node block (thus atria may beat 2 or 3 times faster than ventricle)
  • Saw tooth appearance on ECG
40
Q

TX for Atrial flutter

A
  • carotid sinus massage
  • valsava
  • Cardioversion if unstable
41
Q

Saw tooth ECG may indicate

42
Q

Atrial Fibrillation =

A

Irregularly irregular rhythm

43
Q

Causes for A.fib?

A

hypoxemia, fever, ETOH, PE, pericarditis, Ischemia, MV disease, thyrotoxicosis

44
Q

Tx for A. Fib?

A

tx underlying cause
Slow Ventricular rate (verapamil, digoxin, esmolol)
Cardioversion
Antiocoagulation

45
Q

Atrioventricular Junctional Arrhythmias feature:

A
  • AV Node is acting as pacemaker (40-60bpm)

- protective mechanism in case of sinus brady

46
Q

AV Node reentrant tachycardia

A 
Rate 150-250bpm, sudden onset
Tx
-carotid massage, Valsalva maneuvers
-verapamil, esmolol, dig, adenosine
-cardioversion
47
Q

Pre-excitation syndrome

A

Abn conduction pathway b/w atrium and ventricle leads to early depoloarization of ventricle.

48
Q

Pre-excitation syndrome - PR Interval is

A

shortened < 0.12 sec

AV node is bypassed

49
Q

Wolff-Parkinson -White Syndrome is most common form of

A

Pre-excitation syndrome

50
Q

TX for Wolff Parkinson-White Syndrome?

51
Q

Premature Contractions

AV node or AV Bundle

A

P wave early or inverted (high AV junction)
P wave missing (mid AV Junction)
P wave late or inverted (Low AV Junction)
Impluse travels backward into atria

52
Q

Ventricular Arrhythmias are:

A

PVC’s
Ventricular Tachycardia
V. flutter
V. Fib

53
Q

PVC’s are:

A
  • beat arises directly from ventricle
  • QRS is widened b/c impulse is conducted through muscle which has slow conduction (wider than 0.12 sec)
  • T wave is inverted
  • may occur as isolated beats;; bigeminy, trigeminy, pairs of triplets
54
Q

Triggers for PVC’s:

A

tobacco
caffeine
alcohol
anxiety

55
Q

Treatment for PVC’s

A

no tx for asymptomatic

-trigger avoidance

56
Q

Ventricular Tachycardia =

A
  • V.rate 110-250
  • More than 3 PVC’s in a row
  • “sustained” = 30sec
  • QRS > 0.14 sec
  • AV Dissociation (Hall mark)
  • Cannon “a” wave
57
Q

Hall mark sign of V.Tach

A

AV dissociation

58
Q

Clinical Features of V.Tach

A

-sudden death

59
Q

TX for V.Tach

A
  • Cardioversion
  • IV lidocaine
  • Quinidine (na-ch blocker) increases refractory period of cardiac muscle and can eliminate the problem
60
Q

“Torsade de pointes”

A

V.Tach

-twisting around the baseline

61
Q

Ventricular flutter and fibrillation

A
  • Sine wave pattern; rate 200-300’s
    -chaotic baseline w/o organized QRS
    Lack of ordered contraction of ventricles
    = DEATH (d/t zero CO)
    -some parts of ventricle contract; others relax = little blood flow = no CO
62
Q

Causes for V.flutter/fib

A
  • ischemia

- electrical shock

63
Q

Tx for VF

A

Defibrillation

-may go into V.Fib

64
Q

VFib also called

A

Circus movements

65
Q

“circus movements” occur:

A
  • if pathway is long (dilated heart)
  • if conduction velocity is decreased (blockade of purkinje system, ischemia of muscle, and high K+ levels)
  • if refractory period is shortened (epinephrine)
66
Q

Ventricular Defibrillation

A

1000 volts

  • all parts of heart become refractory and remain quiescent for 3-5 sec; until new pacemaker is established.
  • after 1 min in V.fib; defibrillation is usually no good. heart too weak to correct.
67
Q

The Heart blocks are:

A
  1. Sinoatrial Block
  2. Atrioventricular block
  3. Incomplete HB
    - First degree AV Block
    - Second degree AV Block - type 1 and 2
  4. Third degree (Complete) HB
68
Q

Sinoatrial Block

A
  • Impulses from SA Node are blocked
  • no P waves
  • New pacemaker in region of heart with the fastest d/c rate; usually AV Node
69
Q

Atrioventricular Block

A

impulses through AV node and AV bundle (bundle of his) are slowed or blocked.

70
Q

Causes for AV Block:

A
  1. ) ischemia of AV node/bundle fibers (coronary ischemia)
  2. ) Compression of AV bundle (scar tissue or calcified tissue)
  3. ) AV Node or AV Bundle inflammation
  4. ) Excessive vagal stimulation
71
Q

Hallmark of first degree heart block:

A

Prolonged PR -interval (>0.20 sec)

72
Q

First degree AV Block:

A
  • Delay of >0.20 sec at AV node
  • PR interval prolonged >0.20 sec (WNL = 0.16 sec)
  • Normal P and QRS
  • Asymptomatic
  • No treatment
73
Q

Second Degree AV Blocks are:

A

Type I - wenchebach

Type II - Mobitz

74
Q

Type I - Wenchebach is described as:

A

“Progressive” PR prolongation and then nonconduted P wave “dropped beat”

  • P wave not followed by QRS complex
  • more benign-rarely produces s/s
75
Q

Causes for Type I AV block?

A

inferior wall MI

76
Q

Type II - Mobitz is described as:

A

“Constant” PR interval. Sudden dropped QRS.

-2 P waves: 1 QRS response (2:1 block)

77
Q

Causes of Type II AV Block?

A
  • disease below AV node

- anterior wall MI

78
Q

S/S of Type II AV Block:

A

syncope

“symptomatic bradycardia”

79
Q

Tx for Type II AV Block:

80
Q

Third degree HB (Complete)

A
  • Total block of AV node.
  • No atrial conduction reaches ventricles
  • P wave completely dissociated from QRS
  • Ventricular escape rate may originate in bundle of his –> narrow QRS
  • Rate 25-40 (severe symptomatic bradycardia)
81
Q

TX for Complete HB

A

Permanent pacemaker

82
Q

Stokes Adams Syndrome is

A

Complete AV Block that comes and goes

83
Q

In Stokes Adams Syndrome, what happens to the ventricles?

A

Ventricles stop contracting for 5-30 sec b/c of overdrive suppression (they’re used to atrial drive)
- then ventricles escape occurs w/ AV node of AV bundle rhythm (15-40bpm)

84
Q

S/S associated with Stokes Adams Syndrome:

A

Fainting d/t poor cerebral blood flow

85
Q

TX for Stokes - Adams Syndrome

86
Q

Incomplete Intraventricular block (electrical alternans)

A
  • abn/bizarre QRS waves

- caused by ischemia, myocarditis, and digitalis toxicity

87
Q

Premature Contractions caused by

A

ectopic foci in the heart

88
Q

Causes for ectopic foci are:

A
  1. local areas of ischemia
  2. calcified palques
  3. toxic irritation of AV node; purkinje system or myocardium by drugs
89
Q

Drugs that may be toxic/ irritating to myocardium :

A

nicotine

caffeine

90
Q

Premature Atrial Contractions:

A
  1. PR interval is shortened (if ectopic foci originating the beat are near AV node)
  2. Impulse travels through AVnode, back toward SA node causing d/c of the SA node.
  3. Thus, SA node d/c is late
  4. Early contraction does not allow heart to fill w/blood causing a low SV and weak radial pulse
91
Q

a low SV and weak radial pulse are seen with

92
Q

Cardiac Arrest usually occurs d/t -

A

hypoxic conditions in the heart

93
Q

Hypoxic conditions in the heart prevent

A

muscle and conductive fibers from maintaining their electrolyte gradients

Spring '20/ L. A&P (21 decks)

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