A&P CV 2 Rhythmical Excitation of Heart Flashcards
1
Q
Sinoatrial (SA) node is known as the
A
pacemaker
2
Q
SA node —>
A
Internodal tracts
3
Q
Internodal tracts –>
A
Atrioventricular (AV) node
4
Q
Atrioventricular (AV) node —->
A
Bundle of His
5
Q
Bundle of His —>
A
Bundle branches
6
Q
Bundle branches —>
A
Purkinje fibers
7
Q
Purkinje fibers —>
A
Ventricular muscle
8
Q
Depolarization slows down within
A
the AV Node
think of it as the speeding zone
9
Q
Speed of conduction (secs) to AV node
A
0.03
10
Q
Speed of conduction (secs) to AV bundle
A
0.12
11
Q
Speed of conduction (secs) to bundle branches/ Ventricular septum
A
0.16
12
Q
Speed of conduction (secs) at the SA node
A
0.00
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
14
Q
How long is the brief delay at the AV node?
A
~ 100-150 msec
15
Q
The atrial pause enhances:
A
ventricular filing.
16
Q
This extremely slow conduction through the AV node is due to decreased
A
number of gap junctions
17
Q
A decreased number of gap junctions results in
A
Great Ion resistance ( increased resistance = increased delay)
18
Q
The fastest conduction is in:
A
Purkinje fibers
19
Q
The slowest conduction is in:
A
AV Node
20
Q
P -Wave
A
- atrial depolarization
- does not include atrial repoloarization; which is ‘buried” in the QRS
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
22
Q
QRS complex =
A
ventricular depolarization (<120msec)
23
Q
QT Interval -
A
represents the entire period of DE and REpoloarization of ventricles
24
Q
ST segment-
A
Isoelectric
ventricles are depolarized
25
T Wave
Ventricular Repolarziation
26
Causes of Cardiac Arrhythmia's:
- 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
27
Sinus Tach =
HR > 100bmp
| Normal P wave & QRS
28
Causes of Sinus Tach?
```
Fever
SNS - blood loss; reflex stimulation of heart
Stress
Ischemia
Reduced SV (HF)
Infection
Dehydration
```
29
Tx for Sinus Tach
Tx underlying cause
30
Bradycardia =
slow HR < 60bpm
31
Causes for Bradycardia
```
athletes who have a large SV
Vagal stimulation (carotid Sinus Syndrome)
```
32
carotid Sinus Syndrome can cause what arrhythmia?
Brady
33
TX for bradycardia
atropine
34
SVT (proxysmal atrial tachycardia)
HR 150-250 - rapid HR; transient or continuous
Narrow QRS
P waves buried in QRS or T wave
Occurs by re-entrant pathways
35
TV of SVT
```
-Increase Vagal stimulation
carotid massage
valsalva maneuver
-Drugs
verapamil
beta blockers (esmolol)
digoxin or adenosine
```
36
You'd use beta blockers (esmolol) to tx:
SVT
37
what would you be treating with digoxin or adenosine?
SVT
38
verapamil is an option to tx what?
SVT
39
Atrial Flutter =
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
TX for Atrial flutter
- carotid sinus massage
- valsava
- Cardioversion if unstable
41
Saw tooth ECG may indicate
A flutter
42
Atrial Fibrillation =
Irregularly irregular rhythm
43
Causes for A.fib?
hypoxemia, fever, ETOH, PE, pericarditis, Ischemia, MV disease, thyrotoxicosis
44
Tx for A. Fib?
tx underlying cause
Slow Ventricular rate (verapamil, digoxin, esmolol)
Cardioversion
Antiocoagulation
45
Atrioventricular Junctional Arrhythmias feature:
- AV Node is acting as pacemaker (40-60bpm)
| - protective mechanism in case of sinus brady
46
AV Node reentrant tachycardia
```
Rate 150-250bpm, sudden onset
Tx
-carotid massage, Valsalva maneuvers
-verapamil, esmolol, dig, adenosine
-cardioversion
```
47
Pre-excitation syndrome
Abn conduction pathway b/w atrium and ventricle leads to early depoloarization of ventricle.
48
Pre-excitation syndrome - PR Interval is
shortened < 0.12 sec
| AV node is bypassed
49
Wolff-Parkinson -White Syndrome is most common form of
Pre-excitation syndrome
50
TX for Wolff Parkinson-White Syndrome?
ablation
51
Premature Contractions
| AV node or AV Bundle
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
Ventricular Arrhythmias are:
PVC's
Ventricular Tachycardia
V. flutter
V. Fib
53
PVC's are:
- 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
Triggers for PVC's:
tobacco
caffeine
alcohol
anxiety
55
Treatment for PVC's
no tx for asymptomatic
| -trigger avoidance
56
Ventricular Tachycardia =
- 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
Hall mark sign of V.Tach
AV dissociation
58
Clinical Features of V.Tach
-sudden death
59
TX for V.Tach
- Cardioversion
- IV lidocaine
- Quinidine (na-ch blocker) increases refractory period of cardiac muscle and can eliminate the problem
60
"Torsade de pointes"
V.Tach
| -twisting around the baseline
61
Ventricular flutter and fibrillation
- 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
Causes for V.flutter/fib
- ischemia
| - electrical shock
63
Tx for VF
Defibrillation
| -may go into V.Fib
64
VFib also called
Circus movements
65
"circus movements" occur:
- 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
Ventricular Defibrillation
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
The Heart blocks are:
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
Sinoatrial Block
- 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
Atrioventricular Block
impulses through AV node and AV bundle (bundle of his) are slowed or blocked.
70
Causes for AV Block:
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
Hallmark of first degree heart block:
Prolonged PR -interval (>0.20 sec)
72
First degree AV Block:
- 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
Second Degree AV Blocks are:
Type I - wenchebach
| Type II - Mobitz
74
Type I - Wenchebach is described as:
"Progressive" PR prolongation and then nonconduted P wave "dropped beat"
- P wave not followed by QRS complex
- more benign-rarely produces s/s
75
Causes for Type I AV block?
inferior wall MI
76
Type II - Mobitz is described as:
"Constant" PR interval. Sudden dropped QRS.
| -2 P waves: 1 QRS response (2:1 block)
77
Causes of Type II AV Block?
- disease below AV node
| - anterior wall MI
78
S/S of Type II AV Block:
syncope
| "symptomatic bradycardia"
79
Tx for Type II AV Block:
Pacemaker
80
Third degree HB (Complete)
- 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
TX for Complete HB
Permanent pacemaker
82
Stokes Adams Syndrome is
Complete AV Block that comes and goes
83
In Stokes Adams Syndrome, what happens to the ventricles?
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
S/S associated with Stokes Adams Syndrome:
Fainting d/t poor cerebral blood flow
85
TX for Stokes - Adams Syndrome
pacemaker
86
Incomplete Intraventricular block (electrical alternans)
- abn/bizarre QRS waves
| - caused by ischemia, myocarditis, and digitalis toxicity
87
Premature Contractions caused by
ectopic foci in the heart
88
Causes for ectopic foci are:
1. local areas of ischemia
2. calcified palques
3. toxic irritation of AV node; purkinje system or myocardium by drugs
89
Drugs that may be toxic/ irritating to myocardium :
nicotine
| caffeine
90
Premature Atrial Contractions:
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
a low SV and weak radial pulse are seen with
PAC's
92
Cardiac Arrest usually occurs d/t -
hypoxic conditions in the heart
93
Hypoxic conditions in the heart prevent
muscle and conductive fibers from maintaining their electrolyte gradients
