Block 3 - Conduction and Rhythm Flashcards

(67 cards)

1
Q

What is intrinsic control?

A

Heart depolarizes and contracts w/o NS stimulation

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2
Q

What is extrinsic control

A

Rhythm can be altered by ANS

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3
Q

What factors coordinate heart beat?

A
  1. Gap junctions
  2. Intrinsic cardiac conduction system
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4
Q

What are the components of intrinsic cardiac conduction system?

A
  1. Network of non contractile (auto rhythmic cells)
  2. Initiate and distribute impulses → coordinated depolarization and contraction of heart
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5
Q

Describe the activity of pacemaker cells (action potential)?

A
  1. Pacemaker potential: Repolarization closes K+ channels and opens slow Na+ channels → ion imbalance →
  2. Depolarization:
    Ca2+ channels open → huge influx → rising phase of action potential
  3. Repolarization
    K+ channels open → efflux of K+
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6
Q

Unstable resting membrane potential is caused by?

A

Opening of slow Na+ channels

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7
Q

At threshold, ___ channels open?

A

Ca2+

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8
Q

Explosive Ca2+ influx produces ___

A

Rising phase of action potential

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9
Q

Describe the action potential initiation by contractile cardiomyocytes?

A
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10
Q

Describe the sequence of excitation?

A

SA node → Av node → V bundles → right and left bundle branches → Purkinje fibers (subendocardial conducting network)

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11
Q

What is the purpose of the SA node?

A
  1. Pacemaker of heart in right atrial wall
  2. Depolarizes faster than the rest of the heart
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12
Q

SA node impulse? Inherent rate?

A

75x/min (sinus rhythm)

100X/min

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13
Q

How does AV node differ from SA?

A
  1. Delays impulse 0.1 sec
  2. Smaller fibers → fewer gap junctions
  3. Atrial contraction
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14
Q

Inherent rate of AV nodes?

A

50x/min without SA node input

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15
Q

What is the function of AV bundles?

A

Only electrical connection between atria and ventricles

(not connected by gap junctions)

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16
Q

What is the function of the right and left bundle branches?

A

Carry impulses toward apex of heart

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17
Q

What is the function of subendocardial conducting network?

A
  1. Complete pathway through inter ventricular septum into apex and ventricular wall
  2. More elaborate on left side of heart
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18
Q

Intrinsic rate of Punjenke fibers?

A

Depolarizes 30X/min in absence of AV node input

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19
Q

What happens after Pujenke fibers?

A

Ventricular contraction from apex toward atria

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20
Q

Describe the overal intrinsic cardiac conduction system during action potential?

A
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21
Q

Identify the action potential shapes?

A
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22
Q

What occurs during extrinsic innervation of the heart?

A

ANS via cardiac centers in medulla oblongata
1. Sympathetic → Increased rate and force
2. Parasympathetic → Decrease rate
3. Cardioacceleratory center → stimulate SA, AV, muscles, and coronary arteries
4. Cardioinhibitory center → inhibits SA and AV via vague nerves

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23
Q

What are the components of ECG?

A
  1. P wave – depolarization SA node → atria
  2. QRS complex - ventricular depolarization and atrial repolarization
  3. T wave - ventricular repolarization
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24
Q

What occurs during the PR interval?

A

Beginning of atrial excitation to beginning of ventricular excitation

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25
What occurs during the ST segment?
Entire ventricular myocardium depolarized
26
What occurs during the QT segment?
Beginning of ventricular depolarization through ventricular repolarization
27
Identify the components of the ECG chart?
28
Identify the rhythm
Normal
29
Identify the rhythm
Ventricular fibrilation
30
Identify the rhythm
Second degree heart block
31
Identify the rhythm
Junctional rhythm
32
What is Automaticity?
ability of pacemaker cells to generate an electrical impulse to regulate heart rate in accordance to the body’s needs
33
What is absolute refractory period?
Time after the firing of a nerve fiber during which the nerve fiber cannot be stimulated, regardless of strength of the stimulus applied
34
What causes ischemia in regards to electrolyte imbalances?
Inappropriate Ca2+ entry and K+ exit from cardiomyocytes
35
What are electrolyte imbalances that cause dysthymias?
1. Hyponatremia and kalmia: Actute MI 2. Hypomagnesia: Increased CHD mortality and sudden cardiac death 3. Hypercalcemia: shortens QT inteval
36
What is reentry?
Cycling of electrical impulses Propagating impulse fails to die out after normal activation of the heart and persists
37
Where does reentry take place?
1. Myocardial tissue 2. AV nodal cells 3. Junctional tissue 4. Ventricles
38
What is required to intimate reentry?
1. Areas of slow conduction 2. Unidirectional conduction block 3. Triggering stimulus
39
What is the function of areas of slow conduction?
previously depolarized areas to repolarize adequately to conduct an impulse again
40
What is the function of unidirectional conduction block?
Provides one-way route for original impulse to re-enter, thereby blocking other impulses entering from the opposing direction and extinguishing the reentrant circuit
41
What is the purpose of triggering stimulus?
Extrasystole to start the circuit
42
What is cardiac arrest?
Abrupt loss of cardiac function
43
What is considered normal conduction?
impulses from all Purkinje fibers collide in the ventricle and extinguish themselves → ventricular depolarization
44
What causes reentry?
1. Ischemia 2. Infarction 3. Elevated serum K+ levels 4. Scar issue
45
How can scar tissue cause dysrhythmias?
1. Interrupts normally low-resistance paths between viable myocardial cells 2. Slows conduction 3. Promotes asynchronous myocardial activation 4. Predisposes to unidirectional conduction block
46
What is anatomic reentry?
Involves anatomic obstacle around which the circulating current must pass → an excitation wave the travels to set pathway
47
What are the outcomes of anatomic reentry?
Arrhythmias: PSVTs, A fib, atrial flutter, AV nodal reentry, some ventricular tachycardias
48
What is functional reentry?
Depends on local differences in conduction velocity and refractionaries among neighboring fibers that allow an impulse to circulate repeatedly around an area
49
What are the manifestations of functional reentry?
Spinal reentry: wave of current does not propagate normally after meeting refractory tissue Arrhythmias are polymorphic
50
What is reflection reentry>
Occurs in parallel pathways of myocardial tissue or of the Purkinje network
51
How does reflection reentry differ from true reentry?
The impulse travels along the same pathway in both directions and does not require a circuit
52
What are the categories of peri-infarction dysrhythmias?
1. Supraventricular tachydysrhthmias 2. Accelerated junctional rhythms 3. Ventricular dysrhythmias 4. Intraventricular blocks 5. Bradydysrhythmias
53
Fast heart rate leads to ___
Sufficient ventricular filling
54
Slow heart rate leads to ___
Sufficient perfusion
55
Absent heart rate leads to ___
Pulseless VT or VF → cardiac arrest
56
What are the presentations of Supraventricular tachydysrhythmias?
1. Sinus tachycardia 2. Premature atrial contractions (PACs) 3. Paroxysmal supraventricular tachycardia (PSVT) 4. Atrial flutter 5. A fib
57
What is A fib?
Atria to beat a rapid, irregular rate → pooling and clotting of blood → MI or stroke → Mortality
58
Identify the difference?
Atrial flutter; A fib
59
What is Accelerated junctional rhythms?
Junctional rhythms → Increased automaticity of AV junction tissue and escape rhythm Inferior MI
60
What are the presentation of ventricular dysrhythmia?
1. Premature ventricular contractions (PVCs) 2. Ventricular tachycardia (VT) 3. Ventricular fibrillation (VF)
61
What causes ventricular dysrhythmias?
1. Electrical instability related to electrolyte imbalances 2. Cardiomyopathies related to ischemia or nonischemic causes, structural problems, or heart failure
62
What are the types of intraventricular blocks?
RBBB, LBBB
63
What is RBBB?
Conduction delay that occurs in any part of the right-sided intraventricular conduction system → Death from cariogenic shock
64
What is LBBB?
conduction delay or block from any of the several intraventricular conduction system sites → Reduced survival rates
65
What are the types of Bradydysrhythmias?
1. Sinus bradycardia 2. First-degree AV block 3. Second degree AV block 4. Third degree AV block
66
What are the types of second degree AV block?
1.Mobitz type I – commonly associated with an inferior MI 2. Mobitz type II – commonly associated with an anterior wall MI
67
What is third degree AV block?
anterior and inferior MI Most concerning High mortality rate