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Cardio Final > Rhythm and Arrhythmias > Flashcards

Rhythm and Arrhythmias Flashcards

1
Q

Define Membrane Potential

A

Vital cellular function and the way that cell communication with other and stimulate thing to happen

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2
Q

Action potentials

A

Only some cells can generate action potentials which allow them to stimulate other cells
(Nervous system, muscles and heart)

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3
Q

Define Refractory period

A

Time during cardiac/electrical cycles that cells cannot be stimulated

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4
Q

Refractory periods are important because:

A

You don’t want to excite a myocyte that is already excited

- Disease will cause a decrease or a complete removal of this period

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5
Q

Excitation Contraction Coupling (ECC)

A

The mechanisms by which the action potential cause the myofibrils of the muscles to contract
- Changes in the electrical activity will be reflected by changes in the heart function

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6
Q

Intracellular is usually ___? Extracellular is usually —-?

A

IC: more negative
EC: more positve

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7
Q

Where is potassium and sodium typically found

A

K is within the cell

Na is outside the cell and within the blood

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8
Q

How does a change in membrane potential occure

A

3 Na get pumped out and 2 K are pumped in
With ATP there can be actiation of channels that allow a change to occur
There are also leaky channels that are more leaky for potassium

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9
Q

Define propagation

A

In one section of the membrane the charges are different (positive inside and negative outside)
Depolarization has occurred in this section and it can move down the nerve/muscle/electrical conductive system of the heart

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10
Q

Four Phases of Action Potential

A 
Phase 0: Rapid depolarization (lots of negative in the cells
Phase 1: Small Repolarization
Phase 2: Plateau phase
Phase 3: Repolarization
Phase 4: Resting potential
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11
Q

How are the action potentials in pacemaker cells different?

A

They are less negative than normal cells which means they are closer to the threshold and easier for a AP to go
The don’t have a flat plateau phase, it is constantly increasing back up to threshold
The cells are constantly firing and they excite themselves

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12
Q

Define Ion Channels

A

Passively conduct ions down their electrochemical gradients

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13
Q

Define Pump Transporters

A

Actively transport ions against their electrochemical gradient

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14
Q

Define Exchangers

A

Electrogenically exchange ionic species (i.e. Na/K ATPase

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15
Q

What channels are involved in Phase 0?

A

Fast sodium channels

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16
Q

What channels are involved in Phase 1?

A

Potassium opens

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17
Q

What channels are involved in Phase 2?

A

Slow Calcium Channels open
K+ leaves cells
Blance between Ca and K

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18
Q

What channels are involved in Phase 3?

A

Slow Calcium channels close and membrane permeability for K increase (more potassium is leaving the cell)
This brings the membrane back to threshold

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19
Q

Extracellular Ca causes

A

Myocyte contraction and the strength of contraction of cardiac muscles depends on Ca

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20
Q

Sinoatrial (SA) node

A

Self-excitation bc stage 4 is never stable
Cell membrane is leaky to Na and Ca
Slow Ca is activated at threshold and potassium leaves cells (depolarization is not as fast here)

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21
Q

SA Node has what channels

A

Slow Ca (and Na)
K
The fast Na are inhibited

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22
Q

Rhythmical Excitation of the Heart

A

SA impulses travel through the heart and cause the atria to contract first
SA –> Bundles of His –> Purkinje fibers

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23
Q

Problems with the heart can be based on

A

Generation or conduction of the impulses

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24
Q

The only connections between the atria and ventricle is the

A

SA node and the Bundles of His and this typically prevent arrhythmias

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25
Q

Cardiac cycle

A

Spontaneous generation of an AP in the SA node –> AP travels through both atria and then through the AV bundle after a delay into the ventricles

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26
Q

Diastole

A

Filling

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27
Q

Systole

A

Pumping

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28
Q

What does the P wave represent

A

Generation of the impulses traveling through the SA node to the AV node
Contraction of the atria

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29
Q

QRS represents?

A

Excitation of the ventricles

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30
Q

Impulses are faster ____ and slower ____?

A

Faster: Nervous
Slower: Heart

31
Q

ST represents

A

Repolarization of the ventricles

32
Q

Phase right after QRS reflects:

A

Valvular contraction and ventricle contractions –> increased pressure –> blood flows out

33
Q

SA Node

A

70-80 BPM

34
Q

AV Node

A

40-60 BPM

35
Q

Purkinje fibers

A

15-40 BPM

36
Q

If something happens to one node,

A

the other can take over

If the SA node is damage, the AV node will take over but the BP will be much lower and possibly even too low

37
Q

Parasympathetic

A

Decreases the rate of rhythm at SA and slows transmission of impusles

38
Q

Sympathetic

A

Increases the rate of SA discharge, accelerates conduction and increases contractility

39
Q

NE does what

A

Increase permeability of the membrane to Na and Ca which causes more strength behind each contraction

40
Q

Define Arrhythmia

A

Irregular rhythm
Tachycardia >100
Bradycardia less than 60
- Typically the atrial and ventricle will beat at different frequencies which leads to the ventricles not being able to keep up and blood gets suck

41
Q

Mechanisms of Cardiac Arrhythmias

A

Abnormalities of electrical impulse generation
Abnormalities of electrical impulse conduction
Abnormalites of electrical impulse generation and conduction

42
Q

Define Bradyarrhythmias

A

Disturbances in impulse formation at the level of SA node
OR
Disturbances at any level including exit block from SA, conduction block in AV and impaired conduction in the His-Purkinje system

43
Q

Examples of Conduction Blocks

A

SA block (no P wave)
AV block
Intraventricular block

44
Q

AV block degrees

A 
First degree (minor; delay of conduction)
Second (some impulses do not reach; dropped beats)
Third (complete; no impulses)
45
Q

In third degree AV block will the heart stop beating?

A

No because there are other nodes (SA)

46
Q

Define Stokes-Adams syndrome

A

Symptoms only occur sometimes and are difficult to catch

47
Q

Tachyarrhythmias is caused by:

A

Enhanced automaticitiy
Triggered arrhythmias during or after repolarization
Reentry

48
Q

Define After-depolarization

A

Exciting a myocyte even after it has already been excited

49
Q

Define Reetry

A

Constant excitation of current part of the heart

- MOST COMMON type of tachyarrhythmias

50
Q

Increased automaticity through

A

Sympathetic NS stimulation (beat adrenergic receptors)

Sinus tachycardia > 200 BPM

51
Q

Fast rhythm leads to:

A 
Diastolic shortening which leads to less blood being taken in
Increased pressure (hypertrophy)
Pump function will be impaired
52
Q

Tachyarrhythmias + Ischemia and hypokalemia

A

Reduced Na/K ATPase which leads to reduce repolarization current, less negative membrane potential, closer to the threshold and easier to depolarize

53
Q

Tachyarrhythmias + Mild Hyperkalemia

A

Reduced repolarization current
Less negative membrane potential
These lead to increased HR

54
Q

Tachyarrhythmias + Significant hyperkalemia

A

Depolarization of the membrane potential

Heart becomes unexcitable (cardiac arrest)

55
Q

Atrial and ventricular tachycardia can be caused by

A

Ischemia
Escape rhythms (blocks)
Hyperkalemia (mild)
Ischemia reperfusion injury

56
Q

Ischemia reperfusion injury

A

Restoration of the blood flow after an MI

- Massive amount of blood to the area leads to influx of inflammatory cells and activation of complement

57
Q

Define Triggered Automaticity

A

Impulses initiation that is dependent on afterpolarization

58
Q

Define Afterdepolarization

A

Membrane voltage oscillations that occur during or after an action potential

59
Q

Define Delayed After Depolarization

A

Increased calcium leads to hypoperfusion of tissues, HF, kidney believe it is hypovolemic which increase catecholamines

60
Q

Increased Calcium + Ischemia

A

Release of lysophospholipids with consequent Ca and Na overload
Cell from damged area that survive display spontaneous release of Ca from SR
BOTH LEAD TO TACHYARRHYTHMIAS

61
Q

Define Early After Depolarization

A

Prolongation of QT/AP and reactivation of depolarizing current

62
Q

When the QT is prolonged –>

A

Intracellular Ca increases and L-Type Ca current occurs

63
Q

Afterdepolarization in IHD and CHF

A

Intracellular Calcium overload via EAD and DAD

64
Q

Afterdepolarization with Drugs

A

Anti-arrhythmic with Class IA and III action

65
Q

Reentry explained

A

If we have a block but it is only in one direction, the depolarization wave cannot enter that part of the myocyte but it will go around it
The issue is whether or not this block adds time and the impulse doesn’t get where it is going fast enough (need an optimal refractory time)

66
Q

Define Global Reentry

A

There is a block that prevents the impulses from getting somewhere but then the heart finds another way to get the impulses through = global reentry
Example: Bundle of Kent

67
Q

Diagnostic Workup Includes

A 
History and EKG
Symptoms 
Structural heart disease and MI
FH
Long-term EKG recordings
68
Q

Symptoms can range from

A

Asymptomatic to loss of consciousness

69
Q

Ventricular tacharrhythmias causes

A

Ventricular systolic dysfunction
Chamber dilation
Hypertrophic cardiomyopathy
Sarcoidosis

70
Q

Symptoms of Bradyarrhythmia

A 
Hypotension
Syncope
Presyncope
Fatigue
Weakness
71
Q

Symptoms of Tachyarrhythmias

A 
Palpitations
Racing pulse
Dizziness
Hemodynamic disturbances (heart pump function is reduced)
Angina
VF
72
Q

Atrial Fibrillation

A

Disorganized rapid and irregular atrial activation

Rapid ventricular rhythm (120-160 BPM)

73
Q

Consequences of Afib

A

Loss of atrial contracitlity (stasis)
Fast ventricular response
Loss of contractility and emptying leading to risk of thromboembolic events

Cardio Final (12 decks)

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