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kardiaggeiako > Myocardial action potential-Pacemaker action potential-ΗΚΓ > Flashcards

Myocardial action potential-Pacemaker action potential-ΗΚΓ Flashcards

1
Q

During what phase of the cardiac myocyte action potential does extracellular calcium enter the cell? What is the effect of this calcium?

A

The plateau phase; causes calcium release from sarcoplasmic reticulum (calcium-induced calcium release) and then muscle myocyte contraction

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2
Q

During what phase of the cardiac myocyte action potential does extracellular calcium enter the cell? What is the effect of this calcium?

A

The plateau phase; causes calcium release from sarcoplasmic reticulum (calcium-induced calcium release) and then muscle myocyte contraction

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3
Q

What do the cardiac nodal cells do during diastole?

A

They spontaneously depolarize, as this automaticity is due to the If (funny current) channels that create slow, mixed Na+/K+ inward current

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4
Q

What cellular adaptation allows cardiac myocytes to be electrically coupled?

A

Gap junctions

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5
Q

What is the voltage value of the resting potential of a ventricular myocyte? How is that resting potential maintained?

A

-85 mV; the value is maintained by high K+ permeability through K+ channels

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6
Q

Name the phases of the myocardial action potential, in order.

A

Rapid upstroke/depolarization, initial repolarization, plateau, rapid repolarization, resting potential

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7
Q

At each phase of the myocardial action potential, list the ions that enter and exit cells through the cellular membranes.

A

Phase 0 = Na+ in, 1 = Na+ in (tapering off), K+ out, 2 = Ca2+ in, K+ out, 3 = Ca2+ in (tapering off), K+ out, 4 = K+ out

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8
Q

What are some key features that distinguish cardiac muscle action potentials from skeletal muscle action potentials?

A

Ca2+/K+-mediated plateau, Ca2+-induced Ca2+ release from sarcoplasmic reticulum, If (funny current) channels, gap junctions for coupling

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9
Q

Cardiac myocytes in which locations have pacemaker action potentials?

A

The sinoatrial and atrioventricular nodes

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10
Q

What effect does the resting voltage of the pacemaker cell have on the speed of conduction?

A

Permanent inactivation of voltage-gated Na+ channels slows conduction (how the AV node prolongs transmission from atria to ventricles)

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11
Q

• Compared with the myocardial action potential, which phases are absent from the pacemaker potential?

A

Phases 1 and 2 (initial repolarization and plateau phases)

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12
Q

The slope of which phase in the sinoatrial node determines the heart rate? What neurotransmitters increase and decrease the heart rate?

A

Phase 4; catecholamines increase heart rate by increasing the rate of depolarization; ACh/adenosine decrease depolarization and heart rate

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13
Q

What phase of the cardiac action potential accounts for the automaticity of the pacemaker nodes? How?

A

Phase 4; the If (funny current) channels conduct Na+ and K+, which causes spontaneous depolarization

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14
Q

Sympathetic stimulation ____ (decreases/increases) the possibility that If (“funny current”) channels are open.

A

Increases (as a result, the pacemaker cell depolarizes more frequently and the heart rate increases)

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15
Q

During which phase are K+ channels open?

A

Phase 3 (leading to K+ efflux and repolarization)

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16
Q

Name the phases of the pacemaker action potential, in order.

A

Phase 0 = upstroke, phase 3 = inactivation of Ca2+ channels/activation of K+ channels, phase 4 = slow spontaneous diastolic depolarization

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17
Q

What part of the electrocardiogram represents atrial repolarization?

A

Atrial repolarization is masked within the QRS complex

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18
Q

A 67-year-old man has U waves on his electrocardiogram in the ED. He has a normal heart rate. What is the treatment?

A

Replenish potassium (U waves are caused by hypokalemia or bradycardia, the latter of which this patient does not have)

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19
Q

What is the physiologic benefit of the atrioventricular delay? How long is it?

A

It allows time for ventricular filling; 100 msec

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20
Q

Order the following pacemakers from fastest to slowest heart rate: His-Purkinje system/ventricles, SA node, AV node

A

SA node, AV node, His-Purkinje system/ventricles

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21
Q

Order the following structures from fastest to slowest conduction: AV node, atria, Purkinje, ventricles

A

Purkinje, atria, ventricles, AV node

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22
Q

Outline the conduction pathway starting from the SA node and ending with the ventricles.

A

SA node, atria, AV node, common bundle, bundle branches, fascicles, Purkinje fibers, ventricles

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23
Q

How long is a normal PR interval? QRS complex?

A
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24
Q

A patient has a prolonged QT interval. What does this interval on the electrocardiogram measure?

A

Ventricular depolarization, mechanical contraction of the ventricles, ventricular repolarization

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25
Q

A man had chest pain recently. Inverted T waves are seen on his electrocardiogram. What happened? What does this wave usually represent?

A

He likely had a recent MI; inverted T waves (ventricular repolarization) are a common finding in such patients

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26
Q

A man is given a drug that slows AV nodal conduction. Which segment of the electrocardiogram do you expect to change as a result?

A

The PR interval, which represents the time from start of atrial depolarization to start of ventricular depolarization (AV node conduction)

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27
Q

On a patient’s electrocardiogram, you note oddly enlarged P waves. This may indicate pathology in which part of the heart?

A

The atrium (P waves represent atrial depolarization)

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28
Q

A patient has an MI and loses the SA node pacemaker. The heart, however, still beats. What is happening?

A

The AV node (located in the posteroinferior part of the interatrial septum) can take over if the SA node (inherent dominance) is knocked out

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29
Q

On a man’s ECG, at the end of the QRS complex, before the ST segment begins, you note a small sharp point. Are you worried about pathology?

A

No, as this is likely the J point, which is a normal finding

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30
Q

What do the cardiac nodal cells do during diastole?

A

They spontaneously depolarize, as this automaticity is due to the If (funny current) channels that create slow, mixed Na+/K+ inward current

31
Q

What cellular adaptation allows cardiac myocytes to be electrically coupled?

A

Gap junctions

32
Q

What is the voltage value of the resting potential of a ventricular myocyte? How is that resting potential maintained?

A

-85 mV; the value is maintained by high K+ permeability through K+ channels

33
Q

Name the phases of the myocardial action potential, in order.

A

Rapid upstroke/depolarization, initial repolarization, plateau, rapid repolarization, resting potential

34
Q

At each phase of the myocardial action potential, list the ions that enter and exit cells through the cellular membranes.

A

Phase 0 = Na+ in, 1 = Na+ in (tapering off), K+ out, 2 = Ca2+ in, K+ out, 3 = Ca2+ in (tapering off), K+ out, 4 = K+ out

35
Q

What are some key features that distinguish cardiac muscle action potentials from skeletal muscle action potentials?

A

Ca2+/K+-mediated plateau, Ca2+-induced Ca2+ release from sarcoplasmic reticulum, If (funny current) channels, gap junctions for coupling

36
Q

Cardiac myocytes in which locations have pacemaker action potentials?

A

The sinoatrial and atrioventricular nodes

37
Q

What effect does the resting voltage of the pacemaker cell have on the speed of conduction?

A

Permanent inactivation of voltage-gated Na+ channels slows conduction (how the AV node prolongs transmission from atria to ventricles)

38
Q

• Compared with the myocardial action potential, which phases are absent from the pacemaker potential?

A

Phases 1 and 2 (initial repolarization and plateau phases)

39
Q

The slope of which phase in the sinoatrial node determines the heart rate? What neurotransmitters increase and decrease the heart rate?

A

Phase 4; catecholamines increase heart rate by increasing the rate of depolarization; ACh/adenosine decrease depolarization and heart rate

40
Q

What phase of the cardiac action potential accounts for the automaticity of the pacemaker nodes? How?

A

Phase 4; the If (funny current) channels conduct Na+ and K+, which causes spontaneous depolarization

41
Q

Sympathetic stimulation ____ (decreases/increases) the possibility that If (“funny current”) channels are open.

A

Increases (as a result, the pacemaker cell depolarizes more frequently and the heart rate increases)

42
Q

During which phase are K+ channels open?

A

Phase 3 (leading to K+ efflux and repolarization)

43
Q

Name the phases of the pacemaker action potential, in order.

A

Phase 0 = upstroke, phase 3 = inactivation of Ca2+ channels/activation of K+ channels, phase 4 = slow spontaneous diastolic depolarization

44
Q

What part of the electrocardiogram represents atrial repolarization?

A

Atrial repolarization is masked within the QRS complex

45
Q

A 67-year-old man has U waves on his electrocardiogram in the ED. He has a normal heart rate. What is the treatment?

A

Replenish potassium (U waves are caused by hypokalemia or bradycardia, the latter of which this patient does not have)

46
Q

What is the physiologic benefit of the atrioventricular delay? How long is it?

A

It allows time for ventricular filling; 100 msec

47
Q

Order the following pacemakers from fastest to slowest heart rate: His-Purkinje system/ventricles, SA node, AV node

A

SA node, AV node, His-Purkinje system/ventricles

48
Q

Order the following structures from fastest to slowest conduction: AV node, atria, Purkinje, ventricles

A

Purkinje, atria, ventricles, AV node

49
Q

Outline the conduction pathway starting from the SA node and ending with the ventricles.

A

SA node, atria, AV node, common bundle, bundle branches, fascicles, Purkinje fibers, ventricles

50
Q

How long is a normal PR interval? QRS complex?

A
51
Q

A patient has a prolonged QT interval. What does this interval on the electrocardiogram measure?

A

Ventricular depolarization, mechanical contraction of the ventricles, ventricular repolarization

52
Q

A man had chest pain recently. Inverted T waves are seen on his electrocardiogram. What happened? What does this wave usually represent?

A

He likely had a recent MI; inverted T waves (ventricular repolarization) are a common finding in such patients

53
Q

A man is given a drug that slows AV nodal conduction. Which segment of the electrocardiogram do you expect to change as a result?

A

The PR interval, which represents the time from start of atrial depolarization to start of ventricular depolarization (AV node conduction)

54
Q

On a patient’s electrocardiogram, you note oddly enlarged P waves. This may indicate pathology in which part of the heart?

A

The atrium (P waves represent atrial depolarization)

55
Q

A patient has an MI and loses the SA node pacemaker. The heart, however, still beats. What is happening?

A

The AV node (located in the posteroinferior part of the interatrial septum) can take over if the SA node (inherent dominance) is knocked out

56
Q

On a man’s ECG, at the end of the QRS complex, before the ST segment begins, you note a small sharp point. Are you worried about pathology?

A

No, as this is likely the J point, which is a normal finding

57
Q

Define torsades de pointes.

A

Ventricular tachycardia, characterized by a polymorphic sinusoidal pattern on electrocardiogram

58
Q

What are the most dangerous sequelae of torsades de pointes?

A

Ventricular fibrillation and death

59
Q

A 25-year-old man has a congenital long QT syndrome. What is the most likely cause of the condition? What is he at risk for?

A

Typically due to ion channel defects that disrupt myocardial repolarization; ↑ risk of torsades de pointes & sudden cardiac death

60
Q

Congenital long QT syndromes can be associated with what other pathology?

A

Sensorineural deafness (Jervell and Lange-Nielsen syndrome, autosomal recessive) (Romano-Ward syndrome [autosomal dominant] is pure cardiac)

61
Q

Name five classes of medications that can prolong the QT interval.

A

Antiarrhythmics (IA,III), antibiotics (macrolides), anticychotics (haloperidol), antidepressants (TCAs), antiemetics (ondansetron) (ABCDE)

62
Q

An Asian man’s ECG shows a pseudo&8211;right bundle branch block and ST elevations in V1-V3. You suspect which inherited disorder?

A

Brugada syndrome, which is an autosomal dominant disorder most common in Asian male subjects.

63
Q

An Asian male has Brugada syndrome. What is he at risk for? What preventive measure should you take to help this patient?

A

He is at ↑risk for ventricular tachyarrhythmias and sudden cardiac death; prevent with implantable cardioverter-defibrillator

64
Q

What is Wolff-Parkinson-White syndrome?

A

A disorder with an abnormal fast accessory conduction pathway from the atria to the ventricles, leading to early ventricular depolarization

65
Q

In the lab, you study the heart of a patient with Wolff-Parkinson-White syndrome.

A

You note a pathway bypassing the AV node. What is it?

This is likely the accessory pathway (bundle of Kent) giving rise to the disorder

66
Q

Why are patients with atrial fibrillation at increased risk for stroke? How is it treated?

A

It causes atrial stasis, which can lead to cardioembolic events; treat with rate/rhythm control, antithrombotics, and/or cardioversion

67
Q

A patient has electrocardiogram findings consistent with third-degree heart block. What are they? What is the treatment?

A

P waves and QRS complexes are present but have no relation with one another, because the atria and ventricles beat independently; pacemaker

68
Q

An 18-year-old woman presents with a targetoid rash after hiking in the woods. Without treatment, she is at risk for what heart condition?

A

Third-degree (complete) atrioventricular block from Lyme disease

69
Q

Why does atrial flutter present with sawtooth waves on electrocardiogram? How is it treated?

A

Rapid sequence of identical back-to-back atrial depolarization waves; rate control, anticoagulation, cardioversion, or ablation (definitive)

70
Q

A patient has a PR interval of 250 msec. What type of atrioventricular block is this?

A

First degree (patients will generally be asymptomatic) (benign and no treatment required)

71
Q

Does progressive lengthening of the PR interval occur in Mobitz type I, type II, or both? Which is more likely to progress to third degree?

A

Mobitz type I only; Mobitz type II

72
Q

One can use rate or rhythm control for the treatment of atrial fibrillation. What drug classes are commonly used for each approach?

A

Rate control = β-blockers, non-dihydropyridine Ca2+ channel blockers, digoxin, rhythm control = class IC or III antiarrhythmics

73
Q

During a stroke work-up, it is common to perform both ECG and an echocardiogram. Certain findings may prompt treatment with warfarin. Why?

A

Atrial fibrillation can predispose a patient to cardioembolic events, which can be prevented with antithrombotics such as warfarin

kardiaggeiako (11 decks)

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