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
A man had chest pain recently. Inverted T waves are seen on his electrocardiogram. What happened? What does this wave usually represent?
He likely had a recent MI; inverted T waves (ventricular repolarization) are a common finding in such patients
26
A man is given a drug that slows AV nodal conduction. Which segment of the electrocardiogram do you expect to change as a result?
The PR interval, which represents the time from start of atrial depolarization to start of ventricular depolarization (AV node conduction)
27
On a patient's electrocardiogram, you note oddly enlarged P waves. This may indicate pathology in which part of the heart?
The atrium (P waves represent atrial depolarization)
28
A patient has an MI and loses the SA node pacemaker. The heart, however, still beats. What is happening?
The AV node (located in the posteroinferior part of the interatrial septum) can take over if the SA node (inherent dominance) is knocked out
29
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?
No, as this is likely the J point, which is a normal finding
30
What do the cardiac nodal cells do during diastole?
They spontaneously depolarize, as this automaticity is due to the If (funny current) channels that create slow, mixed Na+/K+ inward current
31
What cellular adaptation allows cardiac myocytes to be electrically coupled?
Gap junctions
32
What is the voltage value of the resting potential of a ventricular myocyte? How is that resting potential maintained?
-85 mV; the value is maintained by high K+ permeability through K+ channels
33
Name the phases of the myocardial action potential, in order.
Rapid upstroke/depolarization, initial repolarization, plateau, rapid repolarization, resting potential
34
At each phase of the myocardial action potential, list the ions that enter and exit cells through the cellular membranes.
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
What are some key features that distinguish cardiac muscle action potentials from skeletal muscle action potentials?
Ca2+/K+-mediated plateau, Ca2+-induced Ca2+ release from sarcoplasmic reticulum, If (funny current) channels, gap junctions for coupling
36
Cardiac myocytes in which locations have pacemaker action potentials?
The sinoatrial and atrioventricular nodes
37
What effect does the resting voltage of the pacemaker cell have on the speed of conduction?
Permanent inactivation of voltage-gated Na+ channels slows conduction (how the AV node prolongs transmission from atria to ventricles)
38
• Compared with the myocardial action potential, which phases are absent from the pacemaker potential?
Phases 1 and 2 (initial repolarization and plateau phases)
39
The slope of which phase in the sinoatrial node determines the heart rate? What neurotransmitters increase and decrease the heart rate?
Phase 4; catecholamines increase heart rate by increasing the rate of depolarization; ACh/adenosine decrease depolarization and heart rate
40
What phase of the cardiac action potential accounts for the automaticity of the pacemaker nodes? How?
Phase 4; the If (funny current) channels conduct Na+ and K+, which causes spontaneous depolarization
41
Sympathetic stimulation ____ (decreases/increases) the possibility that If ("funny current") channels are open.
Increases (as a result, the pacemaker cell depolarizes more frequently and the heart rate increases)
42
During which phase are K+ channels open?
Phase 3 (leading to K+ efflux and repolarization)
43
Name the phases of the pacemaker action potential, in order.
Phase 0 = upstroke, phase 3 = inactivation of Ca2+ channels/activation of K+ channels, phase 4 = slow spontaneous diastolic depolarization
44
What part of the electrocardiogram represents atrial repolarization?
Atrial repolarization is masked within the QRS complex
45
A 67-year-old man has U waves on his electrocardiogram in the ED. He has a normal heart rate. What is the treatment?
Replenish potassium (U waves are caused by hypokalemia or bradycardia, the latter of which this patient does not have)
46
What is the physiologic benefit of the atrioventricular delay? How long is it?
It allows time for ventricular filling; 100 msec
47
Order the following pacemakers from fastest to slowest heart rate: His-Purkinje system/ventricles, SA node, AV node
SA node, AV node, His-Purkinje system/ventricles
48
Order the following structures from fastest to slowest conduction: AV node, atria, Purkinje, ventricles
Purkinje, atria, ventricles, AV node
49
Outline the conduction pathway starting from the SA node and ending with the ventricles.
SA node, atria, AV node, common bundle, bundle branches, fascicles, Purkinje fibers, ventricles
50
How long is a normal PR interval? QRS complex?
51
A patient has a prolonged QT interval. What does this interval on the electrocardiogram measure?
Ventricular depolarization, mechanical contraction of the ventricles, ventricular repolarization
52
A man had chest pain recently. Inverted T waves are seen on his electrocardiogram. What happened? What does this wave usually represent?
He likely had a recent MI; inverted T waves (ventricular repolarization) are a common finding in such patients
53
A man is given a drug that slows AV nodal conduction. Which segment of the electrocardiogram do you expect to change as a result?
The PR interval, which represents the time from start of atrial depolarization to start of ventricular depolarization (AV node conduction)
54
On a patient's electrocardiogram, you note oddly enlarged P waves. This may indicate pathology in which part of the heart?
The atrium (P waves represent atrial depolarization)
55
A patient has an MI and loses the SA node pacemaker. The heart, however, still beats. What is happening?
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
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?
No, as this is likely the J point, which is a normal finding
57
Define torsades de pointes.
Ventricular tachycardia, characterized by a polymorphic sinusoidal pattern on electrocardiogram
58
What are the most dangerous sequelae of torsades de pointes?
Ventricular fibrillation and death
59
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?
Typically due to ion channel defects that disrupt myocardial repolarization; ↑ risk of torsades de pointes & sudden cardiac death
60
Congenital long QT syndromes can be associated with what other pathology?
Sensorineural deafness (Jervell and Lange-Nielsen syndrome, autosomal recessive) (Romano-Ward syndrome [autosomal dominant] is pure cardiac)
61
Name five classes of medications that can prolong the QT interval.
Antiarrhythmics (IA,III), antibiotics (macrolides), anticychotics (haloperidol), antidepressants (TCAs), antiemetics (ondansetron) (ABCDE)
62
An Asian man's ECG shows a pseudo&8211;right bundle branch block and ST elevations in V1-V3. You suspect which inherited disorder?
Brugada syndrome, which is an autosomal dominant disorder most common in Asian male subjects.
63
An Asian male has Brugada syndrome. What is he at risk for? What preventive measure should you take to help this patient?
He is at ↑risk for ventricular tachyarrhythmias and sudden cardiac death; prevent with implantable cardioverter-defibrillator
64
What is Wolff-Parkinson-White syndrome?
A disorder with an abnormal fast accessory conduction pathway from the atria to the ventricles, leading to early ventricular depolarization
65
In the lab, you study the heart of a patient with Wolff-Parkinson-White syndrome.
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
Why are patients with atrial fibrillation at increased risk for stroke? How is it treated?
It causes atrial stasis, which can lead to cardioembolic events; treat with rate/rhythm control, antithrombotics, and/or cardioversion
67
A patient has electrocardiogram findings consistent with third-degree heart block. What are they? What is the treatment?
P waves and QRS complexes are present but have no relation with one another, because the atria and ventricles beat independently; pacemaker
68
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?
Third-degree (complete) atrioventricular block from Lyme disease
69
Why does atrial flutter present with sawtooth waves on electrocardiogram? How is it treated?
Rapid sequence of identical back-to-back atrial depolarization waves; rate control, anticoagulation, cardioversion, or ablation (definitive)
70
A patient has a PR interval of 250 msec. What type of atrioventricular block is this?
First degree (patients will generally be asymptomatic) (benign and no treatment required)
71
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?
Mobitz type I only; Mobitz type II
72
One can use rate or rhythm control for the treatment of atrial fibrillation. What drug classes are commonly used for each approach?
Rate control = β-blockers, non-dihydropyridine Ca2+ channel blockers, digoxin, rhythm control = class IC or III antiarrhythmics
73
During a stroke work-up, it is common to perform both ECG and an echocardiogram. Certain findings may prompt treatment with warfarin. Why?
Atrial fibrillation can predispose a patient to cardioembolic events, which can be prevented with antithrombotics such as warfarin