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Block C: Circulation > Electrophysiology > Flashcards

Electrophysiology Flashcards

1
Q

Why does the CO starts falling, when we get above 150bpm?

A

Because the heart doesn’t have the time to fill up

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2
Q

What is the dominant pacemaker, initiating the first impulse?

A

The sinus (sinoatrial) node

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3
Q

Why does the AV node fires relatively slowly?

A

To prevent tachyarrhythmias

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4
Q

The AV node impulse goes to the ventricles via what?

A

The His-Purkinje system

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5
Q

What is the phase 0 of action potential of cells?

A

Phase 0 takes the cell from its negative polarization to its positive maximum

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6
Q

What are you doing when you’re hyperpolarizing the cell?

A

You make the cell more negative than it is at its resting phase

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7
Q

At resting phase, is there more K+ inside or outside the cell?

A

Inside the cell

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8
Q

At resting phase, is there more Na+ inside or outside the cell?

A

Outside

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9
Q

If cell was permeable to Na+, sodium would flow into the cell only to stop at which electrical charge?

A

+60mV

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10
Q

What happens at resting state phase of the cell membrane action potential?

A

Cell is only permeable to K+; K+ leaves the cell, leaving negative charge; electrical equilibrium potential balances at -85mV

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11
Q

What is phase 2 of the cell membrane action potential?

A

Calcium L-channels open; calcium enters and leaves positive charge, electrical equilibrium potential balances at +40mV

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12
Q

What is phase 0 of the cell action potential?

A

Sodium channels open; Na+ enters and leaves positive charge; electrical equilibrium potential balances at +60mV

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13
Q

What is phase 1 of the cell action potential?

A

Potassium continues to leave the cell, making the cell slightly more negative. Overall charge is still positive.

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14
Q

What is phase 3 of the cell action potential?

A

Delayed K+ channel: Potassium continues to leave the cell, making the cell more negative until it reaches resting phase.

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15
Q

Which phase of the cell action potential governs the action potential duration, or “refractoriness”?

A

Phase 3

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16
Q

What is special about the Phase 4 of the His-Purkinje cells?

A

The calcium channels are open, which creates a slight polarization until it reaches a threshold (at which point Phase 0 begins)

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17
Q

In fast channel action potential, refractoriness is determined by what?

A

APD (action potential duration)

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18
Q

In slow-channel action potential, refractoriness is determined by what?

A

Ca2+ channel recovery

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19
Q

Two examples of a slow channel cells?

A

SA & AV nodes

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20
Q

Example of a fast channel cell?

A

His-Purkinje cell

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21
Q

The ectopic beat characterized by no P-waves and a wide-shaped QRS complex is called what?

A

Premature ventricular contraction (PVC) also called Ventricular Tachycardia

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22
Q

What is called the ectopic beat with an early P wave?

A

Premature atrial contraction (PAC)

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23
Q

What are the two most common tachycardias (and give a clue to how to differentiate them)?

A

Atrial fibrillation

Paroxysmal atrial tachycardia (those start and stop abruptly)

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24
Q

Rate > 100 bpm
Arise elsewhere than in the sinus node
are signs of what?

A

Ectopic tachycardias

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25
By what can a reduction of the slop of phase 4 during cell action potential duration be caused?
Reduction Na+ current in fast channel tissue | Reduction Ca2+ current in slow channel tissue
26
What is "early afterdepolarization" (EAD)?
When a cell becomes fully positive (depolarization) during Phase 2 or 3
27
What is "delayed afterdepolarization" (DAD)?
When a cell becomes fully positive (depolarization) during Phase 4, but before another action potential would normally occur via the normal conduction systems of the heart
28
EADs are caused (and favored) by what?
Excessive action potential prolongation allowing Ca2+ to depolarize the cell Blocked K+ channels Favored by slow heart rates
29
To which phase in the action potential does the T-wave corresponds?
Phase 3
30
In broad terms, how do you treat EAD?
You shorten action potential duration: Stop any drugs blocking K+ channels Normalize K+ concentration if low Increase heart rate (temporary pacemaker)
31
Calcium released by the sarcoplasmic reticulum inside the cardiac cell cause what?
Contraction
32
The release of calcium by the sarcoplasmic reticulum is caused by what?
By the calcium entering the cell wall through Ca2+ channels
33
Reuptake of Ca2+ by the sarcoplasmic reticulum leads to what?
Relaxation
34
What is called the Ca2+ release channel on the sarcoplasmic reticulum?
Ryanodine receptor (RyR2)
35
What does DAD cause?
Reduce the sarcoplasmic reticulum Ca2+ loading | Blocks Na+ channels
36
PR interval goes from where to where on the ECG?
HA! It goes from P wave to Q!! NOT from P wave to R!
37
QT interval goes from where to where on the ECG?
From start of the QRS to end of T wave
38
Name two conditions that shortens the QT interval on the ECG
Hypercalcemia | Tachycardia
39
Name four conditions that lengthen the QT interval on the ECG
Hypocalcemia Hypokalemia Myocardial ischemia Hypomagnesemia
40
Things that alter someone's cardiac electrical axis?
Physical orientation of the heart Ventricular hypertrophy Infarction
41
What is the angle of right axis deviation?
90 to 180
42
What is the angle of left axis deviation?
-90 to -30
43
What is the angle of extreme axis deviation?
180 to -90
44
What is the angle of normal axis?
-30 to 90
45
What axis do you have if you have Positive lead I Positive lead 2
Normal axis
46
What axis do you have if you have Positive lead I Negative lead 2 Negative aVF
Left axis deviation
47
What axis do you have if you have Negative lead I Positive lead 2 Positive aVF
Right axis deviation
48
What axis do you have if you have Positive lead I Negative aVF
Extreme axis deviation
49
What does the P wave represent?
Depolarization of the right atrium followed by depolarization of the left atrium
50
What are the ECG-lead and axis clues indicating a right ventricular hypertrophy?
Upward deflections of V1 and V2 leads | Right axis deviation
51
What are the ECG-lead clues indicating a left ventricular hypertrophy?
R peak is higher than usual on aVL lead and lead I
52
What may cause a bundle branch blocks (and what are those?)?
Right and left bundle branches are offshoots of the bundle of His on the interventricular septum, linking to the fibers of Purkinje. Bundle branch blocks may be caused by ischemic or degenerative damage
53
What is a sign of a right bundle branch block?
Bunny ears in the V1 to V3 leads in the QRS complex
54
What is a sign of a left bundle branch block?
Abnormal QRS in leads I, aVL, V5 & V6
55
Wide, deep and repeated pathological Q waves are signs of what?
Myocardial infarction
56
Repeated wide, deep Q waves in lead V1 & V2 are signs of what?
(right) Anteroseptal infarct
57
Repeated wide, deep Q waves in lead V2 & V4 are signs of what?
(apex) Anteroapical infarct
58
Repeated wide, deep Q waves in lead V5, V6, aVL & lead I are signs of what?
(left) Anterolateral infarct
59
Repeated wide, deep Q waves in lead I, II and aVF are signs of what?
Inferior infarct
60
Tall R waves in leads V1 & V2 are signs of what?
Posterior infarct
61
What is the coronary artery most often responsible for anteroseptal infarct?
Left anterior descending artery | also known as anterior interventricular branch of left coronary artery, or anterior descending branch
62
What is the coronary artery most often responsible for anteroapical infarct?
Left anterior descending artery | also known as anterior interventricular branch of left coronary artery, or anterior descending branch
63
What is the coronary artery most often responsible for anterolateral infarct?
Circumflex artery
64
What is the coronary artery most often responsible for posterior infarct?
Right coronary artery
65
What is the coronary artery most often responsible for inferior infarct?
Right coronary artery
66
What is transient myocardial ischemia?
Momentarily lack of blood flow to the heart
67
What are the ECG signs of transient myocardial ischemia?
T wave inversion | ST depression
68
T wave inversion ST depression No Q waves are signs of what?
Non-ST segment elevation myocardial ischemia
69
What is non-ST segment elevation myocardial ischemia?
A clot is formed inside the heart, leading to an artery partial obstruction
70
What is a ST segment elevation myocardial ischemia?
A clot is formed inside the heart, leading to an artery complete obstruction
71
What is a syncope?
Fainting
72
What is bradyarrhythmias?
<60bpm
73
What is the most common form of bradyarrythmias?
Sick sinus syndrome
74
Sinus node intermittently fails to fire Usually cause syncope (not cardiac arrest) Occurs generally in the elderly what is the Dx?
Sick sinus syndrome
75
What is first degree atrioventricular block?
A slowing in the atrioventricular conduction
76
What is second-degree atrioventricular block of Mobitz Type 1 (also called Wenkebach block)?
Progressive PR interval lengthening until blocked by P-wave | Rarely progress in 3rd degree
77
``` Blocked P-wave without lengthening of PR interval Disease in the His-Purkinje system QRS complex is long Indication for a pacemaker What is the Dx? ```
Second-degree atrioventricular block of Mobitz Type 2
78
What is 3rd degree atrioventricular block and is a good predictor that it will occur?
No sinus impulse gets to the ventricles Requires a pacemakers Second-degree atrioventricular block of Mobitz Type 2 is a good predictor
79
When an atrioventricular block occcurs, the His-Pirkunje system will rely on Escape Rhythms. What is the bpm of His-Purkinje escape rhythm?
30bpm
80
When sinoatrial node fails, the atrioventricular system will rely on Escape Rhythms. What is the bpm of atrioventricular escape rhythm?
50bpm
81
What is the treatment for acute bradyarrythmias?
Atropine to remove cholinergic tone slowing the sinoatrial and atrioventricular nodes Isoproternol to stimulate Beta-adrenergic receptors and accelerate pacemakers
82
What are the supraventricular pacemakers?
Sinoatrial node | Atrioventricular node
83
What is the treatment for chronic bradyarrythmias?
Permanent pacemaker
84
Substained reentry requires what?
It requires the circuit time to be greater than the longest refractory period
85
Atrioventricular node reentry Common among healthy people What is the Dx?
Paroxysmal supraventricular tachycardias
86
How do you stop atrioventricular reentry?
Block Ca2+ channel mediating atrioventricular conduction or Intravenous adenosine or enhancing vagal tone by vasalva or carotid mssage. This will hyperpolarize atrioventricular node by enhancing K+ current and the action potential will be further from threshold (Ca2+ current is unsufficient on its own to allow continued firing)
87
What are the best methods to prevent atrioventricular node reentry?
Eliminate anatomical by remove AV nodal pathway | Block Ca2+ channels mediating AV node conduction
88
Name a not-so effective treatment to prevent atrioventricular reentry
Beta-blockers suppressing adrenergic enhancement of Ca2+ current
89
What is the atria firing for atrial fibrillation?
400-600bpm
90
What is the most common cause of stroke in the elderly and why?
Atrial fibrillation: static blood pool in fibrillating left atrium will embolize
91
What is the therapy for atrial fibrillation?
Reduce ventricular response rate Restore sinus rhythm with drugs that slowly increase atrial refractory period or an electric shock that terminates reentry by depolarizing tissue
92
Explain the risk prediction scheme
``` CHADS: Congestive heart failure Hypertension Age > 65y Diabetes Prior stroke/transient ischemic attack/thromboembolism (2 points) ```
93
What is the atria firing for atrial flutter?
240-300bpm
94
What is the atrial flutter ECG pattern?
Dents-de-scie
95
What is the most effective treatment for atrial flutter?
Ablation: it's simpler because there's only one macroreentrant circuit This and oral anticoagulants
96
What is the typical rate of ventricular tachycardia rhythm?
150-180bpm
97
By what can ventricular tachycardia be caused?
Enhanced automaticity Delayed afterdepolarization Early afterdepolarization Reentry
98
What is the most usual region of the heart where we see ventricular tachycardia?
Ventricular region, of course, but the correct answer is the His-Purkinje system
99
The patient suffered a mycardial infarction and has now an enhanced automaticity that caused ventricular tachycardia. What is the best treatment?
Drugs of class 1 (they block Na+ channels responsible for phase 0 activation in fast channel tissue)
100
Ca2+ loading Abnormal ryanodine receptor function (mutation) are common in what?
Cardiac hypertrophy
101
The patient suffers cardiac hypertrophy and has now a DAD that caused ventricular tachycardia. What is the best treatment?
Drugs of class 1 (they block Na+ channels responsible for phase 0 activation in fast channel tissue)
102
The patient suffers from ventricular tachycardia and Long QT syndrome. What is the best treatment?
Long QT syndrome is associated with EAD, which is caused impaired K+ channel function. Treatment for those are correcting K+ serum and increasing heart rate
103
The patient has ventricular tachycardia and a myocardial scar. What is the cause of ventricular tachycardia and the treatment?
Cause is reentry | Treatment is drugs increasing refractory period
104
What is the treatment for ventricular fibrillation (and prevention)?
(implanted) Electrical defibrillator
105
Typical rate of ventricular fibrillation?
350-500bpm
106
Is there pumping via the escape rhythms during ventricular fibrillation?
No. Ventricular fibrillation is lethal within minutes.

Block C: Circulation (10 decks)

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