Cardiac electrophysiology and Cardiac Arrhythmias Flashcards

1
Q

Draw and describe the phases of cardiac action potential. Which channels areopen and which currents are responisble for each phase?

A

Phase 0: depolarization; Na+ current (open fast Na+ channels)

Phase 1: partial repolarization; Ito (outward K+ current that drives Vm to be more negative)

Phase 2: plateau (sustained depolarization); Ca2+ current

Phase 3: repolarization; Ik (delayed action)

Phase 4: rest

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2
Q

Which cells undergo the fast response? What about the slow response? Why don’t the slow response cells have a Phase 1? Explain the difference between slow and fast response. What are ERP and RRP?

A

Non-pace maker cells undergo the fast response b/c they have fast Na+ channels

Pacemaker cells undergo the slow response b/c they don’t have fast Na+ channels. Instead, the Ca2+ current is responsible for their depolarization (initiated first by If current at Phase 4), and the Ca2+ are slow channels.

ERP = effective refractory period (same as absolute refractory period)

RRP = relative refractory period

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3
Q

What is responsible for maintaining resting Vm in cardiac cells? Do we consider Na+ current when setting resting Vm in cardiac cells? If not, how is Na+ current involved in membrane potential?

A

At phase 4 = resting Vm set by the Inward Rectifying K+ current

Don’t consider Na+ current for resting Vm in cardiac cells b/c K+ current = high; external Na+ concentration determines peak membrane potential

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4
Q

Which currents are involved in AP propagation in pacemakers and at which phases are they active?

A

If

Ica

Ik

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5
Q

What is the effect of Ina in Ventricular Ap propagation? What happens when you add TTX?

What are the effects of Ica and Ik on ventricular AP?

A

Ina = fast Aps; when Ina is reduced, fast APs get converted to slow APs(in which the upstroke will then be due to Ca2+ channels)

TTX blocks Na channels and reduces Na conductance

Ica effect: responsible for Ap plateau

Ik: repolarizes membrane; blocking K+ channels prolongs Aps

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6
Q

Describe pacemaker depolarization. What is the role of I funny channels? During which phase are these channels active?

A

Due to inward current via I funny channels. Channels are slowly activated and drive Vm towards threshold.

Start activating at phase 4 of SA nodal action potentials

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7
Q

In which situations would the cardiac AP be slower?

What is the order of the speed on conduction in the heart and why?

A

Fewer Na+ channels (e.g. using TTX or another Na+ channel blocker)

Fewer Ca2+ channels activated in SA/Av node

If threshold is more positive

Purkinje fibers>Atria + Ventricles>SA/AV nodes

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8
Q

What is the effect of cycle length on the propagation speed of an AP? How are cycle lengthand Heart Rate related?

A

The faster the heart beat, i.e. the shorter the cycle, the faster the AP

HR and cycle length: shorter cycle length = faster HR

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9
Q

On an EKG, what do a P wave, QRS complex, and T wave represent?

A

P wave = atrial depolarization

QRS complex = ventricular depolarization

T wave = ventricular repolarization

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10
Q

Describe the role of NE/E (sympathetic system) on pacemaker AP

A

NE/E = activate Adenylyl cyclase >> increases cAMP >> stimulates If and Ca channels >> increase in inwards If and Ica current >> faster depol of SA/AV nodal cells >> faster AP= faster pacemaker

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11
Q

How do catecholamines like isopterenol increase contractility?

A

They increase Ca2+ conductance (increase in cAMP >> PKA activated >> add P to L type Ca2+ channels >> increase Ca2+ conductance)

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12
Q

Describe the effect of the parasympathetic system (cholinergic agonists i.e. ACh) on pacemaker APs

A

2 ways: increased ACh >> activates Gs beta and gamma subunits >> activates Ik(ach) channels >> increased outward current (less inward current = hyperpolarization in SA/AV nodal cells) >> slower depolarization b/c threshold is now more positive (closer to reversal potential for Ik)

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13
Q

Define an arrhythmia. What are the categories of arrhythmias discussed?

A

Arrhythmia: any rhythm that’s not a normal sinus rhythm

Conduction abnormalities + Abnormal automaticity

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14
Q

Types of Conduction abnormalities discussed

A

1st degree heart block

2nd degree heart block (Mobitz Type I and II)

3rd degree heart block

Bypass conduction

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15
Q

1st degree heart block. How do you id it on an EKG and what does that mean in terms of AP propagation?

A

Prolonged PR interval. Slowing of action potential.

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16
Q

2nd degree HB. How do you ID it on an EKG/how is it different from 1st degree Av block? What’s the pattern?

A

Progressive lengthening of PR interval. 3rd QRS complex dropped. Only some APs propagated; Pattern = Regularly irregular

17
Q

3rd degree HB. How do you ID it on an EKG?

A

Atria and ventricles contract independently of each other. P waves and QRS complexes dissociated.

18
Q

Bypass conduction. How does this happen and how can you ID this on an EKG?

A

Abnormal fast accesory conduction pathway from RA to ventricle (bypasses AV node) >> early depolarization of ventricles

Shorter PR interval; widened QRS complex with presence of delta wave

19
Q

Which disease is caused by bypass conduction? What can this lead to?

A

Wolf Parkinson White Syndrome

May lead to reentry circuit >> supraventricular tachycardia

20
Q

Abnormal automaticities

A

Sinus tachycardia

Sinus bradycardia

Supraventricular tachycardia

Ventricular tachycardia

Fibrillations (atrial vs ventricular)

21
Q

Which abnormal automaticity is this? How do you know?

A

Tachycardia

Shorter P-P interval

22
Q

Which abnormal automaticity is this?

A

Bradycardia

Longer P-P intervals (slow HR)

23
Q

How do you tell the difference between premature atrial and ventricular depolarizations?

A

Premature atrial depolarization: 2nd P wave is early and obscures T wave

Premature ventricular depolarization: 3rd QRS complex = early and bizarre

24
Q

What’s the difference between supraventricular and ventricular tachycardia?

A

Supraventricular tachycardia: AP comes from outside of the ventricles (upstream)

Ventricular tachycardia: AP from within the ventricles; precursor to ventricular fibrillation

25
Q

Which tachycardia is this? How do you know?

A

Supraventricular tachycardia. No P wave, only QRS complexes.

26
Q

Which tachycardia is this? How do you know?

A

Ventricular tachycardia

27
Q

Which automaticity abnormality is this? How do you know?

A

Atrial fibrillation

No P wave, irregularly spaced QRS complexes; irregularly irregular heartbeat

28
Q

Which abnormal automaticity is this? How do you know? Why is this abnormality particularly concerning?

A

Ventricular fibrillation

No discernible rhythm. Blood isn’t pumped from the heart so its fatal if not CPR or defibrillation is given

29
Q

Which abnormality is this? (hint: we talked about it in small group but not in lecture)

A

Atrial flutter. Sawtooth pattern.

30
Q

Define early after-depolarization. What is this caused by?

A

Instead of getting back down to rest (i.e. Phase 4), a new AP starts firing midway through Phase 3 (start depolarizing again)

Likely due to reactivated Ca2+ channels

31
Q

Describe how EADs can lead to a salvo of APs

A
32
Q

Explain how Delayed afterdepolarizations occur

A

Occur when HR is high (cycle length is small)

When Na+/K+ pump is inhibited, NCX reverses direction and brings Ca2+ inside the cell

33
Q

What are the types of blocks discussed in class?

A

Bidirectional block

Unidirectional block

Complete block

34
Q

Describe each of the blocks

A

Bidirectional block: wave can’t travel to the other branch, or back to the S bundle

Complete block: wave doesn’t reach either branch (may result in V fib?)

Unidirectional block: wave can’t travel to one branch but retrograde wave from the other branch can go back to S bundle (may result in WPW syndrome?)

35
Q

Describe Long QT syndrome

What are the variations of Long QT syndrome (i.e. which channels/currents are affected)?

A

Abnormal rhythm disorder

Widened QT interval - takes longer to repolarize b/c of reduced Ikr current (either via mutations in HERG channels or using HERG channel inhibitor drugs)

Romano Ward syndrome: reduced Ikr or Iks current

Timothy syndrome: Reduced Ica