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A&P I (Fall 2022) > Cardiac Electrophysiology pt.2 (Exam IV) > Flashcards

Cardiac Electrophysiology pt.2 (Exam IV) Flashcards

1
Q

Anything greater than ____ bpm is tachycardia, anything lower than this number is bradycardia (for our A&P class specifically)

A

72

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2
Q

What three causes of sinus tachycardia were talked about in lecture?

A
  1. ↑ Body Temp (like malignant hyperthermia)
  2. SNS stimulation (like from blood loss)
  3. Toxic Ischemia
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3
Q

Ischemic tissue has more frequent ______.

A

Depolarizations

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4
Q

What was Lance Armstrong’s peak CO?

A

40Lpm

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5
Q

What occurs with an elite athletes heart muscle? What occurs with the heart rate and the stroke volume as a result?

A
  • Hypertrophy
  • ↓ HR
  • ↑ SV
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6
Q

What is the only EKG parameter that changes in sinus bradycardia?

A

R-R Interval

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7
Q

How does vagal stimulation produce a lower heart rate?

A

Vagal Stimulation to KACh channels will ↑pK⁺ in the SA node = decreased Vᵣₘ = longer time in Phase 4.

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8
Q

Vagal stimulation would change what phase of a nodal tissue’s action potential?

A

Decreased slope of Phase 4

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9
Q

How does removal of β stimulation affect nodal tissue?
Describe the process by which this happens.

A
  • ↓ HR
  • ↓AC = ↓cAMP = closure of HCN channels = longer time in Phase 4.
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10
Q

How would phenylephrine stimulate reflex bradycardia?

A
  • ↑ SVR → Baroreceptors perceive ↑MAP → inhibition of nodal tissue via Vagus nerve.
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11
Q

Where are baroreceptors located?

A

Aortic Arch & Carotid Bifurcation.

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12
Q

What does “Paroxysmal” mean?

A

“comes & goes” Intermittent.

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13
Q

Where does Paroxysmal Atrial Tachycardia originate?

A

SA node still

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14
Q

What method would be needed to catch a paroxysmal rhythm for diagnosis?

A

Holter Monitor

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15
Q

What two EKG tracings may overlap during Supraventricular Tachycardia?

A

P wave & T wave

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16
Q

What three treatments could be utilized (per lecture) for Supraventricular Tachycardia: Paroxysmal Atrial Tachycardia?

A
  • Vagal Reflex
  • βblocker (or maybe CCB)
  • Digoxin
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17
Q

Loss of ___ ______ occurs with Sinoatrial Block. (hint: EKG)

A

P-waves

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18
Q

What p-wave characteristic might be present in a sinoatrial block? Why is this?

A
  • Negative P-wave deflection
  • AV-node depolarization generating an action potential back into the atria.
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19
Q

What is the heart rate generated by by the AV node?

A

40-60 bpm

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20
Q

What five causes of AV block were discussed in lecture?

A
  1. Ischemia of AV Node or Bundle
  2. Compression of AV bundle
  3. AV Node or AV Bundle Inflammation
  4. Excessive Vagal Stimulation
  5. Excess Digoxin
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21
Q

Differentiate the effects of ischemia vs infarction on the AV Node/Bundle.

A
  • Ischemia would lead to slowing of transmission.
  • Infarction would likely lead to total AV block.
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22
Q

What drugs (pertinent to the heart & mentioned in lecture) slow down cardiac scarring?

A

ACE Inhibitors (through growth factor inhibitors)

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23
Q

Where does compression of the AV bundle occur? What causes compression?

A
  • Penetrating portion of the AV bundle.
  • Scar Tissue or Calcified Tissue
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24
Q

The left Vagal nerve influences the ____ node.

A

AV

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25
Q

The SA node is parasympathetically innervated by the ____ ____ ______.

A

Right Vagal Nerve

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26
Q

Manual compression of the vagal nerve will increase or decrease vagal output?

A

Increase Vagal output

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27
Q

1st degree heart block is defined by a PR interval that is……

A

> 0.2 seconds

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28
Q

2nd degree heart block (both I & II) would have PR intervals of what?
What would indicate a more serious arrhythmia?

A
  • 0.25 - 0.45 seconds.
  • 0.45s PR interval would be more serious than 0.25s.
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29
Q

2nd degree Mobitz type I is also known as?
What characterizes this abnormal rhythm?

A
  • Wenckebach Periodicity
  • Varying PR intervals, with the interval increasing, until a QRS complex is dropped.
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30
Q

Between Mobitz I & Mobitz II, which rhythm is generally better tolerated?
When should a patient be paced?

A
  • 2nd Degree Mobitz Type I.
  • Pacing should occur with Mobitz Type II.
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31
Q

Mobitz Type II incomplete heart block arrhthmias are characterized by what two aspects?

A
  • Consistent PR interval with eventual dropped QRS complex.
  • There should be a ratio of normal beats to dropped beats (2:1, 4:1, etc.)
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32
Q

What would characterize the atrial rate in complete heart block?

A
  • Elevated due to SNS activity trying to ↑ CO.
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33
Q

What would the ventricular rate be in complete 3rd degree heart block?
What governs this rate of fire?

A
  • 15 - 40 bpm.
  • Leaky Ca⁺⁺ & leaky Na⁺ channels in the Purkinje Fibers
34
Q

What would the atrial rate be in atrial flutter?
Would the ventricular rate mirror this?
Why or why not?

A
  • Atrial rate: ~200bpm
  • Ventricular rate will be lower (but still high) due to AV node filtering out erroneous atrial action potential.
35
Q

How much do atria contribute to stroke volume in a healthy adult?
When do the atrial help out more?

A
  • 5% of total stroke volume
    1. During exercise
    2. During illness
    3. With bad ventricles
    4. When under anesthesia.
36
Q

Describe Atrial Flutter and its appearance on an EKG strip.

A

Circular reentry arrhythmia of the atria with a set ratio of p-waves (sawtooth patterned) to QRS complexes.

37
Q

What is the atrial rate, denoted by the p-waves, during Atrial Fibrillation?

A
  • No atrial rate, no defined p-waves
38
Q

A-Fib is an arrhythmia characterized by _____ pacemakers and _____ movement resulting in _________ coordination.

A
  • Ectopic
  • Circus
  • No coordination. (disorganized, errant, etc.)
39
Q

When does A-fib often occur?

A
  • Ischemic Atria
  • Overstretched Atria (can occur from stenotic or regurgitative tricuspid valve).
40
Q

Atrial quivering during A-fib can result in what?

A

Clotting from increased turbulent blood flow.

41
Q

What is Stokes-Adams Syndrome?

A
  • Fainting/Syncope secondary to irregular 3rd degree AV block resulting from a delayed ventricular escape beat.
42
Q

What surgeries often precipitate Stokes-Adams episodes?
Why?

A
  • Eye procedures where the Trigeminal (CN5) nerve is stimulated.
  • Pressure on the Trigeminal Nerve can activate the Oculocardiac Reflex resulting in total AV node block.
43
Q

Describe the “5 & Dime” reflex.

A
  • Oculocardiac Reflex characterized by CN5 stimluation overactivating CN10 resulting in AV node block.
  • Involves Cranial Nerves 5 & 10.
44
Q

How long does it take for a patient to faint without a heart beat?
Why does this happen?

A
  • 30 - 60 seconds.
  • Occurs due to brain needing constant supply of O₂ and glucose.
45
Q

Concerning action potentials, why does it take so long for a ventricular escape beat to occur?

A
  • Myocardial tissue has few leaky Na⁺ & Ca⁺⁺ channels so Phase 4 slope is very long.
46
Q

After the 1st ventricular escape beat, what characterizes subsequent beats?

A
  • Subsequent beats occur at a faster clip.
47
Q

What portion of the heart’s conduction system is malfunctioning in Incomplete Intraventricular Block: Alternans?

A
  • Purkinje Fibers
48
Q

What accounts for widened QRS complexes every other beat in an Alternans arrhythmia?

A
  • Purkinje fibers not being utilized ~ Slower conduction through the rest of the myocardium.
49
Q

What two things prevent resetting of the Purkinje system in Alternans?
When is Alternans more likely to occur?

A
  • Ischemia and/or Digitalis toxicity.
  • During V-tach.
50
Q

What causes Premature Atrial Contractions (PACs) ?

A
  • Energy supply restriction to the atria.
    1. Ischemia
    2. Irritation
    3. Calcification
51
Q

Where is the source of PACs more likely to be?
PACs closer to the AV node would be more likely to have what characteristic?
What would p-waves that originate closer to the SA node look like?

A
  • Closer to AV node than SA node.
  • Inverted p-waves = AV node proximity
  • Normal p-waves = SA node proximity
52
Q

PACs result in a _____ pulse deficit leading to what?

A
  • Radial
  • less filling time → ↓SV
53
Q

Premature AV node/bundle contractions will usually have a missing what?

A
  • P-wave (likely hidden in QRS complex)
54
Q

If an AV node/bundle originated action potential had a p-wave, what would it look like?

A

Inverted
- Early & inverted = High AV junction source
- Late & inverted = Low AV junction source.

55
Q

What four things are common causes of PVCs? (Premature Ventricular Contractions)

A
  1. Caffeine
  2. Nicotine
  3. Stress
  4. Lack of sleep
56
Q

What EKG characteristics do PVCs usually possess?

A
  1. Prolonged QRS (from muscle rather than purkinje conduction).
  2. High QRS Voltage (one V depolarizes the other, no cancelled out voltages)
  3. Inverted T-Wave
57
Q

Tachycardia (in general) with decreased filling times results in what for the coronary arteries?

A

Decrease perfusion time.

58
Q

What does the T-wave look like with Paroxysmal V-tach?
What rhythm can be initiated by Paroxysmal V-tach?

A
  • Inverted
  • V-fib
59
Q

The QT interval should be _______ of the R-R interval.

A

< 40%

60
Q

Long QT intervals are usually indicative of what?

A
  • EADs (Early after depolarizations) = Premature Ventricular Depolarizations.
61
Q

Changes in what two ions are common causes of EADs?

A

Hypokalemia & Hypomagnesemia

62
Q

Profound hypokalemia results in closure of what channels? What occurs due to this?

A
  • Closure of KIR, KDR, & VG K⁺ Channels.
  • ↑ Phase III = EADs = Torsades
63
Q

What drugs (in excess) can cause a long QT interval?
Why?

A
  • Cheap gen H1 Antihistamines (Benadryl)
  • ↓ pK⁺ due to mACh receptor blockage = Phase III time ↑ = Long QT.
64
Q

Which two ion channels are particularly important for the return to Vᵣₘ in phase III?
What drugs affect these ion channels?

A
  • KIR & KDR
  • Non-specific K⁺ blockers like TEA.
65
Q

Delayed After-depolarizations (DADs) are premature depolarizations occurring from __________.

A
  • A highly + Vᵣₘ
66
Q

Would a β agonist be an appropriate drug to utilize with long QT syndrome?
Why or why not?

A

No, because the β agonist would ↑ L-type Ca⁺⁺ channel usage & prolong Phase II time.

67
Q

What channels are dysfunctional & opening in a “rogue” manner during long QT syndrome?

A
  • Fast VG Na⁺ Channel
  • L-type Ca⁺⁺ Channels
68
Q

Early Afterdepolarizations, & thus long QT intervals, are precursors to what rhythms?

A
  • Torsades de Pointes
  • V-Fib
69
Q

What type of current is utilized when shocking a ventricular arrhythmia?

A

Direct Current

70
Q

When do T-waves develop a peaked appearance?
Why does this occur?

A
  • Mild - Moderate hyperkalemia
  • ↑pK⁺ due to increased KDR activity.
71
Q

What occurs with membrane potential in mild to moderate hyperkalemia?
How does the heart compensate for this?

A
  • Vᵣₘ increases (more +)
  • opens up more KDR channels help lower Vᵣₘ.
72
Q

Describe the progression of moderate to severe to extreme hyperkalemia.

Vᵣₘ’s in answer are only examples

A
  1. Moderate - Phase 0 prolonged due to incomplete resetting of fast Na⁺ channels (Vᵣₘ ~ -70mV)
  2. Severe - Only L-type Ca⁺⁺ channels able to depolarize (Vᵣₘ ~ -60mV)
  3. Extreme - No depolarization occurs due to no ion channels being able to reset (Vᵣₘ ~ -45mV)
73
Q

What is Dromotropy and how can it be altered?

A
  • Conduction speed (kinda specific to AV node)
  • Altered via β agonism.
74
Q

What is Lusitropy & how can it be altered?

A
  • Relaxation speed (via speeding up of SERCA & resetting Vᵣₘ)
  • Altered via β agonism.
75
Q

Describe Type I Anti-arrhythmics, their effect on action potentials, & what tissue they affect.

A
  • Fast Na⁺ Channel Blockers (-caine derivatives)
  • Slow Phase 0
  • Primarily myocardial tissue, no Nodal Tissue involvment.
76
Q

Describe Type II Anti-arrhythmics, their effect on cardiac channels & overall cardiac effects.

A
  • β-blockers
  • ↓ pHCN = ↓ HR
  • ↓SERCA pump = longer AP.
77
Q

Describe Type III Anti-arrhythmics that we’ve talked about in lecture.

A

K⁺ channel blockers
- TEA (Tetra-ethyl-ammonium)
- 4-5-Aminopyridine
- Amiodarone (Na⁺, Ca⁺⁺, K⁺, & β blocking effects)

78
Q

Name Type IV Anti-arrhythmics, their effect on conduction, contractility & what cardiac ion channels they manipulate.

A
  • CCBs
  • ↓ AV conduction
  • ↓ Inotropy
  • L-Type VG Ca⁺⁺ Channels
79
Q

What side effects of Digoxin were discussed in lecture?

A
  • ↓ HR
  • ↑ Vᵣₘ (more + Vᵣₘ)
80
Q

What adenosine receptors does the heart have?
What is adenosine similar to?

A
  • A1 Receptors.
  • Adenosine is similar to ACh.
81
Q

What does Adenosine do when administered?
Should it be given peripherally or centrally?

A

Slows heart down through huge ↑pK⁺ for very short time. Best if given through central line so its proximate to the heart tissue.

A&P I (Fall 2022) (17 decks)

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