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
2
Q
What three causes of sinus tachycardia were talked about in lecture?
A
- ↑ Body Temp (like malignant hyperthermia)
- SNS stimulation (like from blood loss)
- Toxic Ischemia
3
Q
Ischemic tissue has more frequent ______.
A
Depolarizations
4
Q
What was Lance Armstrong’s peak CO?
A
40Lpm
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
6
Q
What is the only EKG parameter that changes in sinus bradycardia?
A
R-R Interval
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.
8
Q
Vagal stimulation would change what phase of a nodal tissue’s action potential?
A
Decreased slope of Phase 4
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.
10
Q
How would phenylephrine stimulate reflex bradycardia?
A
- ↑ SVR → Baroreceptors perceive ↑MAP → inhibition of nodal tissue via Vagus nerve.
11
Q
Where are baroreceptors located?
A
Aortic Arch & Carotid Bifurcation.
12
Q
What does “Paroxysmal” mean?
A
“comes & goes” Intermittent.
13
Q
Where does Paroxysmal Atrial Tachycardia originate?
A
SA node still
14
Q
What method would be needed to catch a paroxysmal rhythm for diagnosis?
A
Holter Monitor
15
Q
What two EKG tracings may overlap during Supraventricular Tachycardia?
A
P wave & T wave
16
Q
What three treatments could be utilized (per lecture) for Supraventricular Tachycardia: Paroxysmal Atrial Tachycardia?
A
- Vagal Reflex
- βblocker (or maybe CCB)
- Digoxin
17
Q
Loss of ___ ______ occurs with Sinoatrial Block. (hint: EKG)
A
P-waves
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.
19
Q
What is the heart rate generated by by the AV node?
A
40-60 bpm
20
Q
What five causes of AV block were discussed in lecture?
A
- Ischemia of AV Node or Bundle
- Compression of AV bundle
- AV Node or AV Bundle Inflammation
- Excessive Vagal Stimulation
- Excess Digoxin
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.
22
Q
What drugs (pertinent to the heart & mentioned in lecture) slow down cardiac scarring?
A
ACE Inhibitors (through growth factor inhibitors)
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
24
Q
The left Vagal nerve influences the ____ node.
A
AV
25
The SA node is parasympathetically innervated by the ____ ____ ______.
Right Vagal Nerve
26
Manual compression of the vagal nerve will increase or decrease vagal output?
Increase Vagal output
27
1st degree heart block is defined by a PR interval that is......
> 0.2 seconds
28
2nd degree heart block (both I & II) would have PR intervals of what?
What would indicate a more serious arrhythmia?
- 0.25 - 0.45 seconds.
- 0.45s PR interval would be more serious than 0.25s.
29
2nd degree Mobitz type I is also known as?
What characterizes this abnormal rhythm?
- Wenckebach Periodicity
- Varying PR intervals, with the interval increasing, until a QRS complex is dropped.
30
Between Mobitz I & Mobitz II, which rhythm is generally better tolerated?
When should a patient be paced?
- 2nd Degree Mobitz Type I.
- Pacing should occur with Mobitz Type II.
31
Mobitz Type II incomplete heart block arrhthmias are characterized by what two aspects?
- Consistent PR interval with eventual dropped QRS complex.
- There should be a ratio of normal beats to dropped beats (2:1, 4:1, etc.)
32
What would characterize the atrial rate in complete heart block?
- Elevated due to SNS activity trying to ↑ CO.
33
What would the ventricular rate be in complete 3rd degree heart block?
What governs this rate of fire?
- 15 - 40 bpm.
- Leaky Ca⁺⁺ & leaky Na⁺ channels in the Purkinje Fibers
34
What would the atrial rate be in atrial flutter?
Would the ventricular rate mirror this?
Why or why not?
- Atrial rate: ~200bpm
- Ventricular rate will be lower (but still high) due to AV node filtering out erroneous atrial action potential.
35
How much do atria contribute to stroke volume in a healthy adult?
When do the atrial help out more?
- 5% of total stroke volume
1. During exercise
2. During illness
3. With bad ventricles
4. When under anesthesia.
36
Describe Atrial Flutter and its appearance on an EKG strip.
Circular reentry arrhythmia of the atria with a set ratio of p-waves (sawtooth patterned) to QRS complexes.
37
What is the atrial rate, denoted by the p-waves, during Atrial Fibrillation?
- No atrial rate, no defined p-waves
38
A-Fib is an arrhythmia characterized by _____ pacemakers and _____ movement resulting in _________ coordination.
- Ectopic
- Circus
- No coordination. (disorganized, errant, etc.)
39
When does A-fib often occur?
- Ischemic Atria
- Overstretched Atria (can occur from stenotic or regurgitative tricuspid valve).
40
Atrial quivering during A-fib can result in what?
Clotting from increased turbulent blood flow.
41
What is Stokes-Adams Syndrome?
- Fainting/Syncope secondary to irregular 3rd degree AV block resulting from a delayed ventricular escape beat.
42
What surgeries often precipitate Stokes-Adams episodes?
Why?
- 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
Describe the "5 & Dime" reflex.
- Oculocardiac Reflex characterized by CN5 stimluation overactivating CN10 resulting in AV node block.
- **Involves Cranial Nerves 5 & 10**.
44
How long does it take for a patient to faint without a heart beat?
Why does this happen?
- 30 - 60 seconds.
- Occurs due to brain needing constant supply of O₂ and glucose.
45
Concerning action potentials, why does it take so long for a ventricular escape beat to occur?
- Myocardial tissue has few leaky Na⁺ & Ca⁺⁺ channels so Phase 4 slope is very long.
46
After the 1st ventricular escape beat, what characterizes subsequent beats?
- Subsequent beats occur at a faster clip.
47
What portion of the heart's conduction system is malfunctioning in Incomplete Intraventricular Block: Alternans?
- Purkinje Fibers
48
What accounts for widened QRS complexes every other beat in an Alternans arrhythmia?
- Purkinje fibers not being utilized ~ Slower conduction through the rest of the myocardium.
49
What two things prevent resetting of the Purkinje system in Alternans?
When is Alternans more likely to occur?
- Ischemia and/or Digitalis toxicity.
- During V-tach.
50
What causes Premature Atrial Contractions (PACs) ?
- Energy supply restriction to the atria.
1. Ischemia
2. Irritation
3. Calcification
51
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?
- Closer to AV node than SA node.
- Inverted p-waves = AV node proximity
- Normal p-waves = SA node proximity
52
PACs result in a _____ pulse deficit leading to what?
- Radial
- less filling time → ↓SV
53
Premature AV node/bundle contractions will usually have a missing what?
- P-wave (likely hidden in QRS complex)
54
If an AV node/bundle originated action potential had a p-wave, what would it look like?
**Inverted**
- Early & inverted = High AV junction source
- Late & inverted = Low AV junction source.
55
What four things are common causes of PVCs? (Premature Ventricular Contractions)
1. Caffeine
2. Nicotine
3. Stress
4. Lack of sleep
56
What EKG characteristics do PVCs usually possess?
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
Tachycardia (in general) with decreased filling times results in what for the coronary arteries?
Decrease perfusion time.
58
What does the T-wave look like with Paroxysmal V-tach?
What rhythm can be initiated by Paroxysmal V-tach?
- Inverted
- V-fib
59
The QT interval should be _______ of the R-R interval.
< 40%
60
Long QT intervals are usually indicative of what?
- EADs (Early after depolarizations) = Premature Ventricular Depolarizations.
61
Changes in what two ions are common causes of EADs?
Hypokalemia & Hypomagnesemia
62
Profound hypokalemia results in closure of what channels? What occurs due to this?
- Closure of KIR, KDR, & VG K⁺ Channels.
- ↑ Phase III = EADs = Torsades
63
What drugs (in excess) can cause a long QT interval?
Why?
- Cheap gen H1 Antihistamines (Benadryl)
- ↓ pK⁺ due to mACh receptor blockage = Phase III time ↑ = Long QT.
64
Which two ion channels are particularly important for the return to Vᵣₘ in phase III?
What drugs affect these ion channels?
- KIR & KDR
- Non-specific K⁺ blockers like TEA.
65
Delayed After-depolarizations (DADs) are premature depolarizations occurring from __________.
- A highly + Vᵣₘ
66
Would a β agonist be an appropriate drug to utilize with long QT syndrome?
Why or why not?
No, because the β agonist would ↑ L-type Ca⁺⁺ channel usage & prolong Phase II time.
67
What channels are dysfunctional & opening in a "rogue" manner during long QT syndrome?
- Fast VG Na⁺ Channel
- L-type Ca⁺⁺ Channels
68
Early Afterdepolarizations, & thus long QT intervals, are precursors to what rhythms?
- Torsades de Pointes
- V-Fib
69
What type of current is utilized when shocking a ventricular arrhythmia?
Direct Current
70
When do T-waves develop a peaked appearance?
Why does this occur?
- Mild - Moderate hyperkalemia
- ↑pK⁺ due to increased KDR activity.
71
What occurs with membrane potential in mild to moderate hyperkalemia?
How does the heart compensate for this?
- Vᵣₘ increases (more +)
- opens up more KDR channels help lower Vᵣₘ.
72
Describe the progression of moderate to severe to extreme hyperkalemia.
*Vᵣₘ's in answer are only examples*
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
What is Dromotropy and how can it be altered?
- Conduction speed (kinda specific to AV node)
- Altered via β agonism.
74
What is Lusitropy & how can it be altered?
- Relaxation speed (via speeding up of SERCA & resetting Vᵣₘ)
- Altered via β agonism.
75
Describe Type I Anti-arrhythmics, their effect on action potentials, & what tissue they affect.
- Fast Na⁺ Channel Blockers (-caine derivatives)
- Slow Phase 0
- Primarily myocardial tissue, no Nodal Tissue involvment.
76
Describe Type II Anti-arrhythmics, their effect on cardiac channels & overall cardiac effects.
- β-blockers
- ↓ pHCN = ↓ HR
- ↓SERCA pump = longer AP.
77
Describe Type III Anti-arrhythmics that we've talked about in lecture.
K⁺ channel blockers
- TEA (Tetra-ethyl-ammonium)
- 4-5-Aminopyridine
- Amiodarone (Na⁺, Ca⁺⁺, K⁺, & β blocking effects)
78
Name Type IV Anti-arrhythmics, their effect on conduction, contractility & what cardiac ion channels they manipulate.
- CCBs
- ↓ AV conduction
- ↓ Inotropy
- L-Type VG Ca⁺⁺ Channels
79
What side effects of Digoxin were discussed in lecture?
- ↓ HR
- ↑ Vᵣₘ (more + Vᵣₘ)
80
What adenosine receptors does the heart have?
What is adenosine similar to?
- A1 Receptors.
- Adenosine is similar to ACh.
81
What does Adenosine do when administered?
Should it be given peripherally or centrally?
**Slows heart down through huge ↑pK⁺ for very short time**. Best if given through central line so its proximate to the heart tissue.
