Cardiac Electrophysiology (Exam IV) Flashcards
Differentiate the location of PSNS (specifically vagal) and SNS input throughout the heart.
- Vagal input occurs at the SA & AV node.
- SNS input occurs throughout the heart.
Where are the internodal pathways located?
What is the general structure of these?
How many are there and what are their names?
- Right Atrium
- Purkinje-ish (more primitive)
1. Anterior internodal
2. Middler internodal
3. Posterior internodal
Where does the interatrial pathway originate? Where does it run through & end?
What is an alternative name for this pathway?
- Originates from anterior internodal pathway, runs between aorta & SVC, terminates in the left atrium.
- Bachmann’s bundle
What is the purpose of Bachmann’s bundle?
What is the cellular structure like?
- Electrical coordination between right & left atria
- Akin to muscle cells but less myofibrils
What properties are conferred to Bachmann’s bundle by having less myofibrils than the surrounding tissue?
- ↑ Conductance
- ↓ Resistance Ω
What usually damages Bachmann’s bundle?
What is the result of damage to this structure?
- MI (i.e. scar tissue) & overstretching
- Loss of coordination between atria.
How much of a delay occurs in the AV node?
- 0.09sec
How long does it take for an electrical impulse from the SA node to reach the AV node?
How much of a delay occurs in the AV node?
How much of a delay occurs in the penetrating portion of the AV bundle?
How much of a delay occurs in the distal portion of the AV bundle?
- 0.03s
- 0.09s
- 0.03s
- 0.01s
How much of a total delay occurs from the SA node to the beginning portions of the Purkinje fibers in the septum?
- 0.16s
How long does it take for entirety of the ventricles to depolarize?
How long would it take for the heart to depolarize completely and what would be the very last site to depolarize?
- 0.06s
- 0.22s
- Upper lateral aspect of left ventricle
How much time would have passed from SA node depolarization to 1 on the figure below?
0.03s
How much time would have passed from SA node depolarization to 9 on the figure below?
0.16s
What structure is denoted by 8 on the figure below? How much of a delay from SA depolarization occurs here?
- AV node
- 0.09s delay from AV node
What structure is denoted by 6 on the figure below? How much of a delay from SA depolarization occurs here?
- Penetrating Portion of AV bundle
- 0.03s delay
What structure is denoted by 5 on the figure below? How much of a delay from SA depolarization occurs here?
- Distal Portion of AV bundle
- 0.01s delay
How much of delay has occurred (from SA node depolarization) to the circle marked by 9 below?
What would this correlate with on an EKG?
- 0.16s
- PR interval
What characteristics of the AV node cause the conductance delay it exhibits?
- ↓ gap junctions = ↑ Ω
What characteristics do Purkinje Fibers possess that allow for increased conductance?
- Large diameter
- ↑ Gap Junctions
- No myofibrils
- Overall low Ω
Where would one expect to find Bundles of Kent?
- Where the Atria & Ventricles meet laterally.
How long does it take for the right atrium to depolarize completely?
The left atrium?
- 0.07s
- 0.09s
How does Bachmann’s bundle & the internodal pathways compare to the Purkinje Fibers?
- Atria Conduction Tissue = some myofibrils, less developed. Fast, but not as fast as Purkinjes.
- Ventricular Purkinje Tissue = No myofibrils, well developed. Very fast.
What portions of the Purkinje Fiber system were described to us in lecture? (List each in order of depolarization & where it is found)
- Posterior Fascicles (branch from septum into the left ventricle
- Anterior Fascicle (towards the apex of the heart)
- Lateral Fascicle (lateral myocardium of heart)
What functions as an insulator between the atria & ventricles in the heart?
What is the exception to this? (in a healthy heart)
- Cartilage
- Foramen for bundle of His
Are accessory pathways (Bundles of Kent) genetic?
What classifications are there for this anatomic anomaly?
- Yes, genetic
- Type A = Left
- Type B = Right
What condition can occur from accessory pathways?
What electrophysiologic component of the heart is bypassed through these pathways?
How much of a delay is bypassed due to this condition?
- WPW (Wolff-Parkinson-White) Syndrome
- AV node is bypassed
- 0.13s delay bypassed
What occurs to the PR interval with WPW (Wolff-Parkinson-White) Syndrome?
What about the QRS complex?
- ↓ PR interval or no PR interval
- Prolonged QRS complex.
What can occur arrhythmia-wise with WPW (Wolff-Parkinson-White) Syndrome?
What makes one prone to arrhythmias with this syndrome?
- Early atrial or ventricular depolarization
- Ectopic atrial or ventricular foci have a pathway to potentially cause arrhythmias.
What syndrome is linked to sudden, fatal cardiac death in young people (20-24yo)?
?
- WPW (Wolff-Parkinson-White) Syndrome
A p-wave with increased mV magnitude would be associated with what?
- Enlarged right atrium
A broader than normal p-wave would be associated with what?
- Enlarged left atrium.
A notched p-wave (with only positive deflection in lead II) would be associated with what?
How does this compare to a p-wave that is completely biphasic?
- Atrial enlargement
- Even worse atrial enlargement
needs verification
What is the first positive deflection after the p-wave in lead II? (assume healthy heart tissue)
- R-wave
What would a ventricular depolarization wave be called if no R-wave was present?
- QS-wave
What would the presence of a QS wave indicate if noted on Lead II?
- Dead heart tissue
At what point is a wide QRS complex diagnosed?
> 0.12s
What is the normal mV of a QRS complex in a non-precordial lead?
- 1.5-2 mV
Are precordial leads more or less sensitive than limb leads?
What QRS complex mV magnitude might be seen in a precordial lead?
How would this compare to a limb lead?
- More sensitive.
- 3-4mV
- Precordial leads are about double limb leads in terms of mV.
Can atrial repolarization be seen in Lead II?
No, should be hidden in the QRS complex.
Why is negative deflection seen for the Q wave?
When is this especially pronounced?
What lead would you be unlikely to see a Q wave in?
- Initial left side depolarization propagating to the right.
- Pronounced in Lead I.
- Lead III.
How long is the QT interval?
What does this time correlate with mechanically?
- 0.35s
- Length of time that ventricles are squeezing.
What layer of the heart is more prone to ischemia and lighter MI’s?
Why is this?
- Endocardium
- Endocardium is deeper and further away from coronary artery. Contraction of the heart can squeeze microvasculature leading to less blood supply the deeper into heart tissue that you go.
- Endocardium also uses more energy.
wordy & needs verification
How long is the ST segment?
What does this segment symbolize (in healthy tissue) ?
- 0.16s
- Time period where all ventricular tissue has been depolarized.
What are two other names for the ST segment?
Why does it have these names?
- J-point
- Isoelectric point
This is the period in time where no electrical activity should be occurring.
needs explanation for why these are the names
What is very very simplified reason for why T-wave repolarization is a positive deflection?
- Epicardial repolarization occuring before endocardial repolarization. This repolarization is heading towards our lead so it appears +.
needs better explanation & verification
Why is there a noted mV drop from the cellular membrane vs the mV recorded by an EKG?
What, in particular, causes this drop the most? Why?
- mV is lost to surrounding tissue before being picked up by EKG sensors.
- Air in the lungs, air is very insulative.
What two conditions can cause a decreased mV magnitude registered by our EKG leads? Why?
- Obesity = ↑ tissue
- COPD = ↑ air in lungs
What lead is the mean vector through a partially depolarized heart?
Lead II
needs verification
Electric potential is recorded when the ventricular muscle is completely depolarized.
True or False?
How about when the heart is completely repolarized?
- False
- Still false.
What is the typical R-R interval?
How do we determine heart rate from this?
- 0.83 seconds
- 60/R-R interval = bpm
1 small box on an EKG strip equals _____.
1mm or 0.04s
1 large box on an EKG strip equals ______.
5mm or 0.2s
How quickly is paper fed through an EKG machine?
25 mm/s
What would a > 2mV QRS complex in the bipolar limb leads be indicative of?
- Hypertrophy of some sort (more tissue being depolarized)
How would the mV compare from lead II to leads I & III?
Lead II = ↑ mV compared to I & III.
If healthy, both the QRS complex and T-wave should be ______ in leads I, II, & III.
positive.
The mV magnitude of leads I & III added together should roughly equal what?
The mV magnitude of lead II.
What is the mean electrical axis of the heart?
59°
A clockwise shift of the mean electrical axis shift of the heart is indicative of what?
- Right-axis deviation
A counter-clockwise shift of the mean electrical axis shift of the heart is indicative of what?
- Left-axis deviation
How long from SA node depolarization until the ventricles have depolarized completely? (assume a healthy heart)
0.22 s
What percentage of people have Bundles of Kent?
How are these usually acquired?
- 0.2%
- Inherited
Why does infarcting tissue stay depolarized?
- No energy is available for Na⁺K⁺ATPase to reset the Vᵣₘ of the cell.
How would the duration of the action potential of more superficial ventricular tissue compare to the action potential of deeper ventricular tissue?
What is the purpose of this?
- Superficial tissue (outer myocardium & epicardium) = shorter APD (repolarizes sooner)
- Deeper tissue (endocardium) = longer APD (repolarizes after more superficial tissue)
- Helps ensure all of ventricular muscle contracts at the same time.
What tissue in the ventricles depolarizes first after the Purkinje fibers?
- Endocardial muscle cells.
Regarding Lead I, where is the negative terminal connected? How about the positive terminal?
Negative terminal = Right arm
Positive terminal = Left arm
Regarding Lead II, where is the negative terminal connected? How about he positive terminal?
Negative terminal = Right arm
Positive terminal = Left leg
Regarding Lead III, where is the negative terminal connected? How about he positive terminal?
Negative terminal = Left arm
Positive terminal = Left leg
Einthoven’s law states that if Lead I = 1mV & Lead III = 0.5 mV, then Lead II = _______.
1.5mV
Which lead can be used as the determinant of posterior vs anterior injury?
V2
In which precordial lead does the QRS complex have the most magnitude?
V4
What mV is denoted by a small box on an EKG strip?
0.1mV
What mV is denoted by a large box on an EKG strip?
0.5mV
What angle is viewed utilizing aVF?
90°
What angle is viewed utilizing aVL?
-30°
What angle is viewed utilizing aVR?
How does this compare to lead II?
-150°
- aVR is essentially opposite lead II. (not exactly though, Lead II’s negative terminal is -120°)
What are the positive & negative terminals for lead aVR?
Negative = left arm + left leg (+30°)
Positive = right arm (-150°)
What are the positive & negative terminals for lead aVF?
Negative = left arm + right arm
Positive = left leg
What are the positive & negative terminals for lead aVL?
Negative = left leg + right arm
Positive = left arm
What cardiac EKG lead is the least useful in practice but most unique in its position? (this one has a lot of test questions about it)
aVR
What is the axis of Lead I?
0°
What is the axis of Lead III?
120°
Any deviation less than _________ is a left axis deviation.
+59°
Any deviation from _____ to ____ is right axis deviation.
+59° - +180°
What degree change would characterize an extreme axis deviation?
-90° to 180°
What would the mV of this QRS complex be?
+1.5mV
What would the mV of this QRS complex be?
- 1.0mV ( approximation)
Obesity can cause ____ _____ deviation. Why is this?
- Left Axis
- Excess tissue pushes apex of heart up.
Decreased lung volume from paralysis can cause ____ ____ deviation.
left axis
What deviation results from left ventricular hypertrophy? Why?
- Left Axis Deviation due to increased tissue causing ↑ current.
A QRS of -1.0mV in lead III would indicate that the current is heading towards or away from its positive lead?
Away from the positive lead.
A left bundle branch block will cause what axis deviation? Why?
- Left axis deviation due to delayed left side depolarization.
Systemic hypertension will eventually result in what abnormality of your EKG?
- Left Axis Deviation due to ventricular hypertrophy
Determine the mV of leads I & III and subsequently the degree & axis of deviation noted by these strips.
- Lead I ≈ -2.5mV
- Lead III ≈ +1.75mV
- Deviation ≈ inbetween +180° & +120° ≈ 170° due to greater Lead I magnitude. Significant right axis deviation
The EKG strips below are indicative of what pathology?
Right Bundle Branch Block (RBBB)
A notched, wide R wave on Lead V6 would likely be indicative of what condition?
- Left Bundle Branch Block (LBBB)
The EKG strips below are indicative of what pathology?
- Left Bundle Branch Block (LBBB)
If the sum of the voltages of Leads I, II, & III is greater than ______ then this is considered a high voltage EKG.
What causes this most often?
- 4mV
- ↑ ventricular muscle mass (HTN, marathon runner, etc.)
A positive current of injury noted on V2 would be indicative of what?
Posterior MI
A negative current of injury noted on V2 would be indicative of what?
Anterior MI
QRS complexes _______ in magnitude (mV) after injury.
Why is this?
- decrease
- Scar tissue is a bad conductor.
A biphasic T-wave in Lead II would be indicative of what?
- Vᵣₘ reset abnormalities
- ↑ K⁺
- ↑ Na⁺ Channel Blockers (-caine derivatives)
Na⁺ Channel blockers will affect epicardial tissue more than endocardial tissue. T/F ?
True
During this interval, there should be no electrical activity.
T-P Interval
What are the three causes of current of injury?
- Local Ischemia
- Mechanical Trauma
- Infection
Why does damage of cardiac muscle result in perpetually depolarized tissue?
Loss of Na⁺ K⁺ ATPase pump (No ATP)
What are the primary & secondary side effects from digoxin?
- Bradycardia
- Arrythmias
What would a Lead II biphasic T-wave be indicative of?
- A very messed up Vᵣₘ