Cardio - Physiology - Arrhythmias; Heart Sounds Flashcards
What rhythym is shown here?
Normal sinus rhythym
(P –> QRS –> T
every time)
What rhythym is shown here?
Sinus tachycardia
What is a normal PR interval?
What is a normal QRS interval?
0.12 - 0.20 sec
≤ 0.12 sec
How much time is represented by each 1 mm box on an EKG?
How much time is represented by each 5 mm box on an EKG?
How much time is represented by five 5 mm boxes on an EKG?
- 04 second
- 2 second
1 second
What is the internationally standardized speed at which EKG paper moves?
25 mm / sec
(so five large boxes = 1 sec)
If there is one large box (five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
300 BPM
(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)
If there are two large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
150 BPM
(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)
If there are three large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
100 BPM
(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)
If there are four large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
75 BPM
(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)
If there are five large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
60 BPM
(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)
If there are six large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
50 BPM
(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)
If there are seven large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
43 BPM
(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)
Name the heart rate indicated by each of the following intervals of space between adjacent QRS complexes:
4 large boxes (twenty 1 mm boxes)
2 large boxes (ten 1 mm boxes)
1 large box (five 1 mm boxes)
3 large boxes (fifteen 1 mm boxes)
(Just 300 divided by the number of large boxes between adjacent QRS complexes)
75 BPM
150 BPM
300 BPM
100 BPM
Name the heart rate indicated by each of the following intervals of space between adjacent QRS complexes:
1 large box (five 1 mm boxes)
2 large boxes (ten 1 mm boxes)
3 large boxes (fifteen 1 mm boxes)
4 large boxes (twenty 1 mm boxes)
5 large boxes (twenty-five 1 mm boxes)
6 large boxes (thirty 1 mm boxes)
(Just 300 divided by the number of large boxes between adjacent QRS complexes)
300
150
100
75
60
50
What arrythmia is shown here?
Atrial fibrillation
What arrythmia is shown here?
Atrial flutter
What arrythmia is shown here?
Third degree AV block
What arrythmia is shown here?
Premature ventricular beat
(ectopic ventricular beat –> this explains why it is opposite in polarity. It may be starting in the right ventricle)
What are some ways by which arrythmias are classified?
Origin
(SA, atrial, supraventricular, ventricular, etc.)
Pattern & rate
(tachycardia, bradycardia, fibrillation, flutter, etc.)
# of ectopic sites
(unifocal or multifocal)
How can arrhythmias be classified based on their origin?
Sinus, atrial, supraventricular, ventricular, etc.
How can arrhythmias be classified based on their pattern and rate?
Tachycardia, bradycardia;
flutter, fibrillation, etc.
How can arrhythmias be classified based on their number of ectopic sites?
Either unifocal or multifocal
What is an example arrhythmia that could result in the following finding on EKG examination?
An ectopic site in the left atrium
(the green star in the attached diagram)
What is an example arrhythmia that could result in either of the following findings on EKG examination?
A supraventricular ectopic site firing
[either in the AV node (no P wave) or adjacent to it]
(the purple circle in the attached diagram)
What is an example arrhythmia that could result in the following finding on EKG examination?
(Note: the QRS is prolonged and the T wave inverted.)
An ectopic ventricular firing site
(the red star in the attached diagram)
Describe the pattern and rate of each of the following:
tachycardia
bradycardia
fibrillation
flutter
T > 100 BPM; regular
B < 60 BPM; regular
Fibrillation 300 - 600 BPM; chaotic and irregular
Flutter 250 - 400 BPM; regular
If you see multiple morphologies in the same EKG strip, what may be going on?
(See attached image for a simplified version.)
Multifocal ectopic firing
What arrhythmia is shown here?
Ventricular tachycardia
What arrhythmia is shown here?
Torsade de Pointes
[a polymorphic (multifocal) v. tach.]
What is Torsade de Pointes?
A polymorphic (multifocal) ventricular tachycardia
What is a very common cause of Torsade de Pointes?
Many, many medications can cause this
What arrhythmia is shown here?
Ventricular fibrillation
≥80% of all clinically relevant arrhythmias are due to what mechanism type?
Reentrant excitation
(or just, reentry)
What are two common causes of reentrant excitation in cardiac tissue?
disturbance in conduction (e.g. MI);
dispersion of ERPs (effective refractory periods) (e.g. due to atrial stretching in CHF)
What are some examples of arrhythmias for which the mechanism is often reentrant excitation (reentry)?
Ventricular tachycardia (VTach),
atrial fibrillation (AFib),
ventricular fibrillation (VFib),
paroxysmal supraventricular tachycardia (PSVTs),
premature ventricular contractions (PVCs)
Name the mechanism common to each of the following arrhythmias:
Ventricular tachycardia (VTach),
atrial fibrillation (AFib),
ventricular fibrillation (VFib),
paroxysmal supraventricular tachycardia (PSVTs),
premature ventricular contractions (PVCs)
Reentrant excitation
(reentry)
What type of reentrant excitation is associated with ventricular fibrillation and atrial fibrillation?
Multifocal
(many simultaneous rentrant loops)
(atrial shown in the attached image)
What type of reentrant excitation is associated with paroxysmal supraventricular tachycardia (PSVT)?
AV nodal reentry
What is a ‘dispersion of ERPs’ in regards to reentrant excitation in cardiac tissue?
Different sections of cardiac tissue have varying effective refractory periods
(flow is not even through the tissue and may loop around and ‘reenter’ slower tissues)
What are EADs (early after-depolarizations) and DADs (delayed after-depolarizations)?
Abnormal automaticity in cardiac tissue
(i.e. ectopic pacemaker(s) that is(are) repeatedly firing)
What is the cause for most EADs (early after-depolarizations) and DADs (delayed after-depolarizations)?
Medications;
they are most commonly drug-induced arrhythmias
Describe the changes in extracellular potassium and intracellular pH in infarcted cardiac tissue in the following timeframes after infarction has occurred:
the first 0 - 5 minutes
15 - 40 minutes
≥ 40 minutes
The first 0 - 5 minutes
Rapid efflux of potassium; rapid decrease in pH
15 - 40 minutes
Plateaued potassium level; rapid decrease in pH
≥ 40 minutes
Continued efflux of potassium; plateaued pH
In the graph below, cardiac intracellular pH and extracellular potassium are shown plotted against time after infarction.
What is the significance of the potassium plateau between 10 and 40 minutes?
What is the significance of the rising levels of potassium after 40 minutes?
The changes are reversible;
cell necrosis has begun
How long does it typically take for cardiac myocytes to begin to die in ischemic conditions?
30 - 40 minutes
What happens to extracellular K+ levels during infarction?
Why?
They increase;
lack of ATP –> no inhibition of KATP channels;
What type of channel are KATP channels?
Where are they found?
K+ channels that are inhibited by ATP;
cardiac tissue, the pancreas, smooth muscle
What happens to KATP channels if ATP levels fall?
They are unihibited;
massive efflux of potassium out of cardiac cells
What effect do ischemic conditions have on cardiac myocyte resting potentials?
Depolarization;
Na+ channel inactivation
What effect do ischemic conditions have on Na+ channels?
What is the result?
Depolarization –> Na+ channel inactivation
–>
conduction block
What happens when cardiac tissue action potentials run headlong into one another?
They extinguish one another
(due to ERPs)
The attached image shows a subendocardial infarction in the apex of the heart.
Indicate the accepted route that might be taken for a reentrant excitation (reentry) arrhythmia to take place.
What are the three requirements that must be met for a reentrant excitation (reentry) arrhythmia to occur?
- ≥ Two parallel pathways
- Unidirectional block
- Conduction time of the circuit > ERP for the circuit
* (Basically, all just requirements so that the action potential(s) can double back from its normal route and circle around between healthy and affected tissues)*
Why is each of the following necessary to the development of a reentrant excitation (reentry) arrhythmia?
- ≥ Two parallel pathways
- Unidirectional block
- Conduction time of the circuit > ERP for the circuit
- So there is an unrefractory path ‘backwards’ if the action potential swings around and goes back the way it came
- So that when the action potential swings around to go back, it isn’t blocked going backwards
- If the effective refractory periods (ERPs) of some cells were longer, the circuit action potentials would simply hit them and dissipate (i.e. the circuit would not keep flowing around and around)
For a slow-moving reentrant excitation (reentry) arrhythmia in the ventricles (as shown in the apex in the attached image), what might the resulting EKG look like?
(Single or multiple) premature ventricular contractions (PVCs)
(the current can get caught in this loop)
For a _fast-movin_g reentrant excitation (reentry) arrhythmia in the ventricles (as shown in the apex in the attached image), what might the resulting EKG look like?
Ventricular tachycardia
(the current can get caught in this loop)
Describe the mechanism by which atrial or ventricular tachycardia operate.
How does this differ from non-sustained ventricular tachycardia (> 2 beats; < 30 sec)?
A single loop of quick conduction goes around in a reentry (reentrant excitation) pathway
(the attached image shows an example in the ventricles);
NSVT = one transient circuit
What is the simple mechanism for atrial or ventricular fibrillation?
What is atrial flutter’s simple mechanism?
Large number of reentry circuits (reentrant excitation)
a single, large reentry circuit (reentrant excitation)
What is the accepted mechanism for paroxsymal supraventricular tachycardia?
AV nodal reentrant excitation
(reentry arrhythmia –> the conduction current goes around some differential in conduction speen and keeps reexciting its circuit by traveling back up the faster end)
What predisposes individuals to paroxysmal supraventricular tachycardias (PSVTs)?
Large differences in speed and effective refractory period (dispersion of refractoriness) between at least two pathways in the AV node
How do paroxysmal supraventricular tachycardias (PVSTs) often present?
How are they treated? Why?
Palpitations, dizziness — no P waves on EKG;
calcium channel-blockers — AV nodal dysfunction
In atrial flutter (a macroreentry arrhythmia), why is the atrial rate so much higher than the ventricular rate (i.e., why doesn’t each atrial action potential make it to the ventricles)?
The AV node acts as a filter, only letting through 1 for every 3 or 4 atrial beats
(3:1 or 4:1)
What arrhythmia is known for relapsing and recurring?
Atrial fibrillation
(“Afib begets afib”)