Lesson14 by Axilogy

Lesson 14 Arrythmias Larson (based on soft chalk, not all ECGs used) Answers in gray 1. What is the heart rate in order of these ECG tracings?

a. b. c. d.

40, 50, 60, 70, 80, 90, 100 45, 55, 65, 75, 100, 120, 200 50, 60, 75, 100, 150, 300 60, 70, 75, 100, 150 300

1. C: Bradycardia

Normal: 60-100

Tachycardia

Suggested way to calculate heart rate: 60 ÷ # Boxes in R-R interval * .2 OR 1500 ÷ # Small boxes in R-R interval If irregular: 10 x # of “QRS segments” in 30 large boxes 2. What are normal values? I. HR: 60-100 bpm II. PR interval .2 sec (3-5 small boxes) III. QRS interval >.1 sec (>2.5 small boxes) a. I only b. II only c. I & II only d. I, II, & III 2. D. HR is around 60-100 bpm. PR interval is 3-5 SMALL boxes. QRS interval is less than 2.5 small boxes. Small squares at .04sec, large squares at .2sec. A heart rate < 60 bpm is termed bradycardia, one > 100 bpm is called tachycardia. Although the SA node is the normal pacemaker that determines heart rate, if the SA node fails or if conduction to the ventricle is blocked, other regions of the heart that have auto-rhythmicity can serve as pacemakers. Intrinsic rates: atrial tissue > AV junction (40-50 bpm) > ventricular bundle branches & Purkinji fibers (20-40bpm)

3. What can cause bradycardia? a. decreased vagus nerve stimulation b. increased sympathetic stimulation c. beta-1 receptor agonist d. beta-1 receptor blocker 3. D. Activation of B1-receptors by sympathetic nerve NE or Epinephrine will increase HR so blocking it will decrease HR. Vagus nerve (parasympathetic) decreases HR, sympathetic increases HR.

4. Which is not a cause of tachycardia? a. Increased vagal tone b. Increased sympathetic tone (NE) or circulating epinephrine c. Fever, exercise, fear d. B1 receptor agonist 4. A: Decreased vagal tone causes tachycardia 5. What is true about the interval-duration relationship? a. During higher HR (tachycardia) the ventricular action potential for contraction is shorter b. During higher HR (tachycardia) systole and diastole are shortened so filling time between beats is not as drastically altered c. During higher HR (tachycardia) the Q-T interval is shorter d. All of the above 5. D: During higher HR, ventricular contraction is shorter as well diastole and systole so that filling time is less compromised. 6. What does not describe a sinus arrythmia? a. ECG looks relatively normal except for rhythm b. Found in older adults c. Difference between interval varies by more than 4 small boxes (4 * .02 = 16) d. Correlates to inspiration (stretch lung receptors/vagal tone inhibited/HR increases/interval decreases) and expiration (interval increases/HR decreases) 6. B: Sinus Arrhythmia is found in children and is less apparent with age. The ECG looks normal except for the rhythm which is measured by the DIFFERENCE of interval lengths by more than 4 boxes. It correlates to breathing due to vagal inhibition from airway stretch receptors causing increase in HR and decrease in R-R interval upon inhalation.

7. What does not describe a wandering atrial pacemaker? a. The P wave is upright due to being parallel to the mean electric axis on Lead II b. P wave can be upright or inverted c. Depolarization occurs from areas other than the SA node d. Inverted P way must start at a point that is in the opposite direction to normal 7. A: A NORMAL P wave is upright due to this positive upright deflection. Excitation from areas other than the SA node will cause the wave to not be parallel + positive on Lead II thus leading to inversion. It can be inverted or upright and have different morphologies which indicates that it occurs at more than one different point.

8. An atrial flutter consists of: a. Saw tooth waves b. Smaller deflections thus assume it is from atrium c. Caused by reentrant rhythm that cannot spread backward due to conduction block and thus takes longer to circle back d. Dilated atrium being more likely due to time it takes to reach site of origin e. All of the above 8. E. All of the above are a part of atrial flutter. Calculate flutter waves per minute by: # Flutter waves in 5 squares (equal to 1 second length) * 60 second = Flutter waves per minute. QRS complexes have variable frequency and are irregular. With such a high frequency of atrial depolarizations, it is fortunate that not all waves are conducted to the ventricle, because filling would be significantly impaired at that frequency, and life could not be sustained. The AV node has a long refractory period that protects the ventricle from being paced at an abnormally high rate. Therefore, only a fraction of the atrial depolarizations are conducted though the AV node

9. What do atrial fibrillation and atrial flutter have in common? a. Irregular sawtooth waves b. Low amplitude waves c. Chaotic reentry waves d. Unproductive ventricular contractions 9. D: Atrial fibrillation (NOT ATRIAL FLUTTER) has irregular, low amplitude, chaotic waves with more frequency.

10. How can premature atrial contraction can the PR interval to be longer? a. The premature impulse reaches the AV node within its refractory period leading to the conduction velocity being slowed b. The premature impulse reaches the SA node within its refractory period leading to the conduction velocity being slowed c. The premature impulse reaches the SA node before its refractory period leading to the conduction velocity being slowed d. The premature impulse reaches the AV node before its refractory period leading to the conduction velocity being slowed 10. A: The premature impulse reaches the AV node within its refractory period leading to the conduction velocity being slowed and the PR interval lengthened (not always). The premature atrial systole occurs due to a site other than the SA node working as the pacemaker (usually its just one site so one p-wave morphology unlocking wandering pacemaker waves). In order to call it a PAC, it must have a upright P wave.

11. Which of the following correctly aligns the causes of extended P-P interval in PAC to their effects: I. Compensatory pause: The SA node was prematurely excited and fired again after a longer than normal delay because of overdrive suppression. II. SA node resets to fire normally: Prolonged time is due to time for PAC wave to reach SA node + time for SA to reset and fire III. Overdrive suppression: Refractory atrium blocks normal post-PAC impulse: SA node normal P wave will not show up where expected on EKG after a PAC a. I & III b. II only c. I only d. I, II, & III 11. B: Compensatory pause: Refractory atrium blocks normal post-PAC impulse: SA node normal P wave will not show up where expected on EKG after a PAC, Overdrive suppression: The SA node was prematurely excited and fired again after a longer than normal delay because of overdrive suppression, SA node resets to fire normally: Prolonged time is due to time for PAC wave to reach SA node + time for SA to reset and fire The SV associated with the premature complex will be very small because of the short time for filling after the preceding ventricular contraction. The SV of the following beat, on the other hand, will be greater than normal because of the much longer filling period and greater EDV. 12. The shape and duration of a QRS wave indicate that is ventricular depolarization occurred normally. A premature junctional impulse is known to occur above the junctional bifurcation due to the QRS wave (and therefor ventricles) not being affected. What is true about a premature junctional complex (PJC)? a. PMJ are only conducted forward (antegrade) to the ventricle b. PMJ can be conducted retrograde to the atrium (causing atrium to depolarize AFTER ventricle) c. PMJ can be seen as inverted P wave just before every QRS complex d. PMJ originate only in the bundle of His. 12. B. PMJ can be antegrade or retrograde. It is seen as a inverted P wave in some QRS complexes. It can originate in the AV node OR bundle of His.

13. What is true about AV node conduction? a. Low maximum diastolic potential b. Slow rise in AP due to slow inward Ca2+ flow during depolarization c. Low action potential amplitudes d. All of the above 13. D:All of the above are true. AV node has a lower maximum diastolic potential, lower rise in AP, and lower amplitude than SA node. A current that reaches the AV node during its relative refractory period will be even further attenuated (slower conduction).

14. AV blocked can be caused by hypersensitivity of the carotid sinus (++ vagus tone) or degeneration of the AV node. Which of these accurately matches the degree of AV block with the EKG characteristics. a.First degree block is identified as a lengthening of the PR interval (more than 3-5 small boxes) b.Second degree block is the failure of some but not all P-waves to be conducted into the ventricle. (PR lengthens until one drops) c.Third degree block, is complete dissociation of electrical activity in the atria and ventricles.(SA node fires by self + AV node/bundle of His set the rhythm for the ventricle at lower frequency than SA node) d. All of the above 14. D: All of the above.

First degree AV block: Long PR intervals Second degree Mobitz Type I AV block: PR intervals keep getting longer until a P wave drops Second degree Mobitz Type II AV block: P wave drops but PR intervals have consistent frequency Third degree AV block: P & QRS waves have consistent frequency but both independently fire A block with a long QRS means it has a prolonged period of ventricular depolarization which can be explained by a block of conduction in one of the bundle branches

15. Premature ventricular excitation often leaves the ventricle refractory thus preventing excitation from the atrium even though the SA node is firing normally. Based on the number of ventricular areas depolarizing (1 vs many) they can be uniform or multifocal. What is not true regarding premature complexes.

Premature Ventricular Complexes (PJC)

a. In PAC there are upright P waves b. In PJC there is an inverted or absent p wave c. In PVC there is wide and bizarre qrs with no (buried) p wave d. In PVC there is only uniform (unifocal) contractions 15. D is wrong: Use diagrams below in support

16. What is not true about ventricular tachycardia and ventricular fibrillation? a. Ventricular tachycardia can lead to ventricular fibrillation b. Both are organized and consistent c. Not compatible with life d. All are true 16. B: Fibrillation is chaotic not organized.