Advanced Pharmacology Final Verified Exam Questions and Answers
Latest update 2026/2027
Question:
1. What is the most serious type of arrhythmia?
Answer:
Fribrillaton Ventricular fibrillation is fatal and atrial fibrillation (AF), the most common cardiac
arrhythmia, is usually symptomatic.
Question:
2. How are arrhythmias classified?
Answer:
Location (ventricular or supraventricular) Direction of rate change: bradycardia or tachycardia.
Question:
3. Arrhythmias occur in approximately of all surgical patients under anesthesia.
Answer:
25% Most do not require treatment.
Question:
4. When do we treat arrhythmia?
Answer:
?
Question:
5. Causes of Arrhythmia can be:
Answer:
STRUCTURAL:
-CAD, Valvular dz
-Cardiomyopathies
-SSS or prolonged QT syndromes
-WPW
TRANSIENT IMBALANCES:
Stress Electrolyte imbalance or metabolic imbalance Hypoxia Hypercarbia ICD/Pacemaker Surgical
stimulation Anesthetic agents (or lack of)
,Question:
6. Why not give everyone at risk antiarrhythmics?
Answer:
Prophylactic antiarrhythmic therapy is largely unwarranted in CAD and STEMI patients because of
the risk of being proarrhythmic ICDs and radio frequency ablation have superseded pharmacologic
therapy of sustained post-STEMI arrhythmias
Question:
7. Routine use of class I antiarrhythmics is contraindicated post-MI.
True or False?
Answer:
True
Question:
8. Radiofrequency (RF) catheter ablation is the 1st-line therapy/highly effective for:
Answer:
WPW, AV nodal reentry, and Atrial ectopic tachycardia, AF and several types of monomorphic VT
Question:
9. Vaughan-Williams Classification:
Answer:
the system most commonly used to classify antidysrhythmic drugs Class I- interfere with Na+
channel. Subdivided into a, b & c Quinidine, Procainamide, Lidocaine, Phenytoin, Flecainide Class II-
Anti-SNS agents. Beta blockers Class III- Affect K+ efflux. Amiodarone Class IV- Affect the av node.
Ca2+ channel blockers Class V- Work by other or unknown mechanisms Digoxin, Adenosine, and
Magnesium Limitations
Question:
10. Mnemonic for Class I-IV agents:
Answer:
SoBe PoCa (SOBE as in South Beach or the drink, POCA as in Polka dance) Sodium channel
blockers, Beta blockers, Potassium channel blockers, Calcium channel blockers
,Question:
11. Ventricular Myocyte Action Poten- *Rapid Depolarization* tial
Answer:
-Na+ inflow
*Plateau Phase*
-Ca+ inflow
*Repolarization*
-K+ outflow
-Ca+ outflow
*Absolute Refractory*
-Longer than skeletal
Question:
12. Procainamide (Pronestyl, Procan):
nTx of lido/amio resistant ventricular arrhythmia, afib, or PSVT, arrhythmia control in MH after
lidocaine, ACLS algorithms (Class Ia)
Answer:
Increases the effective refractory period and reduces impulse conduction velocity in the atria,
His-Purkinje fibers and ventricular muscle. Variable effect on AV conduction, slowing effect on AV
node Direct myocardial depression level >8 mcg/ml
Question:
13. Procainamide is contraindicated in:
Answer:
-CHB
-SLE
-Torsades
(prolonged QT)
Question:
14. What can occur with administration of procainamide?
Answer:
Hypotension
Question:
15. What may signify procainamide toxcity?
Answer:
QRS widening of >25 %
, Question:
16. Does lidocaine have significant decrease in BP, contractility or CO?
Answer:
No
Question:
17. What class is lidocaine?
Answer:
Class Ib
Question:
18. What arrhythmia can lidocaine be used for?
Answer:
Ventricular arrhythmias, MH and ACLS alg. Effective in suppressing reentry cardiac arrhythmias,
such as PVC's and V-tach
Question:
19. How does lidocaine work?
Answer:
Suppresses automaticity and shortens the effective refractory period. Delays the rate of spontaneous
phase 4 depolarization by diminishing the gradual decrease in K+ ion permeability
Question:
20. Lidocaine Pharmacokinetics
Answer:
Onset: 45-90 sec Peak onset:1-2 min Duration:10-20 min Metabolized in liver by oxidative
dealkylation to monoethylglycinexylidide Dose 1-1.5 mg per kg Infusion 1-4 mg/min Max dose
200-300 mg in 1hr Therapeutic level is 2-5 mcg/ml
Question:
21.
Is lidocaine contraindicated in patients with amide sensitivity?
Answer:
Yes
Latest update 2026/2027
Question:
1. What is the most serious type of arrhythmia?
Answer:
Fribrillaton Ventricular fibrillation is fatal and atrial fibrillation (AF), the most common cardiac
arrhythmia, is usually symptomatic.
Question:
2. How are arrhythmias classified?
Answer:
Location (ventricular or supraventricular) Direction of rate change: bradycardia or tachycardia.
Question:
3. Arrhythmias occur in approximately of all surgical patients under anesthesia.
Answer:
25% Most do not require treatment.
Question:
4. When do we treat arrhythmia?
Answer:
?
Question:
5. Causes of Arrhythmia can be:
Answer:
STRUCTURAL:
-CAD, Valvular dz
-Cardiomyopathies
-SSS or prolonged QT syndromes
-WPW
TRANSIENT IMBALANCES:
Stress Electrolyte imbalance or metabolic imbalance Hypoxia Hypercarbia ICD/Pacemaker Surgical
stimulation Anesthetic agents (or lack of)
,Question:
6. Why not give everyone at risk antiarrhythmics?
Answer:
Prophylactic antiarrhythmic therapy is largely unwarranted in CAD and STEMI patients because of
the risk of being proarrhythmic ICDs and radio frequency ablation have superseded pharmacologic
therapy of sustained post-STEMI arrhythmias
Question:
7. Routine use of class I antiarrhythmics is contraindicated post-MI.
True or False?
Answer:
True
Question:
8. Radiofrequency (RF) catheter ablation is the 1st-line therapy/highly effective for:
Answer:
WPW, AV nodal reentry, and Atrial ectopic tachycardia, AF and several types of monomorphic VT
Question:
9. Vaughan-Williams Classification:
Answer:
the system most commonly used to classify antidysrhythmic drugs Class I- interfere with Na+
channel. Subdivided into a, b & c Quinidine, Procainamide, Lidocaine, Phenytoin, Flecainide Class II-
Anti-SNS agents. Beta blockers Class III- Affect K+ efflux. Amiodarone Class IV- Affect the av node.
Ca2+ channel blockers Class V- Work by other or unknown mechanisms Digoxin, Adenosine, and
Magnesium Limitations
Question:
10. Mnemonic for Class I-IV agents:
Answer:
SoBe PoCa (SOBE as in South Beach or the drink, POCA as in Polka dance) Sodium channel
blockers, Beta blockers, Potassium channel blockers, Calcium channel blockers
,Question:
11. Ventricular Myocyte Action Poten- *Rapid Depolarization* tial
Answer:
-Na+ inflow
*Plateau Phase*
-Ca+ inflow
*Repolarization*
-K+ outflow
-Ca+ outflow
*Absolute Refractory*
-Longer than skeletal
Question:
12. Procainamide (Pronestyl, Procan):
nTx of lido/amio resistant ventricular arrhythmia, afib, or PSVT, arrhythmia control in MH after
lidocaine, ACLS algorithms (Class Ia)
Answer:
Increases the effective refractory period and reduces impulse conduction velocity in the atria,
His-Purkinje fibers and ventricular muscle. Variable effect on AV conduction, slowing effect on AV
node Direct myocardial depression level >8 mcg/ml
Question:
13. Procainamide is contraindicated in:
Answer:
-CHB
-SLE
-Torsades
(prolonged QT)
Question:
14. What can occur with administration of procainamide?
Answer:
Hypotension
Question:
15. What may signify procainamide toxcity?
Answer:
QRS widening of >25 %
, Question:
16. Does lidocaine have significant decrease in BP, contractility or CO?
Answer:
No
Question:
17. What class is lidocaine?
Answer:
Class Ib
Question:
18. What arrhythmia can lidocaine be used for?
Answer:
Ventricular arrhythmias, MH and ACLS alg. Effective in suppressing reentry cardiac arrhythmias,
such as PVC's and V-tach
Question:
19. How does lidocaine work?
Answer:
Suppresses automaticity and shortens the effective refractory period. Delays the rate of spontaneous
phase 4 depolarization by diminishing the gradual decrease in K+ ion permeability
Question:
20. Lidocaine Pharmacokinetics
Answer:
Onset: 45-90 sec Peak onset:1-2 min Duration:10-20 min Metabolized in liver by oxidative
dealkylation to monoethylglycinexylidide Dose 1-1.5 mg per kg Infusion 1-4 mg/min Max dose
200-300 mg in 1hr Therapeutic level is 2-5 mcg/ml
Question:
21.
Is lidocaine contraindicated in patients with amide sensitivity?
Answer:
Yes
