Podcast
Questions and Answers
Which part of the heart has the slowest conduction velocity?
Which part of the heart has the slowest conduction velocity?
- Bundle branches
- Sinus node
- Cranial AV node (correct)
- Ventricle myocytes
Which ion current is responsible for phase 0 depolarization in working myocytes and Purkinje fibers?
Which ion current is responsible for phase 0 depolarization in working myocytes and Purkinje fibers?
- Ca++
- Na+ (correct)
- K+
- HCN
What is the absolute refractory period?
What is the absolute refractory period?
- A period during which a weak stimulus can evoke a response
- A period during which no stimuli can generate another action potential (correct)
- A period during which the heart is incapable of responding to the next normal impulse
- A period during which a more intense stimulus is needed to initiate an action potential
What can cause premature contractions in the heart?
What can cause premature contractions in the heart?
Which phase of the fast action potentials can early afterdepolarizations occur during?
Which phase of the fast action potentials can early afterdepolarizations occur during?
What can cause delayed afterdepolarizations during phase 4 of the fast action potentials?
What can cause delayed afterdepolarizations during phase 4 of the fast action potentials?
What is required for reentry tachycardias to occur?
What is required for reentry tachycardias to occur?
Which class of antiarrhythmic drugs prevent Ca2+ overload and afterdepolarizations?
Which class of antiarrhythmic drugs prevent Ca2+ overload and afterdepolarizations?
Which class of antiarrhythmic drugs is not dependent on heart rate and blocks conduction and effective refractory period?
Which class of antiarrhythmic drugs is not dependent on heart rate and blocks conduction and effective refractory period?
Which class of antiarrhythmic drugs acts by inhibiting potassium channels, leading to an increase in action potential duration?
Which class of antiarrhythmic drugs acts by inhibiting potassium channels, leading to an increase in action potential duration?
Which class of drugs can reduce the number of atrial excitations that are transmitted into the ventricle, and thus reduce the ventricular rate in patients with atrial fibrillation?
Which class of drugs can reduce the number of atrial excitations that are transmitted into the ventricle, and thus reduce the ventricular rate in patients with atrial fibrillation?
Which class of antiarrhythmic drugs blocks calcium channels and reduces conduction velocity in the atrioventricular (AV) node?
Which class of antiarrhythmic drugs blocks calcium channels and reduces conduction velocity in the atrioventricular (AV) node?
Which class of antiarrhythmic drugs primarily block inactivated Na+ channels and reduce action potential duration?
Which class of antiarrhythmic drugs primarily block inactivated Na+ channels and reduce action potential duration?
Which class of antiarrhythmic drugs acts as β-adrenergic receptor blockers and reduces sinus node automaticity?
Which class of antiarrhythmic drugs acts as β-adrenergic receptor blockers and reduces sinus node automaticity?
Which class of antiarrhythmic drugs primarily block open/activated Na+ channels and increase action potential duration?
Which class of antiarrhythmic drugs primarily block open/activated Na+ channels and increase action potential duration?
Which class of antiarrhythmic drugs primarily block inactivated Na+ channels without effect on action potential duration?
Which class of antiarrhythmic drugs primarily block inactivated Na+ channels without effect on action potential duration?
Which class of drugs can potentially slow ventricular rate in patients with atrial fibrillation/flutter?
Which class of drugs can potentially slow ventricular rate in patients with atrial fibrillation/flutter?
Which class of drugs can increase the refractory period and potentially break the atrial re-entry tachycardia?
Which class of drugs can increase the refractory period and potentially break the atrial re-entry tachycardia?
Which class of drugs can reduce the number of atrial excitations that are transmitted into the ventricle, and thus reduce the ventricular rate in patients with atrial fibrillation?
Which class of drugs can reduce the number of atrial excitations that are transmitted into the ventricle, and thus reduce the ventricular rate in patients with atrial fibrillation?
Which class of drugs is indicated for the treatment of atrial fibrillation and can prolong the duration of action potentials?
Which class of drugs is indicated for the treatment of atrial fibrillation and can prolong the duration of action potentials?
Which of the following factors determine the electrical properties of the heart?
Which of the following factors determine the electrical properties of the heart?
What is the term used to describe the ability of cardiac cells to conduct impulses?
What is the term used to describe the ability of cardiac cells to conduct impulses?
Which of the following can lead to ectopic pacemaker activity and reentry tachycardia?
Which of the following can lead to ectopic pacemaker activity and reentry tachycardia?
How do the effects of different classes of antiarrhythmic drugs on the electrical properties of the heart relate to their therapeutic uses and potential adverse effects?
How do the effects of different classes of antiarrhythmic drugs on the electrical properties of the heart relate to their therapeutic uses and potential adverse effects?
Which class of drugs has been shown to reduce mortality in patients with myocardial infarction?
Which class of drugs has been shown to reduce mortality in patients with myocardial infarction?
What are the contraindications for using non-dihydropyridine CCBs?
What are the contraindications for using non-dihydropyridine CCBs?
Which class of drugs reduces SA nodal rate, AV conduction, and inotropy?
Which class of drugs reduces SA nodal rate, AV conduction, and inotropy?
What are the indications for using verapamil or diltiazem?
What are the indications for using verapamil or diltiazem?
What are the unwanted effects of non-dihydropyridine CCBs?
What are the unwanted effects of non-dihydropyridine CCBs?
Why should non-dihydropyridine CCBs not be combined with β-blockers?
Why should non-dihydropyridine CCBs not be combined with β-blockers?
