Class II antiarrhythmics (beta blockers) US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Class II antiarrhythmics (beta blockers). These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Class II antiarrhythmics (beta blockers) US Medical PG Question 1: A 23-year-old woman presents to the emergency department with acute onset of shortness of breath, wheezing, and chest tightness. This is her 4th visit for these symptoms in the last 5 years. She tells you she recently ran out of her normal "controller" medication. Concerned for an asthma exacerbation, you begin therapy with a short-acting beta2-agonist. What is the expected cellular response to your therapy?
- A. Gs protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP (Correct Answer)
- B. Gq protein coupled receptor activates phospholipase C and increases intracellular calcium
- C. Gq protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP
- D. Gs protein coupled receptor activates phospholipase C and increases intracellular calcium
- E. Gi protein coupled receptor inhibits adenylyl cyclase and decreases cAMP
Class II antiarrhythmics (beta blockers) Explanation: ***Gs protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP***
- **Short-acting beta2-agonists (SABAs)** like **albuterol** bind to **beta2-adrenergic receptors** on airway smooth muscle cells, which are **Gs protein-coupled receptors**.
- Activation of **Gs protein** stimulates **adenylyl cyclase**, leading to an increase in intracellular **cyclic AMP (cAMP)**, which triggers downstream relaxation of bronchial smooth muscle.
*Gq protein coupled receptor activates phospholipase C and increases intracellular calcium*
- **Gq protein-coupled receptors** are typically associated with **alpha1-adrenergic receptors** or **muscarinic M1/M3 receptors**, which, when activated, cause **bronchoconstriction** not bronchodilation.
- Activation of **Gq protein** leads to activation of **phospholipase C**, which generates **IP3** and **DAG**, ultimately increasing intracellular **calcium** and promoting contraction.
*Gq protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP*
- This option incorrectly pairs **Gq protein** with the activation of **adenylyl cyclase** and an increase in **cAMP**.
- **Gq protein** signaling primarily involves the **phospholipase C pathway** and **calcium** mobilization, not direct adenylyl cyclase activation.
*Gs protein coupled receptor activates phospholipase C and increases intracellular calcium*
- This option incorrectly pairs **Gs protein** with the activation of **phospholipase C** and an increase in intracellular **calcium**.
- **Gs protein** is specifically coupled to the **adenylyl cyclase/cAMP pathway**, while **phospholipase C** and **calcium** are associated with **Gq protein** signaling.
*Gi protein coupled receptor inhibits adenylyl cyclase and decreases cAMP*
- **Gi protein-coupled receptors** inhibit **adenylyl cyclase** and decrease intracellular **cAMP**, which would lead to **bronchoconstriction**, not bronchodilation.
- This mechanism is associated with **M2 muscarinic receptors** on presynaptic terminals, which regulate acetylcholine release, or alpha2-adrenergic receptors, which are not the primary target for bronchodilation in asthma exacerbations.
Class II antiarrhythmics (beta blockers) US Medical PG Question 2: A 39-year-old woman is brought to the emergency department 30 minutes after her husband found her unconscious on the living room floor. She does not report having experienced light-headedness, nausea, sweating, or visual disturbance before losing consciousness. Three weeks ago, she was diagnosed with open-angle glaucoma and began treatment with an antiglaucoma drug in the form of eye drops. She last used the eye drops 1 hour ago. Examination shows pupils of normal size that are reactive to light. An ECG shows sinus bradycardia. This patient is most likely undergoing treatment with which of the following drugs?
- A. Brimonidine
- B. Dorzolamide
- C. Latanoprost
- D. Pilocarpine
- E. Timolol (Correct Answer)
Class II antiarrhythmics (beta blockers) Explanation: ***Timolol***
- **Timolol** is a **non-selective beta-blocker** used to treat open-angle glaucoma by reducing aqueous humor production
- Can be **systemically absorbed** from eye drops, causing cardiac side effects including **bradycardia, hypotension, and syncope**
- The patient's presentation of **sudden unconsciousness without prodromal symptoms** plus **sinus bradycardia** is classic for beta-blocker toxicity
- Systemic absorption is enhanced with frequent dosing and can occur even with topical ophthalmic use
*Brimonidine*
- **Brimonidine** is an **alpha-2 adrenergic agonist** that reduces aqueous humor production and increases uveoscleral outflow
- Systemic absorption can cause CNS depression, fatigue, and hypotension, but **bradycardia is not a prominent feature**
- Would not typically present with syncope as the primary manifestation
*Dorzolamide*
- **Dorzolamide** is a **carbonic anhydrase inhibitor** that reduces aqueous humor production
- Systemic side effects include metabolic acidosis and electrolyte disturbances with chronic use
- **Not associated with significant bradycardia or acute syncope**
*Latanoprost*
- **Latanoprost** is a **prostaglandin F2-alpha analog** that increases uveoscleral outflow to lower intraocular pressure
- Side effects are primarily local (iris pigmentation, eyelash growth, conjunctival hyperemia)
- Has **minimal systemic absorption** and would not cause bradycardia or syncope
*Pilocarpine*
- **Pilocarpine** is a **muscarinic cholinergic agonist** that causes miosis and increases trabecular outflow
- Can cause cholinergic side effects including bradycardia, but typically accompanied by **miosis, salivation, lacrimation, nausea, and sweating**
- Patient has **normal-sized reactive pupils** and no cholinergic symptoms, ruling this out
Class II antiarrhythmics (beta blockers) US Medical PG Question 3: A 25-year-old female presents to the emergency room with a heart rate of 32 BPM and a blood pressure of 80/40. She was found by emergency medical services with an empty bottle of propranolol that was taken from her grandmother. Her vital signs do not improve despite IV fluids and oxygen. Which of the following is a first line treatment for overdose?
- A. Hemodialysis
- B. Adenosine
- C. Atropine
- D. Vagal maneuvers
- E. Glucagon (Correct Answer)
Class II antiarrhythmics (beta blockers) Explanation: ***Glucagon***
- **Glucagon** is the first-line antidote for severe beta-blocker overdose due to its ability to increase **intracellular cAMP** independently of beta-adrenergic receptors, thereby bypassing receptor blockade.
- This action leads to increased **heart rate** and **contractility**, improving hemodynamic stability.
*Hemodialysis*
- **Hemodialysis** is generally ineffective for propanolol overdose as it has a large volume of distribution and is highly protein-bound, making it difficult to clear from the body.
- It might be considered for other beta-blockers with different pharmacokinetic profiles but is not first-line for propanolol.
*Adenosine*
- **Adenosine** is contraindicated in beta-blocker overdose as it can worsen **bradycardia** and **hypotension** by directly inhibiting AV nodal conduction.
- Its action as an AV nodal blocker would exacerbate the patient's already compromised cardiac function.
*Atropine*
- **Atropine** may be used in beta-blocker overdose to counteract the **bradycardia** by blocking muscarinic receptors and increasing heart rate.
- However, it often provides only a partial or transient effect in severe beta-blocker toxicity and is not as effective as glucagon in restoring hemodynamic stability.
*Vagal maneuvers*
- **Vagal maneuvers** increase vagal tone, which would further slow the **heart rate** and worsen bradycardia in the context of beta-blocker overdose.
- They are used to terminate supraventricular tachycardias, not to treat bradycardia and hypotension from overdose.
Class II antiarrhythmics (beta blockers) US Medical PG Question 4: An investigator is comparing the risk of adverse effects among various antiarrhythmic medications. One of the drugs being studied primarily acts by blocking the outward flow of K+ during myocyte repolarization. Further investigation shows that the use of this drug is associated with a lower rate of ventricular tachycardia, ventricular fibrillation, and torsades de pointes when compared to similar drugs. Which of the following drugs is most likely being studied?
- A. Verapamil
- B. Procainamide
- C. Esmolol
- D. Amiodarone (Correct Answer)
- E. Sotalol
Class II antiarrhythmics (beta blockers) Explanation: ***Amiodarone***
- Amiodarone is a **Class III antiarrhythmic drug** that primarily blocks **potassium channels**, thereby prolonging repolarization and the effective refractory period in cardiac myocytes.
- While it has properties of all four Vaughn-Williams classes, its dominant action as a potassium channel blocker makes it highly effective in preventing and treating various arrhythmias, including **ventricular tachycardia (VT)** and **ventricular fibrillation (VF)**, and it has a relatively lower risk of **torsades de pointes (TdP)** compared to other Class III drugs due to its broader ion channel effects.
*Verapamil*
- Verapamil is a **Class IV antiarrhythmic drug (non-dihydropyridine calcium channel blocker)** that primarily blocks **L-type calcium channels**, slowing conduction through the AV node.
- It is mainly used for **supraventricular tachycardias** and rate control in atrial fibrillation, not typically for ventricular arrhythmias like VT/VF.
*Procainamide*
- Procainamide is a **Class IA antiarrhythmic drug** that blocks **sodium channels** and also prolongs repolarization by blocking some potassium channels, but its primary effect is on sodium channels.
- Class IA drugs are known to **increase the QT interval** and carry a significant risk of **torsades de pointes**, making them less favorable for preventing VT/VF with adverse effect concerns.
*Esmolol*
- Esmolol is a **Class II antiarrhythmic drug (beta-blocker)** that primarily acts by **blocking beta-adrenergic receptors**, thereby reducing heart rate, contractility, and AV nodal conduction.
- While useful in some arrhythmias, its main mechanism is not potassium channel blockade, and it is not typically preferred for the direct prevention of VT/VF in situations with concerns about TdP.
*Sotalol*
- Sotalol is a **Class III antiarrhythmic drug** that primarily acts as a **potassium channel blocker**, prolonging the action potential duration and effective refractory period, and also has **beta-blocking properties**.
- While it blocks potassium channels, sotalol carries a **higher risk of torsades de pointes** compared to amiodarone, especially at higher doses and in patients with underlying heart conditions.
Class II antiarrhythmics (beta blockers) US Medical PG Question 5: A 50-year-old man with a history of atrial fibrillation presents to his cardiologist’s office for a follow-up visit. He recently started treatment with an anti-arrhythmic drug to prevent future recurrences and reports that he has been feeling well and has no complaints. The physical examination shows that the arrhythmia appears to have resolved; however, there is now mild bradycardia. In addition, the electrocardiogram recording shows a slight prolongation of the PR and QT intervals. Which of the following drugs was most likely used to treat this patient?
- A. Metoprolol
- B. Sotalol (Correct Answer)
- C. Propranolol
- D. Verapamil
- E. Carvedilol
Class II antiarrhythmics (beta blockers) Explanation: ***Sotalol***
- **Sotalol** is a **beta-blocker** and a **Class III antiarrhythmic** drug, meaning it blocks potassium channels.
- This dual action explains the **bradycardia** (beta-blockade) and the **prolongation of the PR and QT intervals** (potassium channel blockade), which are characteristic side effects.
*Metoprolol*
- **Metoprolol** is a **selective beta-1 blocker** (Class II antiarrhythmic) that would cause **bradycardia** and **PR prolongation**, but it does not typically prolong the **QT interval**.
- It primarily affects the heart rate and AV nodal conduction without significant potassium channel blocking properties.
*Propranolol*
- **Propranolol** is a **non-selective beta-blocker** (Class II antiarrhythmic) that would cause **bradycardia** and **PR prolongation**.
- Similar to metoprolol, it does not typically prolong the **QT interval**.
*Verapamil*
- **Verapamil** is a **non-dihydropyridine calcium channel blocker** (Class IV antiarrhythmic) that causes **bradycardia** and **PR prolongation**.
- However, it does not prolong the **QT interval**; instead, it can sometimes shorten it.
*Carvedilol*
- **Carvedilol** is a **non-selective beta-blocker** with **alpha-1 blocking properties** (Class II antiarrhythmic), leading to **bradycardia** and **PR prolongation**.
- It does not have effects on potassium channels that would lead to **QT prolongation**.
Class II antiarrhythmics (beta blockers) US Medical PG Question 6: A 70-year-old male presents for an annual exam. His past medical history is notable for shortness of breath when he sleeps, and upon exertion. Recently he has experienced dyspnea and lower extremity edema that seems to be worsening. Both of these symptoms have resolved since he was started on several medications and instructed to weigh himself daily. Which of the following is most likely a component of his medical management?
- A. Lidocaine
- B. Verapamil
- C. Carvedilol (Correct Answer)
- D. Aspirin
- E. Ibutilide
Class II antiarrhythmics (beta blockers) Explanation: ***Carvedilol***
- The patient exhibits classic symptoms of **heart failure**, such as **dyspnea on exertion**, **orthopnea** (shortness of breath when he sleeps), and **lower extremity edema**.
- **Beta-blockers** like carvedilol are essential for managing **chronic heart failure** by reducing myocardial oxygen demand and improving cardiac function.
*Lidocaine*
- **Lidocaine** is primarily an **antiarrhythmic drug** used for acute treatment of **ventricular arrhythmias**, not for chronic heart failure management.
- It works by blocking sodium channels and has no direct benefit in addressing the underlying pathophysiology of heart failure.
*Verapamil*
- **Verapamil** is a **non-dihydropyridine calcium channel blocker** typically used for hypertension, angina, and supraventricular tachyarrhythmias.
- It can have **negative inotropic effects**, which are generally contraindicated or used with extreme caution in patients with **systolic heart failure** due to its potential to worsen cardiac function.
*Aspirin*
- **Aspirin** is an **antiplatelet agent** used for primary or secondary prevention of **atherosclerotic cardiovascular disease** (e.g., in patients with coronary artery disease).
- It does not directly manage the symptoms or pathophysiology of **heart failure** unless there is a coexisting ischemic etiology.
*Ibutilide*
- **Ibutilide** is an **antiarrhythmic drug** specifically used for the rapid conversion of **atrial flutter and atrial fibrillation** of recent onset to sinus rhythm.
- It is not a medication used for the long-term management of **heart failure** symptoms described in the patient.
Class II antiarrhythmics (beta blockers) US Medical PG Question 7: A 77-year-old woman with congestive heart failure is admitted to the hospital for evaluation prior to cardiac transplantation. During her stay at the hospital, the physician prescribes a drug to improve cardiac contractility. The drug works by selectively inhibiting an isoenzyme that is responsible for the degradation of cyclic adenosine monophosphate. Which of the following is the most likely adverse effect of this drug?
- A. Hyperkalemia
- B. QT interval prolongation
- C. Hyperglycemia
- D. Bronchospasm
- E. Hypotension (Correct Answer)
Class II antiarrhythmics (beta blockers) Explanation: ***Hypotension***
- The drug described is likely a **phosphodiesterase-3 inhibitor** (e.g., milrinone), which increases cyclic AMP in cardiac myocytes and vascular smooth muscle cells.
- Increased **cyclic AMP** in vascular smooth muscle leads to **vasodilation**, causing a drop in systemic vascular resistance and subsequently **hypotension**.
*Hyperkalemia*
- **Hyperkalemia** is not a characteristic adverse effect of phosphodiesterase inhibitors. It is associated with drugs like **ACE inhibitors**, **ARBs**, or **aldosterone antagonists**.
- These drugs primarily affect the **renin-angiotensin-aldosterone system** or potassium excretion.
*QT interval prolongation*
- While some **phosphodiesterase inhibitors** can cause **QT prolongation**, it is not the *most likely* adverse effect compared to hypotension, especially in a patient with heart failure.
- Furthermore, **QT prolongation** is a more prominent concern with drugs like **antiarrhythmics** (e.g., amiodarone, sotalol) or certain **antibiotics** (e.g., macrolides).
*Hyperglycemia*
- **Hyperglycemia** is typically associated with drugs that interfere with **insulin secretion** or **insulin sensitivity**, such as **corticosteroids** or some **atypical antipsychotics**.
- Phosphodiesterase inhibitors do not directly cause significant **glucose disturbances**.
*Bronchospasm*
- **Bronchospasm** is a common side effect of **beta-blockers** due to their antagonism of beta-2 adrenergic receptors in the airways.
- Phosphodiesterase inhibitors, by increasing **cyclic AMP**, would theoretically cause **bronchodilation**, not bronchospasm.
Class II antiarrhythmics (beta blockers) US Medical PG Question 8: A 56 year old female comes to the ED complaining of moderate right eye pain, headache, and acute onset of blurry vision, which she describes as colored halos around lights. She was watching a movie at home with her husband about an hour ago when the pain began. On physical exam of her right eye, her pupil is mid-dilated and unresponsive to light. Her right eyeball is firm to pressure. Intraocular pressure (IOP) measured with tonometer is elevated at 36mmHg. Which of the following is the most appropriate emergency treatment?
- A. Laser peripheral iridotomy
- B. Epinephrine ophthalmic solution
- C. Anti-cholinergic ophthalmic solution
- D. NSAID ophthalmic solution
- E. Timolol ophthalmic solution (Correct Answer)
Class II antiarrhythmics (beta blockers) Explanation: ***Timolol ophthalmic solution***
- The patient presents with symptoms and signs consistent with **acute angle-closure glaucoma** (AAGC), including acute eye pain, headache, colored halos, mid-dilated non-reactive pupil, firm eyeball, and elevated IOP. **Timolol** is a **beta-blocker** that reduces aqueous humor production, thereby lowering intraocular pressure.
- Emergency treatment for AAGC focuses on rapidly lowering IOP to prevent permanent vision loss, often involving a combination of topical medications like beta-blockers (e.g., timolol), **alpha-agonists**, and **carbonic anhydrase inhibitors**, along with systemic agents if needed.
*Laser peripheral iridotomy*
- This is a definitive treatment for AAGC, creating an opening in the iris to equalize pressure between the anterior and posterior chambers; however, it is typically performed **after initial medical management** has reduced the IOP.
- While it addresses the underlying anatomical cause, it is not the immediate first-line emergency treatment to acutely lower a critically high IOP.
*Epinephrine ophthalmic solution*
- Epinephrine can cause **pupil dilation (mydriasis)**, which can further exacerbate angle closure in AAGC by pushing the iris into the angle.
- Therefore, it is **contraindicated** in acute angle-closure glaucoma.
*Anti-cholinergic ophthalmic solution*
- Anti-cholinergic agents like atropine cause **pupil dilation (mydriasis)** and relaxation of the ciliary muscle, pulling the iris posteriorly and potentially worsening angle closure.
- These are **contraindicated** in acute angle-closure glaucoma as they can worsen the condition by further narrowing the anterior chamber angle.
*NSAID ophthalmic solution*
- NSAID ophthalmic solutions are primarily used to treat **ocular inflammation** and **pain** in conditions such as postoperative inflammation or allergic conjunctivitis.
- They do not directly lower intraocular pressure and are therefore not an appropriate emergency treatment for acute angle-closure glaucoma.
Class II antiarrhythmics (beta blockers) US Medical PG Question 9: A 73-year-old man presents to his primary care physician with chest pain. He noticed the pain after walking several blocks, and the pain is relieved by sitting. On exam, he has a BP 155/89 mmHg, HR 79 bpm, and T 98.9 F. The physician refers the patient to a cardiologist and offers prescriptions for carvedilol and nitroglycerin. Which of the following describes the mechanism or effects of each of these medications, respectively?
- A. Increased contractility; Decreased endothelial nitric oxide
- B. Decreased cAMP; Increased cGMP (Correct Answer)
- C. Increased cAMP; Increased cAMP
- D. Decreased cGMP; Increased venous resistance
- E. Increased heart rate; Decreased arterial resistance
Class II antiarrhythmics (beta blockers) Explanation: ***Decreased cAMP; Increased cGMP***
- **Carvedilol** is a beta-blocker that *blocks β1 and β2 adrenergic receptors*, leading to a **decrease in intracellular cAMP**, which in turn reduces heart rate, contractility, and blood pressure.
- **Nitroglycerin** acts by releasing **nitric oxide**, which activates **guanylate cyclase** to convert GTP to **cGMP**, leading to smooth muscle relaxation and vasodilation.
*Increased contractility; Decreased endothelial nitric oxide*
- **Carvedilol** (a beta-blocker) causes a **decrease in contractility**, not an increase, by blocking beta-adrenergic receptors.
- **Nitroglycerin** works by **increasing** the production of nitric oxide, not decreasing it.
*Increased cAMP; Increased cAMP*
- **Carvedilol** (a beta-blocker) functions by **decreasing** cAMP, not increasing it.
- While other agents might increase cAMP, this is not the mechanism for nitroglycerin.
*Decreased cGMP; Increased venous resistance*
- **Nitroglycerin** works by **increasing cGMP**, which promotes vasodilation, rather than decreasing it.
- Nitroglycerin causes **decreased venous resistance** (venous dilation) to reduce preload, not increased resistance.
*Increased heart rate; Decreased arterial resistance*
- **Carvedilol** (a beta-blocker) primarily **decreases heart rate**, not increases it.
- While nitroglycerin does cause some arterial dilation, its primary effect at therapeutic doses is **venous dilation** to reduce preload, not just decreased arterial resistance.
Class II antiarrhythmics (beta blockers) US Medical PG Question 10: A 72-year-old man with congestive heart failure is brought to the emergency department because of chest pain, shortness of breath, dizziness, and palpitations for 30 minutes. An ECG shows a wide complex tachycardia with a P-wave rate of 105/min, an R-wave rate of 130/min, and no apparent relation between the two. Intravenous pharmacotherapy is initiated with a drug that prolongs the QRS and QT intervals. The patient was most likely treated with which of the following drugs?
- A. Carvedilol
- B. Verapamil
- C. Flecainide
- D. Quinidine (Correct Answer)
- E. Sotalol
Class II antiarrhythmics (beta blockers) Explanation: **Quinidine**
- Quinidine is a **Class IA antiarrhythmic** that blocks fast sodium channels, prolonging both the **QRS complex** (due to slowed conduction) and the **QT interval** (due to prolonged repolarization).
- The ECG findings of **wide-complex tachycardia** and **AV dissociation** (P-wave rate different from R-wave rate without apparent relation) are consistent with ventricular tachycardia, which Class IA drugs can treat.
*Carvedilol*
- Carvedilol is a **beta-blocker** (Class II antiarrhythmic) that primarily slows heart rate and AV nodal conduction, generally **shortening the QT interval** or having no effect, and would not widen the QRS complex.
- Beta-blockers are typically contraindicated in **decompensated heart failure** and **wide-complex tachycardia** due to their negative inotropic effects and risk of worsening decompensation.
*Verapamil*
- Verapamil is a **non-dihydropyridine calcium channel blocker** (Class IV antiarrhythmic) that mainly slows AV nodal conduction. It would not cause QRS widening and can shorten the QT interval.
- Verapamil is generally contraindicated in **wide-complex tachycardias** of unknown origin as it can precipitate cardiovascular collapse if the arrhythmia is ventricular.
*Flecainide*
- Flecainide is a **Class IC antiarrhythmic** that primarily blocks fast sodium channels, causing significant **QRS widening** but has **minimal effect on the QT interval**, which is contrary to the case description.
- Class IC agents are also generally avoided in patients with **structural heart disease** like congestive heart failure due to increased mortality risk.
*Sotalol*
- Sotalol is a **Class III antiarrhythmic** (beta-blocker with potassium channel blockade) that primarily prolongs the **QT interval** by blocking potassium channels. While it prolongs the QT, it does **not significantly widen the QRS complex**.
- Its beta-blocking effects could exacerbate **decompensated heart failure** in this patient, similar to carvedilol.
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