Use the оutput belоw tо perform а test for model significаnce аt the 1% significance level. ANOVA Table Source Degrees of Freedom Sum of Squares Regression 4 3370.1 Error 60 7611.1 Total 64 10981.2 Coefficients Table Source Coefficients Standard Error Intercept -20.57 8.16 educ 2.16 0.48 exper 0.19 0.13 married 5.92 3.17 metro 3.89 3.26 What is the critical value for the test? Round your answer to the second decimal place.
DRUG THERAPY OF ARRHYTHMIAS Clаss 0 — HCN Chаnnel Blоcker: Ivаbradine Mechanism оf Actiоn Blocks HCN (“funny”) channels in SA node→ ↓ Na⁺ If current→ ↓ slope of phase 4 depolarization→ ↓ HR & ↓ SA node automaticity Pharmacokinetics Oral Metabolized by CYP3A4 → drug interactions Excreted in feces & urine Uses Chronic HF (HR ≥ 70 bpm) Stable angina (HR ≥ 70 bpm) Sinus tachycardia Adverse Effects: Bradycardia Class I — Na⁺ Channel Blockers Class IA: Quinidine, Procainamide, Disopyramide Mechanism Moderate Na⁺ blockade→ ↓ depolarization rate→ ↑ AP duration & ↑ ERP→ Prolong QT Effects ↓ Automaticity ↓ Conduction ↑ Refractory period → ↓ reentry Uses SVT (AF, A-fib) VT/V-fib WPW (procainamide) Adverse Effects ⚠️ Torsades de pointes (QT prolongation) Disopyramide → anticholinergic (CI in myasthenia gravis) Quinidine → cinchonism, hemolysis (G6PD) Procainamide → lupus, bone marrow suppression Negative inotropy → CI in HF Class IB: Lidocaine, Mexiletine Mechanism: Weak Na⁺ blockade → ↓ AP duration Effects ↓ Automaticity ↓ Conduction & ↓ ERP Uses Ventricular arrhythmias (post-MI) Digitalis-induced arrhythmia Adverse Effects CNS toxicity (tremor, seizures) Lidocaine → neurotoxicity (high dose) Mexiletine → hepatotoxicity Negative inotropy Class IC: Flecainide, Propafenone Mechanism: Strong Na⁺ blockade → markedly ↓ depolarization → no change in AP duration Effects ↓ Automaticity ↓ Conduction → ↓ reentry ↑ QT interval Uses SVT (AF, A-fib) Resistant VT WPW Adverse Effects ⚠️ High pro-arrhythmic risk (boxed warning) Flecainide → ventricular arrhythmias Negative inotropy → CI in HF Propafenone → bronchospasm (β-blocking effect) Class II — Autonomic Modulators Class IIa — β-Blockers: Metoprolol, Atenolol, Propranolol, Esmolol, Carvedilol Mechanism: Block β1 → ↓ cAMP → ↓ phase 4 slope Effects ↓ HR (↓ SA node) ↓ AV conduction ↓ QT Uses SVT (especially stress-induced) Premature beats Atrial & ventricular arrhythmias Long QT syndrome Class IIb — β-Agonist: Isoproterenol Mechanism β1 → ↑ HR, conduction β2 → vasodilation Uses Bradycardia AV block (temporary) Torsades (bradycardia-dependent) Adverse Effects Tachyarrhythmias Hypotension Class IIc — M2 Antagonist: Atropine Mechanism: Blocks M2 receptors → ↑ SA automaticity → ↑ AV conduction Uses Bradycardia AV block Adverse Effects Anticholinergic: Dry mouth Blurred vision Urinary retention Tachycardia Class IId — M2 Activator: Digoxin Mechanism ↑ Vagal tone → ↓ HR & AV conduction Inhibits Na⁺/K⁺ ATPase → ↑ Ca²⁺ → ↑ contractility Uses AF (rate control when others not suitable) HFrEF (limited use now) Key Contraindications Hypokalemia Hypercalcemia AV block, bradycardia WPW with AF Adverse Effects Narrow therapeutic index GI, visual disturbances ⚠️ Arrhythmias Class IIe — Adenosine A1 Agonist: Adenosine Mechanism: ↑ K⁺ efflux, ↓ Ca²⁺ influx → hyperpolarization Effects ↓ SA node activity ↓ AV conduction Uses PSVT (first-line emergency) Adverse Effects Flushing, chest discomfort (~1 min) Bronchospasm (CI in asthma) Interactions ↓ effect: caffeine, theophylline Question: A 58-year-old man presents with atrial fibrillation. He has a history of heart failure with reduced ejection fraction (HFrEF). An antiarrhythmic is considered, but the provider is concerned about its strong sodium channel blockade, marked slowing of conduction, and high risk of pro-arrhythmic ventricular arrhythmias. Which of the following medications is most likely being described?