Which of the following molecular actions most likely mediated the positive inotropic action of digoxin in a patient with heart failure?

Correct Answer: C

Rationale: Rationale: 1. Digoxin inhibits Na+/K+ ATPase, leading to intracellular Na+ accumulation. 2. Increased intracellular Na+ reduces the activity of Na+/Ca2+ exchanger, causing Ca2+ to remain in the cell. 3. Elevated intracellular Ca2+ levels enhance cardiac contractility, resulting in positive inotropic effects. Summary: A: Closing of calcium channels would decrease Ca2+ influx, contrary to the inotropic effect. B: Increased release of Ca2+ from the sarcoplasmic reticulum is not the primary mechanism of digoxin's action. D: Activation of the Ca2+/Na+ exchanger would lead to Ca2+ extrusion, opposing the inotropic effect.

Correct Answer: A

Rationale: In this question, the correct answer is A) Digoxin. Digoxin is a cardiac glycoside that acts by inhibiting the sodium-potassium pump, leading to an increase in intracellular calcium levels. This increase in calcium enhances cardiac contractility, making the heart muscle more efficient at pumping blood. Digoxin also predictably prolongs the PR interval by slowing down the conduction of electrical impulses through the atrioventricular (AV) node. This effect is important to note as it can be seen on an electrocardiogram (ECG) when monitoring patients on digoxin therapy. Now, let's discuss why the other options are incorrect: - B) Lidocaine is a local anesthetic and antiarrhythmic drug that primarily works by blocking sodium channels in the heart to prevent abnormal electrical activity. It does not affect the PR interval or increase cardiac contractility. - C) Propranolol is a beta-blocker that decreases heart rate and blood pressure by blocking beta-adrenergic receptors. It does not predictably prolong the PR interval or increase cardiac contractility. - D) Quinidine is an antiarrhythmic medication that works by blocking sodium and potassium channels in the heart. While it can prolong the QT interval on an ECG, it does not specifically prolong the PR interval or increase cardiac contractility like digoxin. In an educational context, understanding the effects of different cardiovascular drugs on the heart's electrical conduction system and contractility is crucial for healthcare professionals, especially those working in cardiology or critical care settings. Recognizing the unique actions of each medication helps in making informed decisions regarding treatment options and monitoring for potential side effects or complications.

Correct Answer: B

Rationale: The correct statement about the action of nitrates on coronary vessels is option B) They preferentially dilate conducting arteries without affecting resistance arterioles. This is the right answer because nitrates primarily act by dilating veins, which reduces preload and consequently decreases cardiac oxygen demand. This dilation also affects conducting arteries, like the large epicardial coronary arteries, leading to increased blood flow to the myocardium. Option A is incorrect because nitrates do not increase total coronary flow significantly; instead, they redistribute blood flow within the coronary circulation. Option C is incorrect because nitrates do not selectively dilate autoregulatory arterioles; their effect is more prominent on conducting arteries. Option D is incorrect because nitrates increase subendocardial blood flow more than subepicardial blood flow due to their preferential dilation of larger coronary arteries. From an educational perspective, understanding the mechanism of action of nitrates on coronary vessels is crucial for healthcare professionals managing patients with cardiovascular diseases like angina pectoris. Knowing how nitrates affect coronary circulation helps in optimizing treatment strategies and ensuring better patient outcomes. This knowledge also forms the basis for further learning about the pharmacological management of cardiovascular conditions.

Correct Answer: B

Rationale: In the context of cardiovascular drugs, the correct answer to the question is B) Depression of cardiac contractility. Quinidine is a class I antiarrhythmic drug that primarily works by blocking sodium channels in cardiac myocytes. The depression of cardiac contractility is not a desirable effect clinically because it can lead to a decrease in cardiac output and exacerbate heart failure in patients with compromised cardiac function. Option A) Shortening of A-V nodal refractory period due to vagolytic action is a useful property of quinidine as it can help in managing certain types of arrhythmias by affecting the conduction of electrical impulses in the heart. Option C) Decrease in the automaticity of the normal pacemaker is also a desirable effect of quinidine as it helps in reducing abnormal electrical activity in the heart and can be beneficial in treating arrhythmias. Option D) Reduction in the slope of slow diastolic depolarization is another useful property of quinidine as it can help in stabilizing the heart's electrical activity and preventing the occurrence of certain types of arrhythmias. From an educational perspective, understanding the pharmacological properties of cardiovascular drugs like quinidine is crucial for healthcare professionals involved in the management of cardiac conditions. Knowing the desired effects as well as the potential adverse effects of these drugs is essential for safe and effective patient care. This knowledge helps in making informed decisions regarding drug selection, dosing, monitoring, and managing potential drug interactions or adverse effects.

Correct Answer: B

Rationale: In this question, the correct answer is B) Beta blocker. Class II anti-arrhythmic agents, such as beta blockers, work by blocking beta-adrenergic receptors in the heart, leading to a decrease in heart rate and contractility. This effect helps in managing arrhythmias by stabilizing the heart's electrical activity. Option A) Calcium channel blocker primarily works by blocking calcium channels, affecting the heart's contractility and conductivity. While calcium channel blockers are used in various cardiovascular conditions, they do not belong to Class II anti-arrhythmic agents. Option C) Sodium channel blocker, like Class I anti-arrhythmic agents, work by blocking sodium channels in the heart, affecting the depolarization phase of cardiac action potentials. This class is different from Class II agents. Option D) ACE inhibitor is not an anti-arrhythmic agent. ACE inhibitors work by inhibiting the conversion of angiotensin I to angiotensin II, primarily used in conditions like hypertension and heart failure. Understanding the classification and mechanisms of action of different cardiovascular drugs is crucial for healthcare professionals to make informed decisions in managing patients with cardiac conditions. Identifying the correct Class II anti-arrhythmic agents, such as beta blockers, ensures appropriate treatment selection and optimal patient outcomes.