Which of the following medications does the nurse identify as a calcium channel blocker used to treat tachycardia and manage heart rate?
Digoxin
Diltiazem (Cardizem)
Nitroglycerin
Nitroprusside (Nipride)
The Correct Answer is B
Choice A rationale:
Digoxin is a cardiac glycoside, not a calcium channel blocker. It works by increasing the force of contraction of the heart muscle and slowing the heart rate. However, it is not typically used as a first-line treatment for tachycardia. It's more commonly used to treat heart failure and atrial fibrillation.
Mechanism of action: Digoxin inhibits the sodium-potassium ATPase pump in cardiac cells, leading to an increase in intracellular calcium. This increased calcium availability enhances myocardial contractility. Digoxin also indirectly affects the autonomic nervous system, leading to a decrease in heart rate.
Key points:
Digoxin is not a calcium channel blocker.
It's used primarily for heart failure and atrial fibrillation.
Its mechanism of action involves increasing intracellular calcium and decreasing heart rate.
Choice B rationale:
Diltiazem (Cardizem) is a calcium channel blocker that is commonly used to treat tachycardia and manage heart rate. It works by blocking the movement of calcium into cardiac cells, which slows down the electrical conduction system of the heart and leads to a decrease in heart rate.
Mechanism of action: Diltiazem blocks L-type calcium channels in cardiac and vascular smooth muscle cells. This reduces calcium influx, leading to:
Decreased myocardial contractility Vasodilation (relaxation of blood vessels)
Negative chronotropic effect (decreased heart rate)
Negative dromotropic effect (slowed conduction through the AV node) Key points:
Diltiazem is a calcium channel blocker.
It's effective in treating tachycardia and managing heart rate.
Its mechanism of action involves blocking calcium channels, leading to various cardiovascular effects.
Choice C rationale:
Nitroglycerin is a vasodilator, not a calcium channel blocker. It works by relaxing the smooth muscle in blood vessels, which widens the vessels and allows more blood to flow through them. This can help to relieve chest pain (angina) and lower blood pressure, but it does not directly affect heart rate.
Mechanism of action: Nitroglycerin is metabolized to nitric oxide, which activates guanylate cyclase, leading to increased production of cyclic guanosine monophosphate (cGMP). cGMP causes smooth muscle relaxation, resulting in vasodilation.
Key points:
Nitroglycerin is a vasodilator, not a calcium channel blocker. It's primarily used for angina and hypertension.
Its mechanism of action involves nitric oxide-mediated vasodilation.
Choice D rationale:
Nitroprusside (Nipride) is a potent vasodilator, not a calcium channel blocker. It is typically used in critical care settings to manage severe hypertension or heart failure. It works by relaxing the smooth muscle in blood vessels, which widens the vessels and allows more blood to flow through them. This can help to lower blood pressure, but it does not directly affect heart rate.
Mechanism of action: Nitroprusside directly releases nitric oxide, leading to vasodilation. Key points:
Nitroprusside is a potent vasodilator, not a calcium channel blocker.
It's used in critical care settings for severe hypertension or heart failure.
Its mechanism of action involves direct nitric oxide release and vasodilation.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Choice A rationale:
Calcium gluconate is the antidote for magnesium sulfate toxicity. It directly counteracts the effects of magnesium on the neuromuscular system, cardiovascular system, and central nervous system. It is essential to have calcium gluconate readily available at the bedside of any client receiving magnesium sulfate, as toxicity can occur quickly and without warning.
Mechanism of action:
Calcium gluconate competes with magnesium for binding sites on cell membranes and proteins. It displaces magnesium from these sites, thereby restoring normal cellular function.
Calcium gluconate also enhances calcium influx into cells, which further counteracts the effects of magnesium. Indications for use in magnesium sulfate toxicity:
Respiratory depression (respiratory rate <12 breaths per minute) Loss of deep tendon reflexes
Seizures
Cardiac arrhythmias (including heart block and cardiac arrest) Hypotension (systolic blood pressure <90 mmHg)
Dosage and administration:
The typical dose of calcium gluconate for magnesium sulfate toxicity is 1 gram (10 mL of a 10% solution) given IV push over 3- 5 minutes.
This dose may be repeated as needed, depending on the severity of the toxicity and the client's response to treatment. Nursing considerations:
Monitor the client's vital signs, respiratory status, and deep tendon reflexes closely during magnesium sulfate infusion and after administration of calcium gluconate.
Have a crash cart and code equipment readily available in case of cardiac arrest. Document the administration of calcium gluconate and the client's response to treatment.
Correct Answer is C
Explanation
Choice A rationale:
Respiratory distress is not a direct side effect of metformin. While metformin can cause a rare condition called lactic acidosis, which can lead to rapid breathing, respiratory distress is not a primary concern with metformin use.
Respiratory distress typically involves difficulty breathing due to other causes such as asthma, pneumonia, heart failure, or chronic obstructive pulmonary disease (COPD).
Choice B rationale:
Seizures are not a known side effect of metformin.
Seizures are typically associated with neurological conditions, such as epilepsy, or metabolic disturbances such as hypoglycemia or electrolyte imbalances.
Metformin does not directly affect the central nervous system in a way that would increase the risk of seizures.
Choice C rationale:
Lactic acidosis:
This is a rare but serious condition that can occur with metformin use.
It happens when lactic acid builds up in the bloodstream, causing the blood to become too acidic. Symptoms of lactic acidosis include:
Rapid breathing Nausea and vomiting Abdominal pain Muscle weakness Unusual sleepiness Feeling cold
Risk factors for lactic acidosis in patients taking metformin include:
Kidney disease Congestive heart failure Liver disease Dehydration
Excessive alcohol intake Recent surgery or heart attack
It's important to note that lactic acidosis is rare, occurring in about 3 to 10 cases per 100,000 people taking metformin per year.
Renal failure:
Metformin is primarily eliminated by the kidneys.
If kidney function is impaired, metformin can build up in the body, increasing the risk of lactic acidosis. Additionally, metformin can potentially cause kidney damage in rare cases, further worsening kidney function. It's crucial to monitor kidney function regularly in patients taking metformin.
Choice D rationale:
Hyperglycemia (high blood sugar) is not a side effect of metformin.
In fact, metformin is a medication used to lower blood sugar levels in people with type 2 diabetes. It works by:
Decreasing the amount of glucose produced by the liver Improving the body's sensitivity to insulin
Slowing the absorption of glucose from the intestines
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