A patient with myocardial infarction develops symptomatic hypotension. The monitor shows a type 1, second-degree AV block with a heart rate of 30. The nurse administers IV atropine as prescribed.
The nurse determines that the drug has been effective on finding a(n).
Decrease in ventricular response.
Increase in peripheral pulse volume.
Increase in the patient's heart rate.
Decrease in premature contractions.
The Correct Answer is C
Choice A rationale
A decrease in ventricular response would indicate a worsening of the bradycardia or an increase in the degree of the heart block. Atropine is an anticholinergic medication that works by blocking vagal stimulation at the sinoatrial node, thereby increasing the firing rate. If the ventricular response decreased, the drug would have failed to counteract the parasympathetic influence, potentially leading to a further decline in cardiac output and worsening of the patient's symptomatic hypotension.
Choice B rationale
While an increase in peripheral pulse volume suggests improved stroke volume and systemic perfusion, it is a secondary effect of an improved heart rate and rhythm. Atropine's primary and direct mechanism of action is the acceleration of the cardiac rate. Pulse volume can be influenced by many factors, including vascular tone and fluid volume, making it a less specific indicator of atropine's direct pharmacological success compared to a measured increase in chronotropy.
Choice C rationale
Atropine is the first-line treatment for symptomatic bradycardia because it inhibits the muscarinic acetylcholine receptors. By blocking the parasympathetic nervous system's slowing effect on the heart, it increases the rate of SA node discharge and improves conduction through the AV node. An increase from the baseline heart rate of 30 towards a more normal range (60 to 100 beats per minute) directly demonstrates that the drug has reached its therapeutic target.
Choice D rationale
Premature contractions are ectopic beats arising from irritable foci in the atria or ventricles. Atropine is not indicated for the suppression of ectopy; in fact, by increasing the heart rate, it may sometimes increase myocardial oxygen demand and potentially exacerbate irritability in an ischemic heart. The primary goal in this clinical scenario is to resolve the profound bradycardia and hypotension resulting from the myocardial infarction, not to manage minor rhythm irregularities like PVCs.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
The correct answer is Choice A.
Step 1 is 28 units ÷ 1 is 28 units.
Correct Answer is B
Explanation
Choice A rationale
Atenolol is a selective beta-1 adrenergic antagonist, meaning it blocks the effects of epinephrine on the heart. Rather than increasing the strength of the heart muscle, it actually has a negative inotropic effect, which reduces the force of myocardial contraction. This helps decrease the heart's workload and oxygen demand. The patient's statement suggesting an increase in muscle strength is physiologically incorrect and indicates a misunderstanding of how the medication functions to prevent angina.
Choice B rationale
Abrupt withdrawal of beta-blockers like atenolol can trigger a phenomenon known as rebound hypertension or a thyroid storm-like state. This occurs because the heart's beta receptors become hypersensitized during therapy. Suddenly stopping the drug can lead to severe tachycardia, intensified angina, or even myocardial infarction due to an exaggerated response to circulating catecholamines. Therefore, emphasizing that the medication should never be stopped suddenly is a critical and accurate component of patient teaching for safety.
Choice C rationale
Shortness of breath is a potential adverse effect of beta-blockers, particularly if they lose selectivity and affect beta-2 receptors in the lungs, causing bronchoconstriction. However, this is not a normal or expected outcome that a patient should simply accept. If a patient feels short of breath while taking atenolol, it may indicate a worsening of heart failure or an underlying reactive airway issue. The goal of teaching is to identify side effects to report, not to expect respiratory distress.
Choice D rationale
While atenolol helps manage angina by reducing the oxygen demand of the heart, it does not primarily work by improving blood flow through the coronary arteries. Nitrates are the class of drugs typically responsible for coronary vasodilation. Atenolol works by slowing the heart rate and reducing blood pressure, which allows more time for the heart to rest between beats. Misunderstanding the primary mechanism of action as a vasodilator suggests that the patient requires further clarification on pharmacological effects.
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