Which adverse effect of an angiotensin converting enzyme inhibitor (ACE inhibitor) will the nurse expect to assess in a hypertensive patient?

Choice A reason: This is the correct statement. Non-selective beta-adrenergic blockers can interfere with the signs and symptoms of hypoglycemia (low blood sugar), such as tachycardia, tremors, and sweating. They can also impair the glucose metabolism and insulin secretion in the body. Therefore, patients with diabetes who take non-selective beta-adrenergic blockers need to monitor their blood glucose levels closely and adjust their insulin or oral hypoglycemic agents accordingly.

Choice B reason: This is not a correct statement. Non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or naproxen, do not interact with non-selective beta-adrenergic blockers. However, they can reduce the effectiveness of other antihypertensive medications, such as diuretics or ACE inhibitors, by causing fluid retention and decreasing renal blood flow.

Choice C reason: This is not a correct statement. Non-selective beta-adrenergic blockers have a rapid onset of action and can lower the blood pressure within hours of administration. Therefore, patients do not need to wait for a few weeks to see if their dosage is effective. However, they may need periodic follow-up visits to monitor their blood pressure, heart rate, and other vital signs.

Choice D reason: This is not a correct statement. Dizziness is a common side effect of non-selective beta-adrenergic blockers, especially when the patient changes position or stands up quickly. This is due to the orthostatic hypotension (a drop in blood pressure when standing up) caused by the vasodilation effect of the medication. However, this does not mean that the patient should stop taking the medication, as this can cause rebound hypertension and other complications. Instead, the patient should rise slowly from a sitting or lying position, drink plenty of fluids, and report any severe or persistent dizziness to their health care provider.

Choice A reason: The cells of the myocardium become hypertrophic in response to increased workload or pressure, not as a result of myocardial infarction. Hypertrophy is an adaptive mechanism that can lead to impaired ventricular function over time.

Choice B reason: The resulting hypoxia leads to ischemic injury and myocardial cell death. This is the main cause of impaired ventricular function after a myocardial infarction. The loss of viable myocardial tissue reduces the contractility and pumping ability of the heart.

Choice C reason: There is a temporary alteration in electrolyte balance that can be corrected. This is not the primary cause of impaired ventricular function after a myocardial infarction. Electrolyte imbalance can occur due to fluid loss, renal impairment, or medication side effects, but it can be managed with appropriate interventions.

Choice D reason: There is too much pressure on the heart and the ventricles begin to dysfunction. This is not the direct cause of impaired ventricular function after a myocardial infarction. Increased pressure on the heart can result from hypertension, valvular disease, or pulmonary embolism, but it is not related to myocardial ischemia or necrosis.