The nurse administers IV nitroglycerin to a client diagnosed with an acute myocardial infarction. In evaluating the effectiveness of this intervention, the nurse should monitor for:

decrease in heart rate.

relief of chest pain.

decrease in cardiac dysrhythmias.

decrease in blood pressure.

Answer and Explanation

The Correct Answer is B

A. Decrease in heart rate: While nitroglycerin can sometimes cause reflex tachycardia (an increase in heart rate) as a compensatory mechanism in response to a decrease in blood pressure, its primary effect is on reducing myocardial oxygen demand through vasodilation. Although heart rate may decrease in some situations due to improved perfusion or as a secondary response to pain relief, a decrease in heart rate is not the most reliable or immediate indicator of effectiveness in this context. The relief of chest pain is a more direct measure of the drug's impact.

B. Relief of chest pain: Nitroglycerin works by dilating blood vessels, which reduces myocardial oxygen demand and improves blood flow to the heart, particularly in cases of acute myocardial infarction (MI). The primary therapeutic goal is to relieve chest pain (angina) and reduce the workload of the heart. Monitoring for relief of chest pain is the most direct and important indicator of the medication's effectiveness. If the chest pain decreases or resolves, it suggests that the medication is helping to alleviate the ischemia caused by the MI.

C. Decrease in cardiac dysrhythmias: Nitroglycerin is not primarily used to treat dysrhythmias, although improved perfusion and reduced myocardial oxygen demand may indirectly reduce the occurrence of dysrhythmias in some cases. However, a decrease in dysrhythmias is not a primary goal of nitroglycerin therapy, and the nurse should not primarily monitor for this outcome. Any dysrhythmias should be managed with other specific interventions if needed.

D. Decrease in blood pressure: Nitroglycerin's vasodilatory effect does lead to a reduction in blood pressure, particularly in patients with high blood pressure or in the context of a myocardial infarction. However, excessive hypotension can be dangerous and may lead to inadequate perfusion of vital organs. The nurse must monitor blood pressure closely to avoid hypotension, but a decrease in blood pressure is not the main goal of therapy. The primary objective is to relieve the chest pain associated with the MI. If blood pressure drops too low, it may indicate a need to adjust the dose or discontinue the nitroglycerin.

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Correct Answer is A

Explanation

A. pH 7.36, PaO2 98 mmHg, PaCO2 27 mmHg, HCO3 16 mEq/L, O2 sat 99%: This set of ABG results is consistent with fully compensated metabolic acidosis. pH 7.36: This is within the normal range (7.35-7.45), indicating that compensation has occurred, as the pH has returned to normal levels. PaCO2 27 mmHg: The PaCO2 is low, suggesting that the respiratory system has compensated for the metabolic acidosis by increasing ventilation to excrete CO2, thus reducing the acid load. HCO3 16 mEq/L: The bicarbonate level is low, which is consistent with metabolic acidosis as the primary disturbance. The PaO2 and O2 saturation are normal, indicating adequate oxygenation. Since the pH is within the normal range and the PaCO2 and HCO3 levels reflect the compensatory changes needed to correct the metabolic acidosis, this is a case of fully compensated metabolic acidosis.

B. pH 7.47, PaO2 91 mmHg, PaCO2 52 mmHg, HCO3 30 mEq/L, O2 sat 96%:

This result indicates alkalosis rather than acidosis. The pH is alkalotic (7.47), and PaCO2 is elevated (52 mmHg), which suggests respiratory acidosis as the primary disturbance. The HCO3 is also high (30 mEq/L), which is consistent with metabolic compensation for respiratory acidosis, not for metabolic acidosis. Therefore, this is not consistent with fully compensated metabolic acidosis.

C. pH 7.45, PaO2 86 mmHg, PaCO2 56 mmHg, HCO3 28 mEq/L, O2 sat 94%:

The pH is normal, but PaCO2 is elevated (56 mmHg), indicating respiratory acidosis rather than metabolic acidosis. The HCO3 is also elevated (28 mEq/L), which is consistent with compensation for respiratory acidosis, not metabolic acidosis. This result suggests respiratory acidosis with compensated metabolic alkalosis rather than metabolic acidosis.

D. pH 7.32, PaO2 88 mmHg, PaCO2 54 mmHg, HCO3 29 mEq/L, O2 sat 94%:

The pH of 7.32 indicates acidosis, but it is not within the normal range, so this is not fully compensated. The PaCO2 is elevated (54 mmHg), indicating respiratory acidosis, and the HCO3 is elevated (29 mEq/L), showing metabolic compensation. However, since the pH has not yet returned to normal (it remains acidotic), this is an example of partially compensated respiratory acidosis, not fully compensated metabolic acidosis.

respiratory acidosis, not fully compensated metabolic acidosis.

A. reports taking an extra dose each day of their anticholinesterase medication. B. is experiencing a respiratory infection and is short of breath. C. has a family history of autoimmune disorders. D. has a past medical history of type 2 diabetes mellitus.

Correct Answer is A

Explanation

A. "Reports taking an extra dose each day of their anticholinesterase medication."
This client is at highest risk for developing a cholinergic crisis. A cholinergic crisis occurs when there is overdose or excessive stimulation of acetylcholine receptors due to too much anticholinesterase medication. Symptoms include muscle weakness, respiratory distress, salivation, sweating, and bradycardia. Taking an extra dose of the medication can result in an overdose of acetylcholine, triggering these symptoms. Therefore, this client is at the greatest risk for a cholinergic crisis.

B. "Is experiencing a respiratory infection and is short of breath."
While respiratory infections can worsen symptoms of myasthenia gravis due to increased muscle weakness, this client is not directly at risk for a cholinergic crisis. Respiratory infections can increase the risk of myasthenic crisis, which is a different complication where muscle weakness worsens to the point of respiratory failure. A myasthenic crisis is caused by insufficient anticholinesterase medication or a disease exacerbation, not an overdose.

C. "Has a family history of autoimmune disorders."
A family history of autoimmune disorders may suggest a genetic predisposition to autoimmune diseases, but it does not increase the risk of a cholinergic crisis specifically. The risk of a cholinergic crisis is more directly related to medication management, not family history.

D. "Has a past medical history of type 2 diabetes mellitus."
Type 2 diabetes mellitus does not directly increase the risk of a cholinergic crisis. While diabetes may influence overall health and immune function, it does not have a direct impact on anticholinesterase therapy or the risk of cholinergic crisis in myasthenia gravis.

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