A patient has been treated with antiparkinson medications for 3 months. What therapeutic responses should the nurse look for when assessing this patient?

A. Diarrhea is not typically associated with ergotamine toxicity. Gastrointestinal symptoms such as nausea and vomiting are more common adverse effects of ergotamine use.
B. Delirium is a potential sign of ergotamine toxicity. At toxic levels, ergotamine can cause central nervous system symptoms such as confusion, hallucinations, and delirium.
C. Hypotension may occur as an adverse effect of ergotamine due to its vasoconstrictive properties. However, hypotension alone may not indicate ergotamine toxicity.
D. Bradycardia is not a typical adverse effect of ergotamine. Ergotamine is more commonly associated with vasoconstriction and can lead to hypertension or tachycardia rather than bradycardia.

A. Diarrhea is not typically associated with ergotamine toxicity. Gastrointestinal symptoms such as nausea and vomiting are more common adverse effects of ergotamine use.
B. Delirium is a potential sign of ergotamine toxicity. At toxic levels, ergotamine can cause central nervous system symptoms such as confusion, hallucinations, and delirium.
C. Hypotension may occur as an adverse effect of ergotamine due to its vasoconstrictive properties. However, hypotension alone may not indicate ergotamine toxicity.
D. Bradycardia is not a typical adverse effect of ergotamine. Ergotamine is more commonly associated with vasoconstriction and can lead to hypertension or tachycardia rather than bradycardia.

A. Decreased urine output is not the primary intended effect of an adrenergic agonist in the

treatment of shock. While adrenergic agonists may increase blood pressure, leading to a decrease in urine output due to vasoconstriction, the primary goal of administering these drugs in shock is to improve tissue perfusion and cardiac output.
B. Increased cardiac output is the primary intended effect of adrenergic agonists in the treatment of shock. These medications stimulate adrenergic receptors, leading to increased heart rate, contractility, and stroke volume, ultimately improving cardiac output and tissue perfusion.
C. Volume restoration may be a secondary effect of administering fluids along with adrenergic agonists in the treatment of shock, but it is not the primary intended effect of the medication
itself.

D. Reduced anxiety is not a primary goal of administering adrenergic agonists in the treatment of shock. While these medications may have anxiolytic effects in certain situations, the primary goal is to improve cardiovascular function and tissue perfusion.