Can you take Lisinopril with Trazodone?

Lisinopril has a major potential interaction with Angioedema.

The use of these agents is contraindicated in patients with hereditary angioedema or a history of idiopathic angioedema. Patients with a history of angioedema unrelated to ACE inhibitors may be at increased risk of angioedema while receiving an ACE inhibitor. Patients should be advised to immediately report any signs or symptoms suggestive of angioedema (swelling of face, extremities, eyes, lips, or tongue, or difficulty swallowing or breathing) and to stop taking the medication until otherwise directed by their physician. Emergency therapy and/or measures to prevent airway obstruction are required for angioedema involving the tongue, glottis, or larynx. Treatment with ACE inhibitors should be discontinued permanently if angioedema develops in association with therapy.

traZODone has a moderate potential interaction with Arrhythmia.

Although less cardiotoxic than the tricyclic antidepressants, trazodone may be arrhythmogenic in some patients with cardiac disease. The use of trazodone has been associated with the occurrence of arrhythmias, including PVCs, ventricular couplets, ventricular tachycardia, atrial fibrillation, and heart block. Myocardial infarction has been reported. Trazodone should not be used during the acute recovery phase following myocardial infarction, and should be administered only with extreme caution in patients with hyperthyroidism and/or cardiovascular disease. Close monitoring of cardiovascular status, including ECG changes, is recommended at all dosages. Many of the newer antidepressants, including bupropion and the selective serotonin reuptake inhibitors (SSRIs), are considerably less or minimally cardiotoxic and may be appropriate alternatives.

traZODone has a moderate potential interaction with Bipolar Disorder.

Adults, young adults and children patients with depression and other psychiatric disorders may experience worsening of their symptoms and may have the emergence of suicidal thoughts and behavior. Patients should be monitored appropriately and observed closely for worsening of their symptoms, suicidality or changes in their behavior, especially during the first few months of treatment, and at times of dose changes. Discontinuing the medication should be considered if symptoms are persistently worse, or abrupt in onset. Phenylpiperazine antidepressants are not approved for use in pediatric patients.

traZODone has a moderate potential interaction with Bipolar Disorder.

All antidepressants may occasionally cause mania or hypomania, particularly in patients with bipolar disorder. Therapy with antidepressants should be administered cautiously in patients with a history of mania/hypomania.

Lisinopril has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

ACE inhibitors may cause bone marrow suppression, rarely in uncomplicated individuals but more frequently in patients with renal impairment, especially if they also have a collagen-vascular disease such as systemic lupus erythematosus or scleroderma. Neutropenia, agranulocytosis, aplastic anemia, hemolytic anemia, eosinophilia and thrombocytopenia have been reported, mostly with captopril. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting blood dyscrasias or complications that may increase the risk of bone marrow depression during ACE inhibitor therapy. Monitoring of blood counts, particularly white blood cells, should be considered.

traZODone has a moderate potential interaction with Cardiovascular Conditions and Disorders.

Although less cardiotoxic than the tricyclic antidepressants, trazodone may be arrhythmogenic in some patients with cardiac disease. The use of trazodone has been associated with the occurrence of arrhythmias, including PVCs, ventricular couplets, ventricular tachycardia, atrial fibrillation, and heart block. Myocardial infarction has been reported. Trazodone should not be used during the acute recovery phase following myocardial infarction, and should be administered only with extreme caution in patients with hyperthyroidism and/or cardiovascular disease. Close monitoring of cardiovascular status, including ECG changes, is recommended at all dosages. Many of the newer antidepressants, including bupropion and the selective serotonin reuptake inhibitors (SSRIs), are considerably less or minimally cardiotoxic and may be appropriate alternatives.

Lisinopril has a major potential interaction with Cerebrovascular Insufficiency.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

traZODone has a moderate potential interaction with Cerebrovascular Insufficiency.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

Lisinopril has a major potential interaction with Collagen Vascular Disease.

ACE inhibitors may cause bone marrow suppression, rarely in uncomplicated individuals but more frequently in patients with renal impairment, especially if they also have a collagen-vascular disease such as systemic lupus erythematosus or scleroderma. Neutropenia, agranulocytosis, aplastic anemia, hemolytic anemia, eosinophilia and thrombocytopenia have been reported, mostly with captopril. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting blood dyscrasias or complications that may increase the risk of bone marrow depression during ACE inhibitor therapy. Monitoring of blood counts, particularly white blood cells, should be considered.

Lisinopril has a major potential interaction with Dehydration.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

traZODone has a moderate potential interaction with Dehydration.

Treatment with trazodone may cause hyponatremia, in many cases secondary to development of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Caution should be used when treating patients at greater risk of developing hyponatremia such as elderly patients, patients taking diuretics or those who are volume-depleted. Discontinuation of trazodone should be considered in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted.

traZODone has a moderate potential interaction with Dehydration.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

traZODone has a moderate potential interaction with Depression.

Adults, young adults and children patients with depression and other psychiatric disorders may experience worsening of their symptoms and may have the emergence of suicidal thoughts and behavior. Patients should be monitored appropriately and observed closely for worsening of their symptoms, suicidality or changes in their behavior, especially during the first few months of treatment, and at times of dose changes. Discontinuing the medication should be considered if symptoms are persistently worse, or abrupt in onset. Phenylpiperazine antidepressants are not approved for use in pediatric patients.

Lisinopril has a major potential interaction with Diabetes Mellitus.

In patients with hyperkalemia, especially those associated with impaired renal function or congestive heart failure, ACE inhibitors may further raise serum potassium levels. Therapy with ACE inhibitors should be administered cautiously in patients with or predisposed to hyperkalemia, and serum potassium levels should be carefully monitored. Risk factors for the development of hyperkalemia during ACE inhibitor therapy include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.

Lisinopril has a major potential interaction with Diarrhea.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

traZODone has a moderate potential interaction with Diarrhea.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

traZODone has a moderate potential interaction with Glaucoma, Narrow Angle.

Some antidepressants exert mydriatic activity that can induce increased intraocular pressure and result in angle-closure (narrow-angle) glaucoma in a patient with anatomically narrow angles who does not have a patent iridectomy. Prior to initiating therapy with these agents, patients should be examined to determine whether they are susceptible to angle closure, and have a prophylactic procedure (e.g., iridectomy), if they are susceptible. The use of these drugs in patients with untreated anatomically narrow angles should be avoided.

Lisinopril has a major potential interaction with Hemodialysis.

Anaphylactoid reactions have been reported in patients undergoing hemodialysis with high-flux polyacrylonitrile membranes and treated concomitantly with an ACE inhibitor. The frequency and mechanism of this interaction have not been established, and it is not known whether the interaction occurs with other membrane types. Therapy with ACE inhibitors should be administered cautiously in patients requiring hemodialysis.

Lisinopril has a major potential interaction with Hemodialysis.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

traZODone has a moderate potential interaction with History - Cerebrovascular Disease.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

traZODone has a moderate potential interaction with History - Myocardial Infarction.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

Lisinopril has a major potential interaction with Hyperkalemia.

In patients with hyperkalemia, especially those associated with impaired renal function or congestive heart failure, ACE inhibitors may further raise serum potassium levels. Therapy with ACE inhibitors should be administered cautiously in patients with or predisposed to hyperkalemia, and serum potassium levels should be carefully monitored. Risk factors for the development of hyperkalemia during ACE inhibitor therapy include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.

traZODone has a moderate potential interaction with Hyperthyroidism.

Although less cardiotoxic than the tricyclic antidepressants, trazodone may be arrhythmogenic in some patients with cardiac disease. The use of trazodone has been associated with the occurrence of arrhythmias, including PVCs, ventricular couplets, ventricular tachycardia, atrial fibrillation, and heart block. Myocardial infarction has been reported. Trazodone should not be used during the acute recovery phase following myocardial infarction, and should be administered only with extreme caution in patients with hyperthyroidism and/or cardiovascular disease. Close monitoring of cardiovascular status, including ECG changes, is recommended at all dosages. Many of the newer antidepressants, including bupropion and the selective serotonin reuptake inhibitors (SSRIs), are considerably less or minimally cardiotoxic and may be appropriate alternatives.

Lisinopril has a major potential interaction with Hyponatremia.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

traZODone has a moderate potential interaction with Hyponatremia.

Treatment with trazodone may cause hyponatremia, in many cases secondary to development of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Caution should be used when treating patients at greater risk of developing hyponatremia such as elderly patients, patients taking diuretics or those who are volume-depleted. Discontinuation of trazodone should be considered in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted.

traZODone has a moderate potential interaction with Hypotension.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

Lisinopril has a major potential interaction with Ischemic Heart Disease.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

traZODone has a moderate potential interaction with Ischemic Heart Disease.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.

Lisinopril has a moderate potential interaction with Liver Disease.

Rarely, elevations of liver enzymes and/or serum bilirubin have occurred with the use of ACE inhibitors. Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receive appropriate medical follow-up.

traZODone has a moderate potential interaction with Liver Disease.

Trazodone undergoes metabolism in the liver. The metabolites, at least one of which is pharmacologically active, are excreted by the kidney. There are no data available concerning the pharmacokinetic disposition of trazodone or its metabolites in patients with renal and/or liver disease. Therapy with trazodone should be administered cautiously in patients with significantly impaired renal or hepatic function. Dosage adjustments may be necessary.

traZODone has a moderate potential interaction with Mania.

All antidepressants may occasionally cause mania or hypomania, particularly in patients with bipolar disorder. Therapy with antidepressants should be administered cautiously in patients with a history of mania/hypomania.

Lisinopril has a major potential interaction with Renal Dysfunction.

In patients with hyperkalemia, especially those associated with impaired renal function or congestive heart failure, ACE inhibitors may further raise serum potassium levels. Therapy with ACE inhibitors should be administered cautiously in patients with or predisposed to hyperkalemia, and serum potassium levels should be carefully monitored. Risk factors for the development of hyperkalemia during ACE inhibitor therapy include renal insufficiency, diabetes mellitus, and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.

Lisinopril has a major potential interaction with Renal Dysfunction.

ACE inhibitors may cause bone marrow suppression, rarely in uncomplicated individuals but more frequently in patients with renal impairment, especially if they also have a collagen-vascular disease such as systemic lupus erythematosus or scleroderma. Neutropenia, agranulocytosis, aplastic anemia, hemolytic anemia, eosinophilia and thrombocytopenia have been reported, mostly with captopril. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting blood dyscrasias or complications that may increase the risk of bone marrow depression during ACE inhibitor therapy. Monitoring of blood counts, particularly white blood cells, should be considered.

Lisinopril has a moderate potential interaction with Renal Dysfunction.

With the exception of fosinopril, ACE inhibitors (and/or their active metabolites in some cases) are primarily eliminated by the kidney and may accumulate in patients with renal impairment. ACE inhibitors can also worsen renal function in some patients by blocking the effect of angiotensin II-mediated efferent arteriolar vasoconstriction, thereby decreasing glomerular filtration. Therapy with ACE inhibitors should be administered cautiously in patients with preexisting renal dysfunction, particularly those with renovascular disease. Patients with moderate to severe renal impairment usually require lower or less frequent doses and smaller increments in dose. In addition, a dosage reduction or discontinuation of any concomitantly administered diuretics may be helpful. Fosinopril probably does not require dosage adjustments unless hepatic function is also significantly impaired.

In patients with bilateral renal artery stenosis or renal artery stenosis in a solitary kidney, ACE inhibitors may reduce renal perfusion to a critically low level. Renal function should be monitored closely for the first few weeks of therapy.

traZODone has a moderate potential interaction with Renal Dysfunction.

Trazodone undergoes metabolism in the liver. The metabolites, at least one of which is pharmacologically active, are excreted by the kidney. There are no data available concerning the pharmacokinetic disposition of trazodone or its metabolites in patients with renal and/or liver disease. Therapy with trazodone should be administered cautiously in patients with significantly impaired renal or hepatic function. Dosage adjustments may be necessary.

traZODone has a moderate potential interaction with Seizures.

The use of most antidepressants is associated with a risk of seizures. There have been only rare reports of convulsions, including grand mal seizures, following the administration of nefazodone or trazodone. Although a causal relationship has not been established, therapy with these agents should be administered cautiously in patients with a history of seizures.

traZODone has a moderate potential interaction with SIADH.

Treatment with trazodone may cause hyponatremia, in many cases secondary to development of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Caution should be used when treating patients at greater risk of developing hyponatremia such as elderly patients, patients taking diuretics or those who are volume-depleted. Discontinuation of trazodone should be considered in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted.

Lisinopril has a major potential interaction with Vomiting.

ACE inhibitors can cause symptomatic hypotension, most often during the initiation of therapy and in patients who are volume- and/or sodium-depleted or treated for congestive heart failure (CHF). Therapy with ACE inhibitors should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if it was recently instituted; those on dietary salt restriction; those with severe or prolonged diarrhea or vomiting; and renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with ACE inhibitors, and the patient should be hemodynamically stable. If concomitant diuretics and/or dietary sodium restriction are employed, reducing or temporarily withholding the dosing of diuretics and/or liberalizing dietary sodium intake for 2 to 3 days in advance can help minimize the risk of severe hypotension in patients who are able to tolerate such adjustments. ACE inhibitors should also be used cautiously in patients in whom excessive hypotension may have serious consequences, such as patients with coronary or cerebrovascular insufficiency. Patients at risk for excessive hypotension should initiate ACE inhibitor therapy under very close medical supervision, and followed closely for the first 2 weeks of treatment and whenever the dosage of ACE inhibitor or diuretic is increased.

traZODone has a moderate potential interaction with Vomiting.

Trazodone has alpha-1 adrenergic blocking activity and may cause hypotension (including orthostatic hypotension) in approximately 5% of patients. Therapy with trazodone should be administered cautiously in patients with hypotension or conditions that could be exacerbated by hypotension, such as a history of myocardial infarction, angina, or ischemic stroke. Patients with dehydration (e.g., due to severe diarrhea or vomiting) may be predisposed to hypotension and should also be managed carefully during therapy with trazodone. Blood pressure should be monitored at regular intervals, particularly during dosage escalation or whenever dosage has been altered, and patients should be advised not to rise abruptly from a sitting or recumbent position.