Drug Interactions between chlorpheniramine / guaifenesin / phenylephrine and potassium citrate

GENERALLY AVOID: Alcohol may potentiate some of the pharmacologic effects of CNS-active agents. Use in combination may result in additive central nervous system depression and/or impairment of judgment, thinking, and psychomotor skills.

MANAGEMENT: Patients receiving CNS-active agents should be warned of this interaction and advised to avoid or limit consumption of alcohol. Ambulatory patients should be counseled to avoid hazardous activities requiring complete mental alertness and motor coordination until they know how these agents affect them, and to notify their physician if they experience excessive or prolonged CNS effects that interfere with their normal activities.

MONITOR: Coadministration of two or more sympathomimetic agents may increase the risk of adverse effects such as nervousness, irritability, and increased heart rate. Central nervous system (CNS) stimulants, particularly amphetamines, can potentiate the adrenergic response to vasopressors and other sympathomimetic agents. Additive increases in blood pressure and heart rate may occur due to enhanced peripheral sympathetic activity.

MANAGEMENT: Caution is advised if two or more sympathomimetic agents are coadministered. Pulse and blood pressure should be closely monitored.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

Administration of potassium salts in severe dehydration may predispose to renal impairment. Therapy with potassium salts should be administered cautiously in patients with acute dehydration (e.g., due to severe or prolonged diarrhea or heat stress). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Administration of potassium salts in severe dehydration may predispose to renal impairment. Therapy with potassium salts should be administered cautiously in patients with acute dehydration (e.g., due to severe or prolonged diarrhea or heat stress). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

Administration of potassium salts may precipitate attacks in familial hyperkalemic periodic paralysis or paramyotonia congenita. Therapy with potassium preparations should be administered cautiously in patients with these conditions.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The use of potassium salts is contraindicated in patients with severe renal impairment characterized by oliguria, anuria, or azotemia. Since potassium is excreted by the kidney, the administration of potassium salts in such patients, particularly by the intravenous route, may produce hyperkalemia and cardiac arrhythmias or arrest. Therapy with potassium salts should be administered cautiously in patients with diminished renal function or other conditions which impairs potassium excretion (e.g. adrenal insufficiency). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium citrate for management of renal tubular acidosis and renal stones is contraindicated in patients with active urinary tract infection caused by urea-splitting organisms. Its ability to increase urinary citrate may be attenuated by bacterial enzymatic degradation of citrate. Moreover, the rise in urinary pH resulting from potassium citrate therapy might promote further bacterial growth.

Hypokalemia in patients with metabolic or respiratory alkalosis should generally be treated with potassium chloride rather than an alkalinizing potassium salt (i.e. acetate, bicarbonate, citrate, or gluconate), since alkali therapy may exacerbate the condition. In addition, hypochloremia may accompany alkalosis, which is best treated with potassium chloride. Close monitoring of acid-base balance, serum electrolytes, electrocardiogram, and clinical status is recommended.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

Sympathomimetic agents may cause increases in blood glucose concentrations. These effects are usually transient and slight but may be significant with dosages higher than those normally recommended. Therapy with sympathomimetic agents should be administered cautiously in patients with diabetes mellitus. Closer monitoring of blood glucose concentrations may be appropriate.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Sympathomimetic agents can induce transient mydriasis via stimulation of alpha-1 adrenergic receptors. In patients with anatomically narrow angles or narrow-angle glaucoma, pupillary dilation can provoke an acute attack. In patients with other forms of glaucoma, mydriasis may occasionally increase intraocular pressure. Therapy with sympathomimetic agents should be administered cautiously in patients with or predisposed to glaucoma, particularly narrow-angle glaucoma.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

Alkalinizing agents act as proton acceptors and/or dissociate to provide bicarbonate ions. Elimination of bicarbonate is decreased in patients with renal impairment and can result in metabolic alkalosis. Symptoms of metabolic alkalosis include hyperirritability or tetany, arrhythmia, and/or seizures (altered pH = altered calcium), or lactic acidosis due to impaired oxygen release. Therapy with alkalinizing agents should be administered with extreme caution in patients with compromised renal function. Clinical monitoring of renal function, acid/base balance and electrolytes is recommended.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.