Term
| Vasopressor and Vasodilators |
|
Definition
• Norepinephrine (Levophed)
• Phenylephrine (Neo-synephrine)
• Dopamine (Intropin)
• Dobutamine (Dobutrex)
• Vasopressin (Pitressin)
• Nitroglycerin
• Morphine
• Sodium nitroprusside (Nipride)
• Hydralazine (Apresoline)
• Inamrinone (Inocor)
• Milrinone (Primacor)
• Digitalis (Digoxin, Lanoxin)
• Furosemide (Lasix) |
|
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Term
| Norepinephrine (Levophed) |
|
Definition
Mechanism of Action
Vasopressor & Sympathomimetic
Endogenous catecholamine
• Potent alpha-adrenergic receptor stimulation
• Increases myocardial contractility due to weaker beta-1 effects
• Arterial and venous vasoconstriction from potent alpha stimulation
• Increased SVR (afterload) increases blood pressure and may diminish cardiac output.
• Due to an increase in myocardial oxygen demand, may worsen myocardial ischemia, especially if coronary vasoconstriction is induced by coronary alpha receptor stimulation. |
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Term
| Norepinephrine (Levophed) |
|
Definition
Indications to Administer
• Hemodynamically significant hypotension refractory to other sympathomimetics
• Cardiogenic shock
• Used more often with low SVR states (e.g., sepsis) than in MI-related hypotension |
|
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Term
| Norepinephrine (Levophed) |
|
Definition
Contraindications
• Hypotension due to hypovolemia (may be used as a temporary agent until volume can be replaced)
• Profound hypoxemia or hypercarbia
• Mesenteric or peripheral vascular thrombosis
• Pre-existing hypertension
• Use with caution in patients with heart disease and/or hyperthyroidism. |
|
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Term
| Norepinephrine (Levophed) |
|
Definition
Side Effects
• Hypertension
• Arrhythmias (baroreceptor-mediated bradycardia)
• Chest pain
• Decreased peripheral perfusion
• Decreased renal perfusion (monitor urinary output and renal function) |
|
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Term
| Norepinephrine (Levophed) |
|
Definition
Dose
• Start at 0.5 - 1.0 mcg/min
• Titrate to desired effect (SBP of 90 - 100 mmHg); up to 30 mcg/min
• Adult dosage commonly 2 - 12 mcg/min
• Mix 4 ml ampule (1 mg/ml) in 500 ml D5W or 0.9% NSS to make 8 mcg/ml |
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Term
| Phenylephrine (Neo-synephrine) |
|
Definition
Mechanisms of Action
• Potent direct-acting sympathomimetic (synthetic) with strong alpha-adrenergic and weak beta-adrenergic cardiac stimulant properties
• Elevates systolic and diastolic pressures due to peripheral arteriolar constriction.
• Constricts capacitance vessels and increases venous return.
• Cardiac output is slightly decreased due to the increase in afterload.
• Coronary blood flow is increased.
• Rise in blood pressure may cause reflex bradycardia due to aortic baroreceptor stimulation.
• Produces little or no CNS stimulation |
|
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Term
| Phenylephrine (Neo-synephrine) |
|
Definition
Indications
• Hypotension from shock, shock-like states, or drug- induced shock
• To overcome PSVT
• During anesthesia to maintain adequate level of blood pressure and prolong anesthesia drug’s effects |
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Term
| Phenylephrine (Neo-synephrine) |
|
Definition
Contraindications
• Severe coronary disease or hypertension
• Hypotension due to hypovolemia
• Ventricular tachycardia
• Cautious use in thyroid dysfunction, diabetes mellitus, myocardial disease, bradycardia, or cerebral atherosclerosis |
|
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Term
| Phenylephrine (Neo-synephrine) |
|
Definition
Adverse Reactions
• Sympathomimetic effects: palpitations, tachycardia, rebound bradycardia (especially in overdoses), extrasystoles, ventricular irritability, hypertension
• Tremors, dizziness, sleeplessness, headache, excitability
• Severe visceral or peripheral vasoconstriction and tissue necrosis if IV infiltrates |
|
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Term
| Phenylephrine (Neo-synephrine) |
|
Definition
Dose
• Titrate 0.1 - 0.18 mg/min until BP stabilizes, then 0.04 - 0.06 mg/min for maintenance infusion.
• Dilute 10 mg in 500 ml D5W or 0.9% NSS to make 0.2 mg/ml concentration. |
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Term
|
Definition
Mechanisms of Action
VASOPRESSOR
• Chemical precursor of norepinephrine
• Low doses = dopaminergic receptor stimulation
• Vasodilation of renal, mesenteric, and cerebral arteries
• Urine output increased, while heart rate and blood pressure are usually unchanged
• Mid-range doses = beta-1 adrenergic receptor stimulation with weak alpha-stimulation
• Increased cardiac output due to increased heart rate and contractility
• Small increase in SVR
• Weaker alpha-1 at this dose antagonized by beta-1 stimulation
• High doses = alpha-adrenergic receptor stimulation
• Renal, mesenteric, and peripheral vasoconstriction
• Increase in SVR and preload
• Doses above 20 mcg/kg/min produce alpha stimulation similar to norepinephrine
• Increases myocardial work without compensatory increase in coronary blood flow |
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Term
|
Definition
Indications
• Cardiogenic shock
• Hemodynamically significant hypotension, in absence of hypovolemia (systolic blood pressure [SBP] < 70 mmHg)
• CHF, in combination with other agents (such as sodium nitroprusside) |
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Term
|
Definition
Precautions
• Excessive vasoconstriction at high doses
• Can compromise circulation to the extremities in some patients (monitor peripheral pulses, color, and temperature).
• Will increase heart rate and may cause supraventricular or ventricular arrhythmias.
• Increased myocardial workload without increase in coronary perfusion can cause or worsen ischemia.
• Taper infusion carefully to avoid acute hypotension.
• Monoamine oxidase (MAO) inhibitors may potentiate effects of dopamine. |
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Term
|
Definition
Contraindications
• Cardiogenic shock
• Uncorrected tachyarrhythmias
• Ventricular fibrillation
• Hemodynamically significant hypotension, in presence of hypovolemia (SBP < 70 mmHg) |
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Term
|
Definition
Adverse Reactions
• Sympathomimetic stimulation: tachycardia, hypertension, ventricular ectopy, angina, anxiety, and decreased peripheral perfusion
• Headache
• Nausea and vomiting
• Decrease in pulse pressure
• Extravasation causes tissue necrosis and sloughing |
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Term
|
Definition
Dose
• Low dose: 2 - 5 mcg/kg/min
• Mid-range dose: 5 - 10 mcg/kg/min
• High dose: > 10 mcg/kg/min
• Titrate dosage to desired hemodynamic effect, using data from right heart catheterization as measure of effects.
• Dilute 400 mg in 250 ml D5W for concentration of 1600 mcg/ml. |
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Term
|
Definition
Mechanisms of Action
VASOPRESSOR
• Sympathomimetic with potent inotropic effects
• Stimulates beta-1 and alpha-adrenergic receptors
• Minor alpha stimulation antagonized by !stronger beta-1 effects
• Less likely to induce tachycardia at therapeutic doses than isoproterenol or dopamine
• Increase in renal and mesenteric blood flow due to increased cardiac output
• May be combined with dopamine to increase cardiac output, SVR, and preload.
• Decreases pulmonary occlusive pressures and peripheral resistance
• Myocardial work is balanced by increased coronary blood flow.
• Does not cause release of norepinephrine |
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Term
|
Definition
Indications
• Hypotension with pulmonary congestion and dysfunction (e.g., CHF, cardiogenic shock)
• Hemodynamically significant hypotension (SBP of 70 - 100 mmHg)
• Drug of choice in low cardiac output states due to RV infarction
• Stress test echocardiography |
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Term
|
Definition
Precautions
• Monitor for arrhythmias and fluctuations in blood pressure
• Insulin effects may be antagonized due to beta-2 stimulation in the pancreas
• Extravasation leads to tissue necrosis
• Cavity obliteration during dobutamine stress echocardiography (DSE)
• Due to myocardial thickening and increased contractility
• walls may “touch” with resultant decrease in heart rate and cardiac output
• May be alleviated by increasing preload (volume infusion) |
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Term
|
Definition
Contraindications
• Idiopathic hypertrophic subaortic stenosis (IHSS)
• LVOT obstructions
• Tachydysrhythmias
• Pre-existing hypertension
• Shock due to hypovolemia
• Acute coronary syndrome with ventricular irritability
• Hypersensitivity to sympathomimetic amines |
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Term
|
Definition
Adverse Reactions
• Tachycardia, arrhythmias, ventricular ectopy, palpitation, hypertension
• Anginal pain
• Peripheral vasoconstriction (may be countered with combined sodium nitroprusside infusion)
• Shortness of breath
• Nausea and vomiting
• Headache
• Anxiety, jitteriness |
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Term
|
Definition
Dose
• Start at 0.5 mcg/kg/min IV and titrate to desired effect
• Usual dose is 2 - 20 mcg/kg/min
• Insertion of Swan-Ganz catheter for continuous pressure monitoring
• Titrate upward so as not to increase heart rate by greater than 10% (unless for stress echocardiogram).
• Dilute 1000 mg in 250 ml of D5W or 0.9% NSS for a concentration of 4 mg/ml. |
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Term
|
Definition
Mechanisms of Action
ANTIDIURETIC & HEMOSTATIC• Anti-diuretic hormone
• Increases permeability of the renal tubular epithelium to adenosine monophosphate and water, promoting reabsorption of water and producing concentrated urine
• Cardiovascular effects related to potent alpha-adrenergic stimulation of vascular smooth muscles, leading to vasoconstriction and increased afterload
• Beneficial redistribution to coronary and cerebral vasculature without beta-1 induced increase in myocardial oxygen demand seen with epinephrine (cardiac arrest benefits) |
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Term
|
Definition
Indications
• Cardiac arrest due to ventricular arrhythmias, asystole, or PEA (alternate to epinephrine)
• Hemodynamic support in vasodilatory shock (e.g. septic shock) refractory to more traditional therapy
• Esophageal variceal hemorrhage |
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Term
|
Definition
Precautions
• Several drug interactions; consult drug reference or pharmacist (except in cardiac arrest)
• May provoke cardiac ischemia and angina
• Monitor for hypersensitivity reactions (urticaria, bronchoconstriction, angioedema, anaphylaxis). |
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Term
|
Definition
Contraindications
• None during cardiac arrest
• Ischemic coronary artery disease or advanced arteriosclerosis
• Renal failure |
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Term
|
Definition
Adverse Reactions
• Tremor, headache, vertigo
• Vasoconstriction with reduced peripheral perfusion
• Hypertension
• Arrhythmias, decreased cardiac output, myocardial ischemia
• Anginal chest pain
• Bronchoconstriction, respiratory congestion
• Abdominal cramps, nausea and vomiting, flatulence |
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Term
|
Definition
Dose
• Cardiac arrest: single bolus of 40 units IV; use epinephrine if no response in 10 - 20 minutes
• Currently acceptable via endotracheal route; no set dosage as of current ACLS guidelines |
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Term
|
Definition
Mechanism of Action
• Antianginal & Vasodilator
• Nitrate smooth muscle relaxant
• Relieves angina via vasodilation of the venous system, which reduces venous return to the heart
• Causes a decrease in preload (ventricular volume, pressure, and wall stress); this decreases ventricular contractility and myocardial oxygen demand
• Dilates collateral circulation, including venous capacitance
• Dilates large coronary arteries and increases collateral blood flow to ischemic myocardial tissue
• Blocks vasospasm at the site of plaque rupture and increases collateral blood flow to ischemic myocardial tissues
• Sublingually, nitroglycerin decreases filling pressures without lowering SVR
• Cardiac output usually falls due to the decrease in preload
• When compared with sodium nitroprusside, nitroglycerin produces greater reduction in preload (venous return) and less reduction in afterload (arteriolar resistance) |
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Term
|
Definition
Precautions
• Patient must be seated or supine when administering nitroglycerin (especially sublingual doses).
• Continuous infusion should be via pump only and using appropriate tubing.
• When applying or removing ointment or paste, wear gloves to avoid accidental exposure. |
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Term
|
Definition
Contraindications
• Hypersensitivity to nitrate and nitrites
• Hypotension (SBP < 90 mmHg; cautious use in postural hypotension)
• Uncorrected hypovolemia
• Severe anemia
• Closed-angle glaucoma
• Intracranial bleeding or head trauma
• Cardiac tamponade
• Constrictive pericarditis
• Sildenafil or other phosphodiesterase-5 (PDE-5) inhibitor use within the preceding 48 hours
• Use with extreme caution in patients with inferior wall MI (likelihood of concomitant right ventricular infarction which requires maintenance of preload). |
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Term
|
Definition
Indications
• Drug of choice for acute angina pectoris attacks that are exertional or typical in nature (sublingual route)
• Unstable angina
• Prinzmetal’s angina (either acutely or to relieve spasm induced during ergonovine studies)
• Acute myocardial infarction
• Congestive heart failure (lowers SVR and increases venous capacitance)
• Cardiogenic pulmonary edema
• Maintenance for chest pain prophylaxis (transdermal ointment) |
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Term
|
Definition
Adverse Reactions
• Headache (most common side effect; treat with aspirin or Tylenol)
• Hypotension (most severe side effect; treat with trendelenberg position and IV fluid bolus)
• Methemoglobinemia
• Change in hemoglobin configuration from
• Fe2+ to Fe3+ state
• Can result in refractory hypoxemia; usually related to high doses or longterm use
• Treated with methylene blue infusion
• Bradycardia (hypotension and bradycardia usually respond to IV fluids or atropine)
• Baroreceptor-mediated tachycardia, palpitations
• Nausea and vomiting
• Syncope or collapse |
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Term
|
Definition
Dose
Sublingually (SL):
• 0.3 - 0.4 mg tablet or metered spray every 5 minutes x 3 doses
• SL nitroglycerine (NTG) is drug of choice in angina or MI
• Evaluate pain scale and blood pressure before first dose and after each dose
• If sublingual NTG fails to relieve pain after three doses, patient should seek medical care ASAP.
• Intravenously:
• Start at 10 - 20 mcg/min and titrate until desired effect (pain free) is noted or to a maximum of 500 mcg/min.
• Bolus with 12.5 - 25.0 mcg, then start infusion
• Best for patients with unstable angina or for continuous treatment for AMI
• Dilute 40 mg with 250 ml D5W or 0.9% NSS for a concentration of 160 mcg/ml.
• Transdermal ointment:
• For chronic therapy, not for acute treatment of chest pain
• 1 - 2 inches of 2% paste applied to the chest wall |
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Term
|
Definition
Mechanisms of Action
•Narcotic analgesic (Opiate)
• Schedule II narcotic (opioid) agonist analgesic and vasodilator derived from the opium poppy
• Naturally occurring narcotic analgesic
• Analgesic effects due to binding at various receptor sites, mimicking the effects of endogenous endorphins and enkephalins
• μ1: main action of this receptor is analgesia
• μ2: euphoria, respiratory depression, bradycardia, physical dependence, and ileus are elicited at this receptor
• Delta: modulates activity of mu receptors; it is thought that mu and delta receptors coexist as a complex
• Increases venous capacitance, reduces venous return, and decreases preload
• Decreases pulmonary congestion
• Reduces pulmonary capillary occlusive pressure
• Facilitates reabsorption of pulmonary edema from the alveoli to the vasculature
• Vasodilation decreases SVR at the arteriolar level and increases stroke volume, cardiac output, and decreases myocardial oxygen demand. |
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Term
|
Definition
Indications
• Moderate to severe pain
• Pain and anxiety relief during acute MI
• Acute cardiogenic pulmonary edema (congestive heart failure) |
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Term
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Definition
Precautions
• Action is potentiated when used in combination with sedatives, hypnotics, or barbiturates.
• Narcotic effects can be reversed by naloxone.
• Encourage deep breathing, coughing, and frequent changes in position to minimize the risk of atelectasis |
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Term
|
Definition
Contraindications
• Hypersensitivity to the drug
• Decreased level of consciousness
• Increased intracranial pressure or head trauma
• Convulsive disorders
• Hypotension
• COPD
• Chemical-irritant induced pulmonary edema (e.g., chlorine, ammonia)
• Ingested poisonings
• Chronic alcoholism
• Undiagnosed intra-abdominal or intracranial conditions
• Patients taking MAO inhibitors |
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Term
|
Definition
Adverse Reactions
• Respiratory depression
• Hypotension (especially in patients with hypovolemia or increased SVR)
• Dose-dependent bradycardia due to vagal stimulation; may be blocked or reversed by use of an anticholinergic (such as atropine)
• Depression of cough reflex and respiratory status may induce atelectasis.
• Constipation and urinary retention
• Nausea and vomiting
• Hypothermia
• Localized allergic reaction with IV administration
• Addiction with long-term use
• High doses or overdose may cause:
• Anaphylaxis
• Cheyne-Stokes respiration or apnea
• Severe myocardial depression
• Tachycardia
• Death |
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Term
|
Definition
Dose
•Dosage varies with patient’s size, age, and renal function.
• Start with 2 - 10 mg slow IV over 3-5 minutes.
• Titrate in small increments (1 - 3 mg) to desired effect, while maintaining adequate respiratory status. |
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Term
| Sodium nitroprusside (Nipride) |
|
Definition
Mechanisms of Action
• Vasodilator
• Anti-hypertensive
• Potent peripheral vasodilator, which affects arteriolar and venous smooth muscles (primarily arteriolar)
• Effects are seen immediately and resolve within minutes of infusion cessation
• Reduces blood pressure:
• Decreases SVR (afterload)
• Increases venous capacitance (preload)
• Increases cardiac output and enhances systolic emptying |
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Term
| Sodium nitroprusside (Nipride) |
|
Definition
Indications
• Hypertensive emergencies (drug of choice)
• Hypertensive emergency associated with neurologic dysfunction
• Treatment of failure (by decreasing preload and afterload, thus myocardial workload)
• Heart failure with pulmonary congestion refractory to diuretics
• Combined with dopamine to produce hemodynamic effects similar to dobutamine |
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Term
| Sodium nitroprusside (Nipride) |
|
Definition
Precautions
• Protect from light with foil and use immediately after mixing.
• Hemodynamic monitoring (arterial and right heart lines) is essential.
• Imbalance between coronary supply and demand may induce or worsen myocardial ischemia.
• Possible coronary “steal”
• May cause right-to-left shunt in presence of atrial septal defect (ASD) or ventricular septal defect (VSD), leading to hypoxia and cyanosis
• Sodium thiocyanate toxicity
• Metabolite from liver
• Most likely if used for over 72 hours
• Monitor patient for altered mental status
• Medication should be a faint yellow, not brown
• Long-term use may cause methemoglobinemia with resultant refractory hypoxemia.
• Prolonged use may cause hypothyroidism
• Reduce doses in the elderly
• Monitor arterial pressure and central venous pressure (CVP) |
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Term
| Sodium nitroprusside (Nipride) |
|
Definition
Contraindications
• Treatment of compensatory hypertension (A-V shunt or coarctation of the aorta)
• Known inadequate cerebral perfusion
• Use cautiously in renal or hepatic dysfunction |
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|
Term
| Sodium nitroprusside (Nipride) |
|
Definition
Adverse Reactions
• Usually occurs due to too rapid rate of infusion – reversible
• Hypotension (most common side effect; may induce or exacerbate ischemia)
• Nausea and vomiting
• Diaphoresis
• Headache
• Restlessness and apprehension
• Muscle twitching
• Palpitations
• Chest or abdominal pain |
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Term
| Sodium nitroprusside (Nipride) |
|
Definition
Dose
• Start infusion at 0.5 mcg/kg/min and titrate every 5 - 10 minutes to desired effect (SBP < 150 mmHg and/or DBP < 60 - 90 mmHg).
• Normal range is 0.5 - 8.0 mcg/kg/min.
• Mix 50 mg with 2 - 3 ml of D5W in the vial, then add 250 ml of D5W for a concentration of 200 mcg/ml. |
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Term
|
Definition
Mechanisms of Action
Class:
• Anti-hypertensive • Direct vasodilator
• Non-nitrate vasodilator and antihypertensive
• Reduces blood pressure mainly by direct effects on vascular smooth muscles of the arterioles, resulting in vasodilation
• Little effect on venous-capacitance vessels
• Diastolic response often greater than systolic
• Vasodilation reduces afterload and substantially improves cardiac output, as well as renal and cerebral perfusion.
• Hypotensive effect may be limited by sympathetic reflexes (increases in heart rate, stroke volume, and cardiac output). |
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Term
|
Definition
Indications
• Moderate to severe hypertension, including acute hypertensive emergency
• Pregnancy-induced hypertension and preeclampsia
• May be used in conjunction with cardiac glycosides or other vasodilators in short-term treatment of CHF
• Unexplained pulmonary hypertension |
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Term
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Definition
Precautions
• Taper drug slowly to avoid sudden possible rise in blood pressure.
• Blood dyscrasia resulting in decrease in hemoglobin and hematocrit
• Obtain baseline and periodic BUN, creatinine, uric acid, serum potassium, blood glucose, and CBC; also obtain ECG.
• Use with caution if used concomitantly with beta-adrenergic blockers.
• Tartrazine may be contained in some products; may cause allergic-type reaction in patients who also have aspirin hypersensitivity. |
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Term
|
Definition
Contraindications
• Coronary artery disease or MI
• Pre-existing hypotension
• Persistent tachycardia
• Advanced renal impairment
• Mitral valve disease |
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Term
|
Definition
Adverse Reactions
• Headache and dizziness
• Palpitations and tachycardia
• Drug-induced hypotension
• Angina
• Nausea and vomiting, diarrhea, anorexia
• Decreased hematocrit and hemoglobin levels
• Hypersensitivity reactions: rash, urticaria, fever, chills, arthralgia, hepatitis, eosinophilia |
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Term
|
Definition
Dose
• Hypertension in adults:
• : 10 - 50 mg QID
• Intravenous: 5 - 40 mg slow IV push over 1 - 2 minutes, may repeat every 4 - 6 hours as needed
• Hypertension in geriatrics: start with 10 mg PO BID or TID and titrate as needed |
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Term
|
Definition
Mechanisms of Action
Class : •Inotrophic agent
• Phosphodiesterase (PDE) inhibitor; noncatecholamine inotropic agent
• Formerly called amrinone
• Inhibits peak III cyclic AMP isoenzyme in cardiac and vascular muscle, resulting in direct inotropic effect and direct arterial vasodilation; effects are linked to inhibition of phosphodiesterase
• Drug acts slightly different than digitalis and beta- adrenergic stimulants.
• Rapid acting, potent inotropic (enhanced contractility) and vasodilator
• Cardiac output increases and SVR and preload decrease at dosages of 2 - 15 mcg/kg/min.
• Higher doses produce tachycardia.
• Hemodynamic effects are similar to dobutamine. |
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Term
|
Definition
Indications
• Severe CHF refractory to diuretics, vasodilators, and conventional inotropic agents
• Additive to digitalis and catecholamine therapy
• Promotion of hemodynamic improvements in patients with CHF from ischemic heart disease |
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Term
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Definition
Precautions
• Clear yellow in appearance
• Store at room temperature and protect from light.
• May increase or induce myocardial ischemia
• Do not mix with furosemide or dextrose containing solutions.
• Adjust dosage frequently to achieve desired effect at the lowest possible dosage. |
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Term
|
Definition
Contra- indications
• Hypersensitivity to inamrinone or bisulfites
• Pre-existing hypotension
• Presence of uncorrected aortic or pulmonic valve obstruction
• Right ventricular outflow tract (RVOT) or left ventricular outflow tract (LVOT) obstruction (IHSS)
• Patients with uncorrected hypokalemia or dehydration |
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Term
|
Definition
Adverse Reactions
• Nausea and vomiting
• Thrombocytopenia due to hepatotoxicity (monitor platelet count daily)
• Dose-dependent tachydysrhythmias, ventricular irritability, hypotension
• Muscular stiffness, myalgias, tenderness, and localized inflammatory reaction at site of infusion
• Hypersensitivity reaction (itching) may occur with long-term use
• Fever |
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Term
|
Definition
Dose
• Loading dose: 0.75 mcg/kg over 2-5 minutes
• Infusion at 5 - 10 mcg/kg/min, titrated to desired effect
• Adjust frequently to achieve optimal effects at lowest possible dose
• Mix 20 ml ampule of 100 mg (5 mg/ml) with 0.9% NSS for 1 - 3 mg/ml concentration |
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Term
|
Definition
Mechanisms of Action
Class: •Inotropic agent
• Phosphodiesterase (PDE) inhibitor; noncatecholamine inotropic agent
• Positive inotropic effect by increasing cellular levels of cAMP (inhibits peak III cyclic AMP isoenzyme in cardiac and vascular muscle)
• Results in direct inotropic effect (increased contractility) and vasodilation with little effect on chronotropic activity
• Vasodilation via direct relaxation of vascular smooth muscles with resultant reduction in afterload
• Overall improvement in myocardial contractility, ejection fraction, and cardiac output |
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Term
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Definition
Indications
• Short-term treatment of CHF refractory to diuretics or digitalis
• To increase cardiac output and to reduce pulmonary capillary wedge pressure (PCWP) and SVR without increasing myocardial oxygen demand
• Chronic heart failure with decompensation |
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Term
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Definition
Precautions
• Use cautiously in patients with atrial flutter or fibrillation due to shortening of AV nodal conduction time and potential for increased ventricular response.
• Avoid infusion in same IV line as furosemide (produces a precipitate).
• Monitor vital signs, cardiac monitor, I&O’s, renal function, and platelet levels.
• Expect dose reduction as cardiac output and urinary output improve. |
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Term
|
Definition
Contraindications
• Hypersensitivity to the drug
• Severe aortic and pulmonary valvular stenosis
• Hypertrophic cardiomyopathy
• Acute MI (initial phase)
• Hypotension |
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Term
|
Definition
Adverse Reactions
• Headache
• Ventricular ectopy, ventricular tachycardia (sustained or non-sustained), ventricular fibrillation
• Hypotension
• Chest pain and cardiac ischemia
• Thrombocytopenia (long-term therapy necessitates daily monitoring of platelet count)
• Local tissue discomfort and necrosis |
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Term
|
Definition
Dose
• Initial loading dose: 50 mcg/kg slow IVP over 10 minutes
• Continuous infusion: 0.375 - 0.75 mcg/kg/min
• Titrate dosage to maximum clinical effects (patient improvement, increase in urinary output, improvement in right-heart hemodynamics)
• Drug is commonly used concomitantly with digitalis and diuretics.
• In patients with renal impairment, the maximum dose is 1.13 mg/kg/day. |
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Term
| Digitalis (Digoxin, Lanoxin) |
|
Definition
Mechanisms of Action
Class: Antidysrhythmic
• Cardiac glycoside
• Mild positive inotropic effect due to increased calcium in the sarcoplasmic reticulum, increasing contractility
• Vasoconstriction of coronary and mesenteric arteries is due to increased calcium levels; increases SVR via increased vascular tone.
• Since digitalis effects are caused by increased calcium concentrations, betablockers have no effects on positive inotropic activity.
• Slows AV nodal conduction by lengthening the refractory period
• Increases aortic root baroreceptor sensitivity
• Results in reduction in heart rate due to increased arterial pressure
• High doses cause increased and potentially dangerous adrenergic activity (binds to muscle as well as in the plasma). |
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Term
| Digitalis (Digoxin, Lanoxin) |
|
Definition
Indications
Effective control of ventricular response in atrial tachydysrhythmias without adversely affecting contractility
• Calcium channel blockers may supplant digitalis as drug of choice for atrial fibrillation.
• If the BP is high, use calcium channel blocker.
• If the BP is normal or low, use digitalis.
• May convert PSVT to normal sinus rhythm
• Congestive heart failure |
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Term
| Digitalis (Digoxin, Lanoxin) |
|
Definition
Precautions
• Toxicity occurs in 20% of all patients
• Toxicity and overdose treated with Digoxin Immune Fab (Digibind)
• Hypokalemia
• Hypokalemia sensitizes the myocardium to digitalis.
• May alter onset and rate of positive inotropic effects
• Hyperkalemia possible in massive digitalis overdose.
• Causes massive coronary vasoconstriction
• May induce or worsen ischemia• Electrical cardioversion can be dangerous in the presence of digitalis toxicity.
• Can precipitate fatal ventricular arrhythmias
• Use lowest energy levels (10 - 20 joules)
• Hypercalcemia may also contribute to serious arrhythmias.
• Many drug interactions
• Verapamil and quinidine can double or triple serum levels of digitalis.
• Beta-adrenergic blockers may increase ectopic beats with digitalis on board.
• Concomitant presence of calcium chloride may increase risk of toxicity.
• Interactions also with loop, thiazine, and potassium-sparing diuretics |
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Term
| Digitalis (Digoxin, Lanoxin) |
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Definition
Contra-indication
Ventricular tachycardia or ventricular fibrillation Acute myocardial infarction
High-degree AV blocks
Digitalis intoxication (relative)
WPW syndrome
Use with extreme caution if at all |
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Term
| Digitalis (Digoxin, Lanoxin) |
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Definition
Adverse Reactions
Increases slope of phase 4 of the action potential
May induce delayed after-depolarizations in the Purkinje cells
Results in ectopy
Alters the ECG:
Increases the PR interval
Depresses the ST segment; characteristic ST segment scooped appearance
Flattens or inverts T waves Shortens the QT interval
• Shortens the QT interval
• Slows impulse transmission through the ventricular conduction system – development of reentry arrhythmias
• Wide range of cardiac arrhythmias: AV blocks, bi- directional ventricular tachycardia, paroxysmal atrial tachycardia with AV block, junctional rhythm and tachycardia, ventricular ectopy
• Extracardiac side effects
• Anorexia
• Nausea and vomiting
• Diarrhea
• Fatigue
• Mental status changes
• Blurred vision
• Yellow-green hue to visual spectrum
• Presence of “haloes” around lights |
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Term
| Digitalis (Digoxin, Lanoxin) |
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Definition
Dose
• Loading dose: 10 - 15 mcg/kg
• IV effects in 5 - 30 minutes and peaks in 1.5 - 3.0 hours
• Maintenancedosingdependentonbodysizeand renal function (monitor creatinine clearance)
• Normal therapeutic range is 0.5 - 2.0 ng/ml.
• Alsoavailableinoralpreparations(0.125,0.25, and 0.50 mg tablets) |
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Term
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Definition
Mechanisms of Action
Class: •Antihypertensive •Diuretic
• diuretic
• Inhibits the reabsorption of sodium and chloride in the proximal and distal tubules and in the loop of Henle
• Decreases renal vascular resistance; increases renal blood flow and urine output |
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Term
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Definition
Indications
• Edema associated with CHF, cirrhosis of the liver, and renal disease
• Initiation of rapid diuresis in acute pulmonary edema
• Volume overload (intrinsic or extrinsic)
• Mild impairment in renal function |
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Term
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Definition
Precautions
• Observe for signs of electrolyte disturbances
• Digitalis may exacerbate metabolic effects of hypokalemia. |
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Term
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Definition
Contraindications
• Anuria (not beneficial in patients with renal failure)
• Hypersensitivity to sulfonamides
• Chronic metabolic alkalosis or hyperkalemia
• Hypotension or severe dehydration |
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Term
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Definition
Adverse Reactions
• Electrolyte depletion: hypokalemia, hyponatremia
• Dehydration, hypotension
• Vascular thrombosis or embolism
• Hyperglycemia
• Nausea, vomiting, diarrhea, cramping
• Headache, vertigo, tremors
• Rash, urticaria
• Leukopenia, anemia |
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Term
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Definition
Dose
• Intravenous: 20 - 80 mg IV, usually in increments of 20 mg
• Oral: 20 - 40 mg initially, titrated for effect |
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Term
| Digitalis (Digoxin, Lanoxin) |
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Definition
Mechanisms of Action
Class: Antidysrhythmic
• Cardiac glycoside
• Mild positive inotropic effect due to increased calcium in the sarcoplasmic reticulum, increasing contractility
• Vasoconstriction of coronary and mesenteric arteries is due to increased calcium levels; increases SVR via increased vascular tone.
• Since digitalis effects are caused by increased calcium concentrations, betablockers have no effects on positive inotropic activity.
• Slows AV nodal conduction by lengthening the refractory period
• Increases aortic root baroreceptor sensitivity
• Results in reduction in heart rate due to increased arterial pressure
• High doses cause increased and potentially dangerous adrenergic activity (binds to muscle as well as in the plasma). |
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Term
| Digitalis (Digoxin, Lanoxin) |
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Definition
Indications
• Effective control of ventricular response in atrial tachydysrhythmias without adversely affecting contractility
• Calcium channel blockers may supplant digitalis as drug of choice for atrial fibrillation.
• If the BP is high, use calcium channel blocker.
• If the BP is normal or low, use digitalis.
• May convert PSVT to normal sinus rhythm
• Congestive heart failure |
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Term
| Digitalis (Digoxin, Lanoxin) |
|
Definition
Precautions
• Toxicity occurs in 20% of all patients
• Toxicity and overdose treated with Digoxin Immune Fab (Digibind)
• Hypokalemia
• Hypokalemia sensitizes the myocardium to digitalis.
• May alter onset and rate of positive inotropic effects
• Hyperkalemia possible in massive digitalis overdose.
• Causes massive coronary vasoconstriction
• May induce or worsen ischemia• Electrical cardioversion can be dangerous in the presence of digitalis toxicity.
• Can precipitate fatal ventricular arrhythmias
• Use lowest energy levels (10 - 20 joules)
• Hypercalcemia may also contribute to serious arrhythmias.
• Many drug interactions
• Verapamil and quinidine can double or triple serum levels of digitalis.
• Beta-adrenergic blockers may increase ectopic beats with digitalis on board.
• Concomitant presence of calcium chloride may increase risk of toxicity.
• Interactions also with loop, thiazine, and potassium-sparing diuretics |
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Term
| Digitalis (Digoxin, Lanoxin) |
|
Definition
Contra-indication
Ventricular tachycardia or ventricular fibrillation Acute myocardial infarction
High-degree AV blocks
Digitalis intoxication (relative)
WPW syndrome
Use with extreme caution if at all |
|
|
Term
| Digitalis (Digoxin, Lanoxin) |
|
Definition
Adverse Reactions
Increases slope of phase 4 of the action potential
May induce delayed after-depolarizations in the Purkinje cells
Results in ectopy
Alters the ECG:
Increases the PR interval
Depresses the ST segment; characteristic ST segment scooped appearance
Flattens or inverts T waves Shortens the QT interval
• Shortens the QT interval
• Slows impulse transmission through the ventricular conduction system – development of reentry arrhythmias
• Wide range of cardiac arrhythmias: AV blocks, bi- directional ventricular tachycardia, paroxysmal atrial tachycardia with AV block, junctional rhythm and tachycardia, ventricular ectopy
• Extracardiac side effects
• Anorexia
• Nausea and vomiting
• Diarrhea
• Fatigue
• Mental status changes
• Blurred vision
• Yellow-green hue to visual spectrum
• Presence of “haloes” around lights |
|
|
Term
| Digitalis (Digoxin, Lanoxin) |
|
Definition
Dose
• Loading dose: 10 - 15 mcg/kg
• IV effects in 5 - 30 minutes and peaks in 1.5 - 3.0 hours
• Maintenancedosingdependentonbodysizeand renal function (monitor creatinine clearance)
• Normal therapeutic range is 0.5 - 2.0 ng/ml.
• Alsoavailableinoralpreparations(0.125,0.25, and 0.50 mg tablets) |
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