Cardio medications Flashcards
(31 cards)
Digoxin
Cardiac glycoside used primarily for SVT; some consensus panelists recommend treatment for stage D patients even those in sinus rhythm
Increases myocardial contraction with increased output; increased diuresis secondary to decrease in sympathetic tone; reduction in heart size, heart rate, blood volume, and pulmonary and venous pressures; decreased conduction velocity through AV node and prolonged effective refractory period; exact mechanism not fully described, but thought to increase availability of calcium to myocardial fibers and inhibit NaK ATPase with increased intracellular Na and reduced K
Contraindications: V fib, digitalis intoxication-monitor levels; most agree contraindicated in cats with HCM
Use with caution in renal disease and heart failure, complex ventricular arrhythmias, subaortic stenosis
AE: typically associated with high blood digoxin concentrations; include almost every kind of cardiac arrhythmia with worsening clinical signs associated with heart failure; GI upset; vesicant
Dobutamine
Rapid acting positive ionotrope
short term adjunctive treatment of congestive heart failure
Direct beta 1 adrenergic agonist that increases cardiac contractility and improves CO
mild beta 2 and alpha 1 adrenergic effects, which balance each other out and cause little direct effect on systemic vasculature
Does not cause release of norepinephrine; mild chronotropic, arrhythmogenic, and vasodilative effects, higher doses can result in tachycardia
Use in extreme caution with patients with atrial fibrillation because it can enhance AV condution.
AE: tachycardia, facial twitching, seizures, bradycardia, Bezold-Jarisch reflex (inhibitory reflex-hypopnea, bradycardia, hypotension), increased pulmonary arterial pressure
higher doses in cats - CNS effects
Pimobendan
Inodilater
both positive ionotropic and vasodilatory effects via inhibition of PDE III and by increasing intracellular calcium sensitivity in cardiac contractile apparatus; contractility enhanced without increased myocardial oxygen demand
some antithrombotic activity, but not at typical clinical doses; occasional adjunct to pulmonary hypertension as it may have some activity against PDE 5
Contraindicated in aortic or pulmonary valve stenosis; caution with uncontrolled arrhythmias, severe hepatic impairment, and in dogs under 6 months, DM, other metabolic disease; can worsen systolic anterior motion of mitral valve in cats
AE: GI, azotemia, dyspnea, ataxia, pleural effusion, syncope, sudden death, ascites, heart murmur; does not appear to be proarrhythmic
Amiodarone
Antiarrhythmic Class III
Blocks potassium channels, but is unique in that it has characteristics of all 4 antiarrhythmic classes -
sodium channel blocking activity of class I, beta blocking activity of class II, and calcium channel blocking of class IV; prolongation of myocardial cell action potential duration and refractory period
trypanocidal - mediated by disruption of calcium homeostasis, sterol production, and blockade of protease cruzipain
Contraindicated - cardiogenic shock, severe sinus node dysfunction with severe sinus bradycardia, second and third degree AV block, bradycardia related syncope; caution with thyroid dysfunction - inhibits peripheral conversion of T4 to T3
AE: GI, hepatopathy, bradycardia, neutropenia, thrombocytopenia, thyroid dysfunction, keratopathy, regen anemia, positive coomb’s, corneal deposits; original solvent formulation (NOT Nexterone) caused histamine release and reaction
Lidocaine
Antiarrhythmic class 1B, analgesic, prokinetic
membrane stabilizing that shortens the myocardial action potential; binds to inactive fast sodium channels, which inhibits recovery after repolarization; rapid rates of attachment and dissociation of sodium channels in ventricular conducting tissue more so than atrial; phase 4 diastolic depolarization attenuation, decreased automaticity, decrease or no change in membrane responsiveness and excitability; analgesic effects not well understood but are likely via several mechanisms, including reducing ectopic activity of damaged afferent neurons and action at different molecular sites, such as Na+, Ca2+, and K+ channels and N-methyl-D-aspartate (NMDA) receptors; Does not demonstrate GI prokinetic effects in dogs; inhibits reactive oxygen species and lipid peroxidation, may improve clinical outcome of GDV
contraindications: severe degree of SA, AV, or intraventricular heart block; adams-stokes syndrome, wolff parkinson white syndrome; cats are more sensitive to CNS and cardiodepressant effects, most clinicians avoid the use of IV lidocaine in cats; caution with liver disease, CHF, shock, hypovolemia, severe respiratory depression, hypoxia, bradycardia, complete heart block
AE: if IV bolus too rapid - dose dependent hypotension, GI, drowsiness, depression, ataxia, muscle tremors, PR and QRS interval prolongation, QT interval shortening; may increase ventricular rate if patient has a fib; proarrhythmic when used with monophasic defibrillating shock
Sirolimus (rapamycin)
Macrolide; apical serine/threonine protein kinase that associates with several proteins to form 1 of 2 multiprotein complexes; complexes have distinct roles in promoting cardiovascular health during embryogenesis and postnatal life with varying up and downstream targets. studies have demonstrated that mTORC1 activation from chronic hemodynamic stressors may be detrimental to the heart, leading to pathologic hypertrophy.
Rapamycin could slow or reverse the thickening of the heart muscle in felines with HCM before patients showed any symptoms of the disease. The drug functions by inhibiting the mammalian target of rapamycin (mTOR) pathway, a central regulator of metabolism and physiology
Oncology:
Rapamycin inhibits mTOR, the pathway involved in both cancer development and aging. Rapamycin and other mTOR inhibitors do not cause tumor death, but they slow cell proliferation and tumor progression. There have been several studies demonstrating the use of mTOR inhibitors in prevention and progression of lung and prostate cancer in mice. These inhibitors have also been investigated in mice for its anti-aging properties and found to extend lifespan. In humans, mTOR inhibitors have been shown to reduce the incidence of various cancers in organ transplant patients where neoplasia risk is typically increased. They have also been used in the treatment of renal cell carcinoma, certain breast cancers, and neuroendocrine tumors
Spironolactone/Benazepril (Cardalis)
Aldosterone antagonist/ACE inhibitor
Spironolactone is an aldosterone antagonist and a potassium-sparing diuretic; it also has an affinity for androgen and progesterone receptors. Aldosterone is competitively inhibited by spironolactone in the distal renal tubules with resultant increased excretion of sodium, chloride, and water, and decreased excretion of potassium, ammonium, phosphate, and titratable acid. In dogs, aldosterone also plays a role in the progression of myocardial fibrosis, vascular remodeling, and endothelial dysfunction in heart failure, and spironolactone has been shown to reduce these effects in dogs. addition of spironolactone to an angiotensin-converting enzyme (ACE) inhibitor treatment regimen helps prevent the unwanted effects of aldosterone synthesized from other (ie, non-ACE) pathways
Benazepril is a prodrug and has little pharmacologic activity of its own. After being hydrolyzed in the liver to benazeprilat, the drug inhibits ACE, preventing the conversion of angiotensin-I to angiotensin-II. Angiotensin-II is a potent vasoconstrictor and stimulates production of aldosterone in the adrenal cortex. By blocking angiotensin-II formation, ACE inhibitors reduce blood pressure in hypertensive patients and vascular resistance in patients with congestive heart failure. Aldosterone breakthrough (ie, insufficient suppression of aldosterone secretion) has been documented with ACE inhibitor administration to healthy dogs
Contraindications: addison’s, hyperkalemia, hyponatremia, pregnancy, cardiac failure from aortic or pulmonary stenosis, pulmonary edema should be stabilized prior to use; use with caution in growing dogs due to antiandrogenic effects and in patients with renal or hepatic impairment; do not give with NSAIDs to dogs with renal insufficiency
Mexiletine
Antiarrhythmic
class IB antiarrhythmic agent and is similar to lidocaine in its mechanism of antiarrhythmic activity. It inhibits the inward sodium current (fast sodium channel), thereby reducing the rate of rise of the action potential, Phase 0. In cardiomyocytes, automaticity is decreased and action potential duration is shortened; however, the effective refractory period is minimally affected. Usually conduction is unaffected but may be slowed in patients with preexisting conduction abnormalities. No effect on sinus automaticity has been noted clinically
Contraindications: second or third degree AV block, cardiogenic shock; single case report of collie with MDR1 gene mutation developed toxicity at standard dose
AE: GI, tremors, incoordination, dizziness, depression, chest pain, rarely, seizures, severe liver injury
Procainamide
Antiarrhythmic
Class 1a
binds and inhibits fast sodium channels; similar cardiac action to quinidine; supraventricular and ventricular antidysarrhythmic; prolongs refractory times in both atria and ventricles, decrease myocardial excitability, depresses automaticity and conduction velocity; anticholinergic properties may contribute to its effects; effects on heart rate are unpredictable; may exhibit negative ionotropic actions on heart, but CO not greatly affected
contraindicated - myasthenia gravis, in humans - lupus, torsade de pointes, second or third degree AV block; extreme caution, if at all use, with cardiac glycoside intoxication; caution with renal and hepatic disease or CHF; has been recommended not to use in dobermans and boxers with DCM or dogs with subaortic stenosis as it may be proarrhythmic in certain patients susceptible to tachyarrhythmic induced sudden death
AE: GI, weakness, hypotension, negative ionotropism, widened QRS and QT intervals, AV block, multiform ventricular tachycardias, fever, leukopenia, profound hypotension
Quinidine
Class IA Antiarrhythmic (similar to procainamide)
Blocks fast sodium channels during depolarization of the action potential (phase 0). Depresses myocardial excitability, conduction velocity, and contractibility. Prolongs duration of the action potential and effective refractory period, which prevents the re-entry phenomenon and increases conduction times. Prolongs QT interval
Also possesses anticholinergic activity which decreases vagal tone and may facilitate AV conduction
Contraindications: AV block, myasthenia gravis, digitalis intoxication; caution with hypokalemia, acid/base disturbances, hypoxia
AE: GI, weakness, hypotension, negative ionotropism, widened QRS complex and QT intervals, AV block, multiform ventricular tachycardias
Verapamil
Calcium channel blocker
slow channel calcium (L type) blocking agent and a phenylalkylamine that is classified as a class IV antiarrhythmic drug; binds L type calcium channels and blocks influx of extracellular calcium ions across membranes of vascular smooth muscle cells and myocardial cells - results in inhibition of the contractile mechanisms of vascular, which causes systemic and coronary vasodilation, and inhibition of contractile mechanisms of cardiac smooth muscle. has inhibitory effects on cardiac conduction system and these effects produce antiarrhythmic properties;
increased effective refractory period of AV node, decreased automaticity, substantially decreased AV node conduction; HR and RR intervals can be increased or decreased; PR and AH intervals are increased; negative effects on myocardial contractility
Used for SVT
P glycoprotein substrate - use in caution with MDR1 gene mutation
Contraindications: cardiogenic shock or severe CHF, hypotension, sick sinus syndrome, second or third degree AV block, digoxin intoxication, hypersensitivity to verapamil, IV administration contraindicated within a few hours of IV beta blocker administration
Atropine
Anticholinergic
competitively inhibits acetylcholine at postganglionic parasympathetic neuroeffector sites; salivation, bronchial secretions, GI motility, and cholinergic mediated sweating are inhibited at low doses; moderate doses: mydriasis, incraesed IOP, increased heart rate (and myocardial oxygen consumption), but HR may decrease initially; high doses - decreased urinary tract motility and very high doses inhibit gastric secretion
Shorter onset and duration of action compared to glycopyrrolate; also causes more profound tachycardia
Contraindicated - narrow angle glaucoma, posterior synechiae, tachycardia secondary to thyrotoxicosis, cardiac insufficiency, myocardial ischemia, HCM, bladder obstruction; contraindicated in treatment of poisoning with isoxazole mushrooms (amanita)
routine use of anticholinergics with or after alpha 2 agonists is neither recommended nor necessary
AE: generally dose dependent; dry mouth, GI, decreased secretions, urine retention, drowsiness, seizures, ataxia, respiratory depression, transient AV block, hypertension, postural hypotension, bradycardia, tachyarrhythmia, circulatory failure
Glycopyrrolate
Anticholinergic
Glycopyrrolate is an antimuscarinic with similar actions as atropine. It is a quaternary ammonium compound, and unlike atropine, glycopyrrolate does not appreciably cross the blood-brain and blood-placenta barriers. Therefore, CNS adverse effects and clinical effects in the fetus/newborn should not be exhibited. Antimuscarinic agents competitively inhibit acetylcholine or other cholinergic stimulants at postganglionic parasympathetic neuroeffector sites. High doses may block nicotinic receptors at the autonomic ganglia and at the neuromuscular junction. Pharmacologic effects are dose related. At low doses, salivation, bronchial secretions, and sweating (not in horses) are inhibited. At moderate systemic doses, glycopyrrolate increases heart rate. High doses decrease GI and urinary tract motility. Very high doses can inhibit gastric acid secretion.
Contraindicated in conditions where anticholinergic effects would be detrimental (eg, narrow-angle glaucoma, tachycardia, ileus, urinary obstruction). Not recommended for use in treating bradycardia secondary to dexmedetomidine
Adverse effects are dose related and anticholinergic in nature, including dry secretions; initial bradycardia, then tachycardia; slowing of gut and urinary tract motility; and mydriasis and cycloplegia
Benazepril
Angiotensin converting enzyme inhibitor
After being converted to benazeprilat, the drug inhibits the conversion of angiotensin I to angiotensin II by inhibiting ACE. Angiotensin II is a vasoconstrictor and stimulates production of aldosterone in the adrenal cortex. By blocking angiotensin II formation, ACE inhibitors generally reduce blood pressure in hypertensive patients and vascular resistance in patients with CHF. Decreased angiotensin II and aldosterone also reduce sodium/water retention and can limit cardiac fibrosis and remodeling. Aldosterone breakthrough (ie, insufficient suppression of aldosterone secretion) has been documented with ACE inhibitor use in healthy dogs and can occur in up to 30% of dogs with MMVD, with or without CHF.30
ACE inhibitors’ proteinuric-reducing effects are most likely a result of preferential vasodilation of the efferent glomerular arterioles which reduces intraglomerular hypertension. Reduction in glomerular hypertension may be accompanied by an increase in serum creatinine concentration.
Used to treat heart failure, systemic hypertension, chronic kidney disease (CKD), and proteinuria in dogs and cats
Not recommended for use in patients with acute kidney injury. Should be used with caution in volume-depleted patients, and in patients with increased serum creatinine, hyponatremia, or coronary or cerebrovascular insufficiency
Adverse effects are uncommon. GI disturbances are the most likely adverse effect, but hypotension, renal dysfunction, and hyperkalemia are possible.
Enalapril
Angiotensin converting enzyme inhibitor
Used to treat congestive heart failure (CHF), hypertension, chronic kidney disease (CKD), and proteinuria in dogs and cats
Enalapril is converted in the liver to the active compound enalaprilat which prevents the formation of angiotensin II, a potent vasoconstrictor, by competing with angiotensin I for ACE. ACE appears to have a much higher affinity for enalaprilat than for angiotensin I. Because angiotensin II concentrations are decreased, aldosterone secretion is reduced and plasma renin activity is increased (due to the negative feedback mechanism). However, aldosterone breakthrough (elevated secretion of aldosterone) has been consistently documented in dogs receiving enalapril and other ACE inhibitors, which may be due to angiotensin II reactivation, alternative renin–angiotensin–aldosterone pathways, or overriding effects in patients with activated ACE. In healthy dogs, enalapril partially blocks activation of the renin–angiotensin–aldosterone system (RAAS) caused by amlodipine and furosemide. Aldosterone breakthrough from ACE inhibition is independent of dose.
The cardiovascular effects of enalaprilat in patients with CHF include decreased total peripheral and pulmonary vascular resistance, mean arterial and right atrial pressures, and pulmonary capillary wedge pressure; unchanged or decreased heart rate; and increased cardiac index and output, stroke volume, and exercise tolerance.
ACE inhibitors increase renal blood flow and decrease glomerular efferent arteriole resistance. In animals with glomerular disease, ACE inhibitors may decrease proteinuria and may help to preserve renal function.
If hyponatremia and/or dehydration are present, correct these conditions prior to enalapril treatment. Should be used with caution in animals with dehydration, increased creatinine, hyperkalemia, hyponatremia, systemic lupus erythematosus (SLE), and hematologic disorders
Adverse effects are uncommon. GI disturbances are the most likely adverse effects, but hypotension, renal dysfunction, and hyperkalemia are also possible.
Amlodipine
Calcium channel blocker
Used for treatment of systemic hypertension
Dihydropyridine L type calcium channel blocker that inhibits voltage gated calcium channels in cardiac and vascular smooth muscle. Amlodipine has a higher affinity for L-type calcium channels and some affinity for T-type calcium channels. In the kidney, L-type calcium channels are found primarily in afferent (prerenal) arterioles. Amlodipine has a greater effect on vascular smooth muscle, where it acts as a peripheral arteriolar vasodilator and reduces afterload. Amlodipine slightly depresses impulse formation (automaticity) and conduction velocity in cardiac muscle. In dogs, amlodipine has mild diuretic activity after an initial dose.
Amlodipine has been shown to activate the RAAS when used as a single agent in healthy dogs at higher doses (≈0.6 mg/kg twice daily); use of amlodipine with an ACE inhibitor partially blocks this effect. Amlodipine also significantly increases plasma renin activity and activates RAAS in healthy and hypertensive cats.
Use in caution with heart disease, liver dysfunction, if at risk of hypotension
AE: anorexia, hypotension, gingival hyperplasia
Telmisartan
Angiotensin II receptor blocker
Selectively blocks AT 1 receptor, aldosterone synthesis and secretion are reduced, causing vasodilation and deceased potassium and increased sodium excretion. plasma concentrations of renin and AG II are increased, but this does not counteract the blood pressure lowering effects of telmisartan. Does not interfere with substance P or bradykinin responses; in cats - does not affect potassium excretion
May be useful in dogs for the adjunctive treatment of proteinuria and systemic hypertension secondary to chronic kidney disease (CKD)
Indicated in cats for control of systemic hypertension; may also be used for treatment of proteinuria associated with CKD
AE: In dogs, adverse GI effects (eg, inappetence, vomiting, diarrhea) and increases in serum creatinine have been reported. In cats, adverse GI effects (eg, vomiting, diarrhea) and lethargy are most commonly reported; hypotension, increases in liver enzymes, and anemia are possible but uncommon.
Diltiazem
Nondihydropyridine Calcium channel blocker
class IV antiarrhythmic; inhibits the transmembrane influx of extracellular calcium ions into cardiac vascular smooth muscle cells. The nondihydropyridines act by blocking inward movement of calcium via L type calcium channels which prolongs the refractory period and slows nodal conduction (negative dromotropy). associated with weak negative ionotropic effects compared with other calcium channel blockers. Slows AV node conduction, prolongs PQ interval and prolongs refractory times. Primary effect for SVT is slowing of AV nodal conduction and improved control of ventricular response rate. rarely affects sinoatrial node activity, but in patients with sinus node dysfunction, diltiazem is contraindicated, as resting heart rates may be reduced.
Used in dogs, cats, and ferrets for supraventricular tachycardias (SVTs) and as adjunctive therapy for systemic or pulmonary hypertension.
Contraindications include severe hypotension, sinus node dysfunction, high-grade atrioventricular (AV) block, concurrent radiographically documented pulmonary congestion or edema, acute myocardial infarction, and hypersensitivity.
Use with caution in geriatric patients or in those with controlled heart failure (particularly if also receiving beta blockers) or hepatic or renal impairment
Hydralazine
Vasodilator
Used for systemic hypertension or adjunctive treatment of CHF
acts upon vascular smooth muscle and reduces peripheral resistance and blood pressure (BP). Hydralazine is a semicarbazide-sensitive amine oxidase (SSAO) inhibitor. It is believed that hydralazine alters cellular calcium metabolism in smooth muscle, thereby interfering with calcium movements and preventing the initiation and maintenance of the contractile state. Hydralazine has more effect on arterioles than on veins
With congestive heart failure (CHF), hydralazine significantly increases cardiac output and decreases systemic vascular resistance. Cardiac rate may be slightly increased or unchanged, while BP, pulmonary venous pressure, and right atrial pressure may be decreased or unchanged.
When hydralazine is used to treat primary or secondary systemic hypertension, increased heart rate, cardiac output, and stroke volume can be noted. Hydralazine may activate the renin-angiotensin system, and in humans, it has been documented to increase sodium and water retention if not given with diuretics.
Parenteral hydralazine administration can cause respiratory stimulation.
Contraindications - hypovoleia, pre-existing hypotension
Caution in patients with severe renal disease, intracranial bleeding, or pre-existing autoimmune diseases
Adverse effects include hypotension, reflex tachycardia, sodium/water retention, GI distress (ex. vomiting, diarrhea), can increase creatinine levels due to decreased renal perfusion.
Nitroglycerine
Venodilator, afterload reducer
Transdermal, oral, & injectable venodilator; occasionally used topically in veterinary medicine for congestive heart failure (CHF) or hypertension
Relaxes smooth muscle, primarily on venous side, but can have a dose related effect on arterioles as well. Pre load is reduced from peripheral pooling of blood and decreased venous return to the heart; afterload may also be reduced; myocardial oxygen demand and workload are reduced and coronary circulation can be improved
Continuous use results in tolerance after 48 to 72 hours.
Contraindicated with anemia; use with caution in patients with cerebral hemorrhage, head trauma, diuretic induced hypovolemia, other hypotension
AE: rash at application site, hypotension, transient headaches
Nitroprusside
vascular, smooth muscle relaxant for acute/severe hypertension
Provides intracellular nitric oxide, which activates guanylate cyclase. produces increase in intracellular cyclic GMP, which inhibits vascular smooth muscle contraction. It is an immediate acting IV hypotensive agent that directly causes peripheral vasodilation independent of autonomic innervation. Produces lowering of blood pressure, increase in heart rate, mild decrease in cardiac output, and significant reduction in total peripheral resistance. Preload, afterload, and left ventricular end diastolic pressures are reduced. Tolerance does not develop.
Used in acute heart failure secondary to mitral regurgitation and in combination with dobutamine for refractory congestive heart failure.
Drug of choice in animals under general anesthesia to treat severe hypertension from phenochromocytoma
contraindicated in compensatory hypertension, inadequate cerebral circulation; use with caution in geriatric patients, those with hepatic insufficiency, severe renal impairment, hyponatremia, cobalamin deficiency, hypothyroidism
Adverse effects include hypotensive effects; potentially - nausea, retching, restlessness, apprehension, muscle twitching, dizziness
Dobutamine
Parenteral, rapid acting positive ionotrope used to improve cardiac output
Direct beta 1 adrenergic agonist that increases cardiac contractility and improves cardiac output; mild beta 2 and alpha 1 adernergic effects which balance each other and cause little direct effect on the systemic vasculature
in contrast to dopamine, dobutamine does not cause the release of norepinephrine. mild chronotropic, arrhythmogenic, and vasodilative effects, but higher doses can cause tachycardia; increased myocardial contractility and stroke volume result in increased cardiac output, which also increases myocardial oxygen demand and coronary artery blood flow
Contraindicated in patients with idiopathic hypertrophic subaortic stenosis; use in caution with patients with pre existing arrhythmias; ensure ventricular rate is controlled in animals with atrial fibrillation prior to administration
AE: facial twitching and tachycardia; tremors, seizures in cats with higher doses
Dobutamine can initiate the Bezold–Jarisch reflex, which is an inhibitory reflex that causes hypopnea, bradycardia, and hypotension
achyphylaxis (a rapid decrease in drug response) may occur within 72 hours of starting dobutamine therapy; increased dosages may be required to achieve the desired effect. In dogs with pulmonary hypertension, dobutamine increased pulmonary arterial pressure
Epinephrine
Alpha adrenergic agonist; beta adrenergic agonist
Endogenous adrenergic agent with alpha and beta receptor activity. Relaxes smooth muscles in the bronchi and iris, antagonizes the effects of histamine, increases glycogenolysis, and increases blood glucose concentration. Low dose directly stimulates beta 1 adrenergic receptors to cause increased heart rate and contractility with resultant increased cardiac output. myocardial work and oxygen consumption increase. in the periphery, epinephrine activates beta 2 adrenergic receptors, causing a decrease in peripheral vascular resistance, which lowers diastolic blood pressure. when administered at higher doses, peripheral vascular resistance increases due to alpha 1 adrenergic effects.
Vasopressor used systemically for treatment of anaphylaxis, cardiopulmonary arrest, and refractory hypotension, as well as to prolong the effects of local anesthetic agents
relative contraindications - closed angle glaucoma, shock due to nonanaphylactic causes, during parturition (may delay the second stage), dilated cardiomyopathy, thyrotoxicosis, acute or uncontrolled hypertension, toxemia of pregnancy
AE: tremors, excitability, vomiting, hypertension, tachycardia, other arrhythmias, pulmonary edema, hyperglycemia, behavior changes, lactic acidosis; Tissue necrosis SC injections, extravasation reaction
Isoproterenol
Beta adrenergic agonist
Beta 1 and beta 2 agonist with no appreciable alpha adrenergic activity at therapeutic doses. result of stimulating cyclic AMP production. primary actions are increased inotropism and chronotropism, relaxation of bronchial smooth muscle, and peripheral vasodilation. May increase perfusion to skeletal muscle. Inhibits antigen mediated releases of histamine and slow releasing substance of anaphylaxis. hemodynamic effects include decreased peripheral resistance, increased cardiac output, increased venous return to the heart, and increased rate of discharge by cardiac pacemakers. Isoproterenol can increase myocardial oxygen requirements while also decreasing coronary perfusion.
Nonselective beta-adrenergic agonist used for acute bronchial constriction, cardiac arrhythmias (complete AV block), and as adjunctive therapy in shock or heart failure
Contraindications include tachyarrhythmias, ventricular arrhythmias that do not require increased inotropic activity, and tachycardia or AV block caused by cardiac glycoside intoxication
Use caution in patients with coronary insufficiency, hyperthyroidism, renal disease, hypertension, or diabetes; not a substitute for adequate fluid replacement in shock
Adverse effects include tachycardia, hypotension, anxiety, tremors, excitability, headache, weakness, and vomiting; more arrhythmogenic than dopamine or dobutamine
