Term
Mechanism of Action for Norepinephrine (Levophed)
•Vasopressor
•Sympathomimetic |
|
Definition
•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. |
|
|
Term
Indications for Norepinephrine (Levophed)
•Vasopressor
•Sympathomimetic |
|
Definition
•Hemodynamically significant hypotension refractory to other sympathomimetics
•Cardiogenic shock
•Used more often with low SVR states (e.g., sepsis) than in MI-related hypotension |
|
|
Term
Contraindications for Norepinephrine (Levophed)
•Vasopressor
•Sympathomimetic |
|
Definition
•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. |
|
|
Term
Mechanisms of Action for Phenylephrine (Neo-synephrine)
•Vasopressor |
|
Definition
•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 |
|
|
Term
Indications for Phenylephrine (Neo-synephrine)
•Vasopressor |
|
Definition
•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 |
|
|
Term
Contraindications for Phenylephrine (Neo-synephrine)
•Vasopressor |
|
Definition
•Severe coronary disease or hypertension
•Hypotension due to hypovolemia
•Ventricular tachycardia
•Cautious use in thyroid dysfunction, diabetes mellitus, myocardial disease, bradycardia, or cerebral atherosclerosis |
|
|
Term
Mechanisms of action for Dopamine (Inotropin)
•Vasopressor |
|
Definition
•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 |
|
|
Term
Indications for Dopamine (Inotropin)
•Vasopressor |
|
Definition
•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) |
|
|
Term
Contraindications for Dopamine (Inotropin)
•Vasopressor |
|
Definition
•Cardiogenic shock
•Uncorrected tachyarrhythmias
•Ventricular fibrillation
•Hemodynamically significant hypotension, in presence of hypovolemia (SBP < 70 mmHg) |
|
|
Term
| Extravasation causes tissue necrosis and sloughing. What should you use? |
|
Definition
| Use Phentolamine (Regitine), 5 - 10 mg diluted in 15 ml of 0.9% NSS to minimize damage). |
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|
Term
Mechanisms of Action for Dobutamin (Dobutrex)
•Vasopressor |
|
Definition
•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 |
|
|
Term
Indications for Dobutamin (Dobutrex)
•Vasopressor |
|
Definition
•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 |
|
|
Term
Contraindications for Dobutamin (Dobutrex)
•Vasopressor |
|
Definition
•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 |
|
|
Term
Mechanisms of action for Vasopressin
•Antidiuretic
•Hemostatic |
|
Definition
•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) |
|
|
Term
Indications for Vasopressin
•Antidiuretic
•Hemostatic |
|
Definition
•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 |
|
|
Term
Contraindications for Vasopressin
•Antidiuretic
•Hemostatic |
|
Definition
•None during cardiac arrest
•Ischemic coronary artery disease or advanced arteriosclerosis
•Renal failure |
|
|
Term
| Drug of choice in low cardiac output states due to RV infarction |
|
Definition
|
|
Term
Mechanisms of Actions for Nitroglycerin (NTG)
•Antianginal
•Vasodilator |
|
Definition
•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). |
|
|
Term
Indications for Nitroglycerin (NTG)
•Antianginal
•Vasodilator |
|
Definition
•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) |
|
|
Term
Contraindications for Nitroglycerin (NTG)
•Antianginal
•Vasodilator |
|
Definition
•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). |
|
|
Term
Mechanisms of Action for Morphine Sulfate
•Narcotic analgesic |
|
Definition
•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. |
|
|
Term
Indications for Morphine Sulfate
•Narcotic analgesic |
|
Definition
| •Moderate to severe pain •Pain and anxiety relief during acute MI •Acute cardiogenic pulmonary edema (congestive heart failure) |
|
|
Term
| Contraindications for Morphine Sulfate •Narcotic analgesic |
|
Definition
| •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 |
|
|
Term
| Less likely to induce tachycardia at therapeutic doses than isoproterenol or dopamine |
|
Definition
|
|
Term
| May be combined with dopamine to increase cardiac output, SVR, and preload. |
|
Definition
|
|
Term
| What is different in the Mechanism of Action when taking Nitroglycerin (NTG) sublingually? |
|
Definition
| It decreases filling pressures of the heart without lowering SVR |
|
|
Term
| Drug of choice for acute angina pectoris attacks that are exertional or typical in nature |
|
Definition
Nitroglycerin (NTG)
-sublingual |
|
|
Term
| Which drug is used for maintenance for chest pain prophylaxis? |
|
Definition
Nitroglycerin (NTG)
-transdermal ointment |
|
|
Term
Mechanisms of Action for Sodium Nitroprusside (Nipride)
•Vasodilator
•Anti-hypertensive |
|
Definition
| •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 |
|
|
Term
| Medication classifications for Sodium Nitroprusside |
|
Definition
•Vasodilator
•Anti-hypertensive |
|
|
Term
| Indications for Sodium Nitroprusside (Nipride) |
|
Definition
•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 |
|
|
Term
| Precautions for Sodium Nitroprusside (Nipride) |
|
Definition
•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) |
|
|
Term
| Contraindications for Sodium Nitroprusside (Nipride) |
|
Definition
•Treatment of compensatory hypertension (A-V shunt or coarctation of the aorta)
•Known inadequate cerebral perfusion
•Use cautiously in renal or hepatic dysfunction |
|
|
Term
| What are the drugs that cause Arteriolar Dilation? What do they decrease? |
|
Definition
-Nitroprusside, Hydralazine, Ca++ antagonists, Alpha blockers, Beta-2 stimulants, Nitrates, Nesiritide
-They decrease Afterload |
|
|
Term
| What are the drugs that cause venous dilation? What do they decrease? |
|
Definition
-Nitrates, Nesiritide, Nitroprusside, Furosemide, ACE inhibitors
-They decrease Preload |
|
|
Term
| What is the medication classifications for Hydralazine (Apresoline) |
|
Definition
•Anti-hypertensive
•Direct vasodilator |
|
|
Term
| Mechanisms of Action for Hydralazine (Apresoline) |
|
Definition
•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). |
|
|
Term
Indications for Hydralazine (Apresoline)
•Anti-hypertensive
•Direct vasodilator |
|
Definition
| •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 |
|
|
Term
| Medication Classification for Inamrinone (Inocor) |
|
Definition
|
|
Term
| Mechanisms of Action for Inamrinone (Inocor) |
|
Definition
•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. |
|
|
Term
| Indications for Inamrinone (Inocor) |
|
Definition
•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 |
|
|
Term
| Medication classifications for Norepinephrine (Levophed) |
|
Definition
| •Vasopressor •Sympathomimetic |
|
|
Term
| Mechanisms of Action for Milrinone (Primacor) |
|
Definition
•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 |
|
|
Term
| Medication Classifications for Milrinone (Primacor) |
|
Definition
|
|
Term
| Indications for Milrinone (Primacor) |
|
Definition
•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 |
|
|
Term
| Use cautiously in patients with atrial flutter or fibrillation due to shortening of AV nodal conduction time and potential for increased ventricular response. |
|
Definition
|
|
Term
| You avoid infusing this drug in the same IV line as Furosemide (Produces a precipitate) |
|
Definition
|
|
Term
| Medication Classification for Digitalis (Digoxin, Lanoxin) |
|
Definition
|
|
Term
| Mechanisms of Action for Digitalis (Digoxin, Lanoxin) |
|
Definition
•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). |
|
|
Term
| Indications for Digitalis (Digoxin, Lanoxin) |
|
Definition
| •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 |
|
|
Term
| Medication Classifications for Furosemide (Lasix) |
|
Definition
•Antihypertensive
•Diuretic |
|
|
Term
| Mechanisms of Action for Furosemide (Lasix) |
|
Definition
•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 |
|
|
Term
| Indications for Furosemide (Lasix) |
|
Definition
•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 |
|
|
Term
| What does Nitroglycerin Dilate? What does this reduce? |
|
Definition
-Dilates collateral circulation, venous capacitance, large coronary arteries
-decreases preload, which decreases ventricular contractility and MVO2 |
|
|
Term
| Which drug increases cardiac output and enhances systolic emptying? |
|
Definition
| Sodium Nitroprusside (Nipride) |
|
|
Term
| What does Dobutamine decrease and what does it enhance? |
|
Definition
-Decreases preload and afterload
-Enhances myocardial contractility, stroke volume and cardiac output.
(Also improves renal blood flow and increases urine output) |
|
|
Term
| What may potentiate the effects of Dopamine (Inotropin)? |
|
Definition
| Monoamine oxidase (MAO) inhibitors |
|
|
Term
| What drug can you use for Heart failure with pulmonary congestion that is refractory to diuretics? |
|
Definition
| Sodium Nitroprusside (Nipride) |
|
|
Term
| You should use this drug with extreme caution in patients with inferior wall MI (likelihood of concomitant right ventricular infarction which requires maintenance of preload) |
|
Definition
|
|
Term
| Inamrinone (Inocor) and Milrinone (Primacor) both cause increased contractility and vasodilation. How do they differ in their Mechanisms of actions? |
|
Definition
-Inamrinone (Inocor) reduces preload
-Milrinone (Primacor) reduces afterload |
|
|
Term
| What drug is indicated for severe CHF refractory to diuretics, vasodilators, and conventional inotropic agents |
|
Definition
|
|
Term
| What drug promotes hemodynamic improvements in patients with CHF from ischemic heart disease |
|
Definition
|
|
Term
| Digitalis (Digoxin, Lanoxin) toxicity is treated with what? |
|
Definition
| Toxicity and overdose treated with Digoxin Immune Fab (Digibind) |
|
|
Term
| Verapamil and quinidine can double or triple serum levels of |
|
Definition
| Digitalis (Digoxin, Lanoxin) |
|
|
Term
| Beta-adrenergic blockers may increase ectopic beats with what drug on board? |
|
Definition
| Digitalis (Digoxin, Lanoxin) |
|
|
Term
| Contraindications for Furosemide (Lasix) |
|
Definition
•Anuria (not beneficial in patients with renal failure)
•Hypersensitivity to sulfonamides
•Chronic metabolic alkalosis or hyperkalemia
•Hypotension or severe dehydration |
|
|
Term
| Drug used for stress test echocardiography |
|
Definition
Dobutamine (Dobutrex)
•Vasopressor
|
|
|
Term
| Drug used to treat hypotension with pulmonary congestion and dysfunction (e.g., CHF, Cardiogenic shock) |
|
Definition
Dobutamine (Dobutrex)
•Vasopressor |
|
|
Term
| Increases aortic root baroreceptor sensitivity |
|
Definition
| Digitalis (Digoxin, Lanoxin) |
|
|
Term
| Digitalis (Digoxin, Lanoxin) has a mild positive inotropic effect due to what? |
|
Definition
Increased calcium in the sarcoplasmic reticulum
(Increases contractility) |
|
|
Term
| May be used in conjunction with cardiac glycosides or other vasodilators in short-term treatment of CHF |
|
Definition
Hydralazine (Apresoline)
•Anti-hypertensive
•Direct vasodilator |
|
|
Term
| What does Digitalis (Digoxin, Lanoxin) do to the action potential? This could result in what? |
|
Definition
Increases slope of phase 4 of the action potential
(May induce delayed after-depolarizations in the Purkinje cells; Results in ectopy) |
|
|
Term
| Digitalis (Digoxin, Lanoxin) alters the ECG. What will happen to the PR interval, ST segment, T wave and QT interval? |
|
Definition
-Increases the PR interval
-Depresses the ST segment; characteristic ST segment scooped appearance
-Flattens or inverts T waves
-Shortens the QT interval |
|
|
Term
| With this drug you should use the vein of the antecubital fossa or a central line to prevent extravasation. |
|
Definition
Phenylephrine (Neo-synephrine)
-Vasopressor
-Sympathomimetic |
|
|
Term
| What is the most common side effect of Nitroglycerine (NTG)? What is the most severe side effect and how should you treat it? |
|
Definition
•Headache (most common side effect; treat with aspirin or Tylenol)
•Hypotension (most severe side effect; treat with trendelenberg position and IV fluid bolus) |
|
|
Term
| What dose of Inamrinone (Inocor) will increase cardiac output, decrease SVR and decrease Preload? |
|
Definition
|
|
Term
| Furosemide (Lasix) inhibits the reabsorption of sodium and chloride where? |
|
Definition
| in the proximal and distal tubules and in the loop of Henle |
|
|
Term
| What drug is best for patients with unstable angina or for continuous treatment of Acute MI? |
|
Definition
|
|
Term
| This drug may cause right-to-left shunt in presence of atrial septal defect (ASD) or ventricular septal defect (VSD), leading to hypoxia and cyanosis |
|
Definition
|
|
Term
| Milirinone (Primacor) causes an overall improvement in what? |
|
Definition
| Myocardial contractility, ejection fraction and cardiac output |
|
|
