Vasodilators Flashcards
Clonidine
1) Indications
2) Onset, Peak, DOA, Half life
3) Metabolism
1) Treat sympathetic hyperreactivity and gastrointestinal hyperactivity seen in withdrawal.
2) "Onset 30-60mins Peak 60-9mins DOA 8 hrs PO E1/2t 9-12hrs E1/2L = 12-24 hrs 30% PB 2L/kg"
3) 50% metabolized in liver, 50% excreted unchanged
Clonidine
1) Class
2) Action
1) Selective Alpha2 adrenergic antagonist
2) “Inhibits sympathetic outflow from the medulla = decreased HR and contractility and vasomotor tone.
Enhance antinociceptive state by inhibiting release of spinal substance P.
Inhibit central thermoregulatory control to decrease vasoconstriction and shivering.
Also affects the function of K+ channels in the CNS = making cell hyperpolarized = decreased anesthetic requirements”
Clonidine: Adverse Effects
"Bradycardia, heart failure Hepatotoxicity Dry motuh Sedation Postural hypotension Skin rash impotence Rebound hypertension with abrupt withdrawal of clonidine Sodium and water retention"
Clonidine
1) Contraindications
2) Dosage
1) “Pregnant women
Prior to surgery
Hypersensitivity”
2) “0.2mg-0.3mg/day
Epidural and SAB = 150-450mcg
Do not dc abruptly”
Hydralazine (apresoline)
1) Class
2) Action
1) Vasodilator
2) “Activates guanylate cyclase = membrane hyperpolarization, K+ channel activation, inhibition of IP3-induced calcium release from SR in vascular smooth muscle
Direct acting vasodilator, decreased MAP
Trigger reflexive tachycardia”
Hydralazine (Apresoline)
1) Indications
2) Onset, peak, & Half life
3) Metabolism
1) “Arteriolar smooth muscle dilation >venous
Potent pulmonary arterial dilator
Moderate to severe HTN
Used in HF with isosorbide
HTn in preeclampsia
Increases splanchnic, coronary, cerebral, uterine, and RBF”
2) "IV onset 5-20mins Peak 15-20mins E1/2t = 4 hrs (16hrs in renal dz) E1/2L = 100hrs bc binding to strong binding to smooth muscle 90% PB"
3) Acetylyzed in the liver with extensive first pass effect.
Hydralazine (Apresoline) : Adverse effects
“Increased ICP, head ache, fever, chills, anxiety, disorientation, depression and coma
RA, Lupus like syndrome, cramps, weakness, tremors, neuritis
Tachycardia, angina, orthostatic hypotension, dizziness, palpitations,
Nasal congenstion, dyspnea
Anorexia, NV, diarrhea, constipation, ileus
Impotence, difficult micturition
Anemias, hepatotoxicity, “
Hydralazine (Apresoline)
1) Contraindications
2) Dosage
1) “Hyperstentivity
Dissecting aortic aneurysm, CAD, mitral valve rheumatic heart disease
Prolonged onset should be considered before redosing”
2) “2.5-20mg IV Q4hrs or prn
10-40mg IM
10-100mg PO Q6hrs
(decreased dose for renal pts)”
Nitroglycerin (NTG)
1) Class
2) Action
1) Organic Nitrate - VENOdilator
2) Generates Nitric Oxide to stimulate production of cGMP to cause periph and smooth muscle vasodilator. Increased venous capacitance decreases the preload to the right side of the heart = decreased right and left end diastolic pressure = decreased Myocardial demand
Nitroglycerin (NTG)
1) Indications
2) Peak & Half life
3) Metabolism
1) “Treat stable and unstable MI, angina, hypetension, heart failure, elevated cardiac filling pressure in CHF, Coronary vasospasm
Cocaine induced MI
Controlled hypotension to decrease surgical bleeding
Dilate sphincter of oddi”
2) “IV peak
3) Metabolism results in nitrate metboliate capable of producing methgb by oxidation of ferrous ion in hgb (treat with methylene blue 1-2mg/kg)
Nitroglycerin (NTG): Adverse Effects
“Dizziness, lightheadedness syncope
Mi, reflex tachycardia, cyanosis, NV
Tachycardia tachypnea, coma, convulsion, death
Increase in ICP with decreased intracranial compliance flushing and increased bleeding time.”
Nitroglycerin (NTG)
1) Contraindications
2) Dosage
1) “Hypertrophic obstructive cardiomyopathy
Severe aortic stenosis, hypotension, shock or mi with love left ventricular filling pressures
Increased ICP,glaucoma, angina, severe anemaia, cardiac tamponade, restrictive cardiomyopathy or pericarditis”
2) “Initial 5-10mcg/min IV, titrate in range of 5-200mcg/min IV (0.1-4mcg/kg/min)
Sublingual 0.15-0.6mg PRN onset 1-5 mins”
Milrinone
1) Class
2) Action
1) Bypyridine inotropic/vasodilator agent with phosphodiesterase inhibitor activity.
2) Selectively inhibits phosphodiesterase III which is a heart specific enzyme responsible for degradation of camp. By preventing the degradation of camp and cGMP in myocardium and vascular smooth muscle the increased concentrations activate protein kinases the promote phosphorylations and intracellular calcium stores. The increased calcium = increased contractility and inotropic effects. Increased cAMP works in vascular smooth muscle to cause vasodilation and decrease periph vasc resistance. This all increases CO.
Milrinone
1) Indications
2) Onset, Peak, Half Life & Vd
3) Metabolism
1) “Short term tx of acute decompensated heart failure
Manamange of acute left ventric dysfunction after cardiac surgery
Tx calcium CB intoxication
Short term IVtherapy for congestive heart failure
Inotrope of choice for severe congestive heart failure in pts taking BB”
2) "Onset 5-15mins Peak after 5 mins E1/2time = 2.5hrs Vd = 0.4L/kg 70% PB"
3) 80% unchanged in the urine
Milrinone: Adverse Effects
"SE: Cardiac dysrhythmias, ventricular arrhythmias, and Supraventric arrhythmias Hypotension Angina Headaches Hypokalemia, tremor, thrombocytopenia"
