Anti-HTN / BBs Flashcards
Hydralazine
Hydralazine
Class: Direct acting vasodilator, arteries > veins
MOA:
Activates guanylate cyclase, increases cyclic GMP, inhibits IP3 release of calcicum+ from SR, leading to vasodilation.
Dilates arteries > veins, leads to decrease in SVR and BP.
Pk:
Onset immediate but peak effect takes 15 minutes.
DOA: 6 hours
E12/T: 2 hours
PB: high
vd ?
Metabolized by liver, excreted in urine.
Dose:
2.5 to 10 mg IV in the OR
5 to 20 mg IV q 4 hours - ICU
SE:
Reflex tachycardia
decrease in DBP can lead to angina with EKG changes
r/f MI - usually perscribed with BB and anti-diuretics
decrease in CO leads to activation of RAAS
can have H2O + Na retention
Increase in ICP r/t cerebral dilation
Lupus like syndrome!!
Tachyphylaxis can occur!!
C/I:
Caution in patients with CAD
MUST wait appropirate amount of time between doses
Sodium Nitroprusside
Sodium Nitroprusside
Direct NON-selective vasodilator.
Equally dilates veins and arteries
MOA:
SNP reacts with ferrous ion on HGB and forms nitric oxide, methemglobin, and cyanide ions. The nitric oxide then activates gaunylate cyclase to increase cyclic GMP and inhibit calcium entry into vascular smooth muscle and increase uptake of calcium into SR resulting in vasodilation.
Lacks significant effect on non-vascular smooth muscle.
Uses:
most potent vasodilator in the OR
Used in pheochromacytoma or to decrease afterload in CHF.
PTs MUST HAVE A-LINE FOR SNP.
Pk:
Onset: immeditate
DOA: short
E1/2T: 5 minutes
requires IV gtt to maintain therapeutic effect
must have A-line.
Metabolism; so SNP interacts with HGB to form three products: NO, cyanide, and methemglobin. 1/5 of the cyanide ions combine with methemoglobin to make cyano-methoglobin with is nontoxic. The other 4/5 of the cyanide are metabolized by the liver and kidneys to thiocynate.
Dose:
0.3 to 10 mcg/kg/min
controlled hypotension: 0.3 to 0.5 mcg/kg/min
normal dose for HTN crisis would be 1 to 2 mcg/kg as a bolus.
R/F cyanide toxicity at rates of 2 mcg/kg/min for prolonged period of time.
Should not be at max dose of 10 mcg/kg/min for longer than 10 minutes.
SE:
increased ICP
Coronary artery vasodilation - r/f coronary steal
reflex tachycardia with increased contractility
attenuate pulmonary hypoxic vasoconstriction, decrease PVR
Can interfere with plt aggregation and increase bleeding time.
Cyanide toxicity 2 mcg/kg/min for long periods of time.
Also thiocyanate toxicity and methemoglobinemia.
SNP must be protected from exposure to light!!!
C/I:
Increase ICP / renal failure
caution in CAD/ hypotension.
c/i in cardio hypertrophy, aortic stenosis.
Labetalol
Labetalol
Non selective beta blocker with weak alpha1 adrenergic antagonism. Relative beta to alpha block is 7:1
MOA:
Blocks adrenergic receptors from stimulation by catecholamines, results in decreased SVR, BP, HR, contractility, but CO IS MAINTAINED.
Pk:
onset: 5 minutes
DOA: 4 hours
E1/2t: 5-8 hours
PB: 50%
Metabolized by CYP2D6, excreted in urine.
SE:
Bradycardia, hypotension
ANGINA
BRONCHOSPASM
Masks hypoglycemia effects
exercise intolerance
worsen PVD symptoms
C/I:
Asthma, COPD
DM
Cardiogenic shock/CHF
EFFECT IS DECREASED BY SALICYLATES, NSAIDs
Avoid concurrent use with CCBs.
Esmolol
Esmolol
Cardioselective beta blocker, class II anti-arrthymic
MOA:
Blocks the effects of catecholamines at B1 receptors, decreases HR by decreasing automaticity at SA/AV node, decreases contractility, decreases BP, decreases myocardial oxygen demand.
Class II anti-arrthymic, blocks the effects of increases SNS stim that are often associated with ischemia. Can attenutate SNS stim from DVL
Pk:
Onset: immediate
DOA: <15 minutes
e1/2T: 9 minutes
Hydrolyzed quickly by plasma esterases.
Dose:
0.5 mg/kg IV bolus followed by
50-300 mcg/kg/min gtt
SE:
At low doses can decrase HR without altering BP
Hypotension, bradycardia, HB
blocks symptoms of hypoglycemia
can have bronchconstriction at high, prolonged doses
C/I:
asthma/copd r/t bronchospasm
DM.
Cardiogenic shock / CHF
Hypotension / bradycardia
EFFECT DECREASED BY SALICYLATES / NSAIDs
avoid concurrent admin with CCBs
Metroprolol
Metroprolol
Cardioselective beta blocker, class II antidysrthmic.
MOA:
Blocks the effects of catecholmines at B1 receptors and inhibits the GPCR GaS signalling cascade, resulting in decrease HR, decrease SA/AV automaticity, decrease BP, decrase contractilty, decrease O2 demand.
Class II anti dysrthymic helps block teh effects of increases SNS stim usually accompanying myocardial ischemia, used in both atrial and ventricular tachyarrthymias.
Pk:
onset: 5 minutes
DOA: 7 hours
E1/2T: 3-4 hours
metabolized by liver, cyp-2d6. Undergoes high first pass if PO. <5% eliminated unchanged in kidneys.
SE:
Hypotension, bradycardia, HB
masks the effects of hypoglycemia
can cause bronchoconstriction at high doses for prolonged periods.
DEPPRESSION, INSOMNIA -> CROSSES BBB
C/I:
DM
Hypoglycemiai
caution in asthma/copd
cardiogenic shock
hypotension, bradycardia
EFFECTED DECREASED BY SALICYLATES, NSAIDs
Avoid concurrent use with CCB
Nitroglycerine
Nitroglycerine
Class: organic nitrate
MOA:
Reacts with mitochondrial aldehyde dehydrogenase, thio containing compound, to produce nitric oxide. NO then activates guanylate cyclase which increases gCMP and then increases protein kinase G. Leads to cascade of events that results in dephosphorylation of myosin light chains and sequetration of calcium into smooth ER, leading to vasodilation.
Decreases preload, venous return without altering SVR, HR. Works primarily on venous capacitance vessels and large coronary arteries. Will dilate coronary arteries to ischemic areas preferentially, avoiding coronary steal phenomenon.
Pk:
Onset: Immediate
DOA: 5 minutes
E1/2t: 1.5 minutes
PB: 60%
VD: Large
Metabolized rapidly with nitrate metabolitethat is capable of producing methemoglobin by oxidation of ferrous to ferric ion in Hgb, <1% excreted unchanged in urine.
dose:
10-20mcg/min = controlled hypotension
50-200 mcg/min is regular dose
200 mcg bolus for SOO spasm
SE:
Vasodilation - Increase ICP, HA
NTG tolerance can occur after 24 hours, need some time without exposure.
Bronchodilation, attenutaes hypoxic pulmonary vasoconstriction
Dose dependent - prolongation of bleeding time, inhbits platelet aggregation
relaxation of sphincter of oddi
C/I:
orthostatic hypotension
cranial surgery or increased ICP
hypertrophic cardiomyopathy
caution for s/sx of methemoglobinemia
do not give within 24 hrs of phosphodiesterase type 5 inhibitors
