Hypotensive agents Flashcards
Change in vessels of older patients
less compliant vessels –> increased workload on heart
–> high systolic and low diastolic = wide PP
Sodium Nitroprusside MOA
relax arterial and venous smooth muscle
-> released NO -> (+) guanylyl cyclase –> cGMP -> relaxation
Sodium Nitroprusside characteristics
potent and reliable
RAPID onset (1-2 minutes)
- photodegradation if exposed to light
*it is metabolized by entering RBC and receives Fe2+
–> forms cyanide that can lead to toxicity
CV Effects of Nitroprusside
decreased preload and afterload -> may get increased CO with CHF
- reflexive tachycardia
- intracoronary steal
CNS Effects of Nitroprusside
- dilates the cerebral vessels -> abolishes cerebral autoregulation => increased CBF and ICP
Pulm Effects of Nitroprusside
- pulmonary vasculature dilation -> decreased perfusion -> increased dead space
Nitroglycerin MOA
relaxes vascular smooth muscle –> predominantly venous dilation
- NO causes vasodilation
CV Effects of Nitro
relieves myocardial ischemia, hypertension and ventricular failure –> with decreased preload you get decreased myocardial stretching
*redistributes blood flow to the coronaries
Metabolism of Nitro
rapid reductive hydrolysis in liver and blood
Hydralazine MOA
relaxes smooth muscle -> precapillary dilation of resistance vessels
- Onset of 15 minutes, lasts 4-6 hrs
- causes reactive tachycardia and contractility
- inhibits cerebral regulation
Hydralazine metabolism
Acetylation and hydroxylation in the liver
Fenoldapam MOA
RAPID vasodilation by selectively activating D1 receptors
- moderate affinity for alpha 2 receptors
Fenoldapam effects
reduces systolic and diastolic blood pressure in patients with malignant hypertension
SE of Fenoldapam
headache, flushing, nausea, tachycardia, hypokalemia
Metabolism of Fenoldapam
conjugation of CyP 450
