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
Effects of Fenoldapam on renal flow
Significantly increases blood flow to the kidneys due to the dopamine receptor action
