Vasodilators Flashcards
Idiopathic HTN
- overactivity of the ANS and an interaction with RASS and factors related to Na homeostasis and intravascular volume
causes of perioperative HTN
- hypercarbia
- hypoxia
- aortic cross clamp
- hypervolemia
- hypothermia
- pain
- airway manipulation
primary cause of peri-op HTN
- increased sympathetic discharge with sympathetic vasoconstriction
prevalence of peri-op HTN
~ 80% of cardiac surgery patients
~ 25% of non-cardiac surgery patients
- does not have to be a diagnosis of HTN
vasodilators MOA
- direct smooth muscle dilation (production of smooth muscle NO)
types of vasodilators
- alpha 1 antagonists (prazosin and labetalol)
- alpha 2 agonists (clonidine, alpha methyldopa)
- ACE inhibitors (captopril, enalapril)
how vasodilators are classified according to their predominate site of action
- arterial dilators
- venodilators
- balanced vasodilators
hemodynamic effects of vasodilators
- pure arteriole dilators cause minimal effects of preload
- pure venodilators do not exist
- balanced vasodilators decrease afterload and preload
reflex response to vasodilators
- reflex increase in HR (baroreceptors)
- redistribution of coronary blood flow (may improve or cause coronary steal)
coronary steal
- narrowed coronaries are already max dilated. Dilating other arteries may cause blood to be shunted away from the coronary vessels
SNP effect on coronary steal
- dilates both epicardial conductance and intramyocardial resistance vessels and in the presence of CAD, shunts blood away from the ischemic zone
NGT and coronary steal
- preferentially dilates conductance vessels and directs more blood toward ischemic zones
hydralazine effects and reflex response
- direct acting arterial vasodilator (alters Ca movement and metabolism)
- has its own receptor
- decreases BP (diastolic > systolic) and SVR
- reflex = (increase HR, contractility, renin activity, fluid retention, CO, SV)
who to avoid hydralazine in
- avoid with CAD, increased ICP, lupus
- increases myocardial O2 demand leading to ischemia (from reflex tachycardia)
side effects of hydralazine
- 5-10% of patients on hydralazine will have a positive ANA (lupus) titer (butterfly rash, joint pain)
- headache, dizziness, tremor, angina, tachycardia, flushing, palpitations, anorexia, agranulocytosis congestion, muscle cramps, edema
pharmacokinetics of hydralazine
- metabolized in the liver
- excreted in kidney
- highly protein bound
- onset 30 min
how nitroglycerine works and what it does to the body
- causes a release of nitric oxide for non-specific relaxation of the vascular smooth muscle
- dilates veins > arteries
- decreases PVR, venous return, myocardial O2 consumption
- relaxes coronary vessels and relieves spasms
nitroglycerin non-cardiac effects
- dilates meningeal vessels (caution with ICP) (causes headaches)
- decreases renal blood flow with decreased BP
- dilates pulmonary vessels
pharmacokinetics of nitroglycerine
- onset 1 min
- duration 3-5 min
nitroglycerine metabolism
- metabolized by glutathione nitrate reductase in the liver
- nitrite ion oxidizes Hgb to methemoglobin
- arterial vessels can build tolerance but not venous vessels
nitroglycerin warnings/ contraindications
- PDE 5 inhibitors (Viagra, Cialis) (usually end in “fil”)
- narrow angle glaucoma
- head trauma / cerebral hemorrhage
- severe anemia
- hypotension
advantages of nitroglycerine
- rapid onset
- coronary vasodilator
- dec myocardial O2 consumption
- no toxicities
- no coronary steal
- reduced PVR
disadvantages of nitroglycerin
- decreased diastolic BP
- reflex tachycardia
- possible hypotension
- tachyphylaxis
- methemoglobinemia
- intrapulmonary shunting
- prolonged bleeding time
sodium nitroprusside actions and effects on the body
- directly vasodilates arteries and veins
- decease BP and HR
- inc cerebral blood flow and ICP
- renal blood flow maintains
- overall reduction in myocardial O2 demand
- with abrupt discontinuation = reflex tachycardia and hypertension
warnings / contraindications w/ sodium nitroprusside
- congenital optic atrophy
- hypovolemia
- compensatory HTN (AV shunting, aortic coarctation)
- increased ICP
- severe renal/ hepatic impairment
presentation of cyanide toxicity w/ sodium nitroprusside
- hypotension, blurred vision, fatigue
- metabolic acidosis
- pink skin
- absence of reflexes
- faint heart sounds
toxic thiocyanide and cyanide levels
- thiocyanate (toxic >30)
- cyanide (toxic >2) (normal 0.2 smoker 0.4)
treatment of cyanide toxicity
- 100% O2
- correct acidosis
- 3% Na nitrate 4-6 mg/kg slow
- sodium thiosulfate
- hydroxocobalamin