Vasodilators:
- what are peripheral vasodilators most often used for?
- what type surgeries are they used in (3 types)?
- -treat hypertensive crisis,
- —deliberate (controlled) hypotension,
- —facilitate left ventricular stroke volume during acute failure
- —attenuate hypertension from aortic cross-clamping intraop - used during neuro, major vascular and cardiac anesthesia
Vasodilators:
- what are the most commonly used vasodilators?
- how do they work?
- nitro vasodilators (nitroglycerine (NTG) and sodium nitroprusside (SNP)
- generate nitric acid (NO) in the cell which stimulates GUANYLATE CYCLASE. this causes increased cGMP which causes smooth muscle relaxation.
vasodilators:
- where does nitric oxide occur (NO) besides in nitro based drugs?
- what effects does nitric oxide (NO) have in the body?
- what effect does NO have on CNS
- exists as an endogenous vasodilator as well
- regulatory effects on cardiac, pulmonary, vascular, CNS, immune and platelet functions
- maintaining wakefulness (suppression of NO by anesthesia increases GABA and enhances anesthetic state).
vasodilators:
- what organ is nitric oxide (NO) have a significant theraputic effect on?
- how is it delivered and what does it do?
- what is a potential problem from NO or its metabolite?
- nitric oxide has theraputic effect with pulmonary disease and pulm hypertension
- given via inhalation causes dilation of pulm vasculature and bronchodilation
- potential pulmonary toxicity from NO or its metabolite NO2
vasodilatiors: sodium nitroprusside
1. what is the action of nipride?
2. what does nipride not have an affect on?
3. what is the onset? duration? d/t duration, what is required for theraputic effect?
4. what actions are needed with a nipride gtt; why?
- SNP (sodium nitroprusside) is a direct acting peripheral vasodilator; works by relaxation of arterial and venous vascular smooth muscle
- no effect on nonvascular smooth muscle(gastric, lungs) and cardiac muscle
- immediate onset of action; short duration; requires IV infusion administration to maintain theraputic effect
- careful titration and continuous monitoring of BP is needed; d/t drug potency
vasodilators: nipride:
1. how does nipride work chemically?
2. what kind of drug is nipride; what is the difference between NO and NTG in how nitric oxide is released?
- SNP interacts with oxyhemoglobin then dissociates immediately to form methemoglobin while releasing NO and cyanide
- SNP spontaneously generates NO thereby functioning as a PRO-DRUG (as opposed to organic nitrates which require presence of thio (sulfur) containing compounds to generate NO.
vasodilators: nipride
1. effects (venous and arterial)
2. which one is affected more?
3. what does decreased BP cause?
4. what happens in the lung vasculature and what does this lead to?
- venous and arterial vasodilation causing a reduction in preload and afterload
- preload primarily affected, decreasing myocardial work and likelihood of ischemia
- decreased BP causes increased myocardial contractility and reflex tachycardia
- dilates pulmonary vasculature which may prevent normal vasoconstrictive response to hypoxia leading to VQ mismatch.
vasodilators: nipride metabolism:
1. metabolized by what? what are the by-products?
2. the by product is metabolized where, by what and into what?
3. what can the by-product lead to that can be deadly?
4. how quickly is the final by-product removed from the kidney?
- metabolized by erythrocytes into cyanide and cyanomethemoglobin
- cyanide is metabolized by rhodanase in the liver into thiocyanate
- cyanide can bind to tissue cytochrome oxidase with interferes with oxygen utilization (causes cyanide toxicity)
- thiocyanate is slowly eliminated by kidneys (4-7 days)
vasodilators: sodium nitroprusside
- treatment of cyanide toxicity:
a. what drug, % solution, dose and over what time?
b. what should be done regarding respiratory?
c. what 2 medications can be given (dose and time frame)
a) methemoglobinemia is treated with methylene blue, 1-2 mg/kg of a 1% solution over 5 minutes
b) patients should be mechanically ventillated with 100% o2 to maximize availability
c) sodium thiosulfate (150 mg/kg over 15 min) or 3% sodium nitrate (5mg/kg over 5 min).
vasodilators: sodium nitroprusside
1. dose:
2. onset:
3. doa:
4. how should it be given; d/t what?
5. what happens in light? what must be done?
- dose:0.3-10 mcg/kg/min (or 10-300 mcg/min) titrate for effect
- onset: 30-60 seconds
- duration: 1-3 min
- must give infusion d/t short duration
- degrades in light, protect from with foil
vasodilators: nitroglycerine:
1. what is nitroglycerine?
2. what is the action?
3. what do higher doses do?
4. what is the result?
5. works by generating NO in the presence of what?
- an organic nitrate vasodilator
- acting mainly on venous capitance vessels (nipride acts on arteriolar and venous vessels)
- relaxes arterial vessels at higher dose.
- results in peripheral pooling of blood volume which decreases preload and left ventricular end diastolic pressure…this leads to decreased cardiac ventricular wall tension
- works by generating NO in the presence of THIO (sulfer) compounds (i.e. intracellular glutathione transferase).
vasodilators: nitroglycerin
1. what all does nitro exert vasodilatory effects?
2. what does it do to these other areas (a,b,c,d)?
- main effects are cardiovascular but also effects smooth muscles in airways and GI tract
- –a)lungs: bronchodilator;
- —–b)GI tract: dilate billiary tract and relax sphincter of odi (from opiate induced spasm)
- —–c)cerebral vasodilation -headache (can increase ICP in patients with decreased intracranial compliance).
- —–d) ureteral, uterine and esophageal smooth muscle relaxation
vasodilators: nitroglycerin
1. what doses cause venous dilation? what does the venous dilation cause?
2. what happens to cardiac output? why?
3. what are effects on heart rate?
4. what does extreme decreases in blood pressure cause (cardiac wise)
5. what effect does nitro have on resistance (what happens to PVR and SVR)?
- venous dilation in doses up to 2 mcg/kg/min (venous dilation causes the decreased BP).
- cardiac output is decreased d/t decreased venous return (has NO DIRECT inotropic effect)
- no change or slight decrease in heart rate
- extremes in decreased blood pressure can decrease coronary blood flow and elicit reflexive tachycardia and increased MRO2
- decreased pulmonary vascular resistance (PVR) but not decreased SVR
vasodilators: nitroglycerin
1. how does nitroglycerin improve coronary blood flow? As opposed to what drug?
2. that is the reason why in WHAT patient population is nitro preferred over nipride?
3. how does nitro affect bleeding time?
- dilates conductance coronary vessels leading to increase flow to ischemic areas (as opposed to nipride which can produce coronary steal syndrome/ phenomenon)
- reason why nitro is preferred over nipride in CAD patients
- nitro can affect plateet aggregation; along with decreased blood pressure and decreased vascular tone all of which prolong bleeding time.
vasodilators: nitroglycerin –uses
1-4 main uses for nitro? and how it works?
5. when would you use nitro in cardiovascular SURGERY?
- angina pectoris (decreases o2 requirements)
- cardiac failure (decreases preload and pulmonary edema)
- acuter hypertension (venous dilation)
- controlled hypotension (not as potent as nipride but has better cardiac profile–no coronary steal).
- attenuation of HTN from cross clamping aorta
vasodilators: nitroglycerin side effects/toxicy
1. neuro:
2. cardiac:
3. blood
- headaches, increased ICP (from increased cerebral blood flow)
- reflex tachycardia, orthostatic hypotension
- nitrate tolerance, potential for methemoglobinemia
vasodilators: nitroglycerine
1. dose (infusion & bolus):
2. onset: (a)iv, b)sublingual, c)transdermal)
3. peak:
4. duration:
- dose:– infusion: 5-200 mcg/min (0.1 to 4mcg/kg/min)
- -bolus: 0.5-2 mcg/kg - onset: –1-2 minutes (IV);
- 1-3 min SL;
- 40-60 transdermal - peak: —-1-5 minutes
- duration: 3-5 min IV, 30-60 min SL
What does nitroglycerine tubing do?
helps decrease absorption of nitroglycerin into tubing
cardiac glycosides:
- name the drug:
- what is it made from?
- uses: (a,b)
- why does dig have a high chance for overdose?
- digitalis (digoxin)
- derived from naturally occuring plants including foxglove plant
- a) cardiac failure
b) to slow rapid ventricular rate in patients with SVT - has a narrow theraputic to toxic range (1.0-2.0), greater than 2.0 can be toxic
- what condition potentiates dig toxicity?
2. why?
- hypokalemia
2. digoxin competes with potassium for binding sites at Na/K+ ATPase binding sites (leaves digoxin unopposed).
