Lecture 19 (Exam 4) - Anesthesia Pharmacology Adjuncts Flashcards
What type of receptors are Alpha Agonists?
What are the two subtypes and give a brief description on what happens when an agonists binds to them.
G-protein coupled receptors
Two subtypes:
1. Occupancy by agonists at alpha-1
- ⬆ synthesis of 2nd messengers: IP3 …⬆ Ca++ release from SR
- Affects vascular smooth muscle
- Determine arteriolar resistance, venous capacity and BP
- Occupancy by agonists at alpha-2
- Decrease release of NE from presynaptic nerve terminals (brainstem) and locus coeruleus.
- ⬆ sleepiness, ⬇️ sympathetic outflow.
(Slide 19)
Is Metoprolol selective or Non-selective Beta antagonist?
Which effects would we expect with Metoprolol?
Selective Beta-1 Antagonist
Leaves B2 functions intact: Bronchodilation, Vasodilation, and metabolic effects
(slide 13)
- What are the doses for Phenylephrine (Neosynephrine)?
- What two forms does it usually come in?
- IVP: 100 mcg per push (can give 50 mcg). Can give 200 - 300 mcg if needed in 100 increments that are spread out.
- Can come in a 100 mcg/mL syringe (Expensive but safer) Can come in 1000 mg/mL vials (Make the math math)
Fun Fact: It is Corndog’s favorite drug <3!
(Slide 20)
What should you worry about when giving Phenylephrine?!
What can you do to fix it?!
Reflex bradycardia with high doses!
You can wait for it to resolve or you can give propofol or VA to counteract the bradycardia!
(Slide 20 )
Is Phenylephrine (Neosynephrine) an alpha or beta agonist?
Is it used in the OR?
Does it do more venous or arterial constriction?
Alpha 1 Agonist!
Clinically mimics NE but less potent and longer-lasting
- Indirectly releases small amount of norepinephrine.
Given everyday in the OR
Venous constriction > arterial constriction
(Slide 20)
Phenylephrine is used to treat hypotension from?
Why do we like it for CAD and aortic stenosis?
- SNS blockade by regional anesthesia and spinal
- Inhaled/injected anesthetics
- Patients not responding to fluids, or you are giving them fluids
- Very useful in CAD and AS –> no tachycardia.
- Commonly used both IVP & IV drip
(Slide 20)
Metoprolol (Lopressor) has 2 PO formulations, what are they and what are their individual elimination 1/2 times?
Metoprolol IV is usually dosed ___mg q___mins in blocks of ___mgs.
Tartrate - E1/2 time of 2-3 hours
Succinate - E1/2 time of 5-7 hours
Metoprolol IV is usually dosed 1 mg q 5 mins in blocks of 5 mgs.
(slide13)
- What drug class is Labetalol?!
- What should you watch out for when giving Labetalol?
- How does Labetalol work?
- Typical doses?
- Selective alpha1, non-selective B1 and B2 antagonist effect
- Beta to alpha blocking ratio is 7:1 for IV form (More HR change than vasodilation) - High incidence of tachyphylaxis
- Lowers systemic BP by ↓ SVR
- Reflex tachycardia attenuated by beta blockade
Maximum effect of IV dose 5-10 minutes - Usual dose 2.5-5 mg IV; may increase to 10mg IV
(Slide 22)
Is Nitric Oxide a vasodilator or constrictor? And what is its MOA?
Vasodilator
It is a chemical messenger that activate cGMP in the cell to inhibit Ca++ entry into smooth muscle and increases uptake by the ER
(slide 42)
With Nitric Oxide, what effects does it have in the body? (6)
Cardiovascular tone relaxation
Platelet regulation
CNS neurotransmitter
GI smooth muscle relaxation
Immune modulation
Pulmonary artery vasodilation
(slide 42)
Mr. Spencer is in your preoperative holding room, scheduled for a CABG x 4 this am. You realize that he has not had his beta blocker this am. Which beta-blocker will you administer???
A. Labetalol
B. Metoprolol
C. Carvedilol
D. Esmolol
E. Propranolol
A or B!
A. Labetalol: It is shorter which will cause a small swing. We do not need a lot of drugs in his system because he will be on bypass and pulseless.
B. Metoprolol: Because CABG will be a long procedure.
C. Carvedilol: For CHF
D. Esmolol: Too short
E. Propranolol: Not Beta specific
(Slide 24)
What are 2 Nitro-Vasodilator drugs we use and what do they do in the body?
Sodium Nitroprusside, Nitroglycerin
↓ SVR….arterial vasodilators…treat effects of vasoconstriction
↓ venous return…venous vasodilators…alleviate pulmonary/systemic congestion
(slide 43)
You are in the process of extubating a patient immediately following a left carotid endarterectomy. His blood pressure is 210/64. Which of the following drugs would be most desirable?
A. Labatolol
B. Metoprolol
C. Esmolol
D. Propranolol
C!
B is also correct if depending on the situation.
A. Labetalol: No because of the alpha component.
B. Metoprolol: DOA too long for this case. Given only if he skipped his BB dose in the AM and is constantly hypertensive!
C. Esmolol: It is short acting, once neck stimulation is over BP will drop back to normal.
D. Propranolol
(Slide 25)
Sodium Nitroprusside (SNP) does what in the body? and does it work on the arteries or veins?
Vasodilator that causes relaxation of arterial and venous vascular smooth muscle
(arterial >venous)
(slide 44)
What is Sodium Nitroprusside (SNP) dose?
What is the onset, duration and special considerations?
Initial dose: 0.3 mcg/kg/min…titrated to 2 mcg/kg/min
Immediate onset, transient duration (hard to titrate, use small amounts)
Requires continuous administration
Requires invasive arterial monitoring
Sensitive to sunlight
(slide 44)
What is a side effect with Sodium Nitroprusside (SNP) that could be dangerous?
Dissociates immediately upon contacting oxyhemoglobin to methemoglobin: releasing cyanide and NO –> cyanide poisoning!
(slide 44)
Why and when do we use Sodium Nitroprusside (SNP)?
Production of controlled hypotension:
- Aortic surgery
- Pheochromocytoma
- Spine surgery
Hypertensive emergencies:
- Carotid surgery
(in instances that need immediate decreases in BP)
(slide 45)
In what instances could Cyanide Toxicity be seen with SNP admin? and What causes it?
With higher IV doses
Cyanide radical accumulate d/t sulfur donors/methemoglobin exhaustion
(slide 46)
What is a treatment for Cyanide toxicity with SNP admin?
How does it treat?
Give Methylene blue – to convert methemoglobin back to oxyhemoglobin
When do we suspect we have a Cyanide toxicity? And what are some indications?
- When Increasing doses SNP needed
- Increased mixed-venous sats….tissues aren’t using/extracting oxygen - will see: SVO2 increasing
- Metabolic acidosis….same
- CNS dysfunction/change in LOC occurs
Use labs to help diagnose!
(slide 46)
What is Nitroglycerin and does it work on arteries or veins?
Vasodilator - Acts on venous capacitance vessels and large coronary arteries
(more venous > than arterial)
(Slide 47)
What is the dose of Nitroglycerin, and what does it do in the body? Also, what can happen in a short period of time with this drug?
Initial dose: 5-10 mcq/min infusion and titrate
Vasodilation:
- Decreases preload to right heart.
(Can cause Venous pooling)
- Relaxation of arterial vascular smooth muscle (high doses)
Can develop Tachyphylaxis very quickly.
(slide 47)
The tachyphylaxis that can happen with Nitroglycerine is due to:
And what can we do to fix it?
- Dose dependent and duration dependent (within 24 hours)
- Limits vasodilation
to fix: Drug free interval for 12-15hrs reverses tolerance (to help reset the receptor) BUT ….rebound ischemia risk (will need to find something to replace or t fix in the mean time)
(slide 47)
When/Why do we use Nitroglycerin?
- Acute MI- Relieves pulmonary congestion, ↓ O2 requirements, limits MI size
- Controlled Hypotension- Less potent than SNP
- Sphincter of Oddi Spasm- During cholecystectomy/opioid induced Glucogon is the first line drug for this)
- Retained placenta- to relax uterus.
(slide 48)
What does SCIP stand for?
Surgical Care Improvement Protocol.
Slide 8
Under SCIP, Beta blockers have to be given within _____ hours of the procedure for what kind of patients?
24 hours
Patients at risk for myocardial ischemia and those already on beta-blockade therapy.
(Pts at risk for MI are; unstable angina, MI in the past, pt who had stent before due to MI, pt’s non-compliant to their statin drug. It’s a guesswork!)
Slide 8
If your patient forgot to take beta-blocker and its almost 24 hours to surgery but your pt’s HR is 63 and BP is 100/65. Would you give beta-blocker to your patient?
Yes, you would, according to the SCIP. But you would give just a small dose. (Play the game. CMS does not know what beta-blocker and how much beta-blocker you gave. Check the box.)
Slide 8
What are three ß1 selective agents that we use most in OR?
Atenolol
Metoprolol
Esmolol
(They do not cause vasodilation, so they are not involved in decreasing afterload.)
Slide 9
About ___% of beta receptors are ß1 in the myocardium.
75%
Slide 9
(25% are not ß1, so ß1 selective drugs are mostly specific.)
Which beta blocker that we do not use in anesthesia but we compare all the other beta blockers with?
Propranolol (Inderal)
Slide 10
(It is not cardio-selective, has an active metabolite and elimination half-time is 2-3 hrs)
What’s the elimination half-time of Esmolol?
0.15 hours (9 mins)
Slide 10
(Very short half-life)
What are the common characteristics of metoprolol, atenolol, and Esmolol?
All of them are cardio-selective, do not have active metabolite, and have low protein binding.
Slide 10
Propranolol (Inderal) are prototypical ________ and it has activity on both ____ and _____ receptors.
Prototypical antagonist
ß1 and ß2 receptors in equally.
Slide 11
Propranolol has a negative ionotropic effect and chronotropic effect. Which effect lasts longer?
The negative chronotropic effect (slow HR) lasts longer than the negative ionotropic effect.
(This is thought to be due to subdivisions of ß1 receptors, like ß1A and ß1B. This is just a proposed idea, nobody knows🤷♀️ )
Slide 11
Propranolol (Inderal) decreases clearance of what two classes of drugs?
Opioids and Amine LA’s.
(Propranolol decreases clearance of amide local anesthetics by decreasing hepatic blood flow and inhibiting metabolism in the liver. Pulmonary first-pass uptake of fentanyl is substantially decreased in patients being treated chronically
with propranolol.)
Slide 11
This is what I found in the book. She did not elaborate on it.
Which is THE most ß1 selective agent that anesthesia do not use very often?
Atenolol (Tenormin)
(Important when ß2 agonist receptor activity is important.)
Slide 12