SS25 Anesthesia Adjuncts (Exam 4) Flashcards
1
Q
What are the subtypes of β receptors and where are they primarily located?
A
- β1 - Heart
- β2 - Lungs
- β3 - Fat/Muscle (disregard β3)
2
Q
What type of receptors are β receptors?
A
GPCR
3
Q
β agonism MOA
A
- Ligand (agonist binds)
- Activates Adenylyl Cyclase (AC)
- cAMP produced
- Enhances Ca influx
- Expected effects occurs
4
Q
What effects occur with β agonism?
A
- Chronotropic
- Inotropic
- Dromotropic
5
Q
What type of antagonism occurs at β receptors?
A
- Competitive antagonism
6
Q
βeta-antagonist prevents ________. from binding at the heart, airway smooth muscle, and blood vessels
A
- catecholamines (or sympathomimetics)
7
Q
Chronic administration of β blockers results in what effect on receptors?
A
- Tachyphylaxis
- Receptor upregulation (aka ↑ # of receptors)
- Desensitization
8
Q
T/F: The selectivity of β blockers is dose-dependent but dose depenendency is lost at high doses
A
- True
- B blockers are dose-dependent
- At high doses, no longer selective works on all receptors (B1, B2, B3)
9
Q
What effects do βeta Antangonist (β-blockers) have?
A
- May restore receptor responsiveness (maybe take a break from drug & switch to new one)
- Protect myocytes from perop ischemia & infarct
- May ↓ arterial vascular tone & ↓ afterload
- ↓ CO & inhibit renin release
10
Q
T/F: Patient on B Blockers must be given dose within 24 hr of surgery
A
True
11
Q
How do β blockers protect myocytes from perioperative ischemia/infarct?
A
- By ↓O₂ demand on the heart
12
Q
T/F. β blockers will potentiate renin release.
A
- False. β blockers will inhibit renin release
13
Q
How will β blockers affect the cardiac foci action potential?
A
- Decrease slope = Prolonged Phase 4
- ↓ rate of spontaneus depolarization
- ↓ dysrhythmias during ischemia and reperfusion (Ex. CABG, TVAR, Ablation)
Myocardium perfuses during diastole
14
Q
Bonus: Myocardium perfuses during diastole
Why?
A
- During systole, aortic valves leaflets are open and it blocks the opening to coronary arteries
- During systole, tiny epicardial vessels are constrictricted as well
- Diastole allows for retrograde flow so better perfusion into coronaries
15
Q
How will β blockers affect diastolic perfusion time?
A
- Increases diastolic perfusion time = ↑ filling time
16
Q
What type of HTN is a possible indication for β blocker therapy?
A
- Essential Hypertension
17
Q
Other β- blocker indications:
A
- Excessive SNS stimulation (noxious stimuli, acute cocaine ingestion)
- Thyrotoxicosis (↑ thyroid)
- Cardiac dysrhythmias
- SCIP
18
Q
What is SCIP?
- Describe the protocol and its goals.
A
- Surgical Care Improvement Protocol
- β-blockers must be given within 24 hrs of surgery for patients at risk for cardiac ischemia and pts already on β-blocker therapy.
19
Q
What percentage of β receptors in the myocardium are β1 ?
A
75%
20
Q
Do cardio-selective β-blockers cause vasodilation?
A
No
21
Q
What non-selective β-blocker has active metabolites and is considered the prototype?
A
- Propanolol (Inderal)
- β1 = β2 activity
22
Q
What were the (3) β1 cardio-selective drugs discussed in lecture?
A
- Atenolol (Tenormin)
- Metoprolol (Lopressor)
- Esmolol (Breviblock)
23
Q
Differentiate the clearance mechanisms:
- Propranolol
- Metoprolol
- Atenolol
- Esmolol
A
- Propranolol: Hepatic
- Metoprolol: Hepatic
- Atenolol: Renal
- Esmolol: Hydrolysis (Plasma cholinesterases via cytosol)
24
Q
Differentiate the E½ of the following:
- Propranolol:
- Metoprolol:
- Atenolol:
- Esmolol:
A
- Propranolol: 2-3 hrs
- Metoprolol: 3-4 hours
- Atenolol: 6-7 hrs
- Esmolol: 0.15 hrs = 9 minutes
25
When propanolol is given, what effect lasts longer, negative inotropy or negative chronotropy?
- Why?
- **Negative Chronotropy (Bradycardia) lasts longer**
- Possibly d/t β1 sub-receptor types (ex. β1A, β1B, etc.)
26
Propanolol will decrease the clearance of which two important anesthetic drug classes?
- **Opioids**
- **AmiNe LAs** (not amides)
27
What drug is the **most selective** β1 antagonist?
**Atenolol (Tenormin)**
28
What are the three benefits of Atenolol?
- Dosed only 1x daily → Good for non-cardiac sx CAD patients (**↓ complications for 2 years**)
- Doesn't potentiate insulin-induced hypoglycemia
- Does **not** cross the BBB (less fatigue)
29
What is the dose for Atenolol?
5mg q10min IV
30
What 3 effects does Metoprolol (Lopressor) have?
- Bronchodilator, Vasodilator, & Metabolic effects of β2 receptors intact
31
What is the dose of metoprolol?
- **1mg q5min** x 5 (for a total of 5 mg)
- repeat set if needed
32
What two PO formulations of Metoprolol are there?
- Metoprolol **Tartate**
- Metoprolol **Succinate**
33
Compare Metoprolol Tartate & Metoprolol Succinate:
- E1/2 times
- dosing
- which one is more commonly prescribed?
- Metoprolol **Tartate**:
-E1/2 = 2 - 3 hrs
-dosing 2-4x day
- Metoprolol **Succinate**
-E1/2 = 2 - 3 hrs
-dosing 1x day
- More likely to Rx Metoprolol **Succinate** d/t increased compliance but less HR cntrl
## Footnote
(typically see Tartate more in hospital setting
34
What β blocker would be used for **treat intraop noxious stimuli (ie: intubation)**?
- dose:
- onset:
- duration:
**Esmolol**
- dose: **20 - 30 mg IV**
- onset: (5 mins)
- duration: 10 - 30 mins
- **rapid on & offset**
35
Caution should be taken when giving Esmolol with which two conditions present?
Why?
- Cocaine and/or Epinephrine absorption
- Can cause pulmonary edema/collapse
36
Based off graph:
- Which drug prevents Tachycardia & HTN associated with intubation?
- Which drug would you give if increased Tachycardia & HTN was rlt to pain?
- Esmolol
- Fentanyl
37
Are the effects of CCBs and β-blockers additive?
No, synergistic
38
What two **conditions should a β1 cardio-selective be used** over a non-selective?
- **DM**: β2 can cause hypoglycemia by insulin potentiation
- **Airway**: β2 potentiates bronchospasm
39
What volatile anesthetic will cause the greatest additive cardiac depression when combined with a β blocker?
- The least additive cardiac depression?
- Why does this not matter?
- Enflurane = greatest additive depression
- Isoflurane = least additive depression (best for myocardium)
- Not significant between 1-2 MAC
40
αlpha receptors:
- subtypes:
- receptor type:
- α1 & α2
- GPCR
41
What occurs with α1 agonism?
1. 2nd messenger synthesis = **IP₃**
2. Ca⁺⁺ release from SR
3. Affect vascular smooth muscle
4. Determines arterial resistance, venous capacity, & BP
42
What occurs with α2 agonism?
- ↓ release of NE from **presynaptic** terminal (brainstem)
43
Is phenylephrine primarily a venoconstrictor or an arterioconstrictor?
More **Venous constriction** effects
44
T/F: Phenylephrine is less potent and short-lasting compared to NE.
False
- less potent & **longer**-lasting
45
Phenylephrine clinically mimics NE and ______ releases small amounts of NE.
- **Indirectly**
46
Indications for Phenylephrine:
- SNS blockade by regional
- Inhaled/Injectable anesthetics
- CAD/A. stenosis (**b/c it doesn't call tachycardia**)
47
What is the normal dose of phenylephrine?
- **100mcg/mL IV push**
- Can also do continuous infusion if requiring frequent IV pushes
48
What adverse effect results from phenylephrine?
- How is it resolved?
- **Reflex bradycardia** d/t very high SVR
- Stop drug
49
What is Labetalol effects?
- **Non-selective β1&2 and Selective α1 antagonist**
- has peripheral effects
- **↓ SVR = ↓ systemic BP and ↑ reflex tachycardia**
50
What is the ratio of β to α blockade for Labetalol?
- **7:1** in IV form
- 7x non-selective β1&2 v. selective α1 antagonist
51
Which of the following receptors does Labetalol antagonize?
A. α1
B. α2
C. β1
D. β2
α1, β1, β2
52
What is the dose for labetalol?
- peak effect:
- **2.5 - 5mg IV; 10mg max**
- 5 - 10 mins
- Tachyphylaxis (+)
53
Which βeta blocker would you administer to patient sceduled for CABG x4 and forgot to take β blocker at home?
- Metoprolol (Lopressor) IV
54
During extubation from L CEA, BP spikes 214/62. Which β blocker would you give?
- Labetalol
- Esmolol
- **Esmolol**
- Rationale: Labetolol could drop the DBP too much
55
Sympathomimetics (Vasopressors) uses:
- **Increase systemic BP**
- Increase myocardial contractility
56
What are 2 AE that can happen if sympathomimetics lack β1 specificity?
- Intense vasoconstriction
- Reflex bradycardia
57
Sympathomimetics: MOA
1. Activate directly or indirectly α or β adrenergic GPCRs
2. cAMP enhance Ca release SRminto cytosol
3. Actin & Mysin interact forcefully (↑ crossbridging)
58
Which drug(s) is an direct-acting sympathomimetic?
- MOA
- **Epi, NE, Phnylephrine, Dopamine**
- Directly activates adrenergic-Rs
59
Which drug(s) is an indirect-acting sympathomimetic?
- MOA
- **Ephedrine**
- Aids in release of NE from **postganglionic** sympatheric nerve endings
60
Image skipped during lecture:
61
Prototype catecholamine
Epinephrine
- cardiac cases & ACLS use only
62
What is the **single bolus IV push dose for Epinephrine**?
- Duration of action
- **2 - 8 mcg IVpush**
- **1 - 5 min**
63
Epinephrine:
- **infusion dose for β2 effects**:
- **infusion dose for β1 effects**:
- **infusion dose for α1 effects**:
- **1-2 mcg/min**
- **4 mcg/min**
- **10-20 mcg/min**
64
What catecholamine will have the greatest effect on heart rate and cardiac output?
- **Epinephrine**
65
What catecholamine will have the greatest effect on SVR?
- **Phenylephrine**
- pure αlpha
66
Ephedrine single IV dose:
- **5 - 10 mg IV**
67
Ephedrine is commonly used in sympathetic depression from what?
- **Inhaled/ injectable anesthetics**
- BP response less intense & last up to 10x longer than Epinephrine
- Tachyphylaxis (+++)
68
Why does tachyphylaxis occur with Ephedrine?
- Ephedrine **depletes NE stores**
69
What is the preferred sympathomimetic for **parturient** (woman in labor) patients?
Why?
- **Ephedrine** can be given d/t hypotension that occurs from spinal SAB
- It doesn't effect uterine blood flow
- **Typically given immediatly after spinal placed for c-section to prevent hypotension**
70
Compared to Phenylephrine, Ephedrine has an equal BP response, but _________ (higher/lower) umbilical pH in neonates.
- **higher**
71
What drug would be utilized for **catecholamine-resistant hypotension**?
- Derivative:
- Single IV dose:
- Vasopressin
-Derivative of Arginine Vasopressin (ADH)
- **Single dose dose: 1-2 units**
72
Vasopressin MOA:
- **Stimulates V1 receptors to cause arterial vasoconstriction**
- Increases renal-collecting duct permeability (more water is reabosorped)
73
Vasopressin side effects:
(Cardiac, GI, Other)
- Cardiac: **Coronary artery vasoconstriction**
_ GI: **Stimluates GI smooth muscle**: abd. pain, cramps, N/V.
- Other: **↓PLT count & antibody formation**
74
T/F: Vasopressin can be used for ACE-Inhibitor resistant hypotension?
- True
75
Review image.
76
You just completed induction on a TKA patient w/ hx of DM, OA, & CAD using Propofol, Vecuronium, & Fentanyl. Pt is intubated on Sevo ET 3%. BP 70/30 HR 54. What is your first intervention?
1. ↓ vaporizer: it's closest & quickest
2. Give Ephedrine and/or IVF
77
Per lecture, what are the 2 pressor(s) of choice for hypotension in CAD patients (place in order)?
1. Ephedrine
2. Phenylephrine
78
β-agonist won't work if fully βeta blocked. You have to give an _____________ agonist.
𝜶lpha agonist
79
During maintanence phase: BP 80/42 HR 92. In addition to an IVF bolus, what is the drug of choice?
- Phenylephrine
- ↑ SVR = ↑ BP without causing tachycardia
80
Pt with hx of uterine cancer and takes ACEIs at home becomes hypotensive and does not respond to Ephedrine pushes x3. What are the next 2 steps?
- IVFs, Vasopressin
- Vasopressin is a good option for patients already on ACEIs
81
Formula to find MAP:
**SBP + (2 * DBP) / 3**
82
Per lecture, which drugs are considered vasodilators?
- Nitrates (ie: Nitroglycerin)
- Sodium Nitroprusside
- Minoxidil
- Hydralazine
83
How does Nitric Oxide cause vasodilation?
- NO → GC → cGMP → Ca⁺⁺ entry inhibited into smooth muscle → increased uptake in SR
84
Which processes are NO involved in? (6)
1. Cardiovascular tone relaxation
2. Plt regulation
3. CNS neurotransmitter
4. GI smooth muscle relaxation
5. Immune moduation
6. Pulmomary Artery Vasodilation
85
Nitro- vasodilators MOA:
- ↓ Systemic BP by:
- ↓ SVR: arterial vasodilators treat effects of vasoconstriction
- ↓ Venous Return: venous vasodilators alleviate pulmonary/systemic congestion
86
How can nitro-vasodilators alleviate pulmonary congestion?
- **By decreasing venous return via venodilation**
87
What vasodilator absolutely requires **continuous monitoring** and an **invasive arterial line monitoring**?
Sodium Nitroprusside
88
Sodium Nitroprusside: MOA
- Relaxation of arterial **and** venous vascular smooth muscle
89
What does **Nitroprusside dissociate on contact with**?
- What is the result?
- Dissociates immediately on contact with oxyhemoglobin → **methemoglobin, NO, and cyanide released.**
- cyanide toxicity risk
90
What is the dose of Nitroprusside?
- onset?
- duration?
- Initial **0.3** mcg/kg/min
- Max: 2 mcg/kg/min
Duration: INSTANT transient onset
91
When is Sodium Nitroprusside (SNP) used?
- Controlled Hypotension: Aortic, Spine, Pheochromocytoma
- Hypertensive emergencies & Carotid sx (CEA)
92
What drug is used to treat cyanide toxicity?
Methylene blue
93
What signs would tip you off to possible cyanide toxicity secondary to nitroprusside administration?
- ↑ dosing need for sodium nitroprusside
- **↑ SvO₂ (mixed venous) & ↑ Metabolic acidosis ↑ b/c tissues are not using O2**
- CNS dysfunction/LOC changes
94
Where does nitroglycerin work?
- **Large coronary arteries**
- **Venous capacitance vessels**
- Lead to venous pooling & relaxation of vascular smooth muscle @ high doses
95
Would nitroglycerin increase or decrease preload?
↓ preload
96
Does nitroprusside or nitroglycerin exhibit tachyphylaxis?
Nitroglycerin
97
What tachyphylactic effects that can occur with NTG?
- Dose & Duration dependent
- Limits vasodilation
- **Drug free interval 12-15 hrs reverses tolerance; may have possibe rebound ischemia .**
98
What is the nitroglycerin dose?
- Initial dose = **5 - 10 mcg/min** infusion and titrateable
- **No max** but ↑ dose not equal ↑resoonse
99
What is the first line treatment for sphincter of Oddi spasm?
What is second?
- Glucagon
- Nitroglycerin
100
What are the indications for nitroglycerin?
- **Acute MI**
-relieves pulm congestion, ↓ O2 requirements, limits MI size
- **Controlled Hypotension**
-Less potent than SNP
- **Sphincter of Oddi spasm**
-Occurs during cholecystectomy/opioid induce
- **Retained placenta**
-Continued bleeding
101
Hydralazine: MOA:
- Direct systemic arterial vasadilator
- ↓ ITP =↓ Ca⁺⁺ release
102
Hydralazine:
Onset:
1/2 Life:
- Peak: 1 hour
- ½-life: 3-7 hours
## Footnote
too slow on & off; not good for sx.
103
What is the initial dose of Hydralazine?
2.5 mg IV
104
Hydralazine: Adverse effects
- Extreme hypotension
- Rebound tachcardia
105
What are the **three types of CaCBs**?
- Include their **selectivity **(**where they act**)
- **Phenylalkylamines** - AV Node
- **Benzothiazepines** - AV Node
- **Dihydropyridines** - Arteriolar Bed
106
- If a CaCB is selective for AV node, the HR will __________ (*decrease/increase*) more.
- If a CaCB is selective for the arteriolar bed, there will be more ______________ (*vasoconstrictive/vasodilatory*) effects.
- decrease
- vasodilatory
107
CaCBs: MOA
1. Bind to L-type V-G Ca channels
2. ↓ Ca⁺⁺ influx
3. Excitation-contraction coupling **inhibited**
108
CaCBs will ______ blood pressure and ________ coronary blood flow.
decrease; increase
109
Effects of CaCBs:
- ↓ vascular smooth muscle contractility
-Peripheral vasodilation = ↓ SVR & systemic BP
-↑ coronary BF
-Dihydropyridines
- ↓ Speed of conduction mainly via AV node
-Phenylalkylamines
-Benzothiazepines
110
Which CCB has the **greatest coronary artery dilation** and **least myocardial depression**?
**Nicardipine** (Cardene)
111
Nicardipine:
- Clinical use:
- Dose:
- E 1/2:
- Clinical use: **short-term severe HTN** (ie: expecting strong stimuli like SBP 220s but wont't need for prolonged time)
- Dose: **5 mg/hr**
-Titrate:(↑ 2.5 mg/**hr** x4 )
-Max 15 mg/hr
- E 1/2: 50% decrease 30 mins after d/c
112
Which antihypertensive works primarily through altering venous capacitance?
NTG
113
Which antihypertensive will worsen the PaO2 (the most) of an end-stage COPDr who needs emergent BP?
Sodium Nitroprusside
114
Surgeon is closing on R CEA. CRNA has reverse muscle relaxant and pt is breathing spontaneously. BP and HR are elevated. What is youre first intervention?
- Give narcotic
- Based off how high BP is, may need to start Nicardipine (Cardene)
