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1
Q

Describe the types of beta recepetors

A

B1, B2, B3

GPCR

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2
Q

Difference in beta action when occupied by agonist vs antagonist

A

agonist
• Activates adenylyl cyclase to produce cAMP
• Enhances Ca++ influx
•Chronotropic, inotropic, and dromotropic effects

antagonist:
inhibition of adenylyl cyclase to produce cAMP
chronotropic, inotropic and dromotropic effects

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3
Q

How do beta-antagonist work

A

Selective affinity for b-adrenergic receptors
NOT necessarily specificity
Selectivity dose dependent response

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4
Q

What type of drugs are beta-antagonist

A

Competitive antagonists

Large concentrations of agonist can out-compete and displace the b-antagonist

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5
Q

benefits of beta blockers

A

 May restore receptor responsiveness
• After desensitization from over exposure to catecholamines (tachyphylaxis)
 Protect myocytes from perioperative ischemia and infarction
 decrease arterial vascular tone and reduce afterload
 Decrease CO
 inhibit renin release

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6
Q

Cardiac effects of beta blockers

A
  • Negative inotrope
  • Negative chronotrope
  • Delay conduction speed through AV node
  • Decrease phase 4 depolarization
  • Increase diastolic coronary perfusion time
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7
Q

Indications for beta blockers

A
  • Excessive SNS stimulation
  • Noxious stimuli, acute cocaine ingestion
  • Thyrotoxicosis
  • Cardiac dysrhythmias
  • SCIP
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8
Q

beta blocker scip protocol

A

Beta blockers w/in 24 hrs
Esp for:
Pt at risk for MI
Pt already on beta blocker

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9
Q

Which beta antagonist would be best used in the asthmatic pt

A

selective B1 antagonist

atenolol, metoprolol, esmolol

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10
Q

Examples of B1 selective agents

A

Atenolol

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11
Q

Benefits of B1 antagonists

B1 selectivity

A

Does not cause:
Vasodilation
Bronchoconstriction

Increases diastolic filling time

Selectivity about 75%

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12
Q

Clearance for metoprolol, atenolol and esmolol

A 
metoprolol= hepatic
Atenolol= renal
Esmolol = plasma hydrolysis
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13
Q

Do metoprolol, atenolol, and esmolol have active metabolite

A

No

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14
Q

Metoprolol
E 1/2 time
protein binding
adult iv dose

A

E 1/2 time = 3-4 hrs
protein binding= low
adult iv dose= 1-15 mg

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15
Q

Atenolol
E 1/2 time
protein binding
adult iv dose

A

E 1/2 time= 6-7 hr
protein binding= low
adult iv dose= 5-10 mg

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16
Q

Esmolol
E 1/2 time
protein binding
adult iv dose

A

E 1/2 time = 0.15 hr (9 min)
protein binding= low
adult iv dose= 10-80 mg

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17
Q

Propranolol
REceptor site
Drawbacks

A

Receptor site: B1 = B2 activity

Drawbacks: HR slowing LONGER than negative inotropic effects

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18
Q

How does dosing differ for propranolol

A

Very pt specific
Can have 20-fold difference in plasma concentrations after PO
Dosing ranges from 40-800 mg/day

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19
Q

Propranolol effects on amide LA and opioids

A

decreases clearance

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20
Q

Which drugs’ clearance are affected by the use of propranolol
Considerations for administration of those drugs

A

amid LAs
opioids

May affect redosing of opioids and LAs

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21
Q

What is the beta antagonist of choice that will still maintain B2 funcion

A

Atenolol

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22
Q

Which beta blocker is the most B1 selective

A

Atenolol

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23
Q

Perioperative cardiac effects of atenolol

A

VERY cardio-protective

May decrease cardiac complications from surgery in CAD pts for up to 2 years

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24
Q

Effects of atenolol on blood glucose

A

does not potentiate insulin-induced hypoglycemia

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25
CNS effects of atenolol
less entering CNS | so less fatigue
26
Atenolol dose
5 mg q 10 min IV
27
Metoprolol formulations | What is the action and dosing difference
Tartrate: E1/2 2-3 hrs bid/qid dosing Succinate: E1/2 5-7 hrs qd dosing
28
Possible drawbacks to metoprolol succinate
May cause withdrawal tachycardia | Could be cause of postop HR increase
29
Metoprolol dosing
1 mg q 5 IV | for total 5 mg
30
which b-blocker has the most rapid onset and offset
Esmolol Onset = 5 min Offset = 10-30 min
31
Which beta blocker would be most useful for rapid blunting of SNS effects from noxious stimuli
esmolol
32
How is esmolol metabolized
Plasma esterases (distinct from plasma cholinesterases)
33
Esmolol dosing
20-30 mg IV
34
Beta blocker drug interactions
Cimetidine Concurrent CCB use Potentiates insulin effects Anesthetic
35
How are beta blockers affected by cimetidine
Metoprolol has decreased 1st pass metabolism
36
Risk of concurrent use of CCBs and b-blockers
bradyarrhythmias | HF
37
What effects do b-blockers have on insulin and blood glucose
Potentiates insulin effects ``` prevents glycogenolysis (specific to B2-antag activity) May cause hypoglycemia ```
38
Possible anesthetic interactions with beta antagonist
* Potential additive(?) myocardial depression * Greatest with enflurane, least with isoflurane * Not significant between 1-2 MAC
39
Which patients would most benefit from b1 selective antagonists
Asthma | Diabetic
40
Example of mixed beta/alpha antagonist
Labetolol | Carvedilol
41
Which selective receptors are affected by labetolol administration
Selective alpha1 | non-selective B1 and B2 antagonist effect
42
Which receptor effect is greater with labetolol use
Beta to alpha 7:1 beta effect 7x greater than alpha
43
Labetolol MOA
•Lowers systemic BP by ↓ SVR (alpha1 antagonist and beta2 agonist effects) NO reflexive tachycardia effects from decreased SVR compensation
44
Which drug may be appropriate for a pt w/ mixed SBP and DBP HTN
Labteolol
45
Labetolol Dose Maximum effect time
Dose: 2/5-5 mg IV (up to 10 mg) Max effect time: 5-10 min IV
46
Use of sympathomimetics
* Increase myocardial contractility | * Increase systemic blood pressure
47
Sympathomimetics that lack B1 specificity may have what effects
* Cause intense vasoconstriction | * Reflex-mediated bradycardia
48
Sympathomimetic MOA
* Activate directly or indirectly beta or alpha adrenergic GPCR * cAMP enhance Ca influx to increase concentrations * Actin and myosin interact more forcefully
49
What are the differences in direct and non-direct sympathomimetics
Direct: • Directly activate adrenergic receptors Indirect: • Evoke the release of norepi from postganglionic sympathetic nerve endings
50
Examples of direct and indirect sympathomimetics
Direct: Epi, norepi, phenylephrine, dopamine Indirect: Ephedrine, phenylephrine (sometimes)
51
Which receptors does epinephrine act on
Alpha, beta1 and beta2 | Beta effects greater than alpha
52
Which receptors dose phenylephrine act on
alpha receptors
53
Comparative CO effects of epinephrine, ephedrine, phenylephrine and vasopressin.
Epi, ephedrine, vaso = INCREASE CO | Phenylephrine has no effect on CO
54
Comparative HR effects of epi, ephedrine, phenylephrine and vaso
Epi and ephedrine = INCREASE HR | Phenyleph and vaso = no HR effect
55
Comparative PVR effects of epi, ephedrine, phenyleph, and vaso
``` Phenylehp = MOST effective on PVR Vaso = mid-range effect on PVR Epi/ephedrine = less effect on PVR ```
56
Receptor effects of epi
Alpha 1 and 2= cutaneous, splanchnic and renal bed vasoconstriction Beta 1 = increased HR and CO Beta2= skeletal muscle vasodilation, bronchodilation
57
Epi effects on renal vessels compared to norepi
Epi has 2-10x greater effect than norepi
58
Dosing and DOA for epi
Single dose = 2-8 mcg | DOA = 1-5 min
59
Infusion dosing and receptor effects of epi
1-2 mcg/min = beta 2 effects 4 mcg/min = beta 1 effects 10-20 mcg/min = mostly alpha effects (decreased peripheral perfusion**)
60
Indications for use of ephedrine
Commonly used in sympathetic depression caused by inhaled or injected anesthetics
61
BP effects of ephedrine
-BP response much less intense (10x
62
Drawback of ephedrine
Increased used leads to tachyphylaxis d/t DEPLETED NOREPI stores
63
Why does ephedrine lead to tachyphylaxis
D/t depleted norepi stores from indirect action of ephedrine to increase availability of norepi Ephedrine effects are dependent on norepi availability
64
Ephedrine use in pregnancy
Generally, the preferred sympathomimetic for hypotension d/t SAB Does not affect uterine blood flow
65
Effects of phenylephrine on parturient patients
Equal BP response to ephedrine Phenyleph increases neonate umbilical pH (so baby is less acidic) May be more beneficial for neonate
66
Vascular effects of phenyleph
Venoconstriction > arterial constriction
67
MOA of phenyleph
DIRECT: Mostly stimulates alpha1 receptors Indirect: releases small amounts of norepi
68
How does phenyleph compare to norepi
Clinically mimics norepi - less potent - longer acting
69
Uses for phenyleph
To treat hypotension d/t SNS blockade by regional Inhaled/injected anesthetics CAD and AS pts
70
Why is phenyleph most useful in AS pateitns?
It maintains afterload | Does not increase heartrate
71
Common phenyleph administration
IVP and IV gtt
72
Drawbacks to phenyleph use?
Reflex bradycardia
73
MOA of vasopressin
* Stimulates vascular V1 receptors to cause arterial vasoconstriction * Increases renal-collecting duct permeability so water is reabsorbed
74
Vasopressin uses
* effective in reversing catecholamine-resistant hypotension | * ACE-I resistant hypotension
75
Side effects of Vaso (CV, GI, hem)
``` CV= coronary artery vasoconstriction GI = stimulates GI smooth muscle (abd pain, N/V) Hem= decreased platelet counts and antibody formation ```
76
Which drugs are more effective at venodilation (minoxidil, SNP, NTG, hydralazine)
Nitrates(NTG) > SNP > Minoxidil > hydralazine
77
Which drugs are more effective at arterial dilation (minoxidil, SNP, NTG, hydralazine)
Hydralazine > minoxidil > SNP > nitrates(NTG)
78
Basic MOA of NO
A chemical messenger that affects cGMP and decreases intracellular Ca ions which relaxes vessels
79
Physiologic actions of NO
``` CV tone relaxation Platelet regulation CNS NT GI smooth muscle relaxation Immune modulation Effector molecule for volatile anesthetic Pulm artery vasodilation ```
80
MOA of SNP
Causes relaxation of arterial and venous vascular smooth muscle More potent arterial dilator
81
Administration considerations for SNP
Immediate onset and offset Requires continuous administration Requires invasive arterial monitoring Can lead to Cyanide toxicity
82
Adverse effects of SNP and why it occurs
SNP dissociates immediately upon contact oxyhgb methemoglobin releases cyanide and NO Cyanide can build up with prolong use
83
Uses of SNP
``` When rapid HTN treatment: Aortic surgery pheochromocytoma Spine surgery Hypertensive emergencies with carotid surgeries ```
84
When may cyanide toxicity be a concern with SNP administration
With prolong use of high doses | Causes accumulation of cyanide d/t sulfur donors
85
What are some suspicions of cyanid toxicity with SNP use
 Increasing doses SNP  Increased mixed-venous sats….tissues aren’t using oxygen  Metabolic acidosis  CNS dysfunction/change in LOC occurs
86
MOA of NTG
Acts on venous capacitance vessels and large coronary arteries with dilatory effects Leads to venous pooling relaxation of arterial vascular smooth muscle (high dose)
87
Problems with prolong use of NTG
Can lead to tachyphylaxis which is Dose and duration dependent Limits vasodilation Requires drug free interval (12-15 hrs)
88
SNP dosing
0.3 mcg/kg/min to 10 mcg/kg/min
89
Dosing of NTG
0.5-1 mcg/kg/min or IVP
90
Uses of NTG
AMI Acute HTN Controlled hypotension Sphincter of Oddi spasm
91
How does NTG aid in treating AMI
relieves pulm congestion decreases O2 requirements Limits MI size
92
How does NTG used in controlled hypotension situations
Less potent than SNP | Relates to intravascular fluid volume d/t venous dilation
93
How does NTG aid w/ sphincter of Oddi spasm
Help determine whether it is chole or opioid related.
94
MOA of hydralazine | Dosing
 Direct, systemic arterial vasodilator • Decreases ITP, ↓ Ca++ release Initial dose = 2.5 mg IV
95
Side-effects of hydralazine
Extreme hypotension | Rebound tachycardia
96
Drawback to hydralazine use
Onset = takes about 1 hour to reach peak plasma concentration
97
What are the types of CCBs and the difference in each.
* Phenylalkylamines: selective for AV node * Benzothiazepines: selective for AV node * Dihydropyrimidines: selective for arteriolar beds
98
MOA of CCBs
* Bind to receptors on VG calcium ion channels (L-type; main pathway) * Decrease calcium influx * inhibits excitation-contraction coupling
99
Effects of CCBs (4)
-Decrease vascular smooth muscle contractility which leads to: +peripheral vasodilation +decrease SVR and SBP - Increase coronary blood flow - Decreases speed of conduction through AV node
100
Use of nicardipine Dosing MAX
Short-term control of HTN Dose: • 5mg/hr (50 ml/hr) • Increase 2.5 mg/hr (25 ml/hr) x 4 to max of 15mg/hr (150 ml/hr) • Decrease to 3mg/hr (30ml/hr) 50% drug decrease 30 minutes after D/C Max = 15 mg/hr
101
``` Nicardipine effects on: HR Myocardial depression SA node depressoin AV node conduction Coronary artery dilation Peripheral artery dilation ```
``` HR = Inc or NC Myocardial depression = slight SA node depression = 0 AV node conduction= 0 Coronary artery dilation= greatest Peripheral artery dilation= Marked ```
102
Comparative HR effects of verapamil, nifedipine, nicardipine, diltiazem
``` Slows = verapamil, diltiazem Inc/NC = nifedipine, nicardipine ```
103
Comparative Myocardial depression effects of verapamil, nifedipine, nicardipine, diltiazem
``` Moderate = verapamil, nifedipine, diltiazem Slight= Nicardipine ```
104
Comparative SA node depression effects of verapamil, nifedipine, nicardipine, diltiazem
``` Moderate= verapamil None= nifedipine, nicardipine slight = diltiazem ```
105
Comparative AV node conduction effects of verapamil, nifedipine, nicardipine, diltiazem
``` Marked= verapamil Moderate= diltiazem none= nifedipine, nicardipine ```
106
Comparative coronary artery dilation effects of verapamil, nifedipine, nicardipine, diltiazem
``` Greatest = Nicardipine Marked= nifedipine Moderate= verapamil, diltiazem ```
107
Comparative peripheral artery dilation effects of verapamil, nifedipine, nicardipine, diltiazem
``` Marked= nicardipine, nifedipine Moderated= Verapamil, diltiazem ```

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