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cardiac constable reading > Chapter 5 Induction of Anesthesia > Flashcards

Chapter 5 Induction of Anesthesia Flashcards

1
Q

What causes hemodynamic changes with induction in the cardiac patient (3 things)

A

Loss of sympathetic tone resulting in 1)vasodilation 2)cardiac depression 3)relative hypovolemia

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2
Q

Why would you chose to hold ACE inhibitors or ARBs?

A

associated with hypotension upon induction of anesthesia, and weaning from CPB

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3
Q

what group of cardiac patients should not be premeditated prior to surgery name 2

A

unstable patients with 1)Heart failure or 2)Symptomatic Aortic Stenosis

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4
Q

What 3 obvious monitors must be utilized during induction

A

1)ECG 2)BP 3)Pulse oximeter

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5
Q

name 3 emergency scenarios in which anesthesia induction comes before placing invasive monitors (PA cath, central lines)

A

1) ruptured thoracic aortic aneurysm
2) cardiac tamponade
3) ventricular rupture

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6
Q

name 3 common opioids given to cardiac patients

A

1) fentanyl (1-2mcg/kg) metabolized in liver, excreted by kidney T1/2 2 to 4 hours mu opioid agonist, respiratory depressant, muscle rigidity no histamine release
2) sufentanyl-most potent opioid-onset 1-2 minutes duration 15-30 minutes dose is 0.1-0.7mcg/kg/min
3) remifentanyl (0.5-1mcg/kg/min for induction dose, for MAC 0.1mcg/kg/min dropped down to .05mcg/kg/min) hydrolyzed by non specific plasma esterase’s, unaffected by renal or liver function) causes muscle rigidity, apnea, T1/2 is 3 10 minutes

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7
Q

name pros and cons for administering iso, des and servo to cardiac patient

A

1)iso is cheap 2)des for rapid titratability 3)sevo for irritable/difficult airway

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8
Q

why would you use the following muscle relaxants 1)sucks 2)pan 3)vec, roc or cis 4)cis

A

1) sucks-difficult airway
2) pan-low heart rates
3) vec or roc cis-hemodynamic instability
4) cis-liver or renal failure

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9
Q

Which anticholinergic would you use (and have drawn up prior to surgery)

A

atropine-tertiary amine crosses the BBB, competes with ACh at muscarinic receptor, causes increased HR, CO, vagal blockade of SA and AV nodes, increases IOP and decreases secretions
dose 0.5 to 3mg

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10
Q

Name some properties of Ephedrine

A

synthetic non-catecholamine, sympathomimetic vasopressor
dose is 5-20mg or 100-200mcg/kg
indirect release of NE at nerve endings which increases BP, CO, HR, PVR and bronchodilation (mixed alpha 1 and beta 1 and 2 agonists)
tachyphylaxis may occur

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11
Q

name some properties of dobutamine

A

beta 1 agonist sympathomimetic drug2-20mcg/kg/min, not to exceed 40 mpg/kg/min

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12
Q

dopamine properties

A 
stimulates dopamergic receptors
alpha and beta effects depending on dose
precursor of NE
renal (dopamergic)1-5mcg/kg/min
cardiac beta 1 2-10mcg/kg/min
alpha receptors 10-20mcg/kg/min to vasoconstrict
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13
Q

epinephrine

A 
sympathomimetic vasopressor
Code dose 1 mg q 3-5 min
1-16mcg/min
low doses 1-2mmcg/min beta 2 alpha 1 effects
2-10mcg/kg/min alpha and beta
>10mcg/min pure beta
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14
Q

phenylephrine

A

pure alpha agonist, 40-200mcg bolus

drip is40-180 mcg/min

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15
Q

norepinephrine

A

dose is 2-30mcg/min, alpha>beta 1 agonist

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16
Q

vasopressin

A

antidiuretic hormone
Dilute 1 unit/ml in a 10 ml syringe
max dose is 1-6 units per hour or 0.1-1unit per minute
arterial vasoconstriction, mesenteric vasoconstriction, H2O reabsorption in renal tubules onset 10-15 minutes
code dose 40 Units

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17
Q

nitroglycerin

A

venous dilator>arterial dilator 0.2-2mcg/kg/min, titrate by 0.1
MOA-NTG converted to NO which stimulates cGMP to cause vasodilation
decreases preload and after load decreases venous return, decreases right to left end diastolic pressure, decreases PVR, may produce coronary steal, abrupt discontinuation may cause coronary vasospasm

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18
Q

nitroprusside

A

arterial and venous vasodilator used to avoid or reverse sudden periods of hypertension-cyanide toxicity
.25-5mcg/kg/min
reduces afterload

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19
Q

nicardipine

A

calcium channel blocker
25mg in 10 ml vial (2.5mg/ml)
dose is 5-15mg/hour, titrate by 2.5
binds to voltage gated ion channels, blocks ca influx into vascular smooth muscle, decreases arterial BP by vasodilation
increases EF, CO in CAD improves LV diastolic distensability
used for hypertension without decreasing HR*

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20
Q

esmolol

A 
beta 1 selective blocker
rapid onset, short acting
*decreases amount of propofol required
0.5mg/kg over 60 seconds
for drip 0.5 to 1mg/kg over 1 minute bolus followed by 50-250mcg/kg/min titrating in increments of 25 to 50 mpg
used in SVT, tachycardia, hypertension
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21
Q

metoprolol

A

selective beta 1 blocker

2.5 5 mg q 5 minutes, max dose 15

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22
Q

diltiazem

A

calcium channel blocker that increases effects of anesthesia=slower emergence
control rapid ventricular response, fib/flutter
5-15mg/hour titrate by 5
bolus of 20 over two minutes

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23
Q

verapamil

A

calcium channel blocker

5-10 mg over 2 minutes for SVT, fib/flutter

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24
Q

lidocaine

A

binds to intracellular Na channels

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25
Q

amiordarone

A

class III antiarrythmic Vfib/Vtach
prolongs phase 3 of cardiac action potential, prolongs QT, PR, QRS which decreasesBP and HR
reduces PVR, relaxes vascular smooth muscle
beta blocker and calcium channel like tendencies on Sa node increases refractory period by na and K channel effects
300mg bolus
than 900 mg for 6 hours 33 ml/hour
than 540 mg for 18 hours=16ml/hour

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26
Q

To be prepared, have which 3 things set up and preprogrammed to pump ready to use

A

one inotrope, one vasopressor, and vasodilator (NTG)

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27
Q

Using conservative drug amounts, being mindful of drug onset times and interactions, and adapting drug doses to physical status of patient for WHAT

A

Attenuation of hemodynamic responses to laryngoscopy and surgery without undue hypotension

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28
Q

Name two common causes of hypovolemia

A

diuretics, prolonged NPO

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29
Q

Why is hypovolemia difficult to access

A

no record of preoperative urine output, and no LV preload assessment

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30
Q

Most CV patients do not tolerate __% depletion of intravascular volume without hemodynamic compromise

A

10%

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31
Q

what compensatory mechanisms that are useful in normal people may be impaired or blunted by cardiac medicine regimen

A

tachycardia and vasoconstriction

32
Q

How do propofol and thiopental reduce BP

A

1) venodilation, peripheral pooling of blood
2) decreasing SNS tone
3) decreasing SVR
4) depressing myocardial contractility
* constable says SVR, MAP CI, and CV decreases

33
Q

from most to least, order the circulatory depression of thiopental, etomidate, midazolam and propofol

A

propofol>thiopental>midazolam>etomidate

34
Q

what is the best way to combat hypovolemia

A

augment intravascular volume by using balanced salt solutions (don’t overdo it!) with mitral valve lesions or CHF

35
Q

Why would you keep a CPB patient dry preoperatively
and what methods do you use to maintain cardiac output
and what is minimum cardiac index goal?

A

conservative use of fluids to prevent hemodilution necessitating blood transfusions, must use vasopressors to perfuse vital organs, keep cardiac index > or equal to 1.8L/min/m2

36
Q

1) Ketamine does this in normal patients

2) ketamine does this in critically ill patients

A

stimulates the SNS and CV system normally
in critically ill its can decrease BP by depleting catecholamines preventing indirect central nervous system mediated sympathomimetic effects to counterbalance its direct negative inotropic and vasodilatory effects

37
Q

with the exception of ketamine, all local anesthetics do this (name 5)

A

1) removing SNS tone
2) decreasing SVR
3) depressing myocardium
4) increasing venous pooling (reduces venous return)
5) inducing bradycardia

38
Q

increasing opioid dose of fentanyl >8mcg/kg fentanyl, .75 ug/kg of sufentanyl, or 1.2 msg/kg/min of remifentanyl does what to stress response

A

does not decrease stress response to intubation (increased BP and HR)

39
Q

in terms of sedative hypnotics, what determines the degree of stress response a)depth of anesthesia or b)central nervous system level of opioid analgesia

A

b)level of opioid analgesia to CNS

40
Q

what is safest way to induce anesthesia to critically ill patients

A

reduce the dose administered

41
Q

When should pancuronium be used

A

patients with a baseline heart rate less than 50

patients with valvular regurgitation

42
Q

ED95 describes what in terms of muscle relaxants

A

-suppression of twitch response in 95% of patients
NDNMB 3 to 7 minutes
-2x ED95 dose 1.5 to 3 minute onset
-3x ED95 dose is 1.5 minutes with Rocuronium

43
Q

using what depolarizing muscle blocker can reduce onset time of NDNMB to 1 to 1.5 minutes

A

succinylcholine

44
Q

describe high dose opioid induction techniques, what are drawbacks of using this

A
  • morphine 1-2mg/kg or fentanyl 50-100mcg/kg used to suppress stress response and hemodynamic stability
  • long post op intubation times,good for high risk patient who will require overnight mechanical ventilation despite anesthetic technique chosen
45
Q

what muscle relaxer is good for high dose opioids

A

pancuronium, give early to reduce chest wall rigidity

46
Q

For the cardiac patient with difficult airway, what is a good technique to use

A

awake intubation using

1) airway anesthesia
2) low to moderate levels of sedation
3) adjuncts to treat hypertension or tachycardia(beta blockers such as esmolol, NTG or cardene, labetalol

47
Q

describe ways provide anesthesia to the airway

A
  • neubulized lidocaine
  • topical cetacaine or topical lidocaine
  • CNIX or SLN blocks (blocks pharynx to vocal cords)
  • transcricoid or transtracheal injection of 4% lidocaine via suction or injection port when reaching VC or trachea
48
Q

what is a good drug to use for awake intubations

A

precedex 1mcg/kg

49
Q

describe the 3 opioid receptors

A

opioid receptors are gamma protein coupled receptors mu, kappa and delta
phenylpiperidine rings

50
Q

what compartment model do synthetic opioids follow

A

3 compartment model

51
Q

what is bioavailability of fentanyl

A

98%

52
Q

how much more potent is Sufentanyl compared to fentanyl

A

7-10 times more potent with a higher pKa and 20% ionized, less protein bound, lower volume of distribution and faster recovery time

53
Q

How is remifentanyl metabolized, what is its onset, what is its recovery time, what do you have to control post operatively

A

1) non specific esterase metabolism, extra hepatic
2) onset is 1 minute
3) recovery time 9-20 minutes
4) post op pain increased

54
Q

etomidate dose, onset, peak, SE

A

0.3-0.6mg/kg, onset 30-40 seconds, peak 1 minute

causes seizures, decreases MAP and SVR and increases HR and CO, adrenal cortical suppression

55
Q

what is unchanged with etomidate administration

A

SV, LVEDP, contractility unchanged in normovolemic patients. preserves myocardial contractility better than any other induction technique except high dose opioids

56
Q

Thiopental onset, CV effects

A

rapid onset, used safely in hemodynamically stable patients, venous pooling, decreased preload, myocardial depression above 2mg/kg, increases HR via baroreceptor reflex, less is more in cardiac patients because more goes to brain and heart, dose related negative inotropic effect from decrease in calcium influx

57
Q

How much will an induction dose of propofol drop BP

A

15-40%

58
Q

with propofol, why does lower BP not cause increase in heart rate

A

resets baroreceptor reflex

59
Q

With propofol what happens to SVR, CI, SC, LV stroke work index

A

decreases all

60
Q

above doses of .75mg/kg, what happens with propofol in terms of the heart

A

direct myocardial depression in doses >0.75mg/kg

use with hemodynamically stable cardiac patients with good ventricular function

61
Q

what property accounts for rapid recovery from propofol

A

extensive redistribution and movement from central to peripheral compartment

62
Q

Name 3 bad things about midazolam, name 2 good things

A

bad things
-difficult to titrate minimum effective dose for induction because of variation in required dose, has a slow onset time to peak in CNS at 3-7 minutes, and when used in conjunction with opioids causes hypotension
good things-amnesic, reduces preload (like NTG) in patients with high filling pressures

63
Q

Is lorazepam useful in cardiac patients?

A

Not really. Very potent, so when small doses are required, sure, but poor choice because of long duration of action. Also has slow onset (peaks 5-10 minutes)

64
Q

What type of anesthesia does ketamine provide, what does ketamine increase, when is it advantageous to use

A

dissassociative anesthesia
extensively redistributed and eliminated, 97% bioavailability with unconsciousness in 20-60 seconds
increases HR, MAP, plasma epi
good for cardiac tamponade, hypovolemia, hemorrhage

65
Q

hemodynamic stimulatory effect of ketamine depends on what 2 things

A

robust myocardium, sympathetic nervous system reserve

66
Q

what are two bad things about ketamine

A

1) coronary blood flow may not be sufficient to meet the increased O2 demand induced by SNS stimulation
2) avoid in patients with increased ICP

67
Q

with iso, sevo and des name 5 things that they cause

A

predominate effect is 1)dose dependent vasodilation that 2)reduce SVR and 3)BP, cause 4)myocardial depression, and 5)dose dependent reflex tachycardia (may be attenuated with b blockers or opioids)

68
Q

When do you not want to use N2O

A

not really used in cardiac cases, but is generally safe for induction. Do NOT use in patients with increased Pulmonary vascular resistance

69
Q

How long does it take to reach MAC >1 with sevo and des

A

2-4 minutes, takes longer with ISO. Des and Sevo can suppress induction stress response faster than iso.

70
Q

drawback to des

A

SNS stimulation with rapidly increased inspired concentration, airway irritant

71
Q

Would you give a NDNMB for intubation

A

difficult airway

72
Q

which NMB has the fastest onset and offset

A

succinylcholine

73
Q

when would you want to give pancuronium

A

if you want beta blockade during high dose opioid induction because vagolytic effects counteract vagal tone and bradycardia caused by opioids

74
Q

which NDNMB are “hemodynamically bland”

A

cisatracurium, rocuronium, and vecuronium

75
Q

which NDNMB would you use for renal or hepatic failure

A

cisatracurium

cardiac constable reading (3 decks)

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