Chapter 5 Induction of Anesthesia Flashcards
What causes hemodynamic changes with induction in the cardiac patient (3 things)
Loss of sympathetic tone resulting in 1)vasodilation 2)cardiac depression 3)relative hypovolemia
Why would you chose to hold ACE inhibitors or ARBs?
associated with hypotension upon induction of anesthesia, and weaning from CPB
what group of cardiac patients should not be premeditated prior to surgery name 2
unstable patients with 1)Heart failure or 2)Symptomatic Aortic Stenosis
What 3 obvious monitors must be utilized during induction
1)ECG 2)BP 3)Pulse oximeter
name 3 emergency scenarios in which anesthesia induction comes before placing invasive monitors (PA cath, central lines)
1) ruptured thoracic aortic aneurysm
2) cardiac tamponade
3) ventricular rupture
name 3 common opioids given to cardiac patients
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
name pros and cons for administering iso, des and servo to cardiac patient
1)iso is cheap 2)des for rapid titratability 3)sevo for irritable/difficult airway
why would you use the following muscle relaxants 1)sucks 2)pan 3)vec, roc or cis 4)cis
1) sucks-difficult airway
2) pan-low heart rates
3) vec or roc cis-hemodynamic instability
4) cis-liver or renal failure
Which anticholinergic would you use (and have drawn up prior to surgery)
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
Name some properties of Ephedrine
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
name some properties of dobutamine
beta 1 agonist sympathomimetic drug2-20mcg/kg/min, not to exceed 40 mpg/kg/min
dopamine properties
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
epinephrine
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
phenylephrine
pure alpha agonist, 40-200mcg bolus
drip is40-180 mcg/min
norepinephrine
dose is 2-30mcg/min, alpha>beta 1 agonist
vasopressin
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
nitroglycerin
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
nitroprusside
arterial and venous vasodilator used to avoid or reverse sudden periods of hypertension-cyanide toxicity
.25-5mcg/kg/min
reduces afterload
nicardipine
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*
esmolol
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
metoprolol
selective beta 1 blocker
2.5 5 mg q 5 minutes, max dose 15
diltiazem
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
verapamil
calcium channel blocker
5-10 mg over 2 minutes for SVT, fib/flutter
lidocaine
binds to intracellular Na channels
amiordarone
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
To be prepared, have which 3 things set up and preprogrammed to pump ready to use
one inotrope, one vasopressor, and vasodilator (NTG)
Using conservative drug amounts, being mindful of drug onset times and interactions, and adapting drug doses to physical status of patient for WHAT
Attenuation of hemodynamic responses to laryngoscopy and surgery without undue hypotension
Name two common causes of hypovolemia
diuretics, prolonged NPO
Why is hypovolemia difficult to access
no record of preoperative urine output, and no LV preload assessment
Most CV patients do not tolerate __% depletion of intravascular volume without hemodynamic compromise
10%
what compensatory mechanisms that are useful in normal people may be impaired or blunted by cardiac medicine regimen
tachycardia and vasoconstriction
How do propofol and thiopental reduce BP
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
from most to least, order the circulatory depression of thiopental, etomidate, midazolam and propofol
propofol>thiopental>midazolam>etomidate
what is the best way to combat hypovolemia
augment intravascular volume by using balanced salt solutions (don’t overdo it!) with mitral valve lesions or CHF
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?
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
1) Ketamine does this in normal patients
2) ketamine does this in critically ill patients
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
with the exception of ketamine, all local anesthetics do this (name 5)
1) removing SNS tone
2) decreasing SVR
3) depressing myocardium
4) increasing venous pooling (reduces venous return)
5) inducing bradycardia
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
does not decrease stress response to intubation (increased BP and HR)
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
b)level of opioid analgesia to CNS
what is safest way to induce anesthesia to critically ill patients
reduce the dose administered
When should pancuronium be used
patients with a baseline heart rate less than 50
patients with valvular regurgitation
ED95 describes what in terms of muscle relaxants
-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
using what depolarizing muscle blocker can reduce onset time of NDNMB to 1 to 1.5 minutes
succinylcholine
describe high dose opioid induction techniques, what are drawbacks of using this
- 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
what muscle relaxer is good for high dose opioids
pancuronium, give early to reduce chest wall rigidity
For the cardiac patient with difficult airway, what is a good technique to use
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
describe ways provide anesthesia to the airway
- 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
what is a good drug to use for awake intubations
precedex 1mcg/kg
describe the 3 opioid receptors
opioid receptors are gamma protein coupled receptors mu, kappa and delta
phenylpiperidine rings
what compartment model do synthetic opioids follow
3 compartment model
what is bioavailability of fentanyl
98%
how much more potent is Sufentanyl compared to fentanyl
7-10 times more potent with a higher pKa and 20% ionized, less protein bound, lower volume of distribution and faster recovery time
How is remifentanyl metabolized, what is its onset, what is its recovery time, what do you have to control post operatively
1) non specific esterase metabolism, extra hepatic
2) onset is 1 minute
3) recovery time 9-20 minutes
4) post op pain increased
etomidate dose, onset, peak, SE
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
what is unchanged with etomidate administration
SV, LVEDP, contractility unchanged in normovolemic patients. preserves myocardial contractility better than any other induction technique except high dose opioids
Thiopental onset, CV effects
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
How much will an induction dose of propofol drop BP
15-40%
with propofol, why does lower BP not cause increase in heart rate
resets baroreceptor reflex
With propofol what happens to SVR, CI, SC, LV stroke work index
decreases all
above doses of .75mg/kg, what happens with propofol in terms of the heart
direct myocardial depression in doses >0.75mg/kg
use with hemodynamically stable cardiac patients with good ventricular function
what property accounts for rapid recovery from propofol
extensive redistribution and movement from central to peripheral compartment
Name 3 bad things about midazolam, name 2 good things
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
Is lorazepam useful in cardiac patients?
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)
What type of anesthesia does ketamine provide, what does ketamine increase, when is it advantageous to use
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
hemodynamic stimulatory effect of ketamine depends on what 2 things
robust myocardium, sympathetic nervous system reserve
what are two bad things about ketamine
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
with iso, sevo and des name 5 things that they cause
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)
When do you not want to use N2O
not really used in cardiac cases, but is generally safe for induction. Do NOT use in patients with increased Pulmonary vascular resistance
How long does it take to reach MAC >1 with sevo and des
2-4 minutes, takes longer with ISO. Des and Sevo can suppress induction stress response faster than iso.
drawback to des
SNS stimulation with rapidly increased inspired concentration, airway irritant
Would you give a NDNMB for intubation
difficult airway
which NMB has the fastest onset and offset
succinylcholine
when would you want to give pancuronium
if you want beta blockade during high dose opioid induction because vagolytic effects counteract vagal tone and bradycardia caused by opioids
which NDNMB are “hemodynamically bland”
cisatracurium, rocuronium, and vecuronium
which NDNMB would you use for renal or hepatic failure
cisatracurium