UBP condescened Flashcards
Extubation criteria
-Adequate oxygenation: SpO2 > 92%, PaO2 > 60 on FiO2 40%
-Adequate ventilation: TV > 5 cc/kg, RR > 7, EtCO2, < 50, PaCO2 < 60
-hemodynamically stable
-reversal of NMB
-neurologically intact
-normal acid/base/lytes/normothermia
-negative inspiratory pressure > 20
-Rapid shallow breathing index < 105
Rapid Shallow Breathing Index
RR/TV in L
Cricoid pressure
-pushes esophagus to side, does not effectively compress the esophagus
-interferes w/ mask ventilation and intubation
-has not been proven to prevent aspiration -> lowers LES tone and may promote aspiration
-proper application of force (30N) is difficult to apply
-if pt begins to vomit -> release cricoid pressure to prevent esophageal rupture
Airway fire protection
-laser tube
-FiO2 30% or less
-avoid nitrous oxide
-inflate cuff with saline
-minimize laser time
Treatment airway fire
-disconnect/turn off O2
-remove ETT
-flood field w/ saline
-mask ventilate with 100% O2
-use rigid bronchoscopy to inspect for airway debris and damage, possible bronchial lavage
-re-intubate
-leave intubated for 24 hours
- steroids
-pulmonary consult
-serial CXR
Contraindications to jet ventilation
severe COPD/respiratory disease that does not allow for proper exhalation
Complications to jet ventilation
PTX
pneumomediastinum
airway fire
gastric distention
aspiration
Airway innervation
posterior oropharynx to epiglottis: glossopharyngeal n
epiglottis to VC: superior laryngeal nerve (internal branch)
VC and below: Recurrent laryngeal n
Airway motor innervation
recurrent laryngeal n: abduction
external branch of superior laryngeal n: cricothyroid m (adduction)
CEA indications:
TIA w/ angiographic evidence of stenosis
reversible ischemic deficits w/ > 70% stenosis
unstable neuro status despite anticoagulation
CEA regional v general
regional: awake for serial neuro exams, requires cooperation, dec CV depression, may not get adequate coverage if extends into territory of CN
general: controlled airway, ventilation, cooperative patient
COPD and CEA pretesting
CXR and room air ABG -> assess pt’s baseline PaCO2 -> if baseline hypercarbic don’t want to fix rapidly in the OR -> cerebral vasoconstriction and ischemia
How to do regional for CEA
-awake pt is best neuro monitor esp if concern of possible plaque rupture
-superficial and deep cervical plexus block.
-superficial cervical plexus block: 10cc along posterior border of SCM
-deep cervical plexus block (C2-C4): draw line from mastoid to anterior transverse process of C6 => at level of cricoid cartilage is C2 -> inject 10cc of local anesthetic at transverse processes of C2, C3, C4
**usually can be done under superficial cervical plexus block alone
How to do a deep cervical plexus block
(C2-C4): draw line from mastoid to anterior transverse process of C6 => at level of cricoid cartilage is C2 -> inject 10cc of local anesthetic at transverse processes of C2, C3, C4
-risks: phrenic n block, epidural, subarachnoid, vertebral artery injection, Horner’s, RLN injury
General plan for CEA
-TIVA (w/ SSEPs)
-if you use volatiles: reverse steel phenomenon (improved cerebral protection and myocardial priming)
Neuromonitoring EEG
-correlates w/ cerebral ischemia, but cannot detect subcortical ischemia
-processed EEG: can detect severe cerebral ischemia, but not focal
Neuromonitoring SSEP
-detects deep brain structure injury, sensitive to anesthetics, hypothermia, hypoTN
Neuromonitoring transcranial doppler
-can detect cross clamp hypoperfusion and shunt malfunction and emboli
-placed at ipsilateral MCA -> detects BF and embolic events
**hard to place
Neuromonitoring cerebral oximetry
simple, but low sensitivty and specificity
-detects regional ischemia, but includes all tissue beds (approximates venous saturation, since mostly venous blood)
-decrease > 20% suggests cerebral ischemia
Neuromonitoring carotid stump pressure
-helps guide need of shunting, no guideline of pressure that shunt should be placed
- < 50 indicates hypoperfusion
*goes in ICA above clamp and measures pressure from collateral flow
CEA reperfusion injury
cerebral hemorrhage or edema after cross clamp removed
-vessels distal to obstruction are maximally dilated -> lost ability to autoregulate -> renewed BF and perfusion is too high
**important to maintain strict BP control
Bradycardia in CEA
surgical manipulation of baroreceptors in carotid sinus
-infiltrate w/ local to prevent recurrence
CEA neuromonitoring change
FiO2 100%
ensure adequate MAP
ask surgeon to release clamp, consider shunt placement
ensure normocarbia
pharmacologic brain protection -> dec CMRO2
CEA Postop delayed awakening
-Residual anesthesia (opioids, volatiles, benzos)
-cardiac failure: hypoperfusion
-metabolic/hypo/hyperglycemia
-hypothermia
-neuro deficits (stroke) -> hematoma compressing artery, stenosis postop (doppler)
CEA postop HTN
-control due to risk of bleeding, MI, arrhythmia, intracerebral hemorrhage, cerebral edema
Causes of postop HTN CEA
hypoxemia
hypercarbia
pain
full bladder
carotid baroreceptor blunting (carotid sinus dysfxn after surgery)
postop HTN CEA tx
correct hypercarbia/hypoxia, tx pain, give hydralazine, NG, beta blocker to lower SBP < 160 or w/i 20% baseline
CEA chemoreceptor dysfunction
Up to 10 months to recover
-loss of response to hypoxia and hypercarbia
-give supp O2, cautious w/ opioids
**esp concerned if b/l CEA in past
CEA cerebral hyperperfusion syndrome
-previously hypoperfused lost ability to autoregulate -> inc systolic pressure and CBF -> focal neuro deficits, edema, HA, sz
CEA neck hematoma, what to do?
apply pressure, call surgeon, transport to OR, have difficult airway equipment ready
Sitting position for posterior fossa surgery: risks
-brain stem ischemia: quadraplegia due to obstruction of carotid or vertebral arteries
-macroglossia/facial edema
-venous air embolism
Oliguria
prerenal: hypovolemia, hypotension, hypoperfusion, renal v or artery thrombosis
intra: ATN (ischemia, toxin, abx, myoglobin, hemoglobin), intrinsic dx (vascular, glomerula, thromboembolism, interstitial nephritis)
post: obstructed catheter, urethral or ureteral obstruction
When should sitting position be avoided for crani surgery?
known intracardiac shut: PFO, ASD/VSD -> inc risk of stroke w/ air embolism
Venous air embolism causes
-inc in pulm a pressure, dec cardiac output, inc deadspace -> mediators released cause inc in PVR
Ways to detect venous air embolism
TEE: most sensitive, but difficult to manipulate under drapes
-precordial doppler: R sternal border b/w 2-4 intercostal
-DECREASED EtCO2, inc in CVP
Treatment for venous air embolism
have surgeon flood the field, apply bone wax, control open blood vessels
-FiO2 100%, d/c nitrous oxide
-Use CVP in RA to aspirate air, manual occlusion of jugular veins
-left lateral decubitus position (keeps air in RA, prevents entry into RV and obstruction of RVOT)
-head below heart
-hemodynamic support: inotropes, fluids
Normal ICP
15
What’s inc ICP
20-25 should be treated
Symptoms of inc ICP
papillema, nausea/vomiting, confusion, Cushings triad (bradycardia, HTN, irregular breathing)
Normal cerebral perfusion pressure
80-100
What cerebral perfusion pressure is considered to be ischemia
< 50
Ideal cerebral perfusion pressure for head injury
60-70
Increased ICP, needs central line, where to place?
subclavian or femoral to avoid head down positioning -> inc ICP
succ and ICP
fasciculations can cause transient inc in ICP -> but hypoxia and hypercarbia w/ difficult airway cause higher inc in ICP
Treatment of inc ICP
-ventriculostomy
-HOB position 30 degrees
-analgesia: blunt pain/symp resp
-avoid hypoxemia
-avoid hypothermia: shivering inc ICP
-osmotic therapy: mannitol, furosemide, hypertonic saline
Hypothermia effects
-inc O2 demand w/ shivering
-inc ICP w/ shivering
-poor wound healing
-coagulopathy
-arrhythmia
glucose and neurosurg
avoid hyperglycemia -> inc brain swelling
-no dextrose containing fliuds -> causes edema w/ injured blood brain barrier
Neurogenic pulm edema
s/p head injury or intracranial bleed
-symp response -> systemic vasoconstriction -> dec LV compliance and inc LA pressure -> pulm edema
-w/ catecholamine surg, inc pulm capillary permeability
-tx: supportive, lung protective
Pseudotumor cerebri
elevated ICP (> 20) w/ normal CSF, normal mentation, no mass lesion
Pseudotumor cerebri treatment
Acetazolamide (dec CSF production)
Furosemide
steroids
lumbar puncture/CSF drain
VP shunt
**no LP before CT head, r/o space occupying lesion
nitrous oxide and ICP
inc CBF, inc CMRO2
Benzos ICP
no change CBF, dec CMRO2
Why ischemia w/ dec PaCO2
cerebral vasoconstriction, left shift of O2-Hgb curve
PaO2 and CBF
Dec PaO2 (<60) -> inc in CBF
Cerebral autoregulation
b/w CPP of 50-150, shifted to the right in HTN
**when MAP above this, or tumor abolishes cerebral autoregulation -> CBF is dpt on MAP
Inc ICP treatment
-HOB up 30 degrees
-avoid hypoxemia
-inc SBP to maintain CPP
-analgesia: blunt pain/symp resp
-avoid hypothermia (shivering inc ICP)
-mannitol, furosemide, hypertonic saline
-avoid hyperglycemia
Etomidate CBF, CMRO2
dec both
N2O and CBF, CMRO2
inc CBF, in CMRO2
Benzos CBF, CMRO2
no change CBF, dec CMRO2
Electrolyte disturbances from SAH
SIADH
CSW
hypoK/hypoCa/HypoMg from diuretics
Preop eval SAH
-neuro deficits/coma
-cardiac dysrhythmias 2/2 catecholamine release
-electrolyte disturbances: SIADH, CWS, hypoK/hypoCa/hypoMg from diuretics
-labs: CBC, T&C
Intraop goals for SAH
-avoid aneurysm rupture: maintain transmural pressure (MAP - ICP)
-maintain CPP
-brain relaxation: hyperventilation (PaCO2 30-25), mannitol, furosemide, CSF drain, avoid hypercarbia, hypoxemia, and nitrous
-blunt symp resp, no succ, no hypoTN
-No dextrose (BG < 180)
cerebral protection during aneurysm clipping
-prop, etomidate, thiopental (dec CBG and CMRO2)
-mild hypothermia (32-34)
-inc MAP (collateral flow)
-minimze occlusion time
-monitor brain function (EEG, SSEP)
-brain relaxation (CSF drainage, mannitol, hyperventilation)
SAH intraop rupture
-control bleeding but maintain CPP
-bleeding control: temp clip or compression ipsilateral carotid artery
-cerebral protection: avoid hyperthermia, hypoxemia, hyperglycemia
Hypothermia complications
-delayed emergence
-HTN if hypothermic w/ emergence
-MI
-wound infxn
-coagulopathy
-dysrhtyhmias
-prolonged anesthetics and muscle relaxants
Post SAH rebleeding timeframe
Usually w/i first 24 hours
Vasospasm post SAH
Starts days 3-12, peak 1 week after
-dx: cerebral angio (gold), transcranial doppler (>200 cm/s)
-cerebral auto regulation impaired
-tx: Nimodipine, angio w/ intra-arterial verapamil
tx for neurogenic pulm edema
Treat CNS cause, lung protective ventilation, diuretics, Hgb > 10, PEEP
SIADH tx
Tx underlying cause, water restriction, hypertonic saline, diuretics
DEMECLOCYLINE (kidneys not sensitive to ADH)
Treatment for SIADH
Treat underlying cause, water restriction, hypertonic saline, diuretics
DEMECLOCYCLINE
Pathophys SIADH
Excessive ADH -> water retention -> hypoNa, normal total body Na, euvolemia, U Na < 100
Cerebral salt wasting
Excessive renal sodium excretion centrally mediated process -> hypoNa
-dehydrated and hypovolemic
Treatment for cerebral salt wasting syndrome
Fluids, salt tabs, mineralocorticoids (fludrocortisone)
Diabetes Insipidus
Inability to concentrate urine due to renal resistance or decreased secretion of ADH
-large volume of dilute urine -> hyperNa
Diabetes Insipidus treatment
Central: desmopressin/DDAVP and hydration
Nephrotoxic: diuretic, hydration, indomethacin
What causes central pontine myelinolysis
Rapid correction of hyponatremia
-locked in syndrome: quadraparesis, dysphagia, dysarthria, diplopia, LOC
-don’t correct faster than 12 mmol/L/day
What are SSEPs measuring?
Ascending sensory pathway (dorsal column pathway)
SSEPs and epidural
-if epidural in place, only give narcotics -> local anesthesia will interfere
MEPs measure what?
Descending motor pathway (lateral corticospinal tract)
**more sensitive to volatiles than SSEP
Contraindications for MEP
Seizure history
Skull fracture
Implanted metal devices
Clips in brain
MEPs and epidural
Only give narcotics through epidural, local anesthesia will interfere
Brain death: how to confirm
-Objective findings of severe insult: documentation, neuro imaging (SAH, infarct, herniation)
-irreversible damage
-no confounding factors: sedation, hypothermia, acid/base, endocrine disturbance
-no cortical response (sternal rub)
-no brainstem function (corneal or gag reflex)
-apnea test
ECT contraindications
-intracranial mass/vascular malformation
-recent SAH, evolving stroke ( <1 month)
-severe cardiac dx: MI < 1 mo, diminished ventricular function
-severe pulm dx
-ASA 4-5
-pheochromocytoma
ECT hemodynamic changes
Parasympathetic then sympathetic!
Multiple sclerosis epidural v spinal
epidural is okay, spinal more likely to cause exacerbation
low back pain, saddle anesthesia, LE weakness, bowel/bladder dysfxn
cauda equina syndrome
-get MRI and emergent neurosug c/s
what happens if ventricular drain dropped to floor whole open
inc drainage of CSF and dec in ICP -> ventricular collapse and tearing of cortical veins
neuraxail w/ spina bifida
AVOID unless MRI shows no tethered cord
which volatile is most cardiac stable?
sevo
-causes the least tachycardia, does cause dose dpt myocardial depression and dec vascular resistance
Normal cardiac index
2.6-4.2
Normal PCWP
2-15
Normal pulm artery pressure
15-30/4-12
normal mixed venous
75%
Hs and Ts PEA
hypoxia, hypoTN/hypovolemia, hypoK/hyperK, hypoglycemia, hypothermia, H+ acidosis
tamponade, tension PTX, toxins, thrombosis (PE/MI), trauma
sinus bradycardia ddx
hypoxia/hypercarbia
beta blocker
succ
anticholinesterase inhibitors
acute inferior MI
vagal stimulation
high sympathetic block
acidosis
inc ICP
reflex bradycardia
atropine dose for sinus brady
0.5 mg
SVT ddx
WPW
thyrotoxicosis
digoxin toxcitiy
PE
preganncy
drug effect
intravascular volume shifts
-heart disease
SVT treatment
-vagal maneuvers
-adenosine (6mg then 12)
-verapamil
-amiodarone
-synchronized cardioversion if unstable
a flutter tx
Diltiazem or esmolol
with a fib, prior to cardioversion?
must r/o thrombi if > 48 hours
Junctional rhythm
HR 40-60
-ectoptic activity inferior to AV node -> abnormal P waves -> normal QRS
-if hypotnesive: atropine/ephedrine/ amio: inc activity of SA node
Causes of PVC/bigeminy
electrolyte imbalances
acidosis
hypoxia
drug intereactions
treatment of PVC/bigeminy
Lidocaine 1.5 mg/kg bolus
-esmolol
-procainamide
-verapamil
-overdrive pacing
treat PVCs
> 5 per min
Vtach w/ a pulse treatment
amiodarone 150 mg over 10 minutes
OR lidocaine 1.5 mg/kg
>3 PVCs, wide QRS, no p waves
Unstable V tach
unsychronized cardioversion 200J
V fib causes
MI, hypoxia, hypothermia, electrolyte imbalance
V fib tx
CPR, O2, unsynchronized debrillation, consider amiodarone 300mg IIV, lidocaine 1.5 mg/kg
LBBB and stress tests
cannot do exercise stress test: assoc w/ low specificity, must do chemical MPI stress
why a fib poorly tolerated w/ aoritc stenosis
inc myocardial O2 demand
-dec time in diastole/dec LV filling time
-dec CPP
-no atrial kick
severe AS transvalvular gradient
> 40 mmhg
mid systolic ejection murmur 2nd right IC space
aortic stenosis
decrescendo diastolic murmur L sternal border
aortic insufficiency
induction w/ Mitral stenosis
be careful w/ dec in afterload -> can’t compensate w/ inc in SV b/c of stenosis to maintain cardiac output -> minimize dec in SVR
what to be careful for after fixing mitral regurge
LV failure -> now has to work harder to pump entire volume against afterload -> was previously splitting b/w
blowing systolic murmur
mitral regurge
causes of Tricuspid regurge
pulm HTN
carcinoid syndrome
ebsteins anomaly
infective endocarditis
HOCM goals
maintain SVR
preload adequate
low HR
avoid PPV if possible
Things that worsen HOCM
tachycardia
hypovolemia
sympathectomy/dec SVR
dysrhythmias
excess PEEP/PPV
inc myocardial contractility
Valsalva
OB and HOCM
-ensure adequate L uterine displacement to maintain preload
-avoid spinal, epidural ok (don’t want a massive dec in SVR)
-can get pulm edema after delivery due to autotransfusion
oxytocin and HOCM
avoid! dec SVR and inc HR!!
Determinants of myocardial O2 consumption
HR
contractility
wall tension
Normal QRS
< 0.12 ms
when to avoid pulm a catheters
when pt has a LBBB -> can cause a RBBB
how to measure cardiac output
10cc room temp or cold saline (whatever programed to) through PAC x3 -> if w/i 10% of each other, accurate
-greater temp change: low CO, less temp change: higher CO
when is pulm artery catheter put in?
poor LV fxn (CVP doesn’t correlate w/ PWCP), pulm HTN, coronary stenosis with valvular lesions, poor RV function, ascending aorta/aortic arch procedure
PCWP v TEE intraop ischemia
TEE is better at assessing regionanl wall motion abnormalities
complications of PAC placement
arrhythmias
PA rupture
VAE
PTX
hemothorax
RBBB
infection
PE
valve injury
treatment for benzo OD
flumazenil
treatment for beta blocker OD
glucagon
HD indications
Acidosis
Electrolytes (hyperK)
Intoxication (ASA, methanol)
Overload of fluids and heart failure
Uremia (encephalopathy, pericarditiis, issues w/ clotting(
Parkland formula
4 x % BSA burned x kg
-half in first 8 hours, 2nd half in 16 hours after
Normal mixed venous
70-75%
what causes high mixed venous
sepsis, high CO states (burns), dec O2 consumption, CO poisoning, cyanide toxicity, L to R shunts, inotropes
what causes low mixed venous
low cardica output, anemia, hypoxemia, high O2 consumption
CI to TEE
esophagectomy
active GI bleed or recent surgery
oropharyngeal trauma
esophageal pathology: stricture, TEF, mallory-weiss tear, scleroderma
stress test indications
-active cardiac conditions
-3 or more RF w/ < 4 METs having high risk surgery and will change management
-pts w/ 1-2 RF w/ < 4 METs undergoing intermediate risk surgery
-1-2 RF > 4 METs w/ high risk surgery
Normal digoxin level
0.5-2
cardiac output and heart transplant
if dec in SVR -> can’t increase HR to compensate to inc CO -> need to inc stroke volume -> dpt on preload
nasal intubation in heart transplant
AVOID: inc risk of infxn w/ nasal flora w/ immunocompromised
NSAIDs and heart transplant
inc risk of toxicity w/ cyclosprine and inc risk of gastritis w/ steroids
AVOID
MAP equation
MAP = SVR x CO
CO equation
CO = SV x HR
roller pumps how works CABG
2 rollers partially compress tubing to promote forward flow
centrifugal pumps how work CAGB
rotational force creates forward flow
heparin dose for bypass
100 U/kg
ACT goal
> 480
glucose goal in bypass
< 150: hyperglycemia causes worse neuro outcomes
hypoTN w/ bypass initiation
hemodilution/dec SVR due to priming solution
-inadequate venous return to reservoir: hypovolemia, caval obstruction, table too low
Getting ready to come off bypass
-Labs normal: pH, pCO2, pO2, Hct 20-24, K 4-4.5, Ca 1.1-1.2, mVO2 > 70%
-anesthesia machine one, benzos to prevent awareness
-EKg stable rhythm/rate
-warmed
air removed from heart
-support drugs available
post bypass coagulopathy
MCC abnormal plt function
-ACT, PT/INR/PTT, CBC, TEG
low mixed venous after off bypass
inadequate tissue oxygenation, needs inc FiO2
pacing post bypass
A pacing preferred -> improved cardiac output w/ preserved atrial kick
-V if complete heart block
Failure to capture w/ pacemaker ddx
MI/conduction abnormalities
lead dislodged
electrolyte abnormalities
acid-base disturbances
-abnormal antiarrhythmic drug levels
difficulty coming off bypass ddx
air in RCA or other coronaries
graft is down
long time on pump
MI
arrhythmias
hypothermia
acidosis
perivalvular leak
type A aortic dissection by Standford
ascending aorta, emergent surgical repair
type B aortic dissection by Stanford
descending aorta, managed medically
AAA complicatiosn
aortic root dilation
ruputure
tamponade
hemothorax
hoarseness (RLN compression)
SOB (trachea/bronchial tree compression)
SVC syndrome
spinal cord blood supply
anterior 2/3: anterior spinal artery, lower by radicular arteries and artery of adamkiewicz
posterior 1/3: posterior spinal arteries
CSF pressure goal w/ drain
8-10
AAA repair, bair hugger?
don’t put warming on clamped lower extremities -> inc acidosis
EVAR complications
endoleak: failure toe separate aneurysm from arterail blood flow
AKI
paraplegia
post implantation syndrome
Post implantation syndrome
EVAR -> endothelial activation due to graft ->< fever, elevate dinflammatory mediators, leukocytosis
**self limited, 2-10 days, give NSAIDs if no renal issues
when to use R sided DLT
distorted anatomy of L main bronchus
compression of L main bronchus by TAA
L pneumonectomy
L lung transplant
pneumonectomy poor outcomes predictors
-ABG: PaCO2 > 45, PaO2 < 50
-FEV1 < 2L
-FEV1/FVC < 50%
-PAP > 40
-FEV1 < 800 cc
FOr a pneumonectomy, who is considered to be high risk
PaCO2 > 45
PaO2 < 60
ppFEV1 < 40%
DLCO < 40%
VO2 max < 15 cc/kg/min
Meds for ECT
-methohexital ideal: rapid onset and recovery, minimal anticonvulsant effects
-prop: Dec sz duration
-Etomidate: may prolong sz
for a pneumonectomy, predicted postop FEV1 < 40%, next steps?
V/Q scan to look for contribution of lung that will be resected and get a TTE (risk of RV failure)
Mediastinoscopy CI
carotid artery dx
CVA due to compression of R brachiocephalic artery
tracheal deviation
c spine disease
TAA
where to put a line in mediastinoscopy
R side to monitor for compression of brachiocephalic artery
mediastinoscopy, what do you need prior to d/c?
CXR to r/o PTX
