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Physiology Flashcards

1
Q

Why do elderly people take longer to wake up.

A

Higher body fat –> higher Vd for lipophilic drugs
Also, decreased GFR, longer effect of drugs due to decreased elimination
Decreased liver volume, phase I metabolism, BF
Decreased albumin (increased FF of drugs)

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2
Q

What happens to the CV system in the geriatric population?

A

Stiffer arteries –> higher pulse pressure, increased afterload–> LVH –> diastolic dysfunction –> more dependent on atrial kick for filling

Decreased SV under stress due to less diastolic filling from less compliant LV
Decreased beta receptor responsiveness, increased
norepinephrine levels

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3
Q

What happens to the respiratory system in the elderly?

A

Decreased tidal volume
Increased dead space, decreased diffusion capacity
Increased closing capacity –> decrease in PaO2, increased shunt
Closing capacity > FRC
Increase in lung compliance
Decrease in chest wall compliance
Diaphragm flattening
Decreased hypoxemic and hypercapnic respiratory drive

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4
Q

What are the CNS effects of aging?

A

Brain mass decrease
Lower NT release and binding sites

Lower MAC and local anesthetic requirements
More spread of local in spinal! And longer duration of action

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5
Q

How do you diagnose postoperative cognitive delirium?

A

Neurobehavioral testing

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6
Q

What are the anesthetic considerations with obesity?

A

Decrease FRC - time to desaturation
Difficult airway - thick neck
Decreased chest wall compliance –> atelectasis
CO2 retention due to airway closure –> hypercapnic respiratory drive is altered, sensitivity to opioids?

Drug administration- large propofol doses for maintenance (based on TBW, higher Vd due to fat content

Increased fibrinogen, factor VII and VIII - procoagulant state –> DVT prophylaxis!

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7
Q

What are the anesthetic considerations for burn patients?

A

More sensitive to benzodiazepines due to decreased albumin (increased Ff of drug)
Opioid resistance due to high tolerance
Increased extrajunctional receptors within 24 H if > 10% TBSA - cannot give succinylcholine for 1 year afterward!
Insulin resistance due to massive catecholamines surge
Decreased alpha glycoproteins - need higher doses of Bb and local anesthetics
Heat loss!
Dehydration : Parkland formula- 4 ml X %TBSA X weight. Then give the first half over 8 hours, then next half over 16 hours

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8
Q

A patient has > 30% of TBSA, what happens with NMB?

A

Develop resistance at 1 week with peak resistance at 4-6 weeks
Slower onset of action, decreased duration, decreased effect because now more receptors.

NEED HIGHER AND MORE FREQUENT DOSING

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9
Q

What are the effects of hypothermia?

A 
Cardiac:
Decreased CO 
Alters cardiac conduction --> arrythmias
Shivering increases myocardial oxygen demand
Decreased oxygen unloading

Metabolic:
Hyperglycemia due to decreased insulin release
Decreased metabolism –> decreased drug clearance

Heme:
Decreased fibrinogen synthesis and platelet dysfunction –> bleeding risk
Decreased immune function –> PNA, wound healing!

CNS:
Decreased respiratory drive
Decreased CMRO2 and CBF –> AMS

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10
Q

You are doing a TURBT on an elderly patient with recent MI, what are you worried about with this case?

A 
TURBT syndrome (from open venous sinuses) causing fluid overload --> CHF and MI from increased demand
AMS due to acute brain swelling and decreased in sodium
Decreased hypotonicity in plasma --> acute intravascular hemolysis
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11
Q

What are other complications of TURBT?

A 
Hypothermia
DIC from release of thromboplastin from prostate 
Dilutional TCP
Prostatic capsule rupture
Sepsis
Bladder perf
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12
Q

Patient has DIC after TURBT, what do you do?

A

Get a TEG, CBC, coags
Start AMICAR, give bolus of 5 grams then start drip at 1 g/hour
Give heparin and clotting factors and platelets
Consult heme

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13
Q

Patient is getting a TURBT, what are all the possible complications?

A 
Bladder perforation 
Fluid overload
Water intoxication 
DIC 
Septicemia 
Hypothermia
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14
Q

What are the advantages of using regional anesthesia?

A

Reduces incidence of venous thromboembolism

Patient awake for mental status checks

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15
Q

How do you treat autonomic hyperreflexia?

A

Remove the stimulus
Deepen the anesthetic!
SL nifedipine

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16
Q

What are the anesthetic considerations for pericardial tamponade?

A

Fast and full
Maintain spontaneous ventilation - avoid PPV!
Avoid phenylephrine due to reflex Brady

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17
Q

What do you want preoperatively for a mediastinal mass?

A

Chest X-RAYS
CT with contrast (not sensitive for obstruction)
High-resolution CT with 3 D airway reconstruction
Bronchoscopy
TEE - to assess heart function, look for tamponade/collapse, rule out for reason for fluid overload (if patient is overloaded). Do supine and standing
Flow volume loops : would show flattening of both inspired and expiratory loops

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18
Q

How would you proceed with anesthesia in someone with a mediastinal mass?

A
  1. Fluid bolus to increase preload and ensure filing of the right heart and ensure no cardiac collapse from external compression
  2. Awake FO intubation sitting up with topicalization and ketamine. ENT standing by to do rigid bronchoscope
  3. Then paralyze with judicious use of NMB (remember if MG - very sensitive to NMB)
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19
Q

What things do you want in the room for a mediastinal mass case?

A

Rigid bronchoscope

CPB by pass machine

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20
Q

Patient has a pacemaker and they are using mono polar electrocautery. The patient has an R on T phenomenon. What do you do?

A

Cease all electrocautery
Remove magnet from ICD - should reinstate it
Zoll pads on (just in case). Do not place directly over device
Shock as appropriate/ACLS

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21
Q

What is platelet transfusion threshold for major elective surgery?

A

< 50 K

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22
Q

What are the advantages of veno-veno bypass in liver transplant?

A

Preserves cardiac output because venous return from the lower extremities and viscera is uninterrupted

Effectively decompressed the portal system and decreases splanchnic congestion

(Cannula in IVC and portal vein to axillary vein)

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23
Q

What is the advantage of a piggy back OLT?

A

Preserves systemic blood flow through a preserved IVC

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24
Q

What happens during reperfusion of the liver?

A

Increase in potassium
Increase in preload
Increase in lactate and hydrogen ions
Get myocardial stunning, increased preload –> bradycardia
Decreased SVR
Increased fibrinolysis from tPA in the graft

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25
Q

What are delayed hemolytic reactions due to?

A

Antibodies to non-D antigens of the Rh system

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26
Q

What are the characteristics of a delayed hemolytic reaction?

A

Happens 2-21 days after transfusion
Symptoms of fever, jaundice, malaise
Dx: Direct Coomb’s

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27
Q

What is a febrile reaction to a transfusion due to?

A

Antibodies to donor WBCs or platelet

No hemolysis occurs

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28
Q

What is urticaria from transfusion due to?

A

Sensitization to plasma proteins

Give antihistamine and steroid

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29
Q

What is R time?

A

Initial clot formation (5-10 minutes)

Function of clotting factor deficiencies, heparinization, TCP

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30
Q

What is k time?

A 
Coagulation rate (1-3 minutes)
Function of clotting factors, platelets, fibrinogen
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31
Q

What is the alpha angle?

A

Rate of fibrin build up and cross-linking (50-70 degrees)

Function of fibrinogen

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32
Q

What is MA

A

Maximal amplitude = clot stability (50-70 mm)

Function of platelets and fibrinogen

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33
Q

What is LY30?

A

Degree of lysis (0-8 percent)

Need anti fibrinolytic therapy

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34
Q

What is a phase 1 block?

A

It is a depolarizing block due to perijunctional sodium channels that inactivate with continued depolarization and cannot reopen until the end plate repolarizes.

The end plate cannot repolarizes as long as the depolarizing muscle relaxant binds Ach receptors

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35
Q

What is a phase II block?

A

When there is conformational change in the Ach receptor

Can happen after prolonged depolarization

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36
Q

What is fade of train of four from?

A

Blocking prejunctional receptors that play a role in mobilizing Ach for sustained contraction.
Indicative of a phase II, nondepol block

Clinical recovery = no fade

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37
Q

What is posttetanic potentiation?

A

It is the ability of a tetanus stimulation (sustained stimulus of 50-100 Hz for 5 seconds) to cause Ach mobilization in the NMJ.

If no posttetanic twitches - you are fully blocked

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38
Q

Why is a drop in afterload detrimental in aortic stenosis?

A

Because these patients have a fixed cardiac output and inability to increase cardiac output.
Usually LVH due to increased afterload from stenosis valve –> at risk for sub endocardial ischemia with hypovolemia and tachycardia

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39
Q

Why is Afib bad in aortic stenosis?

A

It significantly increases myocardial oxygen demand, decreases diastolic (coronary perfusion) time in an already hypertrophic muscle, LV filling time and atrial kick contribution to LV filling which leads to significant reduction in CO

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40
Q

What are EKG signs of PE?

A 
New Rbbb
Peaked P waves
ST changes
Right axis deviation 
SVT arrythmias
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41
Q

How would you treat a PE?

A 
ABCs
100% FiO2, secure airway if needed
Vasopressors to support the heart and decrease PVR - milrinone 
ICU transfer
Anticoagulation
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42
Q

What are your concerns with SVC syndrome?

A

Impairment of venous drainage causing mucosal and airway edema
Increased ICP/impaired CPP
Unreliable drug delivery in the right arm
Potential for massive hemorrhage
Fluid management - too much will lead to more engorgement
Postop respiratory complications secondary to edema and mass compression
Avoid coughing and bucking during emergence because could cause acute airway obstruction

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43
Q

What are you concerns with mediastinoscopy?

A 
Right innominate artery compression (need right radial arterial line or oximeter)
Venous air embolism 
PTX
Rupture of artery
Pericardial tamponade
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44
Q

What are the contraindications to mediastinoscopy?

A 
Severe tracheal deviation
CVA
Severe cervical spine disease with limits neck extension
Previous chest radiation 
Thoracic aortic aneurysm
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45
Q

What concerns you about a patient with longstanding hypertension?

A

They are at increased risk for blood pressure lability, cerebral ischemia secondary to rightward shifted cerebral auto regulation, intraoperative end organ ischemia, arrythmias, CHF, hypotension, HTN, stroke.

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46
Q

For a patient with longstanding uncontrolled hypertension, what would you do preoperatively and then intraoperatively?

A

I would get a thorough history focused on blood pressure medications, BP control, causes of the HTN and presence of end organ damage

Tests: EKG, BMP

Maintain within 20% of baseline or around 140/90

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47
Q

Who would you delay elective surgery in for hypertensive control?

A

SBP readings over 180
DBP over 110
End organ damage
Cardiac, carotid, or pheo resection

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48
Q

What are signs/symptoms of SVC syndrome?

A

Cough, dyspnea, JVD, headache, Orthoptera, hoarseness, papilledema, facial cyanosis, dysphagia, chest pain

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49
Q

How would you induce a patient with SVC syndrome?

A

Head up for drainage

Awake FO

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50
Q

How would you manage hypotension?

A 
Check pulse and other monitors
EKG for arrythmia or cardiac ischemia 
Ensure adequate oxygenation/ventilation
Auscultation for PTX, HTX, bronchospasms, endobronchial intubation
Reduce volatile
Open fluids, give vasopressors
Trendelenburg
Send ABG
If these interventions failed to resolve the problem, I would consider placing CVC, TEE, Precordial Doppler
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51
Q

What is base excess?

A

The amount of strong acid or base needed to return 1L of whole blood back to a ph of 7.4 and PaCO2 of 40.
Represents the nonrespiratory component of acid-base disturbance
Used as a marker for volume resuscitation

Negative = acidosis
Positive = alkalosis
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52
Q

What is the Hamburger shift?

A

Bicarbonate anions exchange for extracellular chloride (part of the hemoglobin buffer for H+ made when CO2 combines with water and then dissociates to make bicarbonate by carbonic anyhdrase

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53
Q

What would you do for someone with hemolytic anemia ?

A

Do physical exam - look for pallor, fatigue, SOB
Check labs: CBC with reticulocyte count, LFTs, BMP, UA
Eliminate causes: hypoxia, hypothermia, acidosis, hyperglycemia, infection, drugs
Give fluids and mannitol

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54
Q

What is DIC?

A

A pathological activation of the coagulation system resulting in widespread microthrombi, consumption of coag factors, TCP, hemolytic anemia, diffuse emboli, thromboembolic events.

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55
Q

What are risk factors for DIC.

A

Amniotic fluid exposure
Hypovolemia
Vascular endothelial injury
Pre-eclampsia

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56
Q

What is TACO?

A

Large volumes of fluids causing increased pulmonary blood flow and therefore increased pulmonary capillary blood pressures

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57
Q

How can you tell the difference between TRALI and TACO.

A

TRALI:
PAOP less than 18
Normal BP, euvolemia, normal heart function
High plasma protein content of edema

TACO:
HTN, S3, peripheral edema, JVD, impaired cardiac function, higher BNP, low plasma protein content of edema

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58
Q

What is the pathophysiology of TRALI?

A

Anti-donor HLA antibodies causing neutrophil activation which leads to endothelial damage, cap leakage and ALI

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59
Q

What is the treatment for TACO?

A

Diuretics
Inotropes as needed
Ensure adequate Hct for oxygen carrying capacity and lowering pulmonary blood flow

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60
Q

What is the treatment for TRALI?

A

No diuretics or steroids (don’t confer benefit)

Stop transfusions. Supportive ventilation. Usually recover within 96 hours

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61
Q

What tests confirms diagnosis of pheochromocytoma?

A

Urine and plasma metanephrines

Clonidine suppression test (doesn’t decrease catecholamines in patients with a pheo)

62
Q

What is the optimal duration of alpha blockade prior to surgery?

A

10-14 days

Discontinue 24-48 hrs before surgery to decrease the risk of hypotension after vascular tumor isolation

63
Q

What drugs should be avoided in pheochromocytoma?

A

Succinylcholine (fasciculations and histamine release)
Morphine (histamine release)

Drugs that increase SNS activity:
Pancuronium
Atropine
Ketamine 
Ephedrine
Halothane
Nitrous oxide
Metoclopromaide
Dropper idol
64
Q

What is a normal dibucaine number?

A

80

65
Q

What would you do if you suspected bladder perforation in a TURBT.

A

Rule out MI with EKG and ensure adequate oxygenation and ventilation
Alert surgeon, ask if there is diminished return of irrigation fluid
Stop procedure
Suprapubic cystotomy

66
Q

What are the advantages of using neuraxial technique for a patient getting TURBT?

A

Allows for an awake patient which facilitates early detection of intraoperative myocardial ischemia, cerebral edema, bladder perf

Reduce risk of periop venous thrombosis
Reduce detrimental effects of volume overload by increasing venous capacitance
Reduce risk of aspiration by maintaining airway reflexes
Control postop pain

67
Q

What are the concerns with glycine irrigation?

A

Hyperammonemia

Visual loss - no reactive pupils, normal fundoscopic exam

68
Q

Would a HbA1C be helpful and how is it helpful?

A

Yes, because it can assess the patient long term glycemic control and risk of end organ damage

Can help indicate the long term problems with diabetes:
Autonomic neuropathy (hypothermia, gastroparesis,
HTN
Retinopathy
Vascular disease
Peripheral neuropathy
Renal insufficiency

69
Q

What is the optimum periop glucose control?

A

120-180 mg/DL

Avoid poor wound healing, reduce infections, mortality and hospital length of stay

70
Q

How would you manage a patient’s blood sugar perioperatively?

A

Reduce long acting night time insulin to 2/3 dose or insulin infusion by 30%
Reduce intermediate or long acting morning of by 1/2
Hold short acting insulin

Check preop glucose and then every 1-2 hours
Treatment with insulin pushes or infusion

71
Q

How would you assess someone getting a CEA preoperatively?

A
  1. Neuro status - CN exam, mental status, strength exam, sensory
  2. Cardiac - EKG, get METS, chest pain history checking for unstable angina, murmur?, LE edema, rate and rhythm –> echo if none within last 12 months (and known LV dysfunction or new symptoms)
  3. Respiratory - CXR to check for cardiomegaly, COPD, PNA, pulm edema
  4. Check for signs of autonomic neuropathy if diabetic
  5. Check baseline BP

4.

72
Q

What are the advantages of using a regional anesthetic for a CEA in a patient with cardiac disease?

A

Provide better hemodynamic stability
Provide a surrogate for monitoring adequate cerebral perfusion
Reduced incidence of postop hematoma (likely because not coughing against the tube)
Reduced need for vasopressor and therefore less stress on the heart

73
Q

What are the disadvantages of using a regional anesthetic for CEA?

A

Phrenic nerve paralysis
Limited access to an unsecured airway
High level of patient cooperation
Pain due to sympathetic afferent of the carotid sheath

74
Q

How do you perform a deep cervical plexus block?

A

Draw a line from mastoid process to the level of the cricoid cartilage
Palate the C2 TP 1-2 cm caudad to mastoid

10 cc at TPs of C2, 3, 4

75
Q

How do you perform a superficial cervical plexus block?

A

Inject 10 cc of local along posterior border of the SCM

76
Q

What are the complications of cervical plexus blockade?

A 
Epidural and SAH injection
Vertebral artery injection
Recurrent laryngeal nerve palsy
Horner's
Phrenic nerve palsy
LAST
77
Q

Why is there destruction of auto regulation in patients with a stenosis carotid artery?

A

Because you have maximal dilation of the cerebral vessels due lack of oxygen to the brain and now cerebral perfusion is pressure dependent

78
Q

Why would you not use a superficial cervical plexus block alone in a CEA?

A

Because inadequate regional could result in a sympathetic response that would result in HTN and detrimental effects in the heart, cause need for IV anesthetic which may cause respiratory compromise and need for urgent airway control and steal phenomenon in the brain due to hypercapnea induced vasodilation of no ischemic areas

79
Q

What are the available options for Neuro monitoring in a patient for CEA?

A

Awake patient - assessment of speak, consciousness, contralateral handgrip
Stump pressure (> 50 is good) = CPP above clamp
EEG
SSEPs
TCD
CEREBROX
Measurement of regional cerebral blood flow
Jugular venous oxygen saturation

80
Q

How do you measure regional CBF?

A

IV or ipsilateral carotid artery injection of radioactive xenon with subsequent analysis

Expensive

81
Q

What are the disadvantages of using EEG for Neuromonitoring?

A

May not detect sub cortical or small infarcts
False negatives especially if had preexisting Neuro condition
Nonspecific (affected by temp, BP, anesthesia)

82
Q

How do TCD help with Neuromonitoring?

A

Measure of ipsilateral MCA and calculates the mean blood flow velocity and detection of microemboli
Analyze shunt function
Manage hyperperfusion

83
Q

What information does jugular bulb venous oxygen saturation provide?

A

Global cerebral oxygen saturation

84
Q

What is myocardial preconditioning?

A

When exposure to a drug serves to protect to myocardium from ischemia and reperfusion injury.

Volatile agents at MAC of 0.25 can do this by opening K ATP
channels which prevent calcium overload

85
Q

What does slowing of an ipsilateral EEG indicate after carotid cross clamp?

A

Cerebral ischemia

Ask surgeon to unclamp and place a shunt
Ventilate with 100% FiO2 
Ensure adequate MAP
Normocarbia 
Consider decreasing CMRO2 if hemodynamics can tolerate
86
Q

If you have delayed awakening in a CEA case, what could you do to assess brain function before CT scan?

A

Use the US to check flow in the carotid
Use EEG to monitor brain function
TCDs

87
Q

What is cerebral hyperperfusion syndrome?

A

Result of sudden perfusion of previously hypoperfused areas in the setting of destroyed cerebral auto regulation resulting in headache, seizure, cerebral edema, ICH

88
Q

Your patient who just had CEA is hypertensive if PACU, what would you do?

A

Give NTG, nicardipine, beta blocker or hydralazine

Correct hypoxemia, hypercarbia
Bladder distention
Pain

89
Q

What would you do if the patient had an expanding neck hematoma in PACU.

A

Check vital signs –> apply pressure to the wound
Call for help/surgeon
Transport to OR if time for intubation
Have surgeon and trach kit and difficult airway equipment close

emergent intubation if needed (avoid tachycardia and HTN!)

90
Q

At what level of potassium should you delay an elective case?

A

Above 5.5

91
Q

If you proceeded with a patient with ESRD and hyperkalemia, how would you do it?

A

Analyze EKG for prolonged PR, wide QRS, and peaked T waves
Give calcium to stabilize cardiac membranes
Avoid sux and potassium solutions
Treat metabolic acidosis
Treat with insulin/glucose, albuterol, hyperventilation, and bicarbonate
Have defibrillator in the room
Monitor K and ECG

92
Q

What kind of blood should you give someone with a transplant?

A

Leukocyte reduced, irradiated and CMV negative to avoid GVHD and alloantibody production

93
Q

What kind of cardiac issues do you expect with ESRD patients?

A 
Dilated cardiomyopathy due to volume overload
CHF
CAD
Arrythmia
Pericarditis due to uremia
94
Q

How can a capnogram aid in assessing hypoxia?

A 
Esophageal intubation - flat line
Incompetent valves (doesn't return to baseline)
Obstructive disease or bronchospasm (more rounded during initial phase, deceased slope )
Curare cleft - inadequate muscle relaxant
95
Q

How do you treat sickle cell crisis

A 
Oxygen supplement 
Hydration
Pain control
Hct 30-40%
Treat infection 
Heme consult
96
Q

What are the concerns in a liposuction case?

A 
Fat embolism
LAST 
Fluid overload 
Systemic epinephrine uptake
Pulmonary edema
97
Q

What is the max recommended dose of lidocaine for liposuction according to the Academy of Derm?

A

55 mg/kg

98
Q

What could you do to limit risk of LAST in liposuction surgery?

A

Used diluted tumescent solution with epi
Limit surgery to less than 3000 ml of fat removal
Have lipid emulsion kit ready

99
Q

What are the systemic effects of growth hormone?

A 
Tissue overgrowth --> Difficult airway, large tongue, tonsils, epiglottis, glottic stenosis 
Cardiomyopathy 
Diabetes
Accelerated atherosclerosis 
Osteoarthritis 
OSA
100
Q

How would you evaluate to atlantoaxial subluxation in an RA patient?

A

Detailed history and physical
AP cervical spine films with flexion/ extension and open mouth Odontoid views
Consult neurosurgeon if the separation of the anterior Odontoid process from the posterior arch of the atlas was greater than 3 mm

101
Q

What are the signs and symptoms of porphyric crisis?

A 
HTN, tachycardia
N/v, severe abdominal pain
Electrolyte abnormalities
Seizure, psych disturbance
CN palsy, peripheral neuropathy
Skeletal muscle weakness 
Respiratory failure, bulbar weakness
102
Q

How would you treat porphyric crisis?

A

Stop inducing drugs
Ensure oxygenation, ventilation, normal electrolytes
Hydration, pain control, anxiety control
10% glucose with saline
Treat N/V, seizure, HTN/tachy

103
Q

How can you reduce the risk of porphyric attack?

A 
Hydration
Anxiolytics
10% glucose in solutions
Avoid drugs that use P459 
Treat infection
104
Q

What degree of burns should you intubate a patient?

A

10% full thickness

25% partial thickness

105
Q

How would you intubate a patient with suspected inhalational injury?

A

Awake fiber optic

106
Q

What are the effects of carbon monoxide?

A

Direct myocardial depressant from mitochondrial function
Leftward shift of oxyhemoglobin dissociation curve
Decreased oxygen carrying capacity

107
Q

Why would you not administer sodium bicarbonate to treat metabolic acidosis?

A

Leads to generation of more CO2 which diffuses into cells and worsens intracelluar acidosis (bad for patients with pulmonary compromise)

Causes leftward shift of oxyhemoglobin dissociation curve resulting in impaired tissue delivery of oxygen

108
Q

Why is PaO2 and SpO2 normal in carbon monoxide poisoning?

A

PaO2 is a measurement of dissolved oxygen in the blood, doesn’t depend on Hb
SaO2 is a percentage of heme binding sites that are saturated with oxygen.

SpO2 derived from PaO2 so can be false in poisoning
Also, COHb absorbs the same amount of light at 660nm as oxyhemoglobin

109
Q

What CV changes do you see following burn injury?

A

Cardiac depression in 24-48 due circulating myocardial depressants, decreased preload from extravasation of plasma proteins, increased SVR, decreased response to catecholamines, decreased coronary BF.
After adequate resuscitation, capillary integrity improves, then you get reabsorption of interstitial fluid, increased metabolic demand, increased CO (hyperdynamic), reduced SVR

110
Q

What happens in bone cement implantation syndrome?

A

Hardening and expansion of the cement cause increased intramedullary pressure and bone marrow embolization causing increased PVR, RH strain and V/Q mismatch
Circulating methyl methacrylate causes decreased SVR

111
Q

How would you treat hypothalamic mediated hyper metabolism after burns?

A

Heat the room to decrease energy expenditure on maintaining adequate core temperature
Aggressive pain control
Adequate nutrition via TPN (25 Kcal/kg +40 per % TBSA per 24 h)
Closely monitor electrolyte, glucose, LFTs

112
Q

How would you adjust your IV anesthetics in an obese patient?

A

Theoretically, lipophilic drugs have a higher volume of distribution, therefore it is reasonable to use TBW for initial dosing. This also makes higher clearance so you can reduce the maintenance doses.
Hydrophilic drugs should be given based on IBW

I would calculate initial doses based on IBW and then Titrate up as necessarily using clinical judgment

113
Q

What is the difference between anaphylaxis and anaphylactoid reaction?

A

Anaphylaxis is IGE mediated (requires previous exposure)

Anaphylactoid is triggered by direct interaction with allergens

114
Q

What is the pathophysiology of anaphylaxis

A

Degranulation of mast cells and basophils to elapse histamine, leukotrienes, bradykinin, TNF,PGs that lead to bronchoconstirciton, peripheral vasodilation

115
Q

How can you confirm the diagnosis of anaphylaxis?

A

Get a tryptase level

116
Q

What are the advantages of preoperatively paracentesis?

A

Improved V/Q mismatch
Decreased risk of aspiration
Increase CO due to increased preload from less compression of IVC
Decreased renin and aldosterone levels, creatinine, BUN, and portal pressures

But risk circ collapse with rapid reaccumulation and anesthesia

117
Q

What is hepatopulmonary syndrome?

A

PaO2 less than 70 on room air
A-a gradient greater than 20
Orthodeoxia (arterial deoxygenation in the upright position)

118
Q

What is hepatorenal syndrome?

A

Cr > 1.5
Renal failure due to vasoconstriction of renal vasculature

Hyperosmolar urine, urine Na less than 10 (sodium retention), normal renal histology and tubular function

119
Q

What is the prehepatic stage of liver transplant?

A

Liver is dissected and mobilized until it is only attached by the IVC, portal vein, hepatic artery, CBD

120
Q

What is the anhepatic stage?

A

Starts with clamping of the hepatic artery
Remove native liver
Implant donor liver

121
Q

At the start of the anhepatic phase, the surgeon clamps the IVX and the BP drops, what will you do?

A

Ask surgeon to unclamp the IVC

Evaluate for other causes and volume load the patient and consider veno-venous bypass to preserve preload

122
Q

What are the EKG findings of hypocalcemia?

A 
Narrow pulse pressure
Prolonged QT 
Flat t waves
Hypotension 
Elevated CVP
123
Q

What are the perioperative concerns in aortic aneurysm or dissection?

A

Propagation of aneurysm or dissection
Exsanguination from burst
MI or tamponade from disruption of coronaries
Stroke from disruption of left common carotid
Paraplegia from blood loss or disruption of radicular arteries to anterior spinal cord
Difficult airway from tracheal deviation or compression, SVC syndrome
Renal failure due to blood loss, clamp time, disruption of bvs
Transfusion related injury

124
Q

What are the ways to decrease risk of spinal cord ischemia in aortic repair?

A

Place lumbar drain and drain to 8-10 mmHg
Avoid hypotension, hyperglycemia
Monitor with SSEPs, MEPs
Give steroids, CCBs, Mg, naloxone, dextrometorphan, papaverine

125
Q

What is an endoleak?

A

Failure to isolate the aneurysmal sac

126
Q

Which type endoleaks are benign?

A

Type II and IV

127
Q

Which endoleaks require urgent intervention?

A

Type I and III

Structural failures of the graft associated with aneurysmal rupture

128
Q

How do you provide a motionless field for graft deployment in aortic repair?

A

Adenosine or inducing ventricular fibrillation

129
Q

Why wouldn’t you use neuraxial for endovascular aortic repair?

A

High likelihood of open repair
Duration of procedure
Need for motionless field for deployment
Difficult airway management if emergent GA was required

130
Q

What is your differential for persistent hypotension after graft deployment?

A 
Persistent hemodynamic effects of providing motionless field
Aneurysm rupture
Vascular damage 
MI/arrythmia 
Embolism
Anaphylaxis
Inadvertent med administration
131
Q

How do you provide renal protection during aortic aneurysm repair?

A

Maintain adequate intravascular volume
Minimize clamp time
Give mannitol, vit C, sodium bicarbonate infusion
Use dye that is no ionic or low osmolality
Hypothermia

132
Q

How does mannitol protect the kidneys?

A

Increases renal cortical BF
Free radical scavenger
Increases renal PGs (vasodilation)
Reduces cell edema

133
Q

How does fenoldopam help?

A

D1 agonist

Preferentially causes vasodilation of splanchnic and renal BF

134
Q

What are the complications of TPN?

A 
Hypokalemia
Hypomagnesemia 
Hypophosphatemia
Hyperglycemia, hypoglycemia 
Hypercarbia
Metabolic acidosis 
Fatty liver
135
Q

What should you think of when you hear thyroiditis?

A

Myasthenia gravis

136
Q

What are the potential causes of prolonged neuromuscular blockade?

A 
MG
pseudocholinesterase deficiency 
MS
Lambert Eaton
ALS
Muscular dystrophy
Drug error
Lithium, aminoglycoside 
Botulism toxin
Defective nerve stimulator
137
Q

Why is succinylcholine effect sometimes increased in MG?

A

If the patient is on anticholinerases, these also inhibit pseudocholinesterase and thereby decrease its metabolism

138
Q

What are the risks associated with retrobulbar block?

A 
Optic ischemia
Increased IOP
Brain spread
Hemorrhage
Globe perforation 
IV or intraneural injection
139
Q

What are the physiologic effect of intra-abdominal compartment syndrome?

A

Impaired ventilation
Cardiac depression due to impaired venous return
Increased afterload
Increased ICP secondary to decreased venous outflow
Oliguria
Decreased lactate clearance (liver dysfunction)
Bacterial translocation and bowel ischemia

140
Q

How do you evaluate for intra-abdominal compartment syndrome?

A

Measure pressure via NG tube or Foley

CT scan showing collapsed IVC, bowel edema,

141
Q

What would you do to manage DKA.

A 
Administer a bolus of insulin and infusion 
Check ABG, BMP
Start IVF
Check the gap
Replace K, Mg, ca, phosphate as needed
142
Q

How rapidly would you correct the glucose in DKA?

A

By 75-100/hour to prevent cerebral edema

143
Q

When would you add glucose to the insulin infusion?

A

When glucose level dropped below 250 to provide energy source and avoid hypoglycemia

144
Q

What are the contraindications to ECT?

A 
Intracranial hemorrhage
Mi within the last 3 months
Stroke within the last month
Increased ICP
Pheo 
Intracranial mass lesions
Vascular malformations
145
Q

How would you evaluate oliguria?

A

Check patients VS, BP, hypoxia, Cvp, CO
Check Foley for obstruction
Give fluid challenge

Get BMP, urine electrolytes
Consult a nephrologist if ATN

146
Q

How do you diagnosis CIN.

A

When there is a 0.5 mg/DL increase in creatinine within 3 days of admin

147
Q

What is type I vWF disease?

A

Most common, quantity defect

Defective release, normal stores

148
Q

What is type III vWF?

A

Due to low levels, severe

Lots of bleeding abnormalities

149
Q

What is the first line treatment for type I vWF?

A

Desmopressin

150
Q

How would you provide prophylaxis for a major surgery in someone with vWF?

A

Give cryo or Humate P to maintain levels of factor VIII and vWF above 100 and above 50 for 7-10 days after surgery

151
Q

What is Humate P?

A

A purified commercial preparation of factor VIII-vWF concentrate containing large vWF multimers

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