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Clinical Entrance Exam > extra (after exam 3) and specifically what he wants us to know for the final > Flashcards

extra (after exam 3) and specifically what he wants us to know for the final Flashcards

1
Q

BMI, what is considered under weight, normal weight, obese I and morbid obesity III?

A 
Underweight: < 18.5
Normal weight: 18.5 - 24.9
Overweight: 25 - 29.9
Obese I:  30 – 34.9
Obesity II:  35 – 39.9
Morbid Obesity III:  > or equal to 40
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2
Q

What BMI does morbid obesity start at?

A

40 (equal to or greater)

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3
Q

What are the three types of body fat distributions (body types and how you gain fat)

A

Android (central obesity)
Visceral fat
gynecoid

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4
Q

Android, visceral fat, and gynecoid… how do these body types differ in how they gain fat?

A

ANDROID: CENTRAL OBESITY: ADIPOSE TISSUE IS LOCATED PREDOMINANTLY IN THE UPPER BODY (TRUNCAL DISTRIBUTION) AND IS ASSOCIATED WITH INCREASE OXYGEN CONSUMPTION AND INCREASE INCIDENCE OF CARDIOVASCULAR DISEASE

VISCERAL FAT: PARTICULAR ASSOCIATED WITH CARDIOVASCULAR DISEASE AND LVD (LEFT VENTRICLE DYSFUNCTION)

GYNECOID: PERIPHERAL OBESITY: ADIPOSE TISSUE IS LOCATED PREDOMINANTLY IN THE HIPS, BUTTOCKS, AND THIGHS. THIS FAT IS LESS METABOLICALLY ACTIVE SO IT IS LESS CLOSELY ASSOCIATED WITH CVD.

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5
Q

What kind of issues will you likely have (in relation to your heart) if you have sleep apnea that is not treated?

A

Right ventricular issues

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6
Q

what does waist circumference correlate with?

A

abdominal fat and is an independent risk predictor of dz

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7
Q

what drug is phentermine similar to in that it can have the same effects?

A

amphetamine (think of adipex (phentermine) as legal meth lol)

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8
Q

Most effective treatment for morbid obesity class III?

A

Bariatric surgery

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9
Q

Should surgery be the first thing morbidly obese people try in order to lose weight?

A

No!

There are multiple less invasive techniques

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10
Q

If someone is obese will this result in increased or decreased lung compliance?

A

DECREASED LUNG COMPLIANCE: FAT ACCUMULATION ON THORAX AND ABDOMEN RESULTS IN DECREASE CHEST WALL AND LUNG COMPLIANCE

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11
Q

What position results in even further reduction in chest wall compliance and increased elastic resistance for obese patients, and what results?

A

Supine, thus resulting in rapid breathing and limited maximum ventilatory capacity.

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12
Q

What is the most commonly reported abnormalities of pulmonary function in obese patients?

A

Decreased FRC and ERV

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13
Q

Anesthesia and supine position in an obese patient can decrease FRC up to how much? how does that compare to a non obese patient?

A

decreases FRC up to 50% in obese, compared to 20% in non obese patient.

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14
Q

What condition increases O2 consumption and CO2 production even at rest?

A

obesity

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15
Q

Gold standard diagnostic test for OSA is?

A

polysomnography (OPS)

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16
Q

CO increases with increasing weight by as much as how much ml/kg? Why?

A

20-30ml/kg increase in CO.

Due to ventricular dilation and increased SVR

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17
Q

Obese individuals have an increased blood volume, what is obese blood volume per kg compared to non obese blood volume per kg?

A

non obese 50ml/kg

obese 70ml/kg

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18
Q

systolic and diastolic changes in BP due to being obese?

A

3-4 mm/Hg INCREASE IN SYSTOLIC AND 2mm/Hg INCREASE IN DIASTOLIC ARTERIAL PRESSURE FOR EVERY 10 Kg OF WEIGHT GAIN

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19
Q

Obese individuals are more likely to have OSA due to excess soft tissue, tell me some physiological abnormalities R/T OSA?

A

HYPOXEMIA, HYPERCAPNEA
PULMONARY HPTN, SYSTEMIC VASOCONSTRICTION
SECONDARY POLYCYTHEMIA FROM RECURRENT HYPOXEMIA
INCREASED RISK OF ISCHEMIC HEART DISEASE
CEREBROVASCULAR DISEASE
RV FAILURE D/T HYPOXIC PULMONARY VASOCONSTRICTION

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20
Q

If someone has sever OSA what can you consider for them before surgery?

A

pre-op CPAP

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21
Q

What is pickwickian syndrome?

A

OBESITY HYPOVENTILATION SYNDROME (OHS) OR PICKWICKIAN SYNDROME RESULT FROM LONG TERM OSA. SEEN IN 5-10% OF MORBID OBESE

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22
Q

If you are obese, what does that do to your gastric volume and acidity?

A

increase acidity and gastric volumes.

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23
Q

obese individuals have up to 75% larger stomach volumes, this increases risk for what? (a lot of risks, just name some- general idea) ULTIMATELY increasing risk for?

A

INCREASED RISK OF HIATAL HERNIA, GERD, DELAYED GASTRIC EMPTYING, HIGHER ACIDITY, INCREASED ABD PRESSURE….
ALL of the above results in INCREASED RISK for aspiration and pneumontis!

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24
Q

what % of obese patients potentially have subclinical hypothyroidism?

A

25%

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25
Q

hypothyroidism associated with?

A

HYPOGLYCEMIA, HYPONATREMIA, AND IMPAIRED HEPATIC DRUG METABOLISM

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26
Q

what are some considerations in the OR for obese patients, in relation to oxygen therapy, positioning, and apnea allowance?

A

O2 ASAP!!! PRE-OXYGENATION WHILE PREPARING FOR INDUCTION. SAT DROPS QUICKLY AFTER INDUCTION D/T ↓ FRC AND ↑ O2 CONSUMPTION

HEAD UP POSITION OR SEMI-SITTING POSITION AT APPROX 25 DEGREES FROM HORIZONTAL, PROVIDES THE LONGEST PERIOD OF APNEA WITHOUT DEVELOPMENT OF HYPOXIA DURING INDUCTION

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27
Q

Would you want to use PEEP during induction on an obese patient?

A

Yes! will combat peri-induction hypoxemia (APL valve PEEP)

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28
Q

What type of intubation might you consider on an obese patient?

A

RSI MAY BE CONSIDERED D/T GASTRIC REGURGITATION, ASPIRATION RISKS

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29
Q

What type of paralytic is recommended for obese patients due to potential airway difficulty?

A

SUCC

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30
Q

Which gas hides in the fat?
What is the drawback to the alternative gas?
Which gas should be limited bc of high 02 demand of obese patient?

A

Sevo supposedly hides in fat (somewhat controversial) Thus you would then want to use Des, but Des has transient HR increase which increases 02 demands on a patient that does not have any 02 to spare, but it is only transient.
N20 should be limited due to the high 02 demand of obese patients.

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31
Q

How can you tell if your vent settings are good to go?

A

If the patient is saturating well and blowing off a good amount of CO2

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32
Q

Tidal Volumes for obese patients? WHY?

A

6-8ml/kg PWD tidal volumes.

Higher tidal volumes offer no added advantages during mechanical ventilation of anesthetized morbidly obese patients.

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33
Q

IS THE ONLY VENTILATORY PARAMETER THAT HAS CONSISTENTLY BEEN SHOWN TO IMPROVE RESPIRATORY FUNCTION IN OBESE SUBJECTS.

A

PEEP

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34
Q

What do you monitor cont. on MAC cases (I would think on all cases)

A

02 and CO2

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35
Q

Gold standard monitoring for patients during surgery or on the vent?

A

CO2

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36
Q

When placed in Trendelenburg for an abd or lap procedure you should be in what vent control setting?

A

you should be in pressure control over volume control.

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37
Q

If you have CSF leaking out of your epidural needle, what does that mean?

A

you have administered a spinal and not an epidural now, you need to pull out, patch, and go one space above.

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38
Q

what can you combine with local anesthesia to decrease the need for opioids and thus decrease respiratory depression?

A

NSAIDS

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39
Q

How to calculate PBW of a male and of a female?

A

MALE: PWB (KG) = 50 + (0.91 X HEIGHT IN CM – 152.4)

FEMALE: PWB (KG) = 45.5 + (0.91 X HEIGHT IN CM – 152.4)

(typically comes out super close to IBW)

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40
Q

Anticholinergic syndrome treatment?

A

Treatment would be a cholinergic medication, physostigmine!

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41
Q

What is anticholinergic syndrome?

A

Anticholinergic syndrome is characterized as mad as a hatter, hot as a hare, dry as a bone, red as a beat and blind as a bat. Caused by too much anticholinergic such as atropine (you would give too much atropine maybe when treating pesticide poisoning)

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42
Q

What type of patients would you prefer to use cisatracurium with?

A

Kidney issues or dz

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43
Q

Cisatracruium intubating dose? Time in min. to return to less than 25%? and how is it metabolized?

A

.1mg/kg
20-35 min
Hydrolysis in plasma (degradation by Hofmann elimination)

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44
Q

MOA rocuronium?

A

competes with ACh for a-subunites at the POSTjunctional nicotinic cholinergic receptors and prevent changes in ion permeability. DEPOLORIZATION can not occur (why it is a nondepolorizing NMB) and skeletal muscle paralysis develops.

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45
Q

Isoproterenol - what cardiac issues are we worried about? Therapeutic plasma concentration monitoring, why?

A

non selective Beta stimulation. B1 greater than B2.
adverse affects are tachycardia and arrhythmias.
longer half life than that of endogenous catecholamines.

PS- can be given during anaphylaxis reaction as a secondary treatment 1-5mcg/min. Barash table 9-6

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46
Q

Morphine MOA?

A

Morphine binds to Mu receptors and produces analgesia. This is mainly inhibitory and the effect is mainly due to hyperpolarization of the cell and reduced excitability. Active metabolite morphine 6 also produces pain relief.

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47
Q

CTM, where is it located?

A

Cricothyroid membrane. Located between the thyroid cartilage and cricoid cartilage.

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48
Q

2nd gas effect?

A

the ability of a high volume uptake of one gas (first gas, typically N20) to accelerate the rate of increase of the PA of a concurrently administered “companion” gas (2nd gas)

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49
Q

pH? What blood pH’s are acidemia and alkalemia?

A

measure of the concentration of H+ present.
below 7.35 = acidemia
above 7.45 = alkalemia

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50
Q

Anion gap formula?

Normal anion gap?

A

anion gap = sodium - (chloride + bicarb)

normal = 8-12 mEq/L

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51
Q

Cardiac arrest with spinal why? (M&P pg 298)

A

rare and not well understood. hypoxemia and over sedation may contribute. Associated with spinal not epidural techniques. (I assume a high spinal will make this happen) (happens with epidurals bc it goes into the CSF with larger amounts of medication)

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52
Q

What regional tech. is associated more often with post dural HA?

A

Spinal

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53
Q

Only absolute contraindication to spinal or epidural?

A

patient’s refusal (and obviously an infection at the site you want to use)

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54
Q

lidocaine 5% plane time and vasoconstriction time?

Bupivacaine 0.75% plane time and vasoconstriction time?

A

lidocaine -60-75min
with vasoconst - 60-90 min

Bupiv- 90-120
with vasoconst - 100-150

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55
Q

most influential factor affecting level of Spinal anesthetic?

A

dosage amount

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56
Q

dermatome level of xiphoid

A

T6

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57
Q

dermatome level of nipples

A

T-4

cardiac accelerators are t4-t-5

58
Q 
IN ADULTS
most used spinal interspace?
largest interspace?
spinal cord ends at?
dural sac ends at?
A

most used = L3-L4
largest = L5-S1
ends = L1-L2
dural = S2

59
Q

PDPH how to identify?

A

starts 24-48 hours after puncture. back of head and neck. Improves in supine position, may have double vision, blurred vision and tinnitus.

60
Q

Nausea after a spinal means what?

A

possibility of systemic hypotension sufficient to produce cerebral ischemia.

61
Q

if platelets are below 120 can you do a spinal or epidural?

A

Yes, the limit is below 100, if below 100 then you do not do spinal or epidural

62
Q

spinals, what 2 physiological changes occur?

A

decrease in BP and HR

63
Q

NMS, what causes it typically and how do you differentiate between MH?

A

psych meds typically cause NMS.

You give a non- dep NMB, if they relax then its NMS and not MH.

64
Q

Risk factors for PONV?

What two drugs are known to reduce it PONV?

A 
Risk factors are:
age less than 50
female gender
hx of PONV or motion sickness
nonsmoker
swallowed blood
type of surgery (middle ear and eye muscle surgery)
narcotic use, inadequate hydration, post op movement
duration of surgery

zofran and dexamethasone.

65
Q

equipment in the OR and electrical status?

A

electrical power is ungrounded in the OR and equipment is grounded.

66
Q

If you can legitimately recall events that occurred during your surgery then that is known as which type of memory? (conscious recall)

A

explicit memory

67
Q

being able to respond to commands but lacking conscious recall of intraoperative events is what type of memory?

A

implicit memory

68
Q

influenzae type A or B causes epiglottitis?

A

type B

69
Q

Mast cells are found where?

A

Skin, lungs, intestines

70
Q

Which type of fighter cell is the least common?

A

Basophils

71
Q

What cells are associated with anaphylaxis?

A

Mast cells and basophils

72
Q

How quickly can a reaction occur (and typically does) after IV use of a drug?

A

5 min

73
Q

How long does it take a latex allergy to show up typically?

A

30 min

74
Q

antigen?

examples of atigens?

A

molecules stimulating an immune response.
foreign substance in the body that the body recognizes as foreign, usually proteins or carbohydrates.

protamine and dextrans are antigens.

75
Q

haptens?

A

SMALL MOLECULAR WEIGHT SUBSTANCES SUCH AS DRUGS OR DRUG METABOLITES THAT BIND TO HOST PROTEINS OR CELL MEMBRANES TO SENSITIZE PATIENT . Haptens are not antigenic by themselves.

76
Q

B cells?

A

B-CELLS REPRESENT A SPECIFIC LYMPHOCYTE CELL LINE THAT CAN DIFFERENTIATE INTO SPECIFIC PLASMA CELLS THAT SYNTHESIZE ANTIBODIES, A STEP CONTROLLED BY BOTH HELPER AND SUPPRESSOR T-CELL

77
Q

T cells, how are they formed, what are they, what types are there and what does each type of t cell do?

A

immature lymphocytes which are thymus derived.
activated by binding to foreign antigens and secrete mediators that regulate the immune response.
two types- T helpers (t4) and T suppressors (T8).

HELPER CELLS: IMPORTANT FOR KEY EFFECTOR CELL RESPONSES

SUPPRESSOR CELLS: INHIBIT IMMUNE FUNCTION

78
Q

What are the diff. types of IG’s? Tell me how they differ (little description of each)

A

5 MAJOR CLASSES OF ANTIBODIES: IgG, IgA, IgM, IgD, AND IgE

79
Q

eosinophils, whats their job, when do they come into play, where do they come from?

A

inflammatory cells recruit eosinophils to collect at the sites of parasitic infections, tumors, and allergic reactions.
formed in the bone marrow. exact function is unclear.
take 8-12 hours to arrive where they need to be.
seen in allergic dz’s such as asthma, autoimmune dz, and hay fever.

80
Q

basophils, when are they seen? What do they do? What do they function like?

A

Least common
IgE receptors on the surface of basophils and function similar to mast cells.
seen in acute/chronic allergic dz’s such as anaphylaxis, asthma, dermatitis. Contributes to resistance to internal parasites, and ticks.

81
Q

mast cells, what are they important for? Where are they located? How do they work?

A

Important cells for immediate hypersensitivity responses
they are tissue fixed and located in teh perivascular spaces of the skin, lungs, and intestines.
IgE receptors are on the surface of the mast cells and bind to specific antigens.

82
Q

cytokines and chemokines?

A

part of humoral immunity, protein mediators that are released initially by inflammatory responses, thus bringing other immune cells to the site of injury or infection and thus cause further inflammation.

83
Q

Which two cells have IgE receptors?

A

mast cells and basophils

84
Q

Kinins, where do they come from and what do they do?

A

KININS ARE SYNTHESIZED IN MAST CELLS AND BASOPHILS TO PRODUCE VASODILATION, INCREASED CAPILLARY PERMEABILITY AND BRONCHOCONSTRICTION

85
Q

Type 1 reaction?

A

TYPE I REACTION: ANAPHYLACTIC. PHYSIOLOGICALLY ACTIVE MEDIATORS ARE RELEASED FROM MAST CELLS AND BASOPHILS AFTER ANTIGEN BINDING TO IgE ANTIBODIES ON THE MEMBRANES OF THESE CELLS. THIS INCLUDES ANAPHYLAXIS, EXTRINSIC ASTHMA, ALLERGIC RHINITIS

86
Q

Type two reaction?

A

TYPE II REACTION: ANTIBODY-DEPENDENT CELL-MEDIATED CYTOTOXIC HYPERSENSITIVITY OR CYTOTOXIC REACTIONS. MEDIATED BY EITHER IgG OR IgM ANTIBODIES DIRECTED AGAINST ANTIGENS ON THE SURFACE OF FOREIGN CELLS

87
Q

what type of allergic reaction is mediated by IgE?

A

type 1

88
Q

What type of allergic reaction is mediated by IgG or IgM?

A

type II

89
Q

Blood transfusion reaction would be which type of reaction (classification)

A

type II

90
Q

example of type III REACTION?

A

serum sickness after snake antisera.

91
Q

Type IV reaction?

when is this immunity important?

A

delayed hypersensitivity reaction. (18-24 hours, peak 40-80 hours, disappear 72-96 hours)
important in tissue rejection, graft vs host, contact dermatitis such as poison ivy and TB.

92
Q

most common life threatening manifestation of allergic reaction in the anesthetized pt?

A

circulatory collapse, reflects vasodilation with resulting decrease in venous return.

93
Q

Can an anaphylactic reaction occur without prev. exposure?

A

No, you MUST have prev. exposure to the antigen to produce sensitivity/ reaction.

94
Q

what type of Ig response is anaphylactic reactions?

A

IgE

95
Q

protomine, what is it for and why do people have reactions with it?

A

used to reverse hep. if someone has an anaphylactic reaction to this why, surely they have never used it before? bc it is in ladies makeup, eye makeup.

96
Q

what cell comes into play with acute allergic reactions?

A

eosinophils

97
Q

refractory hypotension occurs most often with use of what drugs?

A

ACE inhibitors

98
Q

Biggest reaction to orthopedic surgeries?

A

Cement

99
Q

Most common cause of drug induced allergic reactions in the OR?

A

NMB, specifically Roc and sux

100
Q

Anaphylaxis is initiated by?

A

an antigen binding to IgE antibodies.

101
Q

upon re-exposure what cells are responsible for releasing stored mediators? What are those mediators?

A

mast cells and basophils release stored mediators which are histamine, trypase, and chemotactic factors.

102
Q

The released mediators (from arachidonic acid metabolites) produce a symptom complex of?

A 
Bronchospasm
Upper airway edema in respiratory system
Vasodilation
Increased capillary permeability in the CV system
Urticaria
103
Q

Histamine receptor H1 does what?

A

when activated releases endothelium derived relaxing factor (nitric oxide) from vascular endothelium, increases capillary permeability, and contracts airway and vascular smooth muscles

104
Q

Histamine receptor H2 does what?

A

Activation causes gastric secretion, inhibits mast cell activation and contributes to vasodilation.

105
Q

What happens when histamine is injected into the skin? What histamine receptor is responsible for this?

A

When injected into the skin, histamine produces the classic wheal and flare…(Wheal: increased capillary permeability producing tissue edema: Flare: cutaneous vasodilation)

H2

106
Q

Tell me simply how histamine is released?

A

Can happen in an anaphylaxis reaction which is inititated by antigen binding to IgE antibodies (mast cell or basophils) and this is a re-exposure. The binding to IgE creates a bridge which then allows for the release of histamine.

107
Q

In the anesthetized patient what changes about anaphlaxis?

What s/s would you look for?

A

onset may be delayed 2-20 min.

S/S could be:
laryngeal edema
decreased pulmonary compliance
pulmonary edema
acute resp. failure
hypotension
tachycardia
dysrhythmias
decreased SVR
cardiac arrest
pulmonary HTN
hives
flushing
periorbital edema
108
Q

another word for antibodies?

A

immunoglobulins (Ig’s)

109
Q

What drugs can cause a histamine release?

A 
antibiotics (vanc)
hyperosmotic agents
muscle relaxants (atracurium)
opioids (morphine, meperdine, codeine)
thiobarbiturates
110
Q

Management of anaphylaxis during GA?

A
  1. stop administration of antigen.
  2. maintain airway and give 100% 02.
  3. d/c all anesthetic agents.
  4. start IV volume expansion (2-4L crystalloid with hypotention)
  5. Give epi (5-10mcg IV with hypotention titrate as needed; 0.1-1.0 mg IV with cardiovascular collapse).

2ndary treatment would be to manage symptoms- give antihistamines, catecholamine infusion for BP, bronchodilators, sodium bicarb.

111
Q

is histamine release dependent on mu receptors?

A

No bc fentanyl and sufentanil do not release histamine in human skin

112
Q

what is the only cell population that releases histamine in response to both drugs and endogenous stimuli.

A

human cutaneous mast cells

113
Q

True or false, Pretreatment of antihistamines before giving drugs known to release histamine does inhibit histamine release?

A

false, it does NOT inhibit histamine release, but rather compete with histamine at the receptor and may attenuate decreases in SVR.

114
Q

Tell me the concentration of EPI you give if someone is having an anaphylaxis reaction under GA?

A

5-10mcg IV for hypotention, titrate as needed.

0.1-1 mg IV for cardiovascular collapse.

115
Q

why are you turning your anesthetic gas off during an anaphylaxis reaction?

A

if the patient is hypotensive (which they most likely will be) the gas is causing vascular dilation as well as bronchial dilation (you want bronchial but not vascular), you will effectively have no circulation in a patient who really needs it.

116
Q

If a patient is having an anaphylactic reaction but they are normotensive, how will you give the epi?

A

Subq, no IV epi in patients with normal BP.

117
Q

If a patient is having refractory hypotension what do you give?

A

1-2 units vasopressin

118
Q

What is the time we want patients to stop smoking for before surgery (even tho it is most likely not going to happen.)

A

4-8 weeks before orthopedic surgery. (will help with wound healing).

119
Q

Name an independent risk factor for infection with surgery?

A

DM

120
Q

after an anaphylactic reaction THIS DRUG may also be important in attenuating the late-phase reactions reported to occur 12 to 24 hours after anaphylaxis

A

Corticosteroids

121
Q

What is innate immunity?

A

The first line of defense against non-self pathogens is the innate, or non-specific, immune response. The innate immune response consists of physical, chemical and cellular defenses against pathogens. The main purpose of the innate immune response is to immediately prevent the spread and movement of foreign pathogens throughout the body.

122
Q

after NMB what else is a drug induced leading cause of anaphylaxis in the OR?

A

ANTIBIOTICS

Penicillins and cephalasporins (ancef) are number one for allergy reporting and sulfaonamides are 2nd.

123
Q

What type of NMB are more likely to cause direct mast cell degranulation?

A

Benzylisoquinolinium compounds (tubocurarine, atracurium, mivacurium)

124
Q

what type of reaction is a latex allergy?

Who is at risk?

A

type 1 bc it is IgE mediated.
People who have frequent contact with latex are more likely to have allergy ex. spina bif. healthcare workers, people allergic to certain fruits.

125
Q

if a reaction is non IgE mediated what does that mean?

A

reactions involving direct histamine release from mast cells and basophils and are directly related to the rate of drug infusion

126
Q

true or false, abx are mostly for gram (-) pathogens?

A

False. Attention is focused on resistant gram positive organisms such as MRSA but there is virtually no development or abx that are active against resistant gram negative pathogens.

127
Q

Thoracic outlet obstruction – how to position patient?

A

arms down at side

128
Q

What type of abx needed for small bowel entrance?

A

gram negative

129
Q

what type of abx coverage needed for large bowel and female genital tract surgeries?

A

anaerobic (no oxygen)

130
Q

What has been shown to reduce the incidence of SSI in the hospital?
what increases it?

A

decrease= chlorhexidine and treating surgical pain, having the patient warm enough.

increased = hypothermia, DM

131
Q

which fentanil has a very rapid onset and offset?

A

remifentanil

132
Q

most potent fentanil? (and opioid period)

A

sufentanil, 1000x more potent than fentanyl

133
Q

75-100 times more potent than morphine with a more rapid onset?

A

fentanyl

134
Q

short acting fentanil after single bolus injection, reaches peak concentrations quickly.
unpredictable hepatic metabolism?

A

alfentanil

135
Q

fentanil that is good for neuro cases?

A

remifentanil

136
Q

Surgeries that are typically done in deep trendelenburg?

A

Hysterectomies and proctectomies

137
Q

IAP should not exceed?

A

15 mm Hg

138
Q

What is subcutaneous emphysema? How does it occur? What are some predictors for it to happen?

A

same as subq air.
occurs due to inadvertent extra peritoneal insufflation in subcutaneous, pre-peritoneal or retroperitoneal tissues.
Predictors of SE = operative time greater than 200 min. use of 6 or more surgical ports.

139
Q

what is capnothorax?
what are s/s of it?
Treatment?

A

rare, potentially life threatening, occurs in procedures near the diaphragm, need chest x-ray to confirm.
increased airway pressures that are unexplained, hypoxemia, hypercapnia, unequal chest expansion, BULGING DIAPHRAGM, subq emphysema in head and neck.
Treatment= deflation of the abd and supportive tx. hyperventilation and use of peep can inflate the lungs adn resolve capnothorax.

140
Q

DVT/PE and procedures with high and low risks?

A

Lymph node dissection during radical prostatectomy carries a significant risk of DVT and PE postop. Lower risk of performed robotically.

141
Q

If a lap procedure is occurring and the HR drops, what do you do?

A

why did it drop? may need fluids? if it is a significant drop you can give atropine. The reason for the drop will dictate treatment if patient is stable.

Clinical Entrance Exam (21 decks)

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