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Advanced Anes. Spring 21 > 1 - Obesity & Thermal Injury > Flashcards

1 - Obesity & Thermal Injury Flashcards

1
Q

What is the primary factor in the development of obesity?

A

genotype -environment also plays a role

-fat is considered an organ

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2
Q

___% of american adults have a BMI > 30

A

35%

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3
Q

BMI calculations

A

weight (kg)/Height (m^2)

(weight (lbs)/height (in^2) x 703

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4
Q

BMI Class & ASA)

A

25-29.9 = overweight

30-34.9 = obese class I

35 - 39.9 = obese class II

40-44.9 = obese class III / extreme (not morbid)

obese >45 = obese class IV/ severe

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5
Q

IBW

A

Broca’s index:

male = height (cm) - 100

female = height (cm) - 105

*may underdose obese because Vd is bigger

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6
Q

LBW

A

lean body weight = IBW x 1.3

*best to calc dose

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7
Q

Andriod

A

Apple heart disease, DM, HTN, dyspilidemia, death

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8
Q

Gynecoid

A

Pear varicose veins, joint disease

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9
Q

Obestiy: Cardiac

A
  • increased metabolic demand
  • increased CO (0.1 L/min for each kg of fat)
  • increased workload to meet demand
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10
Q

What leads to HTN in the obese?

A

increased volume + RAAS activation

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11
Q

CAD

A

independent factor with obesity

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12
Q

HTN in obesity

A

SBP>140

DBP>90

OR BOTH (2x risk in obesity)

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13
Q

HTN and obesity characteristics…

A

increased: blood viscosity, mineralocorticoids, sodium reabsorption, RAA activation

And…hyperinsulinemia, comression of kidneys

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14
Q

Obesity: respiratory

A
  • decreased compliance, FRC, ERV, VC, TLC
  • F/V loop = restrictive
  • increased dead space
  • RV, CC, FVC and FEV1 dont change
  • hypoventilation, hypercarbia, acidosis
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15
Q

OSA

A

definition: excessive episodes of apnea (10 sec) and hyponea.

>5 episodes per hour or 30/night

risk factor: BMI > 30, abdominal fat dist, large neck

  • BMI>35 - OSA in 71-77%
  • hypoxia, hypercapnia, systemi and pulm HTN, cardiac arrythmias
  • gold standard - polysomnography
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16
Q

STOP-BANG

A

-93% sensitivity

Snoring

Tiredness

Observed apnea

high blood Pressure

BMI >35

Age

Neck (>40 cm)

Gender

0-2 = low risk

3-4 = Intermediate

>5 = high risk

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17
Q

Obese Hypoventilation (Pickwickian) Syndrome

A
  • somnolence, cyanosis induced polycythemia, resp acidosis, R sided heart failure…
  • elevated PaCO2
  • right sided heart fail d/t hypoxic pulm vasoconstriction
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18
Q

DM

A

80% of NIDDM pts are obese, risk linear to BMI

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19
Q

Metabolic Syndrome

A

glucose intolerance, DM2, HTN, dyslipidemia, CVD

CV risk 50-60% above normal

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20
Q

Obesity: Pharmacology

A

-increased Vd (lipid soluble), increased blood volume, increased CO, decreased total body water, altered protein binding

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21
Q

IBW vs TBW

A

low lipophilicity = LBW, mainly goes to lean tissue

highy lipophilicity = TBW (usually), equal distribution to fatty and lean tissue, lipi soluble drugs

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22
Q

Obesity: GA and resp

A
  • 50% reduced FRC compared to 20% in non-obese
  • PEEP 6-10 ml/kg of IBW
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23
Q

Volume replacement - Obese

A

increased TBV, decreased estimated blood volume 45-55 ml/kg

24
Q

1st degree burn

A
  • limited to epidermis (superficial)
  • heals spontaneously
25
Q

2nd degree burn

A
  • extends to dermis (deep/ superficial partial thickness)
  • may need graft
26
Q

3rd degree burn

A
  • extend to subcutaneous (full thickness)
  • skin grafting needed, no pain d/t nerve damage
27
Q

4th degree burn

A

-muscle, fascia, bone -extensive

28
Q

Major Burn

A
  • 2nd degree = >10% for adults, >20% extremes of age
  • 3rd degree = >10%
  • electrical burn
  • inhalation inolvement
29
Q

Mortality estimate

A

age + TBSA% = (>115 moratlity is >80%)

double if inhalation

30
Q

Rule of 9’s: infant

A
31
Q

Rule of 9’s: adult

A
32
Q

Rule of 9’s: child

A
33
Q

Electrical Burn

A

myoglobinurea and renal failure

34
Q

1st Phase of Burn Resuscitation

A

Dx and Tx of airway injury early intubation

succs ok in first 24 hrs

35
Q

Succinylcholine

A
  • denervation-like phenomenon
  • proliferation of ACH receptors, K+ release
  • no succs after 24 hrs, ok after wound closed and pt gaining weight
  • resistnat to NMB agents d/t upregulatio of cholinergic receptors
36
Q

CO Poisoning

A

CO binds to Hgb, 200x affinity more than O2

  • tissues cannot extract oxygen
  • disrupts oxidative phosphorylation
  • metabolic acidosis at cellular level
  • shift curve to the Left, pulse oximetry not accurate
37
Q

CO Poisoning Treatment

A

100% oxygen decreases CO half life from 4 hrs to 40 min

38
Q

Burns and Hypovolemic Shock

A

-fluid loss greatest in 1st 12 hrs, begins to stabilize after 24 hrs

39
Q

Burns - fluid shifts from…

A

intravascular to interstitium

  • leads to plasma depletion and hypovolemia
  • edema
40
Q

Fluid Resuscitation

A

Adults:

Ringers lactate 2-4 ml x kg x BSA%

Child:

Ringers lactate 3-4 ml x kg x BSA%

  • half of estimated volume should be given in first 8 hours after burn. Remaining half should be given in subsequent 16 hrs
  • infants and children should recieve fluid with 5% dextrose at maintenance rate in addition to resus fluid volume
41
Q

Brooke Formula

A

First 24 hr:

crytalloid = 2 ml LR / % burn / kg crystalloid

(no colloid)

*half in first 8 hr, half in next 16 hr

Second 24 hr:

crystalloid = D5W maintenance rate AND

colloid = 0.5 ml / % burn / kg

42
Q

Parkland Formula

A

First 24 hr:

crystalloid = 4 ml LR / % burn / kg

(no colloid)

*half in first 8 hr, half in next 16 hr

Second 24 hr:

crystalloid = D5W maintenance

colloid = 0.5 ml / % burn / kg

43
Q

Minimum urinary output: Burns

A

Adults: 0.5 mL/kg/hr

Children weighing less than 30 kg: 1 mL/kg/hr

Pts w/ high voltage electrical injury: 1-1.5 mL/kg/hr

44
Q

Hypermetabolic/ Hyperhemodynamic Phase

A

Usually after 48 hrs s/s: hyperthermia, tachypnea, tachycardia, increased serum catecholamines, increased oxygen consumption, increased catabolism, increased basal metabolic rate

45
Q

hallmark of burn shock?

A

decreased CO -occurs w/i minutes

  • inititally preserved by catecholamine (inc HR and vasoconstrict)
  • losses overcome
  • myocardial depressants released from burned tissue
46
Q

Pulmonary Fx: Burns

A
  • decreased overall function
  • decreased chest wall compliance, FRC
  • ventilation can increase from 6 L/min to 40 L/min
47
Q

What is the leading cause of death in burn pts?

A

sepsis adults = 75%

peds = near 100%

48
Q

Burns: Renal

A

ARF increases mortality r/t: hypovolemia, decreased CO, increased catecholamines

-myoglobinemia: sodium bicard for tx

49
Q

Burns: GI/ Nutrition

A
  • increased caloric requirement
  • enteral feeds, stop 4 hrs for non-tubed, don’t stop if tubed
  • do not stop TPN
50
Q

Fluid & Blood replacement: Burns

A
  • can be very bloody
  • 200-400 mL EBL for each 1% debridement
51
Q

Capacities:

FRC

ERV

VC

TLC

A

Decreased with obesity:

FRC = 2,500

ERV = 1,000

VC = 4,500

TLC = 5,500

52
Q

Decreased FRC to < CC?

A

hypoxia, dead space increased, VQ mismatch, shunt

53
Q

LBW meds

A
  • propofol induction dose (loading dose determined by distribution)
  • meaintenance of fentanyl and sufentanyl

*water soluble drugs

54
Q

TBW meds

A

propofol maintenance (determined by clearance)

succinylcholine

suggamedex

loading dose of fentanyl, sufentanyl

*lipid soluble drugs

55
Q

IBW

A

roc, vec, cis

remifentantyl

56
Q

Anesthetia and burn pts…

A
  • profound effect of agent due to hypovolemia
  • NSAIDS - may inhibit platelet aggregation
57
Q

highly lipophilic medications

A

digoxing, procainamide, remifentanil

Advanced Anes. Spring 21 (7 decks)

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