physiology of obesity and aging Flashcards
define obesity
WHO defines obesity based on BMI
less than 18.5 - underweight
18.5-24.9 normal
25 to 29.9 overweight
30-34.9 obese 1
35 to 39.9 obese 2
more than 40 obese 3
what are the limitations of BMI? any alternatives?
doesnt include muscle mass
waist circumferance could be used.
what are the different forms of fat distribution?
android and gynaecoid
android = central obesity - worse for myocardial health
what is metabolic syndrome?
group of conditions including
obesity
diabetes
HTN
hypercholesterolaemia
increases risk of IHD, Strokes, and mortality
describe the physiological pathways for hunger control..
The hypothalamus coordinates and regulates hunger. paraventricular nucleus and arcuate nucleus
inputs
- leptin - secreted by adipose tissue. inhibits hunger. hence more fat, negative feedback to reduce hunger
- insulin - after a meal carbohydrates cause insulin to rise and this will inhibit the hunger pathways in hypothalamus
outputs
- sends signals to give sensation of fullness.
- also increases BMR via sympathetic NS
however hunger and eating is more complex than this
* involves food reward pathways and dopamine
* emotional attachment
* addiction
what is the pathophysiological of obesity development?
a number of pathological process
* insulin sensitivity
* hyperinsulinaemia - deposition of fat
* increased leptin levels and hypothalamic insensitivity / different set point
* dopamine reward pathways enhanced.
how does obesity affect anaesthesia
AIRWAY
* more likely to have a difficult airway
* more subcutaneous fat
* more likely to obstruct when anaesthesised - need a guedel
* harder to manoeuver head and hold mask - likely to need 2 person technique
* harder to find cricoid / front of neck
BREATHING
* more likely to desaturate - higher BMR and lower FRC
* reduced FRC - more weight on chest wall and diaphragm pushed up by abdo contents
* therefore closing capacity likely to be larger than FRC and hence atelectasis - more shunting and hence hypoxaemia, likely to need to use PEEP
* better to sit them up / oxford pillow
* likely to have higher airway pressures, as more force needed to inflate lungs
CIRCULATION
* more likely to have cardiovascular disease, HTN hence more at risk of strokes / MI
* may need to increase MAP target if normally HTNs
* likely to need increase CO to keep up with higher BMR
* difficult IV access
DISABILITY
* more likely to need more anaesthetic
* slower recovery from anaesthetic - fat soluble
* may be hyperglycaemic
other
* difficulties with moving an handling can result in injuries / poor positioning
what are the effects of pneumoperitoneum on morbidly obese patient
A - displacement of ET as diaphragm is pushed up
B - atelectasis , reduced FRC, shunting, hypoxaemia, increased airway pressures
C - reduces venous return from increased abdo pressure - can drop cardiac output
D - poor renal perfusion and sphlanchnic perfusion from increased abdo pressures - risk of abdo compartment syndrome and AKI
E: increased intracranial pressure
why can obese people have chronically elevated CO2?
may have obstructive sleep apnoea or obesity hypoventilation syndrome
both result in chronic high CO2 and increased bicarb in CSF to compensate - the set point for responding to CO2 is increased.
in anaesthesia these patients are likely to respond less to hypercarbia and hence may be apnoeic for longer, especially when opioids used. can be hard to wean off the ventilator
what is obesity hypoventilation syndrome?
defined as a raised CO2 ( more than 6kpa) while awake in association with BMI of more than 30 kg/m2
absence of other causes of raised CO2
how is BMI calculated?
height in meters
divided by
weight in kg squared
what is obstructive sleep apnoea?
sleep disorder whereby there is intermittent airway obstruction resulting in periods of apnoea
in turn results in hypoxia and hypercarbia
More likely in obesity
patients will wake up with a sudden gasp of air but will be unaware.
This results in
Neuro - loss of REM sleep so chronic tiredness, poor concentration, anxiety
CVS - HTN, MI, AF
endocrine - impaired glucose tolerance, increased cortisol
resp - high PCO2, pulmonary vasoconstriciton and hence pulm. HTN
how does obesity change your anaesthetic plan?
Pre op
* history
* any associated problems with obesity - diabetes, HTN, OSA - and how are these managed
preparation
* advice from senior college
* obesity is ASA 3 so usually senior should be involved
* regional if possible - although might be hard
* cannulation - USS available
* monitoring - correct size BP cuff, may need arterial line for accuracy.
* consider anaesthetising in theatre to avoid moving and handing issues - discuss with team.
* bariatric table etc
induction
* long time for pre-oxygenation
* use of oxford pillow
* have difficult airway trolley available, McGrath
* consdier high flow TRIVE
* I gel likely to be avoided
intraop
* optimise ventilation - PEEP, may need to compromise on positioning with surgeon
emergence
* very good pre-oxygenation and sat up
* may take a while to emerge, be patient
* awake extubation
* could use high flow again.
which drugs are given for total body weight and lean body weight ?
actual body weight - succinylcholine , midazolam
lean body weight - non-depolarising NMBA, induction dose propofol, remifentanil , LA
adjusted body weight - suggamadex
what is the difference between lean body weight and adjusted body weight?
lean BW represents the weight of non-fat tissue in the body, including muscle, organs, bones, and fluids. It excludes body fat.
adjusted body weight = a modified weight that accounts for excess body fat in obese individuals while recognizing that fat tissue still plays a smaller role in drug distribution than lean tissue.
can you draw a graph to show how closing capacity and FRC change with age
all increase, CC to greater extent
FRC reduced when supine + anaesthesia
hence around age 50 start to get atelectasis and shunting and hypoxaemia.
