Physiology - Extremes of Age, Obesity, and Obstetrics Flashcards
(23 cards)
Define obesity
BMI > 30kg/m^2
NICE categories are as follows:
18.5-24.9 = normal
25 - 29.9 = overweight
30 - 34.9 = obesity class 1
35 - 39.9 = obesity class 2
>40 = obesity class 3
Over 60% of UK adults are overweight or obese, particularly in lower socioeconomic groups
2021 PErioperAtive CHildhood obesitY (PEACHY) study demonstrated worryingly high rates of obesity in children requiring surgery under GA.
BMI = Mass/height²
When does obesity impact perioperative risk
Once BMI reaches 40kg/m², or if there are significant comorbidities.
Obesity hypoventilation syndrome and OSA are of concern, and patients are more sensitive to respiratory depressant effects of opioids.
BMI >50 likely precludes day surgery
Previous bariatric surgery can delay gastric emptying
Central obesity (apple shape) has greater perioperative risk than thigh and waist obesity (pear shape)
What are the anaesthetic implications of obesity?
Cardiovascular
Stroke and PE risk
HTN & IHD
Arrhythmias
Heart Failure
Difficult IV access
Respiratory
Difficult airway (reduced mouth/neck range of motion), large neck & soft tissues, raised intragastric pressure & reflux risk
Obesity Hypoventilation Syndrome
OSA & Opioid sensitivity
Pulmonary HTN
Reduced thoracic compliance
Worse V/Q mismatching
Smaller FRC and larger closing capacity, causing ‘wheeze’
Neurological
Headache, poor sleep, depression
GI
Gallstones, fatty liver
Deranged liver enzymes
Hiatus hernia
Metabolic
Hypercholesterol, DM, Increased BMR
GU
Menstrual issues, erectile dysfunction, fertility problems, PCOS
How does obesity change your anaesthetic plan?
Induction
Difficult cannulation may require US
Monitoring (such as BP cuffs) may need changing
Additional staff/equipment for moving & handling
Consider regional if possible
RSI isn’t essential unless specifically indicated
Consider performing in theatre to reduce risk during transfer from anaesthetic room
Optimal patient positioning (Oxford HELP & ramped position - align tragus to sternal notch)
Preoxygenate (consider THRIVE)
Consider videolaryngoscopy
Call for help early
Anticipate early desaturation & functionally difficult airway
Higher risk of awareness, particularly with volatile agents and prolonged airway manipulation
Intraop
Recruitment manoeuvres
Caution with airway pressures, especially in reverse trendelenburg
Pressure areas
Side extensions on operating table
Table weight limit - especially if traversing
Extubation
Greater risk of desaturation (loss of FRC & increased closing capacity) - ideally sit patient up
Extubate only once fully awake, avoid post-op opioids
Be ready to reintubate
Consider extubation onto BiPAP/THRIVE
What is metabolic syndrome?
A group of conditions:
Obesity
Impaired glucose tolerance
Hypercholesterolaemia Hypertension
Significantly increases mortality for all classes of obesity:
Cardiac/pulmonary complications
AKI
Stroke
Sepsis
How does obesity affect drug dosing and pharmacokinetics?
NEEDS FIXING
Dosing depends on fat-solubility & volume of distribution of the drug.
Total, ideal, and lean body weight are used.
Lean body weight: (Boer/James/Hume Formulae)
Propofol, Thiopentone, Opioids, Non-depolarising NMBDs, local anaesthetics
Ideal/Adjusted body weight: Propfol, neostigmine, sugammadex, antibiotics
Total body weight: Suxamethonium, LMWHs
Absorption
Gastric stasis, IM more difficult to administer
Distribution
Fat soluble drugs have a larger VD, and there is increased body water, plasma volume, and CO
Metabolism
Slightly increased hepatic enzyme activity, increased esterase levels in blood & tissues
Elimination
Increased CO increases renal clearance
What ages correspond to neonates, infants, and children?
Neonates up to 1 month
Infant 1 month - 1 year
Child up to 16
Adolescent between 13-16
What airway factors complicate intubation of young children & babies?
Bigger head, more prominent occiput
Small pharynx & larynx, with anterior, higher larynx at C3-4
Cricoid is narrowest point, not glottis
Short, narrow trachea with higher risk of endobronchial intubation
Soft floppy tissues make airway collapsable
Longer, floppier, and more deeply V shaped epiglottis to facilitate nasal breathing while feeding.
Larger tongue with smaller receding chin
Prominent lymph nodes & tonsils
Smaller FRC & higher BMR - faster desaturation, less intubating time
Describe the physiological differences seen in paediatrics compared with adults.
Unlike adults, children need to enable growth, rather than homeostasis.
Respiratory
Closing capacity exceeds FRC below 6yrs
Increased RR with poor ability to increase TV (horizontal ribs)
WoB higher, over 10% of O2 consumption
Ventilation mainly diaphragmatic with nasal breathing
Cardiovascular
Complex transition from foetal to adult circulation
Increased HR with CO relatively 40% higher
Minimal ability to increase SV, CO dependent on HR
Small blood volume, minimal reserve
Metabolic
High BMR & O₂ consumption
High surface area to volume ratio (rapid heat loss)
Risk of hypoglycaemia
Neurological
Spinal cord terminates at L3
Sympathetic system underdeveloped
Myelination of peripheral nerves not complete unti 6yrs
Immature BBB
GI & Hepatic
Immature liver enzymes
Renal
Extracellular compartment drastically higher in infants (effects volume of distribution)
Reduced GFR & renal tubular function (high renal vascular resistance)
Reduced ability to concentrate urine
Haematological
RBCs have up to 80% HbF at delivery, dropping to 5% by 3 months
Hb elevated at birth, nadirs at 3 months
Reduced Vit-K dependent clotting factors
Musculoskeletal
Fatigue quickly
How is fluid deficit calculated in an infant?
Deficit = 10 x body weight in kg x % dehydration
% dehydration calculated by measuring peripheral temperature
New fasting guidelines (Sip-till-send) allow clear fluids orally until 1 hour pre-op, in low risk elective settings.
How do pharmacokinetics and pharmacodynamics differ in the neonate?
Absorption
Gastric stasis, reduced fat digestion, and higher muscle blood flow (IM drugs well absorbeD)
Distribution
Increased volume of distribution (at birth 75% body water compared with 60%, which is eliminated in urine within a few days)
Reduced plasma protein & drug binding
Blood pH is lower (Affecting ionisation, and therefore distribution/speed of onset)
Blood-brain barrier is immature - larger, more polar molecules may enter the brain.
Metabolism
Regional blood flow (Organs are relatively bigger, and a larger proportion of CO goes to the brain - in particular the liver is much larger, but less efficient)
Enzymes - Neonatal enzymes may be immature - plasma cholinesterase and CYP450 enzymes reduced
Excretion
Nephrons are immature and fewer in number
Creatinine clearance much lower - 10% per kg of adult rate
Pharmacodynamics
Neonates have a higher MAC requirement, with reduced FRC resulting in faster onset of volatiles.
Ductus arteriosus closure triggered by NSAIDS
Describe the Foetal circulation
A parallel cirucit circulatory system that allows the foetus to receive oxygen from the mother rather than its own lungs, which are collapsed and submerged in amniotic fluid.
Foetal blood is oxygenated to 90% in the placenta (as a result of the higher HbF affinity for O2)
It returns to the foetus via the umbilical vein, with 60% bypassing the liver through the ductus venosus after the left hepatic portal vein, and the remaining 40% oxygenating the liver.
Now at 65% saturation, the blood enters the RA from the IVC, and crosses the foramen ovale into the LA.
At 60% saturation, it passes through the LV, aorta and carotids, with some diversion ot the coronary arteries. The afterload to the LV is provided by the resistance of the upper body and cerebral circulations.
It returns to the RA via the SVC with 30% saturation, and down into the RV after mixing with blood from the IVC.
It is pumped into the pulmonary artery, but given the high resistance of the collapsed pulmonary circulation, almost 90% crosses the ductus arteriosus to the descending aorta to supply the rest of the body.
The umbilical arteries arise from the internal iliacs, returning deoxygenated blood to the placenta.
Streaming is the process by which the RA can manage two separate streams of blood.
What is streaming?
In context of foetal circulation
It is the process that allows oxygenated and deoxygenated blood to reach different destinations in the foetal RA.
Oxygenated blood from the placenta is guided by the Eustachian valve along the dorsal RA towards the foramen ovale.
Deoxygenated blood returning from the brain via the SVC is streamed anteriorly across the tricuspid into the RV.
The Eustachian valve is a flap of tissue between the IVC and the right atrium.
What is the foramen ovale?
The foramen ovale is a flap-valve in the inter-atrial septum that facilitates right-to-left flow of oxygenated blood from the placenta in-utero.
It closes functionally at birth, and completely by 6 weeks.
Up to 25% of adults have a patent foramen ovale (PFO), which can allow emboli from the right side of circulation (venous) to cause cerebro-vascular events.
Functional closure of the foramen ovale reflects the drop in right heart pressure caused by perfusion of the lung bed and reduced IVC inflow after clamping of the umbilical vein, resulting in left atrial pressure (which has increased with the blood entering from the pulmonary vein), exceeding that of the RA.
What is the ductus arteriosus?
A wide, muscular conduit allowing blood to flow between the pulmonary artery and aorta within foetal circulation.
It is a right-to-left shunt that allows blood to bypass the collapsed lungs (and therefore high pulmonary vascular resistance), prioritising bloodflow to the lower half of the body.
Its presence in-utero is maintained by low oxygen content, a high pulmonary:aortic pressure gradient, and vasodilatory Prostaglandin (PGE2).
It closes functionally after 3 days, and permanently as a result of thrombosis and fibrosis at 21 days.
What changes occur immediately after birth?
With the first breath, lung volume increases, PVR drops significantly, (further decreased by a reduction in hypoxic pulmonary vasoconstriction) - RV pressures drop.
RA pressure drops because of reduced RV afterload and reduced IVC inflow (from clamping of umbilical vein).
LA pressure increases with increased pulmonary vein inflow.
LA > RA pressure for the first time, and the foramen ovale closes functionally
This can be reversed if the pressure balance changes, and only closes irreversibly at 6 weeks.
The ductus venosus closes via unclear mechanisms after a few hours, and completely by 10 days.
Clamped umbilical arteries raise SVR and aortic pressures.
Aortic > Pulmonary artery pressure for the first time, causing flow reversal in the ductus arteriosus, which closes functionally after 3 days, and anatomically after 2 weeks.
This is the final step in the process, and marks the conversion of a parallel system to one where the ventricles are in series with each other.
Pulmonary artery pressures, blood flow, and vascular resistance reach adult values at 4-6 weeks.
What are the physiological effects of increasing age?
General Considerations Progressive (often undiagnosed) comorbidity in each system
IHD, HTN, COPD, Cognitive dysfunction & sensory impairment, cancer
Polypharmacy - drug interactions & SE)
Autonomic dysfunction
Airway
Teeth - may be edentulous or have expensive bridges/dentures
TMJ dysfunction, cervical spondylosis/arthritis
Respiratory
Reduced FRC, encroaching on increasing closing capacity - small airway closure occurs with tidal breathing when supine.
Reduced sensitivity to hypoxia/hypercapnoea
Increased V/Q mismatch, increased A:a gradient
Reduced compliance (although increased compliance with gas trapping in emphysaema)
Higher risk of Post-op atelectasis & pneumonia
Cardiovascular
Reduced CO
About 20% reduction by 60 years (reduced HR, SV & contractility)
Reduced sensitivity to catecholamines, vasopressors & inotropes
Orthostatic hypotension
Higher risk of thromboembolism
Neurological
Cerebral atrophy (10% reduced brain weight) - worse short term memory, higher risk of delirium
Reduced cerebral blood flow & metabolism - lower MAC required, and increased sensitivity to benzos/opioids
GI
Hiatus hernia, delayed gastric emptying
Renal & Hepatic
Reduced blood flow & GFR (40% lower), reduced drug clearance
Reduced hepatic metabolism
Metabolic & Endocrine
Reduced BMR, less effective temperature regulation
How does increasing age affect pharmacokinetics?
Volume of distribution
Older people have proportionally more fat & less muscle
This is particularly relevant for remifentanil, as it relies on muscle esterases for much of its metabolism
Clearance
Hepatic enzymes slow down, and renal clearance decreases
Comorbidity
Older patients are statistically more comorbid, which may result in direct changes to pharmacokinetics as a result of the disease, or as a result of polypharmacy and interactions.
What physiological changes are seen in pregnancy?
3 categories:
Improving uterine oxygen delivery
Protecting against blood loss during parturition
As a result of a gravid uterus
Most change happens in the first trimester, stimulated by progesterone & oestrogen - highest risk of teratogenicity.
In the second trimester, the mechanical impact of the enlarged uterus increases.
Cardiovascular
CO increases by 50% (30% by end of first trimester), peaking at end of second trimester. Can further increase by 40-50% during labour.
This can unmask undiagnosed cardiac disease
Caval compression reduces cardiac output anytime after 20 weeks.
Stroke volume increases by 35% (peaking at end of second trimester), HR increases by 25%
SVR drops
Heart is displaced cranially and to the left, with LV hypetrophy - causing left axis deviation, ST depression, flattened T waves.
Respiratory
Anatomical changes (mucosal oedema & engorgement) - may need smaller ETT, higher bleeding risk
Fluid overload PIH & pre-eclampsia
Thoracic changes - breast enlargement, diaphragmatic splinting (4cm elevation), but take deeper breaths and hyperventilate.
Compensatory increase in transverse & antero-posterior chest diameters.
VC, Total capacity & FEV1 remain equal.
From 20 weeks until term, the following decrease progressively by 20%
Expiratory reserve volume, residual volume, FRC, Closing capacity.
Inspiratory reserve volume increases
Physiological
Increased O2 consumption & CO2 production (60%), reduced FRC & higher closing capacity make pre-oxygenation less effective.
pCO2 Hyperventilation to 4.1kPa by end of first trimester, TV increasing by 40% and RR by 15%.
PaO2 increases in third trimester, until CO becomes limiting factor, with increased A:a gradient.
Increased 2,3-DPG
Neurological
Reduced epidural space volume (venous engorgement)
Increased sensitivity to hypnotics
Haematological
Anaemia of pregnancy, reduction in platelets
Blood volume - increases from 6 weeks, peaks at 34 weeks, returns to normal 10-14 days post-partum. Progesterone and oestrogen activate RAAS, increasing total body water retention.
Breast tissue, uterus, mucosa and skin all engorge.
Uterine contraction at delivery delivers approx 500ml auto-transfusion, which can delay signs/symptoms of MOH
Renal EPO increases, RBC mass increases by up to 30%, but less than plasma, so haemodilution to approx 120g/L
White cells rise during pregnancy until after delivery, which may mask sepsis
Increased fibrinogen & all clotting factors bar 11 and 13 - normal clotting but reduced fibrinolysis
Renal
Increased perfusion & GFR (50-60%)
Lower urea/creatinine
Small amount of proteinuria/glycosuria
Reduced plasma osmolarity (water retention via RAAS)
Increasd bicarbonate excretion, buffering respiratory alkalosis
Increased risk of UTI (smooth muscle relaxation via progesterone)
Uterus can compress ureters in later pregnancy
Endocrine
Enlarged pituitary, increased T4/T3
Increased insulin production & resistance (via human placental lactogen) - allows glucose across placenta into foetal circulation
Maternal hyperglycaemia causes foetal hyperinsulinaemia & risks post-natal hypoglycaemia
Diabetic mothers have macrosomic babies - insulin is anabolic.
GI
Increased intragastric pressure
Reduced lower oesophageal sphincter tone (upper is striated so not affected by progesterone)
Increased reflux, especially supine (hence the use of PPI & prokinetic, plus sodium citrate for emergency LSCS)
Gastric stasis in labour (worsened by opioids)
Increased ALP (3x normal - produced by placenta)
Gallstones more frequent
What pharmacokinetic & pharmacodynamic changes occur in pregnancy?
Increased volume of distribution (prolonged elimination half-life)
Redcued plasma cholinesterase (clinically insignificant increase in suxamethonium duration)
Reduced MAC requirement
Absorption
Nausea & vomiting, and gastric stasis
Distribution
Increased body fluid, adipose tissue, and reduced alpha-1-glycoprotein (higher sensitivity to local anaesthetics)
Metabolism
Enzyme induction by progesterone, competition by oestrogen for enzyme active sites, reduced plasma cholinesterase activity
Elimination
Increased GFR, but increased volume of distribution
Other
30% reduced MAC requirement, reason unknown. Higher alveolar ventilation with lower FRC (speed of onset of volatiles is faster), but increased CO slows this down, distributing the anaesthetic around the body more quickly.
What is aortocaval compression, and how should it be managed?
From week 20, the uterus compresses the IVC & Aorta in supine position
This reduces venous return, increasing afterload, with a fall in CO
Compression of aorta may reduce renal & uterine blood flow, compromising foetal blood supply.
Women should lie on a tilt, usually left side down, displacing the uterus.
GA and neuraxial both suppress the sympathetic autonomic response (which usually compensates for supine hypotension), increasing the importance of adequate tilt)
How does pregnancy affect administration of anaesthesia?
GA:
Risk of foetal depression
Increased MV and reduced FRC causes faster onset of inhaled agents
Reduced MAC requirement of up to 30%
Neuraxial:
Increased lumbar lordosis and intra-abdominal pressure, with epidural venous engorgement means smaller volume of local anaesthetic required
What is teratogenicity?
A permanent abnormality, induced by a drug due to its effect on foetal development - usually multiple factors rather than one clear causative pathway
