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Primary FRCA > Physiology 19 > Flashcards

Physiology 19 Flashcards

1
Q

What preoperative factors can contribute to the stress response to surgery?

A
  • Personality
  • Preoperative mental state
  • Dehydration
  • Partial starvation
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2
Q

Define the stress response

A

The combination of hormonal, inflammatory, metabolic and psychological changes which occur in response to trauma or surgery

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3
Q

What perioperative factors can contribute to the stress response to surgery?

A
  • Haemorrhage
  • Hypothermia
  • Pain
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4
Q

What postoperative factors can contribute to the stress response to surgery?

A
  • Pain
  • Immobilisation
  • Hypoxia
  • Alterations in diurnal rhythm
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5
Q

Outline the pituitary response to stress

A

Increased anterior pituitary secretion of:

  • ACTH
  • GH
  • β endorphin
  • Prolactin

Increased posterior pituitary secretion of:
-ADH (vasopressin)

TSH, LH and FSH may be increased or decreased

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6
Q

What are the key endocrine organs involved in the response to stress?

A 
Pituitary
Adrenals
Pancreas
Kidneys
Thyroid
Gonads
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7
Q

Outline the adrenal response to stress

A

Increased:

  • Catecholamines
  • Cortisol
  • Aldosterone
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8
Q

Outline the pancreatic response to stress

A

Increased:
-Glucagon

Decreased:
-Insulin

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9
Q

Outline the renal response to stress

A

Increased renin production

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10
Q

Outline the gonadal response to stress

A

Decreased:

  • Testosterone
  • Oestrogen
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11
Q

Outline the thyroid’s response to stress

A

Decreased:

-Tri-iodothyronine

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12
Q

What is the main cytokine associated with the surgical stress response?
What its profile following insult?

A

IL-6

Levels rise 2-4h after start of surgery and peak between 12-24h.
Amplitude of peak reflects severity of tissue damage

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13
Q

How does IL-6 affect the systemic response to stress?

A

IL-6 (and IL-1) have been shown to stimulate pituitary secretion and thus the stress response.

Cortisol release has a negative feedback effect on cytokine gene expression

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14
Q

What are the acute phase proteins associated with the stress response?

What is the effect of this production?

A 
Fibrinogen
CRP
Complement
Amyloid P
Amyloid A
Caeruloplasmin

This results in reduced production of other proteins eg. albumin + transferrin

This results in a reduction in circulating cations eg. Zn, Fe

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15
Q

What are the psychological and behavioural responses associated with surgery?

A

Anxiety/depression
-Usually brief and self-limiting

Fatigue/malaise
-May last several months

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16
Q

What is known about the physiology of postoperative fatigue?

A

Little

  • Poorly defined/measured
  • Not inevitable after major surgery
  • Unknown cause and no known treatments
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17
Q

What is known about the psychology of postoperative fatigue?

A
  • May be component of motivational response. For example joint arthroplasty has low rates of post-op fatigue, possibly due to the positive intended effects of surgery whereas abdominal surgery is rarely life-enhancing and has high rates.
  • Preoperative fatigue may predict postoperative fatigue
  • Association between anxiety/depression and postop fatigue
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18
Q

What surgical/anaesthetic perioperative factors may affect stress response?

A
  • Choice of induction agents
  • Volatile agents
  • High-dose opioid anaesthesia
  • Regional
  • NSAIDs
  • Minimal access surgery
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19
Q

How does etomidate affect the stress response?

A
  • Inhibits adrenal steroidogenesis
  • Acts on mitochondrial 11β-hydroxylase step and 17α-cholesterol cleavage part of the biosynthetic pathway
  • May inhibit cortisol and aldosterone porduction for up to 8h post single induction dose
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20
Q

How may benzodiazepines given at induction affect the stress response to surgery?

A

Diazepam and midazolam inhibit cortisol production in vitro and midazolam has demonstrated this effect in human surgical studies and may have a direct effect on ACTH secretion

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21
Q

What effect do volatile anaesthetic agents have on the stress response to surgery?

A

Unlikely to have a significant effect on HPA axis - from studies mainly on halothane

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22
Q

What effect does high-dose opioid have on the stress response to surgery?

A
  • Inhibition of HPA axis mediated via the hypothalamus

- Fentanyl 50mcg/kg abolishes cortisol response in pelvic surgery, 100mcg/kg in upper abdo surgery

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23
Q

Discuss the effects of regional anaesthesia on the surgical stress response

A
  • Complete afferent blockade (ie. somatic and autonomic) required for blockade of HPA axis
  • Pelvic surgery requires extensive T4-S5 block
  • Very difficult to prevent cortisol secretion in upper abdo surgery with reqional techniques
  • Limb and eye surgery are amenable to complete blockade
  • Regional does not prevent the cytokine response
24
Q

Outline the evidence relating to spinal/epidural anaesthesia on clinical outcomes

A
  • Evidence of beneficial effects of spinal/epidural anaesthesia on outcomes after major surgery are controversial
  • Some evidence does suggest a reduction in DVT and 30-day mortality following hip fracture repair with regional
  • Evidence suggests that epidural anaesthesia provides better pain relief and shortens intubation time on ITU following some major abdo surgery eg. aortic surgery
  • Significant benefit in reduced occurrence of postop respiratory failure with epidural following major abdo surgery
25
Q

What effect does NSAID use have on the surgical stress response?

A
  • No effect on HPA axis
  • Perioperative diclofenac may show reduced IL-6/10 and WCC response but must be started at least 24h prior to surgery for effect
26
Q

What effect may endoscopic surgery have on the stress response?

A

-Endoscopic surgery does not affect the neuroendocrine response to surgery but does reduce the acute phase response and is associated with relatively preserved immune function relative to open techniques

27
Q

List the possible health risks of obesity

A

Neuropsychiatric

  • Headaches
  • Poor sleep
  • Depression
  • Poor self-esteem

Cardiovacscular
-HTN, IHD, CVA, HF, arrhythmia

GI

  • Gallstones
  • HH
  • NASH -> cirrhosis

Resp

  • OSA
  • OHS

Metabolic

  • T2DM
  • Dydlipidaemia

GU

  • Infertility, dymenorrhoea, PCOS
  • ED

Ortho

  • Joint disease
  • Mobility impairment
28
Q

Summarise the pathways governing energy balance

A

NTS receives two types of signal:

  1. Adiposity signals:
    - From fat mass via leptin and insulin -> arcuate nucleus -> paraventricular nucleus and lateral hypothalamus (neuropeptide Y is stimulatory; Pro-opiomelanocortin is inhibitory) -> anabolic or catabolic signals to NTS
  2. Satiety signals:
    - From liver and GIT via autonomic afferents directly to NTS

The integrated response is then transmitted via ANS efferents

29
Q

What mechanism is implicated in the food reward response?

A

Insulin acts to reduce dopamine clearance

30
Q

Summarise the role of leptin in energy balance

A
  • Hormone released from adipose tissue, signalling adipose mass to the CNS
  • Increases melanocyte-stimulating hormone and inhibits neuropeptide Y
  • Reduces drive for food intake and permits increased energy use via sympathetic stimulation
31
Q

Summarise the role of insulin in energy balance

A
  • Acts in CNS to increase melanocyte-stimulating hormone and inhibit neuropeptide Y (in a manner similar to leptin)
  • Reduces drive for food intake and permits increased energy use via sympathetic stimulation
32
Q

What is the effect of leptin level on metabolism?

A

Reduced leptin levels eg. with prolonged starvation, reduces basal metabolic rate, in order to limit weight loss

33
Q

Which dopamine receptors are implicated in the food reward system?

A

D2

34
Q

What role may insulin resistance have on the food reward response?

A

Insulin resistance in the ventral segmental area may lead to dopamine accumulation in the nucleus accumbens -> enhanced pleasure response to food

35
Q

What are the main categories of fat distribution?

A

Android / Gynaecoid

Android:

  • Central obesity with peripheral sparing
  • Higher cardiovascular risk association

Gynaecoid:
-More peripheral distribution (arms, legs, buttocks)

36
Q

How does obesity affect lung capacities in anaesthesia?

A

For BMI >30:

  • Reduced FRC
  • VC reduced by 40% of baseline in laparotomy
  • Compared to reduction of 10% in lean patients
37
Q

How does rate of absolute energy consumption differ between the obese and non-obese patient?

How does this impact anaesthesia?

A

Absolute energy requirements (and thus O2 consumption and CO2 production) are increased for the obese patient.

This has implications for low-flow anaesthesia and minute volumes

38
Q

Elaborate on the possible respiratory consequences of obesity in anaesthesia

A
  • Risk of airway obstruction/collapse
  • Possible pre-existing OSA/OHS
  • Increased mass of chest wall and IA pressure leads to:
  • Reduced FRC and VC
  • Increased A-a gradient
  • Increased closing capacity
  • Increased shunt
39
Q

What are the diagnostic criteria for obesity hypoventilation syndrome?

A
  • Awake PaCO2 of >6kPa
  • BMI > 30
  • Absence of other cause of hypercarbia
  • OSA present (supportive - 83% of OHS also have OSA)
40
Q

What are the possible anaesthetic consequences of OSA/OHV?

A
  • Respiratory alkalosis at normocapnia
  • Difficult or impossible ventilatory weaning
  • Prolonged postoperative respiratory depression
41
Q

What are some possible anaesthetic techniques to limit the problems associated with obesity?

A
  • Increased PEEP to prevent derecruitment
  • Recruitment manoeuvre immediately following induction (when majority of atelectasis occurs)
  • Use of CPAP during induction
  • Possible reduction in atelectasis if FiO2 of <1.0 used prior to intubation
42
Q

What are the possible physiological effects of pneumoperitoneum for the obese patient?

A
  • Reduced venous return
  • Reduced CO
  • Increased PAP
  • Increased ICP
  • Raised IA pressure and risk of splanchnic ischaemia and surgical emphysema
  • Raised PaCO2 -> resp acidosis
  • Sympathetic activation -> arrhythmia, increased SVR
43
Q

What is the effect of obesity on cardiac myocytes?

A
  • Mechanical effect from myocardial adipocytes

- ‘Cross-talk’ with adipocytes reduces fibre-length and peak intracellular calcium

44
Q

What is the effect of obesity on the vascular endothelium?

A
  • Endothelial dysfunction and increased SVR.

- Possibly through leptin-mediated expression of myocardial endothelin-1

45
Q

How does muscle blood flow increase from resting to exercise?

A

Resting: 4ml/100g/min
Exercise: Up to 100ml/100g/min

46
Q

What is the difference between endurance and resistance training in terms of cardiovascular changes

A

Main difference is that endurance training increases CO, whereas resistance training has little effect

47
Q

How much energy does a mole of ATP produce?

A

7.3 kcal (30.7 kJ)

48
Q

What are the routes to ATP production relevant to immediate use in exercise?

A
  1. Stored ATP
  2. Phosphocreatine system
  3. Adenylate kinase reaction:
    - ADP + ADP = ATP + AMP
49
Q

Summarize the sources of ATP production at different durations of exercise

A

2-20 secs:
-ATP-phosphocreatine system

20 - 45 secs:
-Anaerobic glycolysis

45 s - 10 min:

  • Aerobic
  • Glycolysis
  • Phosphocreatine

10 min+
-Aerobic metabolism, reaching steady state

50
Q

What is the anaerobic threshold?

A

aka. lactate threshold. AT is the point at which serum lactate starts to rise significantly with increasing VO2

51
Q

What are the possible mechanisms for the anaerobic threshold?

A
  • Reduced O2 in muscles
  • Accelerated glycolysis
  • Recruitment of fast-twitch fibres (which favour lactate production)
  • Reduced lactate removal
  • Failure of ETC to keep up with glycolysis (excess NAHD in sarcoplasm promotes lactate conversion)
52
Q

What is the ‘crossover concept’ in exercise?

A

As exercise increases, relative proportion of carbohydrate : fat use increases due to recruitment of slow-twitch fibres.

The crossover point is around 35% of VO2max

53
Q

What effect does duration of exercise have on source of energy?

A

At constant exertion, increasing duration of exercise increases the ratio of fat : carbohydrate metabolism

The crossover point is around 20 mins

54
Q

Describe and explain the relationship of VO2 with exercise over time

A

On starting exercise, it takes some time for VO2 to reach steady state. The resultant lag between energy production and O2 consumption implies the contribution of anaerobic metabolism -> O2 deficit.

Following cessation of exercise, it takes some time for VO2 to return to the resting level, this excess of post-exercise O2 consumption is termed O2 debt. It has two main components:

Rapid debt:
-Resynthesis of phosphocreatine and replenishment of O2 ‘stores’

Slow debt:
-Metabolism of lactic acid

Factors such as ongoin ^work of breathing/tachycardia, elevated hormones and hyperthermia also contribute to oxygen debt

55
Q

What are the factors that contribute to VO2max?

A

Central / Peripheral:

Central:

  • Pulmonary function - usually only relevant at altitude or with pulmonary disease
  • Cardiac - Increased CO via SV is important, and likely the limiting factor determining DO2 (and thus VO2max) at maximal exercise
  • O2 carrying capacity - Generally does not limit VO2, but VO2max may be increased by increasing CC (eg. EPO abuse)

Peripheral:

  • Number of mitochondria in skeletal muscle influences O2 extraction but is not a limiting factor for VO2max
  • Increasing muscle capillary density increases O2 extraction and may increase VO2max
56
Q

What is the maximum efficiency of conversion of energy sources into muscular work?

What are the consequences of this?

A

20-25%

This means that increased exercise creates excess heat, which must be dissipated to avoid heat exhaustion

Primary FRCA (34 decks)

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