Describe the cardiovascular changes that occur with morbid obesity
Morbid obesity:
BMI > 35
Extent depends on extent and duration of obesity.
Main issue:
- Increase in adipose tissue
- —> Leads to increase of hormones produced by adipose tissue, e.g. leptin, angiotensinogen.
—-> Stimulate SNS, causes increased RAAS activation (absolute increased blood volume), increased HR, Increased BP, increased VO2, increased CO2 production, polycythaemia and increased CO to preserve DO2.
CO: increased
Vascular resistance:
- decreased as fat is added in parallel circuits not in series.
Left ventricle:
- Increased afterload due to systemic hypertension, LVH, volume overload.
Right ventricle:
- Hypertrophy due to HPV due to OSA
ECG changes:
- Microvoltage
- Right or left ventricle strain/axis deviation
- tachycardia
- Cor pulmonale
(a) Describe the mechanisms by which heat is transferred between the body and its environment (30%)
(b) Describe methods by which body heat may be conserved under anaesthesia (70%)
Mechanisms by which heat is transferred between the body and its environment.
Define heat:
- A form of energy
Temperature will determine which direction heat energy will flow.
5 ways of heat transfer in the operating theatre:
- Radiation Approx 50%
- Convection
- Conduction
- Evaporation
- Respiration ~5%
Methods used to preserve body heat under anaesthesia. NEED to include heat loss and heat gain
Radiation:
- Warm theatres (e.g. for paediatric or trauma case)
- Cover patient with hot blanket
- Reflective blankets and/or hats
- –> Prevent IR radiation from being transferred to operating theatre
Convection and conduction:
- Ensure skin is covered where possible
- Use of bare hugger
- ensure patient isn’t laying in substance easily conductable i.e water, blood, metal table.
- Warmed IV fluids
Evaporation:
- Due to latent heat of vaporisation
- Lost through things like chlorhexidine wash
- Lost from body cavities
- –> Ensure organs are wrapped in plastic bags if exposed
Respiratory:
- HME filter
Briefly outline the functions of the kidney
Candidates were required to give a broad list of functions including water and electrolyte homeostasis and excretion of metabolic waste products PLUS at least two other functions. It was further required that there was some discussion about the significance of these functions and underlying mechanisms.
Functions:
• Regulation of the volume, composition and pH of body fluids
• Excretion of nitrogenous / metabolic waste
• Excretion of drugs and toxins
• Metabolic and synthetic - Endogenous / Exogenous substances
• Endocrine - Synthetic / Target organ
• Long term regulation of arterial pressure
Regulation of water and electrolytes:
- Variable excretion of water and electrolytes to maintain homeostasis.
- Kidneys can concentrate urine up to 1400mOsm to reduce renal water loss.
- Minimum volume is 0.25ml/kg/hr
Excretion of waste:
- especially nitrogenous waste, creatinine from muscle, uric acid, bilirubin
Metabolic and synthetic:
- Hormone production (renin, EPO, active for of Vit D)
Acid base:
- By varying excretion of HCO3 and H+ ions, PO4 ions.
Discuss the determinants of RBF.
Normal renal blood flow is approximately 25% of CO
~1500ml/min in adult.
Flow = delta pressure / resistance
Delta pressure is MAP - CVP
Resistance (as renal flow usually laminar) = 8nl/pi r^4 /
Therefore anything that effects these can change renal blood flow.
Decreased MAP (i.e. haemorrhagic shock)
Increased CVP i.e. from IVC thrombosis
Increasing viscosity i.e. from polycythemia
Decreased radius of blood vessels, predominantly from afferent arteriolar constriction.
Two intrinsic ways in which the kidney autoregulates its blood flow.
- Myogenic autoregulation.
- As stretch increases on the walls of the afferent arteriole blood vessel, increased intracellular calcium is released, causing increased contraction of the vascular smooth muscle of AA. This decreases the radius of the vessel, thereby increasing the resistance, therefore decreasing the flow. - Tubuloglomerular feedback:
- If increasing perfusion to the glomerular apparatus, there will be an increase in the filtrate. This is sensed by the macula densa osmoreceptors in the juxtaglomerular apparatus (in the distal convoluted tubule). This then causes either a release of adenosine and ATII if the perfusion is too great, or a release of NO if the perfusion is too small. Adenosine is a potent vasoconstrictor, thereby decreasing AA radius and decreasing flow and vice versa for NO.
Extrinsic:
- SNS involvement
- Decreases radius of AAs thereby decreasing flow
