SAQs 2016 Flashcards
discuss the determinants of spinal cord perfusion
Essentially the same as determinants for cerebral blood flow.
Intro:
- Arterial anatomy
- Physiology of spinal cord flow
- Control of spinal vascular resistance
Arterial supply:
- Via circle of willis
- predominantly from basilar artery.
- Anterior spinal artery to anterior 2/3
- Two posterior spinal arteries each do posterior 1/6th.
- Segmental reinforcement via thoracic and lumbar arteries
- Main reinforcement by artery of Adamkiewicz (usually T11)
Physiology of spinal cord flow:
- Similar determinants to CBF
- -> Spinal cord blood flow (SCBF)
SCBF = MAP - (SCP or CVP, whichever is greater) / spinal vascular resistance.
Therefore factors which increase SVR, SCP or CVP will decrease flow, and factors which decrease MAP will decrease flow.
Factors which will increase SVR:
- R = 8nl/pi.r^4
therefore reduction in arterial size or increase in viscosity will increase SVR, and decrease SCBF
Describe the physiological effects of sleep on the brain and the respiratory system.
Sleep: A necessary state of rousable unconsciousness which can be reversed by physical stimulus.
Structure:
- Sleep architecture,
- Sleep EEG signature
- Sleep neurochemistry
- Resp changes
Sleep architecture:
- Cycle
- –NREM stages 1-4 then REM
- Reduced in adults, highest in neonates
Sleep EEG signature: - Wave types Beta: 13-30Hz, low amplitude Alpha: 8-13Hz Theta 4-8 Delta <4, high amplitude
NREM1: Alpha and theta
NREM2: theta, sleep spindle (high frequency, low amplitude burst), k complex (low frequency, high amplitude pattern)
NREM3+4: Theta and delta waves (all low freq, high amplitude)
REM: Beta waves, similar to awake EEG (i.e. paradoxical)
Resp effects: NREM: TV decreased RR unchanged Decreased response to PaCO2 and PaO2 Decreased pharyngeal motor tone
REM:
- decreased RR
- Decreased TV
- Very decreased response to hypoxaemia and hypercapnoea
- Muscular atony w/ exception of diaphragm and extraoccular muscles –> pharyngeal obstruction (OSA), no use of intercostals for breathing
Explain the physiological processes that cause oliguria in response to hypovolaemic shock
Oliguria in the presence of shock is designed to preserve intravascular volume.
Oliguria is when the obligatory urine output is not met. This is 430ml/day, or 0.25ml/kg/hr of urine.
Urine production is determined by the balance of glomerular filtrate vs the ability of the kidney to concentrate this filtrate.
Hypovolaemic shock is when inadequate tissue oxygen occurs as a result of intravascular depletion i.e. in haemorrhage or dehydration.
GFR = Kf x NFP.
Hypovolaemic shock will decrease Kf (via stimulation of baroreceptors –> Increase SNS activity –> reduction of surface area for filtration), and will decrease NFP (NFP is determined by starling’s forces –> Decreased MAP, if dehydrated may have increased albumin concentration).
Increased osmolarity or volume depletion will be sensed by the hypothalamus, which will lead to increased production and release of ADH.
ADH acts on V2 receptors which increase transcription and the insertion of AQ2 channels into the collecting duct, which allows for the water in the collecting ducts to be exposed to the high osmolality of the interstitium (established by the CCM and CCE).