hypoxia Flashcards
hypoxia
specific env and ste of conditions
specifically PO2 in the env
hypoxaemia
describes the blood env
PaO2
Ischemia
tissue receiving inadequate oxygen eg forearm ischemia
Factors that cause hypoxic stress on the body
altitude
exercise - but physiological response is efficient so not experienced- more O2 is supplied
disease - COPD
what is the O2 cascade
describes the decreasing O2 tension from inspired air to respiring cells ]
ambient air - highest PO2
reduction in upper airway - humidification
biggest loss in alveoli - mixing - have tio ventilate
small loss in arteries for bronchiole drainage
big loss in tissues - O2 diffusion
vol perfusion matching
cardiac output
thickness of membrane
factors affecting the O2 cascade
o2 therapy increase start PO2
breathing inhaled air decrease start
hyperventilation - reduce affect of mixing - faster
hypoventilation exacerbate mixing
diffusioin affect reduce PO2 in post alv cap
exercise reduce PO2 in tissue - diffusion, increase PCO2
PCO2 and PO2 in O2 cascade
changes are not same
O2 - sigmoid shape
CO2 - linear change
Oxygen cascade on Everest
lower starting PO2
gradient less to work with
Fick’s law
of diffusion flow rate proportional to pressure grad Vgas = area/thickness * diffusibility * PP grad structural disease reduce area fluid in alveoli - increase thickness hypoxic gas reduce PP grad hyperoxic gas increase PP grad
Gas transport change at altitude
boiling point inversely proportional to altitude
need pressurised suit at high altitude - allow breathe and stop body fluids evaporating
hypoxia - less O2 in the air
thermal stress: -7degrees for 1000m, wind chill
solar radiation- sun and reflection
hydration - water lost humidifying inspired air - hypoxia induced diuresis - breathe dry air
hypoxia induced confusion and miscoordination
Oxygen dissociation curve
how much O2 bidn is dependant on PP
Type 1 resp failure
failure of pul gas exchange V/Q inequality hypoxic O2 into blood impaired CO2 out - fine because it is more diffusible PaO2<8KPa PaCO2 - low/normal hypoventilation diffusion abnormality pul oedema pneumonia atelectasis - collapse or closure of the lung - worse GE
Type 2 resp failure
hypercapnic resp failure getting gas there problem V/Q problem PaO2<8KPa - low but not really the problem - O2 down greater conc grad so fine PaCO2 >6.7KPa increased CO2 production decreased VCO2 elimination decreased CNS drive increased work of breathing pul fibrosis neuromuscular disease increased physiological dead space obesity
good Physiological response to high altitude
low atm O2 reduced PAO2 reduced PaO2 activation peripheral chemoreceptors - carotid bodies increase sympathetic outflow increase vent reduce PaCO2 increase PH alkalosis detected by carotid body increase HCO3 excretion ODC normalises increased O2 unloading
good ‘side effects’ of physiological response to attitude
increased symp outflow =
increased HR and Flow
increased O2 loading
increased vent =
increased PAO2
increased O2 loading
decreased PaO2 = increased erythropoietin increased erythropoiesis increased O2 loading increased ox loading increase oxidsative enzymes small increase in 2,3-DPG in RBC right shift ODC increase O2 unloading increase O2 utilisation
bad ‘side effects’ of physiological response to altitude
reduced PaCO2 =
loss of central drive to breathe
reduced vent
reduced O2 loading
increased pH =
left shift ODC
decrease O2 unloading
Prophylaxis of altitude treatment
acclimation - from artificial exposure to the environment
acetazolamide - carbonic anhydrase inhibitor, accelerate the slow renal compensation to hypoxia induced ventilation - reduce initial alkolytic response
Innate developments to prevent altitude sickness
barrel chest - larger TLC and capillarisation - more O2 in
increased haematocrit (vol % RBC in blood) - greater O2 carrying capacity - more O2 carried
larger heart to pump through vasoconstricted circulation - greater perfusion
increased mitochondrial density - greater oxygen utilisation at cellular level - more O2 used
because of exposure through childhood and genetics
not all expressed in all populations
Chronic mountain sickness
Monge’s disease
acclimatised people spontaneously acquire chronic mountain sickness
cause unknown
pathophysiology of chronic mountain sickness
secondary polycythaemia - increase blood viscosity (haematocrit is increased)
sludge through cap beds- impede O2 delivery
symptoms of c nmountain sickness
cyanosis
fatigue
consequences of c mountain sickness
ischemic tissue damage
heart failure
eventual death
treatment
no interventional treatment
forced to go down the hill
causes of acute mountain sickness
maladaptation to high altitude env
recent ascent- onset in 24 hours - last a week
pathophysiology of a mountain sickness
associated with mild cerebral oedema
fluid accumulate in the cranium
symptoms of a mountain sickness
nausea vomiting irritability dizziness insomnia fatigue dyspnoea disappear after 48hours of increased kidney compensation
consequences of a mountain sickness
development to high altitude pul oedema
development to high altitude cerebral oedema
treatment of a mountain sickness
monitor symptoms stop ascent analgesia - pain killer acetazolamide hyperbaric O2 therapy
cause of High altitude pulmonary oedema
rapid ascent
inability to acclimatise
pathophysiology of high alt oedema
vasoconstriction pul vessels -response to hypoxia
increased pul pressure
increased fluid leakage from caps
fluid accumulates - when exceed max lymph drainage
symptom of high alt oedema
dyspnoea
dry cough
bloody sputum
crackling chest sounds
consequences of high alt pul oedema
impaired GE and ventilatory mechanics
treatment of high alt pul oedema
descent hyperbariac O2 therapy nifedipine - Ca channel blocker - vasodilate pul cic salmeterol - relax airway sm sildenafil - affect Bp
cause of high altitude cerebral oedema
rapid ascent
inability to acclimatise
pathophysiology of high alt cer oedema
vasodilation of vessels - hypoxia
more blood to cap - increased leakage
cranium in sealed box -cant expand
intracranial pressure increases
symptoms of high alt cer oedema
confusion ataxia - stumbling behaviourala change hallucinations disorientation - confusion - middle ear
consequences of hugh alt cer oedema
irrational behaviour
irreversible neuro damage
coma
death
treatment of high alt cer oedema
immediate decent
O2 therapy
hyperbaric O2 therapy
dexamethasone
H0w can we hold our breath for along time
wet suit - protect form the cold external environment
hyperventilate with O2 - move the blackout and CO2 threshold
cold water over face - slows breathing and heart rate
how do you calculate a persons total blood vol
5l/70kg = 71ml/kg 71*weight = vol of blood
how do you calculate the amount of Hb in the blood
multiply Hb conc in g/L against blood vol in L
how do you calculate cardiac output from ESV and ejection fraction
ESV/(100-EF) = SV
SV - ESV
stages of acclimatisation to high altitude
low atmospheric O2 reduced PAO2 reduced PaO2 hypoxia detected by carotid bodies increased vent increased PAO2 reduced PACO2 increased PaO2 reduced PaCO2 reduced [H+] increased pH pH imbalance detected by carotid bodies increased HCO3- excretion via the kidneys increased H+ and reduced pH
blood gases after 2 weeks at altitude
pH - unchanged- kidneys will have compensated by now
PCO2 - low - reduced because of increased ventilation
BE low
PO2 low
maximum altitude for permanent human residence
5500m
oxygen transport - partial pressure
age related decline in lung func
tissue use a lot of O2 - PP wise
