- Respiratory Physiology 1
- cascade
- hypoxia
- hypoxaemic
- altitude
- Cascade
- Alveolar gas equation
- Reduced FiO2
- Reduced Pb
- Same SVP of H20
- Increased VA, so decreased PCO2
- Oxygen content
- Reduced sats
- Increased Hb
- Acute: reduced plasma volume (approx 20%), causes haemoconcentration
- Hours: increased erythropoietin, leading to more red cells in days, continuing for weeks
- Oxygen delivery
- Increased sympathetic activity causes tachycardia
- SV decreases slightly due to reduced preload
- Oxygen release
- Acute: alkalosis shifts curve to left
- Days: increased 2,3-DPG corrects it to right
- In the tissues
- Unclear
- Changes in cellular oxygen consumption
- Disease
- AMS
- HAPE
- HACE
- High altitude deterioration
- Hypothermia
- Cold injuries
- Ultraviolet radiation injuries
- Cold injuries
- Higher trauma risk
- Higher thrombosis risk
- Tx: PREVENTION IS BETTER, oxygen, decent, dexamethasone, acetazolamide (alkalinises the urine, causing a metabolic acidosis, shifting dissociation curve to the right more quickly), nifedipine, hyperbaric chamber e.g. Gamow bag
- mismatch
- V/Q = 0/1 = zero = low = shunt
- causes
- intrapulmonary
- blood/pus/water/tumour in alveolus
- reduced FRC
- extrapulmonary
- R-L heart defect
- Bronchial veins
- Thebesian veins
- ‘REMEMBER Right By Them’
- NOT AZYGOUS (drains into SVC) OR CORONARY SINUS (drains into R atrium)!
- Alveolar - arterial gradient = PAO2 - PaO2
- increased by
- shunting
- increased oxygen extraction (CaO2 - CvO2)
- Reduced diffusion capacity
- normal = 0.5 - 1 kPa
- shunt equation
- Qs/Qt = (CcO2 - CaO2) / (CcO2 - CvO2)
- CcO2
- = pulmonary capillary oxygen content
- estimated by oxygen content equation using PAO2 (so also need to do alveolar gas equation)
- CaO2 and CvO2
- estimated simply by Oxygen content equation using arteral/venous sats and arteral/venous PO2’s!
- V/Q = 1/0 = infinity = high = dead space
- increase in PaCO2 and ETCO2 difference
- does not cause hypoxia
- Bohr equation
- CO2 IS DEAD (space) BOHRING!!!
- West zones
Link:www.youtube.com/watch?v=HF__ZUaIY_4
- I = PA>Pa>Pv
- only in IPPV or haemorrhage
- dead space, higher V/Q
- II = Pa>PA>Pv
- III = Pa>Pv>PA
- shunt, lower V/Q
- most of healthy lung
- constant blood flow
- hypoxic pulmonary vasoconstriction (HPV)
- NO mediated vasoconstriction in response to hypoxia to divert blood away from areas of low ventilation in the lungs
- bad in chronic hypoxia —> pulmonary hypertension
- COPD
- altitude: HAPE
- cardiac shunts
- increased by ‘HHANAH’S TEA’
- hypoxia
- hypercapnia
- acidosis
- noradrenaline
- adrenaline
- histamine
- 5-HT
- thromboxane A2
- extremes of lung volume (think TEA graph)
- angiotensin
- (beta blockers and Cox inhibitors)
- decreased by
- vasodilators
- bronchodilators
- volatiles
- NOT AFFECTED BY IV INDUCTION AGENTS
- beta-agonists
- PVR and lung volume
- is increased below FRC
- collapsed extra-alveolar vesels
- TEA down left side of graph
- is increased above FRC
- stretched and distorted capillaries
- resistance = ((MPAP - MCWP) / CO ) x 80
- <250 dynes.sec/cm5
- (SVR 1000-1500 dynes.sec/cm5)
- equations
- PAO2 = FiO2 (Pb - PH20) - PACO2/R
- RQ = CO2 eliminated / O2 used
- pure carb = 1
- pure protein = 0.9
- pure fat = 0.7
- DO2 = CO x (1.34 x Hb x sats/100) x (PaO2 x 0.0.23)
- Hypoxia contd..
- cytotoxic
- Cyanide
- caused by sodium nitroprusside
- >8micrograms/mL
- confusion, dizziness headache, decreased arteriovenous O2 difference, lactic acidosis
- Treatment
- Dicobalt editate
- Sodium/amyl nitrite
- increases formation of metHb, which can bind to CN- to form non-toxic cyanometHb
- Sodium thiosulphate
- provides sulphydryl groups to promote formation of thiocyanate
- normal PaO2, raised PvO2
- stagnant
- normal PaO2 and PvO2
- e.g. cardiogenic shock
- anaemic
- oxygen dissociation curve
- left shift
- myoglobin
- carries 1 molecule of Hb
- hyperbolic as no conformational change
- fetal Hb
- pregnancy
- stored
- has lower 2,3 DPG due to acidosis!
- methaemoglobin
- Ferric rather than ferrous iron (Fe3+)
- subunit can’t carry O2, but increases binding capacity of other subunits so shifts curve to the left
- increased by
- prilocaine
- amyl nitrates
- antidote for cyanide poisoning
- INC GTN!
- treatment
- methylene blue (in propofol dose!)
- carboxyhaemoglobin
- 250x affinity for CO over O2
- prevents Hb from releasing O2 to the tissues
- CHERRY RED CHEEKS
- quantities
- 2% - normal
- 6% - smokers
- 10 - 30% - headache, weakness, D&V
- 60% - convulsions, coma, death
- 2 PROBLEMS
- peripheral baroreceptors register normal pO2
- pulse oximetry is normal
- treatment
- RA
- T 1/2 of carboxyHb = 4 hrs
- oxygen
- hyperbaric if severe
- right shift
- raised CO2
- Acidosis
- raised 2,3-DPG
- increased by thyroid hormones, GH & androgens and CHRONIC ANAEMIA
- Exercise
- raised Temperature
- HbS
- ‘CADETS’
- normal PaO, reduced PvO2
- CO2 carriage
- arterial = 50mL/100mL blood
- bicarbonate = 45mL/100mL
- carbamino = 2.5mL/100mL
- carbonic acid = 2.5mL/100mL
- venous = 54mL/100mL blood
- bicarbonate = 47.5mL/100mL
- carbamino = 3.5mL/100mL
- carbonic acid = 3mL/100mL
- Haldane effect
- = increased ability of deoxygenated blood to carry CO2
- 2 things
- increased affinity of deoxyHb for CO2 (70% of effect)
- more carbamino groups formed
- increased buffering ability of deoxyHb
- when Hb becomes deoxygenated, its imidazole groups conformationally change, making them more able to accept H+, so HHB equation is shifted to the right
- more bicarbonate formed
- pKa 6.8
- Oxygen cascade
- ODC