Gaseous diffusion and transport Flashcards
Factors affecting O2 carriage
pO2 is proportional to conc dissolved in blood. Hb
How to calculate O2 carrying capacity of normal blood
max O2 1g of Hb can combine with x normal blood Hb concentration=Oxygen capacity of normal blood
O2 saturation of blood entering pulmonary capillaries and leaving
enter=75% leave=97-100%
What is the haem group
iron porphyrin compound attached via histidine N to globin. O2 binding is oxygenation, iron remains in Fe2+ strate after O2 released
When does 2,3 DPG increase
hypoxia, anaemia
What is anaemia and what causes it
when there is reduced content of functional Hb in blood. Caused by defect Hb production or red cell numbers. O2 carrying capacity reduced
How is Hb association curve affected in anaemia? sketch
venous pO2 will be lower so tissue pO2 also low. Extraction of O2 during exercise limited
What are the negative effects of CO binding to Hb
reduces amount of O2 bound to Hb
shifts O2 binding curve to left, increases O2 affinity of remaining binding site decreasing unloading of O2
Sketch O2 dissociation curve for CO poisoning
tissues still remove 5mldl-1 of blood. Venous PO2 even lower (2kPa)=tissue PO2
HbF binds DPG more or less than HbA
less
Cyanosis what is it
If supply of O2 to tissues is deficient, content of de-oxyHb in tissue capillary increases because of hypoxia. De-oxy Hb has blue-ish tinge causing discolourisation of tissues
2 types of cyanosis
Peripheral-reduced blood flow to region resulting in hypoxic tissue causing blue-ish tinge in extremities. Cause=cardiovascualr shock, low temp, reduced CO, poor arterial supply
central=arterial hypoxaemia, buccal mucosa and lips used to spot.
Cause=chronic respiratory disease e.g. COPD (~8kPa), right to lef shunt reduces O2 sat
At which point is cyanosis observable
Arterial blood containing >1.5-2g/dl of deoxyHb, canosis is observable even in well-perfused tissues. OCcurs when O2 sat <85% if [Hb] is normal
How are CO2 carried and state the proportions
HCO3-=60%
Hb-CO2=30%
Dissolved CO2
CO2+H2OH2CO3H+ +HCO3- describe
Reaction 1: slow in plasma but fast in RBC because of presene of carbonic anhydrase
Reaction 2 aided by buffering o f {H+] by deooxy-Hb. Bicarbonate formed by reaction 2 diffuses out down its conc grad via antiporter into plasma in exchange for Cl- (chloride shift)
How do carbamino compound form
RNH2+CO2->RNHCOOH (lysine, arginine side chains)
Mostly formed with deoxy-Hb in red cell, a little with plasma proteins. Oxygenation of Hb inhibits reaction and aids CO2 being breathed out
How are various forms of CO2 unloaded in lung
CO2 dissolved in plasma: diffuses down partial pressure grad
carbamino compound: CO2 comes off assisted byy oxygenation of Hb and diffuses into alveoli
HCO3- from plasma: taken back into RBC, combines with H+ which comes off as O2 binds to Hb forming H2 CO3. H2 CO3 dissociates into CO2 via carbonic anhydrase
What is the haldane effect and why does it occur
at any given PCO2, CO2 quantity carried is greater in deoxygenated than oxygenated
Cause:
1. Hb forms carbamino compounds easier when deoxygenated
2. Hb binds to H+ better when deoxygenated which favours formation HCO3-
Sketch CO2 dissociation curve and note key points
not sigmoidal, no plateau, approx linear over physiological range.
More total CO2 carrying capacity than O2. Haldane effect. mixed venous CO2 content-mixed arterial=amount of CO2 produced at rest for 100ml blood passing
What is the Henderson-Hasselbach equation and what is pKa of
pH=pKa+log([HCO3-]/[CO2])
pKa=-log(dissociation constant of H2CO3)
What is the relationship between alveolar pCO2 and alveolar ventilation
Inversely proportional. If one doubles, other halves
How to measure O2 consumption
1) FIck principle: O2 consumption by tissues=COx(arterial-venous O2 content)
2) respiratory measurements:
CO2 produced in tissues=COx(venous-arterial CO2 content)
What is the respiratory quotient
CO2 produced: O2 utilised
What is hyper and hypoventilation
Hyper: over ventilation in proportion to metabolism leading to lower arterial PCO2 below normal values
Hypo: under ventilation in proportion to metabolism results in higher arterial PCO2 levels
Why does hyperventilation not equate to increased ventilation
e.g. exercise increases ventilation but so does metabolic rate so arterial PCO2 remains relatively constant
What does hyperventilation lead to
Hypocapnia=low arterial PCO2->reduces [H+] causes respiratory alkalosis
Hyperventilation cause
anxiety, pain, excessive mechanical ventilation, diseases contribiting to metabolic acidosis
What are the consequences of hyperventilation
1) low PaCO2->cerebral vasoconstriction->cerebral hypoxia resulting in dizziness
2) alkalosis-> decrease plasma free [Ca2+] (more binds to proteins)->increase exitable cells (VGCC open at lower threshold potentials)->disturbed sensation and unwanted muscle contractions
What does hypoventilation cause and what is it caused by
hypercapnia=high arterial PCO2->increases {H+] causes respiratory acidosis. Caused by head injury impairing respiration, anaesthetic drugs, chronic lung disease
Consequences of increased PCO2 due to hypoventilation
Increasing arterial PCO2 causes peripheral vasodilation, flushed skin, full pulse, extra systoles
Very high PCO2 depresses CNS function causing drowsiness, coma and death
What are the normal values of: PAO2, PaO2, arterial O2 content, Arterial Hb saturation, Mixed venous PO2, mixed venous O2 content, mixed venous Hb saturation
PAO2=13.3kPa/100mmHg
PaO2=12.5kPa/94mmHg, arterial O2 content=200ml/l,
Arterial Hb saturation=97%, M
ixed venous PO2=5.3kPa/40mmHg, mixed venous O2 content=150ml/l,
mixed venous Hb saturation=~75%
What are the normal values for: PACO2, PaCO2, arterial CO2 content, Mixed venous PCO2, mixed venous CO2 content, arterial pH, arterial [HCO3-]
PACO2=4.7-6.1kPa/35-45mmHg, PaCO2=4.7-6.1kPa/35-45mmHg, arterial CO2 content=480ml per litre,
Mixed venous PCO2=6.1kPa/46mmHg, mixed venous CO2 content=520ml/litre, arterial pH=7.44-7.36, arterial [HCO3-]=21-27mmol/litre
