V:Q mismatch, ventilatory depression and gas toxicities (physio) Flashcards
What is the O2 cascade?
O2 transfer from air to tissues
Consequence of O2 cascade
When one starts of w/ low pO2 than at sea lvl -> cascadic effect -> subsequent O2 levels at alveolus and systemic arteries are much lower -> compromise O2 supply at tissue
Changes in atmospheric pO2 at high altitude
pO2 decreases
How does ventilation change at high altitude?
Ventilation increases -> decreased pCO2 and H+ and increased pH
Symptoms of acute mountain sickness
Fatigue, headache, dizziness, nausea, palpitations
What is acute mountain sickness due to?
Hypoxia
Consequence of acute mountain sickness
Alkalosis -> decreased H+ -> increased pH
How does body acclimate to sustained low pO2 levels to relieve hypoxia?
Increase 2,3 DPG in RBC -> reduced Hb affinity for O2 -> more O2 released to tissues
Increased erythropoietin -> increased RBC -> more O2 carried in blood
How does body acclimate to high altitudes to relieve alkalosis?
Restoration of pH by kidneys -> H+ excretion decrease and HCO3- reabsorption decrease
Solns to acute ascent problems
Physio -> strong hypoxic drive to increase ventilation
Human intervention -> artificially increase atmospheric O2 in the internal environment
Describe oxygenation of blood at normal alveolar capillary unit
Alveolar ventilation and capillary diffusion matched such that there is oxygenation of blood flow thru unit and CO2 is removed -> pO2 rise from 40-60mmHg
- efficient gas exchange takes place -> at steady state -> ventilation and perfusion well matched
Define dead space
Vol of air inspired which doesn’t undergo gas exchange
How does alveolar dead space affect gas exchange?
Alveolar is ventilated but there is no perfusion -> gas exchange decreases
What is a shunt?
Deoxygenated blood returns to systemic circulation w/o passing thru ventilated alveoli
What happens to gas exchange during shunt condition?
No alveolar ventilation but there continues to be capillary perfusion thru the alveolar capillary unit -> gas exchange decreases
How to describe alveolar dead space and shunt in terms of ventilation/perfusion?
Alveolar dead space = wasted ventilation
Shunt = wasted perfusion
How does alveolar dead space and shunt affect arterial blood gas?
Decreased O2 uptake -> decreased pO2
Increased CO2 retained -> increased pCO2
Normal V/Q ratio and what it indicates
Normal = 1
- there is ventilation and perfusion
What does V/Q value of infinity indicate?
Alveolar dead space -> have ventilation but no perfusion
What does V/Q value of 0 indicate?
Shunt -> have ventilation but no perfusion
Describe gas composition when V/Q ratio is infinity
Resembles that of atmospheric gas composition as air continues to be replenished by atmosphere
Describe gas composition when V/Q ratio is normal
Resembles that of capillary blood that leaves alveolar capillary unit due to replenishment of alveolar gas w/ atmospheric air as alveolar is being ventilated and gas exchange w/ capillary blood that flows through
Describe gas composition when V/Q ratio is 0
No ventilation -> no replenishment of air from atmosphere but gas exchange takes place btw air in alveolus and blood that comes to it -> alveolar gas resembles blood that comes to alveolar capillary unit b4 it’s oxygenated/CO2 removal takes place/similar to gas composition of venous blood that enters right heart
Eg of conditions causing alveolar dead space
Pulmonary circulation blocked by blood clots -> pulmonary embolism
Eg of conditions causing shunt
Pneumonia
Collapsed alveoli/alveoli w/ fluid
What effect does hypoxic vasoconstriction do to shunt?
Reduces effect of shunt
- local response to low alveolar pO2n -> smooth muscle walls of arterioles contract -> redirects blood to better ventilated regions
Blood flow in pulmonary shunt
De-O2 blood returns to systemic circulation w/o passing thru ventilated alveoli -> no gas exchange
Blood flow in vascular shunt
Blood flow bypasses alveoli into systemic circulation -> aft supplying tissues w/ O2, bypasses alveolar capillaries -> left heart
Eg of normal shunt in vascular sys
Bronchial capillaries drain directly into pulmonary veins -> left heart
Eg of abnormal shunt in vascular sys
Direct connection btw R and L heart
Do airways need oxygenated blood for metabolism?
Yes
How are airways supplied w/ O2?
Aorta -> systemic arteries -> bronchial arteries and capillaries -> supply oxygenated blood to bronchi and pleura -> deoxygenated blood flow to bronchial veins -> systemic veins -> RA and RV -> pulmonary artery -> alveoli -> pulmonary veins -> LA and LV -> systemic arteries
Blood flow in normal shunt
Aorta -> systemic arteries -> bronchial arteries and capillaries -> supply oxygenated blood to bronchi and pleura -> deoxygenated blood flow to bronchial veins while some blood bypasses alveoli
- blood that flows to bronchial veins -> systemic veins -> RA and RV -> pulmonary artery -> alveoli -> pulmonary veins -> LA and LV -> systemic arteries
- blood that bypass alveoli -> pulmonary veins -> LA and LV -> systemic arteries
What can blunt ventilatory response?
Altered response to arterial pCO2
Depression of respi control centres in brain
How can normal response to increase in arterial pCO2 be altered?
Chronic increase pCO2 -> adaptation of central chemoreceptors -> less ventilation response (compared to acute setting)
What can depress respi control centre in brain?
Sedative and narcotic drugs
Anaesthetics and alcohol
Changes in arterial blood when respi control centre is depressed?
Decreased ventilation and normal ventilatory response -> CO2 accumulates -> increase in arterial pCO2
- increase in pCO2 usually stimulates ventilation but severely increased pCO2 depresses CNS -> depress respi control centre in brain -> CO2 narcosis -> ventilation decreases further
Eg of toxic gases
CO2
CO
N2
O2
What is CO2 narcosis?
Severely increased pCO2 -> depress CNS and ventilation
Source of CO
Incomplete combustion
Pathophysio of CO poisoning
CO binds Hb w/ greater affinity than O2 -> COHb (carboxyhaemoglobin) -> prevents Hb from carrying O2 -> no O2 delivery to tissues
Colour of COHb
Cherry-pink
What is cyanosis?
Blue discolouration of tissues due to lack of O2 -> excess deoxygenated Hb in blood
If cyanosis isn’t detected in a pt, does it mean that the pt’s O2 saturation is normal?
No
- absence of cyanosis doesn’t mean normal SaO2 -> doesn’t rule out that pt may have decreased SaO2
Treatment for pt w/ CO poisoning
100% O2 at high atm pressure
What happens to inert gases at high atmospheric pressure?
They become toxic
How do you get N2 narcosis?
Breathing compressed air during diving -> rapid ascent from deep diving
- N2 dissolves into tissues during diving and comes out of tissues during rapid ascent -> obstruct blood flow and and cause pain in joints
Pathophysio of N2 narcosis
Increase in pN2 affects CNS -> anaesthetic-like effect
Symptoms of N2 narcosis
Euphoria, loss of coordination, coma, disorientation
Treatment for people w/ decompression sickness
Recompression in a hyperbaric/high pressure chamber then slow release of atm. pressure till surface pressure released -> prevent N2 from coming out as bubbles
When does O2 become toxic?
At high pressure and percentage
Eg of O2 toxicity
80-100% O2 administered for many hrs -> irritation of respi passages
100% O2 administered at vry high atm pressure -> CNS toxicity -> muscle twitching, convulsions
What is hyperbaric O2 therapy? What are some precautions to take?
100% O2 administered at moderately high atm pressure for treatment but only for limited period
Eg of conditions that are treated w/ hyperbaric chamber
High O2 pressure to treat
- decompression sickness
- CO poisoning -> high pO2 to displace CO from Hb
High pO2 improves tissue oxygenation for acute ischaemic injury and bad wounds
