Gas exchange (chapter 2) Flashcards
Measurement of arterial PO2
- with modern blood gas electrodes
- blood taken by puncturing radial artery or from an radial artery catheter
- measure by polarographic principle - test measures the current that flows when a small voltage is applied to the electrodes
Normal value for PO2
95 mm Hg (85-100 mm Hg)
-normal value decreases with age (approx 85 at 60 years old)
Hypothesis fall in PO2 with age
-probably due to increasing ventilation-perfusion inequality
Two important points on normal oxygen dissociation curve
- Arterial blood (PO2, 100; O2 sat 97%)
- Mixed venous blood (PO2 40; O2 sat 75%)
Above 60 mm Hg the O2 saturation exceeds 90% so the curve is fairly flat
What shifts the oxygen dissociation curve to the right
-increase in temperature
-increase PCO2
-increase H+ concentration
(favor unloading of O2 i.e. require higher PO2 to maintain same satruation of O2)
-increase 2,3 DPG inside the red blood cells (part of glycolysis, high in pregnancy - more able to give off O2 to fetus)
when is 2,3 DPG increased in the RBC
During prolonged hypoxia
Causes of hypoxemia
- Hypoventilation
- Diffusion impairment
- Shunt
- Ventilation - perfusion inequality
(reduction of inspired PO2 –i.e. high altitude)
Hypoventilation
the volume of fresh gas going to the alveoli per unit time (alveolar ventilation) is reduced
Hypoventilation –> hypoxemia
-when the resting O2 consumption is not correspondingly reduced in the face of hypoventilation hypoxemia ensues
Features of hypoventilation
- Always causes a rise in PCO2 (diagnostic feature
2. Hypoxemia can be abolished easily by increased the inspired PO2 by delivering O2 via a face mask
relationship alveolar ventilation and PCO2
In the alveolar ventilation equation
PCO2 = VCO2/VA * K
-whre CO2 output is the alveolar ventilation and K is the constant
-therefore if alveolar ventilation is halved PCO2 is double
Alveolar gas equation and treatment of hypoventilation
PAO2 = PIO2 - PACO2/R + F
where F is small corretion fator
If arterial PACO2 and respiratory exchange ratio (R) remain constant (as they will if alveolar ventilation and metabolic rate remain unaltered) every mm Hg rise in inspired PO2 (PIO2) produces a corresponding rise in alveolar PAO2
Why cant the arterial PO2 fall to very low levels from pure hypoventilation
Referring to the alveolar gas equation
if R = 1 the alveolar PO2 falls 1mm Hg for every 1 mm Hg rise in PCO2
-therefore severe hypoventilation sufficient to double PCO2 only decreass alveolar PO2 ???
Causes of hypoventilation (9)
- Depression of the respiratory center by drugs (barbiturates and morphine derivatives)
- Diseases of the medulla (encephalitis, hemorrhage, neoplasms)
- Abnormalities of the spinal cord (following high dislocation)
- Anterior horn cell disease (i.e. poliomyelitis)
- Diseases of the nerve to the respiratory muscles (Guillain Barre syndrome or diphtheria)
- Diseases of the myoneural junction (myasthenia gravis, anticholinesterase poisoning)
- Diseases of the respiratory muscles (progressive muscular dystrophy)
- Thoracic cage abnormalities (crushed chest)
9 .Upper-airway obstruction (tracheal compression by enlaged lymph nodes)
Sleep apnea -types
1) central -where there is no respiratory efforts
2) obstructive - despite the activity of the respiratory muscles there is no airflow
When does central sleep apnea occur
-in patients with hypoventilation because respiratory drive is depressed during sleep
Breathing during REM sleep
Is often irregular and unresponsive to chemical and vagal drives
Really only response to hypoxemia
Obstructive sleep apnea -what cause airway obstruction
- Backwards movement of the tongue
- Collapse of pharyngeal walls
- greatly enlarged tonsils or adenoids
- other anatomic causes of pharyngeal narrowing…
Noticeable symptoms of sleep apnea
- loud snoring
- waking violently after an apneic episode
- chonic sleep depivation (can lead to daytime somnolence, impaired cognitive function, chronic fatigue, morning headaches and personality disturbances - paranoia, hostility and agitated depression)
Treatment of sleep apnea
-continuous positive airway pressure (CPAP) during sleep
Sudden infant death syndrome (SIDS)
- child found dead in crib typically with no apparent cause
- hypothesis is that nervous control of ventilation is not fully developed and respiratory muscles are poorly coordinated
Diffusion impairment -meaning
Equilibration does not occur between the PO2 in the pulmonary capillary blood and alveolar gas
Time equilibration PO2 under normal resting conditions
Capillary blood PO2 almost reaches that of alveolar gas after about 1/3 of the total contact time of 3/4 second available in the capillary
i.e. plenty of time in reserve
Time equilibration PO2 under severe exercise
Contact time reduced to as little as 1/4 seconds and still equilibration occurs (but less reserve)
Why equiibration may be incomplete
Blood-gas barrier is thickened and diffusion is so slowed that equilibration may be incomplete
-any hypoxemia at rest would be further exaggerated on exercise due to reduced contact time between blood and gas
Diseases in which diffusion impairment may contribute to hypoxemia (especially on exercise)
- asbestosis
- sarcoidosis
- diffuse interstitial fibrosis (including idopathic pulmonary fibrosis, interstitial pneumonia)
- connective tissue diseases affecting the lung (scleroderma, rheumatoid lung, lupus erythematosus, Wegener’s granulomatosis, Goodpasture’s syndrome)
- alveolar cell carcinoma
Real cause of arteril hypoxemia in patients with diffusion impairment
- diffusion impairment acounts for some of the hypoxemia however normal lung has lots of diffusion time in reserve, some may only be important with exercise
- also the people have such abnormal architecture that relationship between blood flow and ventilation is surely not preserved - and this accounts for more of the hypoxemia
Correction of hypoxemia by diffusion impairment
Can be corrected by administering 100% oxygen
-large increase in alveolar PO2 can easily overcome the increased diffusion resistance of the thickened blood-gas barrier
Diffusion impairment effect on CO2 elimination
- generally unaffected
- the arterial PCO2 is slightly lower than normal because ventilation will be overstimulated either by hypoxemia or intrapulmonary receptors
Shunt -what does it do
Allows some blood to reach the arterial system without passing through ventilated regions of the lung
Cause of intrapulmonary shunts
=Arterial-venous malformations
-consolidated area (will be unventilated but perfused)
Cause of extrapulmonary shunts
-those that occur in congenital heart disease through atrial or septal defects or a patent ductus arteriosus (but must have rise in right sided heart pressure to cause shunt from right to left)
Effect of giving oxygen to breathe in person with shunt
-arterial PO2 levels fail to rise during 100% O2 breathing
Why is it possible to detect even small shunts by measuring the arterial PO2 during 100% O2 breathing
Because the PO2 of shunted blood is as low as venous blood -when a small amount of shunted blood is added to arterial blood the O2 concentration is depressed –> causes lare fall in arterial P2 because the O2 dissociation curve is so flat in its upper range
Determining the magnitude of a shunt during O2 breathing
Using the shunt equation
Qs/Qt = (Cc-Ca)/(Cc-Cv)
where Qs and Qt = shunt and total blood flow
Cc, Ca, Cv = O2 concentrations of end-capillary arterial and mixed venous blood
Cc= calculated from alveolar PO2
Mixed venous sampled with a catheter in pulmonary artery
Affect of shunt on PCO2
- does not usually result in raised arterial PCO2
- the tendency for CO2 to rise is countered by chemoreceptors which increase ventilation if the PCO2 increases (so often find PCO2 is lower than normal because of additional hypoxemic stimulus to ventilation)
Ventilation-perfusion inequality
- ventilation and blood flow are mismatched in various regions of the lung
- results = gas transfer inefficient
How common is ventilation-perfusion inequality as a cause of hypoxemia
- extremely common
- responsible for most, if not all, of the hypoxemia in COPD, interstitial lung disease and vascular disorders (such as P.E)
How to identify ventilation perfusion inequality as a cause of hypoxemia
Usually identified by excluding the other three causes of hypoxemia: hypoventilation, diffusion impairment, and shunt
Normal ventilation-perfusion inequality
- All lungs have some degree of it
- takes the form of a regional pattern with the ventilation -perfusion ratio decreasing from apex to base
How pathologic ventilation-perfusion inequality is different than normal ventilation-perfusion inequality
-disorganization of normal pattern ventilation-perfusion inequality (i.e no longer just decreasing from apex to base)
Situations which exagerrate hypoxemia of ventilation- perfuson inequality
1 Concomitant hypoventilation (ex if patient with COPD is overly sedated)
2. Reduction of cardiac output
How to assess the severity of ventilation - perfusion inequality from arterial blood gases
Calculate the alveolar-arterial difference for PO2
-calcuate an ideal alveoar PO2 = value that lung would have if there were no ventilation perfusion inequality
PAO2 = PiO2 - PACO2/R +F
Factors that determine the delivery of oxygen to the tissues
1) Oxygen concentration of the blood
2) Cardiac output
3) Distribution of blood flow to the periphery
Arterial PCO2 measurement
PCO2 electrode = glass pH electrode
- surrounded by bicarbonate buffer which is separated from the blood by a thin membrane through which CO2 diffuses
- CO2 alters the pH of the buffer which is measured by the electrode
Normal arterial PCO2
37-43 mm Hg
What normally affect arterial PCO2
- relatively unaffected by age
- tends to fall slightly during heavy exercise and to rise slightly during sleep
Cause of increased arterial PCO2
1) Hypoventilation
2) Ventilation - perfusion inequality
Explanation of how hypoventilation causes increased PCO2
alveolar ventilation equation
PACO2 = VCO/VA * K
-if less ventilation increased PACO2
How to treat increased CO2 retention
Can only be treated by increasing the ventilation! (may require mechanical assistance)
Ventilation-perfusion inequality an increase in PCO2
-idea that ventilation-perfusion inequality does not interfere with CO2 elimination because overventilated regions make up for underventilated is wrong!
-certain patients may have normal PCO2 because
1) Chemoreceptors respond to increased arterial PCO2 and raise ventilation to the alveoli
2) Arterial PCO2 returns to normal level but arterial PO2 is only slightly increased by increased ventilation (not all the way back to normal) –> look at shape of O2 dissociation curve –> strongly depressive action on the arterial PO2
DONT UNDERSTAND THIS!!!
Why some subjects with ventilation-perfusion abnormality never get return to normal PCO2
-because have trouble breathing due to a gross increase in airway resistance
Measurement of arterial pH
Usually measured with glass elecrode concurrenttly with arterial PO2 and PCO2
-related to arterial PCO2 and bicarbonate concentration through the henderson- hasselback equation
pH = pK + log (HCO3-)/0.03 PCO2
Acidosis
Acidosis is a decrease in arterial pH
acidemia = actual fall in pH in the blood
What can cause acidosis
- Respiratory abnormalities
- Metabolic abnormalities
(or both!)
Cause of respiratory acidosis
CO2 retention (increases PCO2 -i.e. denominator in henderson-hasselbach equation then decrease pH) -either by hypoventilation or ventilation-perfusion inequality
Acute vs chronic CO2 retention
Acute:
- little change in bicarbonate concentration (numerator in henderson-hasselbach)
- therefore pH falls as rapidly as PCO2 rises
Chronic:
- kidneys retain bicarbonate in response to increased PCO2 over time in the renal tubular cells
- increases numerator in henderson-hasselbach equation (partially compensated for respiratory acidosis) so that have smaller fall in pH
Cause of metabolic acidosis
Primarily caused by a fall in HCO3-
Effect of metabolic acidosis on PCO2
-fall in arterial pH stimulates peripheral chemoreceptors -this increases ventilation and lowers PCO2 –> therefore as
(look at figure!!!)
Graph arterial pH vs. arterial PCO2 for:
a) Metabolic acidosis
b) Metabolic alkylosis
c) Chronic hyperventilation
d) Acute hyperventilation
e) Acute hypercapnia
f) Chronic hypercapnia
XX
Alkalosis (alkalemia)
Result fro an increase in arterial pH
Causes of alkalosis
- Respiratory alkalosis
2. Metabolic alkalosis
Respiratory alkalosis cause
-seen in acute hyperventilation
Metabolic alkalosis
-seen in disorders such as severe prolonged vomiting when plasma bicarbonate concentration rises
Four types of acid-base disturbance + primary effect + compensation
Acidosis
a) respiratory
- primary : Increase PCO2
- compensation: Increase HCO3-
b) metabolic
- primary: decrease HCO3-
- compensation decrease PCO2
Alkalosis
a) respiratory
- primary: decrease PCO2
- compensation: decrease HCO3-
b) metabolic
- primary: increase HCO3-
- compensation often none
Measurement of diffusion capacity (DCO)
- patient takes vital capacity breath of 0.3% CO and 10% helium
- holds breath for 10 seconds and then exhales
- the first 750 ml of gas is discarded because of dead space contamination and the next liter is collected and analyzed
He = indicates the dilution of inspired gas with alveolar gas (gives initial alveolar PCO)
diffusing capacity = volume of CO taken u per minute per mmHg alveolar PCO
Why use CO to measure diffusion capacity
- partial pressure of CO in ulmonary capillary extremely low in relation to alveolar value as a result CO is taken up by the blood all alng the capillary (in contrast O2 just taken up in first 1/3 )
- thus uptake CO determined by diffusion properties of blood-gas barrier and the rate of combination of CO with blood not saturation of blood with CO
What do the diffusion properties of the alveolar membrane depend on
- its thickness
- its area
What reduces the rate of combination of the blood with CO
-when the number of red cells in the capillaries is reduced
What diseases cause increased thickness of the alveolar membrane
1) interstitial fibrosis
2) sarcoidosis
3) asbestosis
What diseases cause reduced surface area of the blood-gas barrier
Pneumonectomy
+ fall in diffusion capacity that occurs in emphysema is partly caused by the loss of alveolar walls and capillaries
Causes of decrease rate of combination of the blood with CO
- anemia
- diseases that reduce the capillary blood volume (pulmonary embolism)
