Ventilation: Excretion of CO2
Which of the following is NOT a direct determinant of arterial blood carbon dioxide tension (PaCO2)?
CO2 dependent on excretion and consumption from fundamental metabolism, dependent on oxygen consumption! 3. Minute hydrogen ion production (correct) >Other way around! ------- 1. Minute O2 consumption >Production of CO2 and excretion of CO2 >O2 consumed, carbon dioxide produced 2. Minute CO2 production 3. Minute hydrogen ion production: THIS is dependent on CO2 4. Respiratory quotient 5. Minute exhaled ventilation
CO2 Production
CO2 production is determined by our underlying metabolic rate (VO2) and the type of nutritional substrates that we are utilizing -O2 consumption leads to CO2 production >Basal >Stress >Respiratory Quotient (RQ): CO2 produced /O2 consumed >Substrates *Metabolic rate determined by oxygen consumption and respiratory quotient*
Exhaled vs. Alveolar Ventilation
Exhaled minute ventilation (VE) is the product of breathing frequency and tidal volume -Alveolar ventilation is the sole determinant of CO2 excretion and is equal to the total exhaled ventilation minus dead space ventilation (VA= VE-VD). -Normal anatomic dead space is about 1mL per pound of lean body mass or about 30% (VD/VT). -Anatomic dead space is relatively fixed so it is more efficient to increase tidal volume to increase alveolar ventilation in times of stress and increased CO2 production than to increase breathing frequency. -By increasing only breathing frequency, we waste more of our total exhaled minute ventilation-> VE in our anatomic dead space.
Ventilation Requirements for CO2 elimination
For CO2 to be eliminated... 1.) CO2 delivery to lungs via *perfusion* 2.) CO2 *diffuse* across alveolar capillary membrane. 3.) CO2 undergoes *mechanical exchange* as gas moves out of the alveoli (ventilation)
Dead Space Ventilation
Ventilation is defined as the wasted ventilation which occurs with gas movement into areas of the pulmonary system that DO NOT result in CO2 excretion -Conducting airways and un-perfused alveoli. *Assume anatomic dead space is 150 mL (~33% of Vt)*
Anatomical dead space
Volume between the entry point of gas into the body and the respiratory bronchioles (AKA: the conducting airways) -The dead space receives the *first inspired gas of each breath* and expels inspired gas at the beginning of each exhalation. -The normal anatomical dead space is about one mL per pound of lean body weight. -Conducting airway dead space can hold 150mL
Quantifying ventilation
Volume of gas reaching perfused alveoli each minute -Breathing frequency (f): Breaths per minute (breath/min) -Tidal volume (VT): mL per breath (mL/breath) -Exhaled minute ventilation (VE): L/min >VE= f* VT >Total ventilation or total exhaled ventilation= minute ventilation (not necessarily gas that can be exchanged but all gas present) -Dead space ventilation (VD): Gas movement NOT CONTRIBUTING to CO2 ELIMINATION! -Effective alveolar ventilation (VA) is determined by the volume of gas reach adequately perfused alveoli each minute. >Total exhaled ventilation-dead space ventilation *Alveolar ventilation: VA= VE-VD*
Primary Lung Functions (Pathway)
Wasted perfusion: Right-to-left shunting
Dead space vs. Ventilation
Wasted ventilation or *dead space* is primarily the result of our normal anatomic conducting airways -Gas moving in and out of the conducting airways DOES NOT result in CO2 elimination. -Only ventilation of perfused alveoli results in CO2 elimination.
Anatomic dead space (Nitrogen washout)
We can measure the uniformity of dead space by taking a single breath of 100% oxygen and measuring the EXHALED nitrogen concentration -The *first gas to leave is the anatomic dead space*- so this gas will be 100% oxygen leaving FIRST and will contain NO NITROGEN -The next gas exhaled will indicate the uniformity of alveolar ventilation and perfusion and will contain a mixture of gas from dead space and perfused, ventilated alveoli (N2+O2) >This gives the sigmoid shape to the exhaled nitrogen curve -The majority of exhaled gas contains gas from perfused, ventilated alveoli that has a nitrogen concentration in equilibrium with that of the subject's tissues and blood. >This gives the flat, plateau to nitrogen concentration curve.
Ventilation-perfusion ratios
We have a spectrum of ventilation-perfusion ratios that range from zero to infinity -Normally ventilation is equal to perfusion and this results in *optimal gas exchange* (V=Q) -At the ends of the spectrum we have: >*Dead space* which is defined as ventilation with zero perfusion (V/Q= Infinity) >*Shunt* which is defined as perfusion with zero ventilation (collapse) (V/Q=0) -Between these extremes are areas of high and low ventilation-perfusion ratio. >Low V/Q: Alveolus inflated some with some volume change-> not enough ventilation >High V/Q: More ventilation of an alveolus but acts similarly to dead space due to low perfusion. -These *V/Q ratios are critical to the understanding of gas exchange abnormalities*
CO2 Excretion
*Alveolar ventilation!* -Alveolar ventilation (VA) -Dead Space (VD) -Total exhaled ventilation (VE) >Frequency (f) >Tidal volume (VT) Alveolar ventilation is the difference between our total exhaled minute ventilation and the ventilation that is wasted as dead space ventilation >VA= VE-VD -Total exhaled ventilation is the product of breathing frequency and tidal volume >VE= VT X f
Perfusion (Lung function)
*Blood to alveoli* Blood flow in the lung -No ventilation: Wasted blood >R-to-L shunt (anatomic or physiologic)
Ventilation
*CO2 excretion* -Mechanical process for excretion: Producing gas movement in the lungs resulting in CO2 elimination -*Alveolar ventilation* is the only process by whig CO2 is eliminated. -The arterial CO2 partial pressure is equal to a constant (k) times carbon dioxide production dived by alveolar ventilation. >*PaCO2= K X VCO2/ VA* >Double VCO2 then DOUBLE VA! >Double PaCO2, then HALF VA! -During rest: Carbon dioxide production is relatively constant. >Therefore: *Arterial partial pressure of carbon dioxide is inversely proportional to alveolar ventilation* -Oxygen is not involved in ventilation -Oxygenation is separate and independent
Ventilation (Lung function)
*Gas into alveoli* Mechanical process of moving gas into and out of the lungs that results in *CO2 elimination* -With no perfusion: Wasted air >Dead Space: Upper airway, conducting airway, physiologic
Diffusion (Lung function)
*Gas to alveolar-capillary barrier* Movement of GAS across alveolar-capillary membrane.
RQ
*Respiratory Quotient* -Volume of CO2 produced per volume of O2 consumed: Produced CO2/Consumed O2 -RQ= VCO2/VO2 C6H12O2 + 6O2-> 6CO2 + 6H2O >High VO2 during exercise, stress, infection Utilization of.... -Carbohydrate= 1.0 -Protein/ NORMAL RQ= 0.8 -Fat= 0.7 -Ketone body formation during starvation= 0.6 Synthesis of... -Fat synthesis= >1 >Overfeeding that results in fat synthesis increases the inspiratory quotient to greater than one >Overload of CO2: DONUTS! *The respiratory quotient is a major predictor of carbon dioxide production*
What causes a lower tidal volume?
*Restrictive lung disease*
Case #4 continued
-Repeated blood gas analysis shows PO2= 50 on 40% oxygen ia face make; PaCO2=65, pH=7.23; HCO3=30 -CXR shows increasing infiltrate in RML (now involving Right middle lobe) and RLL (Right lower lobe) -Increasing PaCO2: Poor ventilation >2/5 lobes infiltrated >Less base flow to the areas >Severe acidemia (ventilatory) -Hypoventilation so has hypercapnea
A patient with chronic lung disease has an elevated arterial PCO2. Which of the following contribute to this finding?
1. A large dead space fraction (ANSWER) ---- 2. A fast breathing rate ( f ) 3. A pattern of deep breathing: SHOULD LOWER CO2 4. A prolonged expiratory time 5. The finding of hypoxemia: INDEPENDENT PROCESS
Dead space is defined as....
1. Lung volume that *is ventilated without perfusion*: Dead space and NOT anatomical *VENTILATION BUT NO PERFUSION!* ----- 2. Lung volume that is perfused without ventilation: wasted blood flow NOT gas flow 3. Lung volume where perfusion balances ventilation - so net effect is zero 4. The gross anatomy lab!
What is the PO2 of gas contained in the anatomic dead space?
1. The same as the inspired PO2 (correct) ---- 2. The same as the expired PO2 3. The same as the arterial PO2 4. The same as the mixed venous PO2
Primary lung functions
3 primary lung functions that affect gas exchange: *Ventilation, perfusion, and diffusion*
How do dead space and residual volume influence lung function?
3. Residual volume exchanges gas (Correct) -There is a volume in there that is changed -Normal tissue-> gas exchange can occur -Ventilated and perfused ----- 1. Dead space excretes CO2: FALSE! 2. Residual volume is less than dead space: No correlation 4. Both exchange gas: Dead space does not 5. Neither exchange gas: Residual volume does
Recalling the Fick eqn for diffusion, why does diffusion of CO decrease in patients with emphysema?
A) Increased surface area B) Increased thickness of alveoli capillary membrane C) Decreased surface area D) increased diffusion distance E) B and C F) C and D ------ Fick's Law for diffusion: (P1 - P2) x D x A/d In emphysema, the area for diffusion decreases because alveoli are destroyed, and the distances for diffusion increase. Each of these independently will decrease the diffusion of CO in the lung (c and d).
Determinants of PaCO2
Arterial PCO2 levels are the result of balance between CO2 production and excretion.
Alveolar ventilation vs. Partial Pressure
Arterial PCO2 may be estimated as the product of constants times the carbon dioxide production divided by alveolar ventilation. (PCO2= K X VCO2/VA) -Alveolar ventilation is the body's SOLE means of eliminating CO2. -A a constant CO2 production (200mL/min), a greater alveolar ventilation results in a lower partial pressure of CO2 in the arterial blood. -Halving alveolar ventilation DOUBLES arterial PCO2 and doubling alveolar ventilation HALVES arterial PCO2 (inverse relationship). -Normally, the arterial PCO2 is tightly controlled at 40 +/- 2 mmHg. -Alveolar ventilation is around 4 mL/min during rest. >Increasing VCO2 will increase it; but will not change PACO2 as there is increased ventilation for the increased CO2 production. -Graph: Disregard O2 *Greater alveolar ventilation lower arterial PCO2*
When would partial pressure of oxygen be the greatest?
In which of these areas is the partial pressure of oxygen (PO2) normally the greatest? A) Inspired air B) Alveolar air C) Expired air D) Pulmonary capillaries E) Tissue capillaries --- The PIO2 = FIO2 (PB-47 mmHg). In all of the other options, some of the oxygen has been replaced with CO2 which reduces the partial pressure of oxygen. -INSPIRED AIR as you will have most oxygen in body compared to CO2
Ventilatory Failure
Inadequate *alveolar* gas exchange resulting in abnormally high arterial CO2 tension (Increase in PaCO2) -VA decreases as PaCO2 increases -HYPOVENTILATION occurs >Inadequate alveolar ventilation for the level of CO2 production= elevated CO2 >Hypercarbia (-Capnea) occurs as a result-> PaCO2=>45mm Hg
Hypoventilation
Inadequate alveolar ventilation for the level of CO2 production -Elevated PaCO2.
VE
Minute ventilation (f*VT) -Resting would be ~ 6 L/min -Walking would be less than 20 L/min -Running is >20 L/min
Normal anatomic dead space is...
Normal anatomic dead space of the upper airways and conducting airways wastes about *30 percent of our tidal volume* *VD/VT= 0.30*
Case #4 (Conclusion)
Severe COPD with acute bacterial pneumonia and ventilatory failure -Had pus in 2 lungs-> Increased ventilation in other parts of the lungs -Treat pneumonia with appropriate antibiotics -Support physiology with mechanical ventilation until process clears >Adjust tidal volume, frequency, FiO2, and mode of support as needed. -Provide nutritional support -Had to get a tracheostomy-> reduce dead space
Alveolar Gas Law (CO2 vs O2)
Since CO2 diffuses *2o times faster than oxygen*, CO2 reaches the alveolus before fresh inspired oxygen reaches the alveolus -Therefore: *Carbon dioxide determines the partial pressure of oxygen in the alveolus* -The one-to-one rule states that for ever mmHg change in alveolar CO2 there will be an OPPOSITE change in the partial pressure of oxygen. -The 1-to-1 rule is the major source of interplay between the process of ventilation and oxygenation. -If PACO2 increases, PAO2 decreases -If PACO2 decreases, PAO2 increases -PAO2 changes, NO AFFECT on PACO2: CO2 reaches first and will have the primary effect. -Hyperventilation: PCO2 decreases, but PO2 increases (hypocarbia)
A healthy subject who weighs 150 lbs and is breathing at 20 breaths/min, has an exhaled minute ventilation of 14 L/min. He has a sudden change in his respiratory status and his alveolar ventilation becomes 7 L/min. If tidal volume and respiratory frequency do not change, what is his new dead space to tidal volume ratio (VD/VT)?
Since his minute ventilation is still 14 L/min but his alveolar ventilation is only 50% of his minute ventilation, then his dead space ventilation must have increased to 50% or a ratio of VD/VT of 0.50 -Air he can exchange/total minute ventilation-> 1-the ratio->In this case it would be split in half 50% wasted/exchangd.
What is the most effective means to increase CO2 excretion during exercise?
Tables shows the effect of increasing breathing frequency (f), tidal volume (Vt), or both on exhaled ventilation (VE) and alveolar ventilation (Va) during exercise. -All changes increase minute exhaled ventilation but *changes that increase TIDAL volume have a greater effect on alveolar ventilation.* -The work and energy cost of breathing is determined by the VE but the effectiveness of ventilation is related to VA since this is the means of CO2 excretion.
Bohr Equation (Pathway)
The Bohr equation is used to calculate the ratio between the dead space ventilation and tidal volume: VD/VT PaCO2-PECO2/PaCO2 Big number- small number/big number!!!
Alveolar Gas Law
The alveolar gas law is a variant of Dalton's Law (approximately the same) -Dalton's law states that the total pressure of a mixture of gases is equal to the sum of partial pressures of the individual gases. -In the alveolus the total pressure of the gases must equal barometric pressure -While breathing room air, the vast majority of the gas in the alveolus is NITROGEN. >The nitrogen is in equilibrium with the nitrogen in the inspired gas, the plasma, and all body tissues. -Therefore: the partial pressure of nitrogen does not change. -Similarly, water vapor is present in the alveoli. >The partial pressure of water vapor is determined by body temperature and does NOT change significantly (47mmHg) -Therefore: The only two gases that can change significancy are oxygen and carbon dioxide. Dalton: PB =PO2 +PCO2 +PWV +PN2
PaCO2 Determinants
The determinants of PaCO2 are production and excretion -CO2 production is determined by basic metabolism and the nutritional substrates that are used -CO2 excretion occur SOLELY by the process of alveolar ventilation. -Alveolar ventilation is the difference between total exhaled ventilation and dead space ventilation. -Total exhaled ventilation is the product of breathing frequency and tidal volume. *Under conditions of constant CO2 production, PaCO2 is inversely proportional to alveolar ventilation (VA)*
Intrapleural pressure is greatest at which point of the ventilatory cycle?
The end of forced exhalation (ERV) ----- 1. The end of maximal inspiration (TLC): Most volume in thoracic cavity (most negative pressure) 2. The end of relaxed exhalation (FRC)
Partial pressure of Oxygen and CO2
The partial pressure of oxygen and CO2 exhaled from the anatomic dead space is equal to the partial pressures of the inspired gases -NO OXYGEN is extracted from and no CO2 is added to the dead space-> The ventilation is wasted -Partial pressures of CO2 and oxygen in the mixed exhaled gas lie between the partial pressures of inspired gas and alveolar gas.
What is the PCO2 of gas in the anatomic dead space?
The same as inspired gas: From dead space has to be close to inspired gas -Should be zero CO2 though but if there was any! --------- 1. Zero (There could be some!) 2. The same as inspired gas (Best answer) 3. The same as mixed venous blood 4. The same as arterial blood 5. The same as expired gas
Dead space sources
The sources of dead space are the upper airways and the conducting airways -Pathologically: Additional dead spaces occurs at the alveolar level in disease states.
For this question use the following information:PaO2 = 100 mm Hg, SaO2 = o.99, PaCO2 = 40 mm Hg, pHa = 7.40, FIO2 = 0.21,hemoglobin = 15 g/L, SvO2 = 0.75, PvO2 = 40 mm Hg, FECO2 = 0.028, barometric pressure = 760 mm Hg,water vapor pressure at body temp = 47 mm Hg,O2 consumption (VO2) = 140 mL/min/m2,CO2 production (VCO2) = 120 mL/min/m2What is the dead space to tidal volume ratio (Vd/VT)?
To answer this you need to recall that VD/VT = (PaCO2 - PECO2)/PaCO2. Since PECO2 = FECO2 * 760 = 21 and you are given PaCO2 = 40, then (40-21)/40 = 0.48 which is closest to 0.50.
Bohr Equation (Use)
Used to calculate the fraction of each tidal volume breath that is dead space (physiologic dead space) -Assumes 2 compartment lung model >1: perfect match between ventilation and perfusion -> PACO2= PaCO2 >2: Ventilation but no perfusion (dead space) -> PACO2= 0 -Calculates ratio between compartments -Modified for clinical use by Enghoff *Bohr equation is used to calculate the ratio between dead space ventilation and tidal volume: VD/Vt*
Alveolar Ventilation
VA= VE-VD VA= (f x VT)-VD VA= (f x VT)-(VE x VD/VT) VA= f(VT- VD) 3 factors determine alveolar ventilation: breathing frequency, tidal volume, and dead space to tidal volume ratio (VD/Vt) -The volume of air that is *available for gas exchange per minute* >Alveolar ventilation= F X (VT-VD) *Imbalance between alveolar ventilation (CO2 excretion) and CO2 production will result in alteration of arterial PCO2.*
Bohr Equation (Variables)
VD/VT= PACO2-PECO2/PACO2 -> Enghoff's modification VD/VT= PaCO2-PECO2/PaCO2 -VD= Dead space ventilation -VT= Tidal volume -PACO2= Alveolar -PECO2= MIXED expired; Partial pressure of CO2 measured in a timed collection of MIXED EXPIRED gas. >PECO2= Barometric Pressure X FECO2 -PaCO2= Arterial; Carbon dioxide partial pressure measured in arterial blood -VD/Vt ratio is important in assessing patients with plasma CO2 abnormalities -Find VD: Multiply fraction from PaCO2-PECO2/PaCO2 to VT. *Calculate the fraction of each breath that is wasted= Not eliminate CO2!*
Alveolar ventilation
VE= VT X f VA= VE-VD VA= VE-VE (VD/VT) Normal VD/VT= 0.30 >30% of each breath is *wasted ventilation (no CO2 elimination)* ->30% of each tidal volume breath is water as dead space -Sounds like QT= SV X HR for heart
Dead space
Ventilation WITHOUT PERFUSION! -Anatomic (about 1 mL/pound LEAN body mass) >Oro/Nasopharynx >Trachea >Bronchi: Except respiratory bronchioles -Physiologic: Addition is normally very LOW >High V/Q areas in disease ->Q= perfusion -Normally: VD total phsyiologic= VD anatomic and alveolar dead space=0 Pathological example: Pulmonary embolism- disease that can cause a sudden increase in dead space >Total dead space can increase as alveolar or pathologic dead space increase.
