VENTILATION
CHAPTER 4
DR. CARLOS ORTIZ
BIO-208
PARTIAL PRESSURES OF RESPIRATORY
GASES
• AIR IS A GAS MIXTURE OF MOSTLY N2 AND O2. THIS TRACES
OF ARGON, CARBON DIOXIDE, AND OTHER GASES. THE
TOTAL COMBINED PRESSURE EXERTED BY THESE GASES,
THE BAROMETRIC PRESSURE(PB) CAN BE MEASURED BY A
Hg BAROMETER. AT SEA LEVEL THE PB IS EQUIVALENT TO
THE WEIGHT OF A MERCURY COLUMN OF 760 mmHg. THUS
STANDARD PB IS 760 mmHg.
• ACCORDING TO DALTON’S LAW , THE PRESSURE OF EACH
GAS COMPRISING AIR IS INDEPENDENT OF THE OTHER GAS
PRESSURE AND EXERTS A PARTIAL PRESSURE
PROPORTIONAL TO ITS FRACTIONAL CONCENTRATION IN AIR.
• OXYGEN CONSTITUTES 20.93% OF DRY ATMOSPHERIC AIR,
ITS PARTIAL PRESSURE (PO2) AT SEA LEVEL IS AS FOLLOWS:
•
PO2= 0.2093 X760 =159 mm Hg
PARTIAL PRESSURES OF RESPIRATORY
GASES
• IN PHYSIOLOGICAL CALCULATIONS THE PCO2 OF INSPIRED
AIR IS CONSIDERED O.
• INSPIRING AIR HEATS IT TO BODY TEMPERATURE (37ºC) AND
SATURATES IT WITH WATER VAPOR ( 100% RELATIVE
HUMIDITY). THE WATER PRESSURE AT 37ºC AND 100% RH IS
47mmHg. THEREFORE 47 MOST BE SUBSTRUCTED FROM PB
TO CALCULATE PGAS IN THE LUNG OR BLOOD.
• IN THE TRACHEA THE PO2 IS CALCULATED AS FOLLOWS:
•
P02= 0.2093 X ( 760 -47) = 149 mmHg.
CLASIFICATION OF VENTILATION
• MINUTE OR TOTAL VENTILATION
• MINUTE VENTILATION(VE) IS USUALLY DEFINED AS THE
VOLUME OF FRESH AIR ENTERING THE LUNG EACH MINUTE.
IN CLINICAL PRACTICE, VE IS USUALLY MEASURED BY
ADDING THE COLLECTIVE EXHALED VTS OBTAINED OVER 1
MINUTE. VE IS CALCULATED AS FOLLOWS:
• VE = VT x RR
• FOR EXAMPLE : VE = 500 mL x 12/ min = 6000mL OR 6.O L/min
• NOT ALL THE VE REACHES THE ALVEOLI BECAUSE THE LAST
PART OF EACH INSPIRATION STAYS IN THE CONDUCTING
AIRWAYS TO BE REMOVED WITH THE NEXT EXPIRATION.
THUS PART OF THE VE VENTILATES ALVEOLI, ALVEOLAR
VENTILATION(VA). THE REMAINING PART VENTILATES
CONDUCTING AIRWAYS, DEAD-SPACE VENTILTION(VD)
DEAD SPACE VENTILATION
• ANATOMICAL DEAD SPACE
• THE CONDUCTING AIRWAYS FROM THE MOUTH AND NOSE
DOWN TO AND INCLUDING TERMINAL BRONCHIOLES
CONSTITUTE ANATOMICAL DEAD SPACE(VDANAT) .
• DEAD SPACE IS WASTED VENTILATION AND IT TAKES NO
PART IN RESPIRATION. DEAD SPACE IS DEFINED AS LUNG
AREAS THAT ARE VENTILATED BUT NOT PERFUSED BY THE
PULMONARY CIRCULATION.
• VDANAT DOES NOT CHANGE UNLESS SURGERY REMOVES
PART OF A LUNG OR UNLESS AN ARTIFICIAL AIRWAY (ET
TUBE) BYPASSES UPPER AIRWAY DEAD SPACE.
• FOR CLINICAL MONITORING PURPOSES, VDANAT VOLUME IS
CONSIDERED CONSTANT AT ANY TIME.
• MEASURING VDANAT
• VDANAT IS RELATED TO LUNG SIZE; IN NORMAL ADULTS,
ANATOMICAL DEAD SPACE IS APROXIMATELY 1mL PER
POUND OF IDEAL BODY WEIGHT.
ALVEOLAR AND PHYSIOLOGICAL DEAD SPACE
• ALVEOLAR DEAD SPACE(VDA) IS THE VOLUME CONTAINED IN
NONPERFUSED ALVEOLI, OR ALVEOLI WITH NO BLOOD FLOW.
VDA IS ABNORMAL. ANY FACTOR DECREASING PULMONARY
BLOOD FLOW, SUCH AS EXTREMELY LOW CARDIAC OUTPUT
OR A PULMONARY EMBOLUS, INCREASES VDA.
• PHYSIOLOGICAL DEAD SPACE IS THE SUM OF VDANAT AND VDA.
•
VD= VDANAT + VDA
• VD IS INCREASED NOT ONLY BY DECREASED PULMONARY
BLOOD FLOW BUT ALSO BY AN INCREASED BREATHING
RATE. DOUBLING THE BREATHING FREQUENCY DOUBLES
THE NUMBER OF TIMES THE VT MOVES THROUGH THE VDANAT,
THUS DOUBLING THE VDANAT .
ALVEOLAR VENTILATION
• VA IS THE AMOUNT OF GAS ENTERING OR LEAVING THE
ALVEOLI PER MINUTE. VA= VE – VD.
• PRACTICALLY SPEAKING , ALL CO2 IN EXHALED GAS COMES
FROM VENTILATED, PERFUSED ALVEOLI. THE SOURCE OF
THIS CO2 IS TISSUE METABOLISM. NORMAL AEROBIC
METABOLISM PRODUCES CO2, WHICH IS CARRIED BY
VENOUS BLOOD TO THE LUNGS. THE MIXED VENOUS PCO2
(PvCO2) APPROACHING THE ALVEOLI IS SEVERAL mmHg
HIGHER THAN ALVEOLAR PCO2 (PACO2). THUS CO2 DIFFUSES
INTO THE ALVEOLI.
• THE BALANCE BETWEEN METABOLIC CO2 PRODUCTION PER
MINUTE (VCO2) AND ITS RATE OF ELIMINATION (VA)
DETERMINES THE PCO2 OF THE BLOOD LEAVING THE LUNG.
HYPERVENTILATION AND HYPOVENTILATION
• IF VA REMOVES MORE CO2 PER MINUTE THAN IS
METABOLICALLY PRODUCED, ALVEOLAR AND BLOOD PCO2
DECREASE AND A STATE OF HYPERVENTILATION EXISTS.
• IF VA REMOVES LESS CO2 THAN THE BODY PRODUCES,
ALVEOLAR AND BLOOD PCO2 RISE AND A STATE OF
HYPOVENTILATION EXISTS.
• ARTERIAL BLOOD ARISING FROM THE LEFT VENTRICLE HAS
THE SAME PCO2 AS THE ALVEOLI (PACO2 = PaCO2)
• VA DETERMINES ARTERIAL PCO2 BECAUSE IT CONTROLS
ALVEOLAR PCO2. THE PaCO2 OBTAINED CLINICALLY
THROUGH ABG ANALYSIS IS THE DEFINITIVE INDEX OF VA .
• HYPERVENTILATION AND HYPOVENTILATION ARE DEFINED
BY VA RELATIVE TO CO2 PRODUCTION, A RELATIONSHIP THAT
CAN BE KNOWN ONLY BY MEASURING PaCO2.
• IF PaCO2 IS ABOVE NORMAL HYPERCAPNIA,
HYPOVENTILATION EXISTS; IF PaCO2 IS BELOW NORMAL
HYPOCAPNIA, HYPERVENTILATION EXISTS.
• VA AND PACO2
• IF VA IS INVERSELY RELATED TO PACO2; IF VA IS REDUCED BY
HALF, PACO2 DOUBLES. IF VA DOUBLES, PACO2 ( AND PaCO2) IS
REDUCED BY HALF.
• RATIO OF DEAD SPACE TO VT
• VA CAN BE CALCULATED IF IT IS KNOWN WHAT FRACTION OF
THE VT IS DEAD SPACE (VD/VT). NORMALLY, ABOUT 20% TO
40% OF THE INSPIRED VT REMAINS IN CONDUCTING
AIRWAYS, NEVER REACHING ALVEOLI.
• SHALLOW VTS INCREASE THE VD/VT RATIO BECAUSE
CONDUCTING AIRWAY VOLUME REMAINS CONSTANT.
• DEEP BREATHS DECREASE THE VD/VT FOR THE SAME
REASON, CAUSING A LARGER PERCENTAGE OF THE
INSPIRED VOLUME TO REACH THE ALVEOLI.
• THE VD/VT RATIO CAN BE CLINICALLY MEASURED THROUGH
AN ANALYSIS OF MIXED-EXHALED CARBON-DIOXIDE
CONCENTRATIONS. THE PHYSIOLOGICAL DEAD-SPACE
EQUATION, KNOWN AS THE BOHR EQUATION, ALLOWS THE
VD/VT TO BE CALCULATED.
• CAPNOMETERS ARE USED IN THE CLINICAL SETTING TO
ANALYZE EXHALED CO2. CAPNOGRAPHY REFERS TO THE
PCO2 CHANGES OF EXHALED VTS GRAPHYCALLY DISPLAYED
AS A WAVEFORM (CAPNOGRAM). CAPNOGRAMS ALLOW THE
PCO2 TO BE IDENTIFIED AT THE END OF A TIDAL EXHALATION
(PETCO2), WHICH CORRESPONDS TO AVERAGE ALVEOLAR
PCO2 (PACO2 = PETCO2).
• THE VD/VT RATIO IS A MEASURE OF VENTILTORY EFFICIENCY.
A HIGH VD/VT MEANS MUCH OF THE VE IS WASTED IN
VENTILATING NONPERFUSED ALVEOLI, REQUIRING HIGHENERGY EXPENDITURE TO ACCOMPLISH A RELATIVELY
SMALL AMOUNT OF VA.
VENTILATORY PATTERN, DEAD SPACE, AND VA
• THE RATE AND DEPTH OF VENTILATION AFFECT VA AND THE
VD/VT RATIO. VE IS NOT A RELIABLE INDICATOR OF VA .
• IN A, B AND C VDANAT AND VE ARE IDENTICAL. (VE IS 8000
ml/min AND VDANAT IS 150 ml IN EACH INSTANCE).THE FIGURE
B, REPRESENTS A NORMAL VT AND RESPIRATORY RATE.
DEAD SPACE VENTILATION IS THE PRODUCT OF
RESPIRATORY FREQUENCY AND DEAD SPACE VOLUME
(
VD= VD X F).
• FIGURE B, VD EQUALS 16 MULTIPLIED BY 150, WHICH EQUALS
2400 ml/min. THE VA OF 5600 ml/min IS EQUAL TO VE MINUS VD
(8000-2400=5600). FOR THE FOLLOWING DISCUSSION, IT IS
ASSUMED THAT THIS VA MAINTAINS A NORMAL PaCO2 OF 40
mmHg, REPRESENTING NEITHER HYPERVENTILATION NOR
HYPOVENTILATION.
EFFECT OF VENTILATORY PATTERN ON ALVEOLAR
AND DEAD-SPACE VENTILATION
VENTILATORY PATTERN, DEAD SPACE, AND VA
• FIGURE A, ILLUSTRATES THE INEFFICENCY OF
RAPID(TACHYPNEA), SHALLOW (HYPOPNEA) BREATHING. THE
LUNG STILL ACHIEVES A VE OF 8000 ml/min. HOWEVER, VD
NECESSARILY INCREASES ( VD= 32 X 150 = 4800 ml/min,
COMPARED WITH A VD OF 24OO ml/min IN FIGURE B. THIS
LEAVES ONLY 3200 ml/min FOR VA, COMPARED WITH 5600
ml/min IN B. THE VD/VT INCREAES ALSO; IN B IT IS 150/500,
WHICH EQUALS 30%, AND IN A IT IS 150/250=60%.
• THUS 70% OF THE VE IS INVOLVED IN GAS EXCHANGE IN
FIGURE B, WHEREAS ONLY 40% IS SIMILARLY INVOLVED IN
FIGURE A. RAPID SHALLOW BREATHING IS A COMMON
SIGNAL OF RESPIRATORY DISSTRESS AND POSSIBLE
VENTILATORY FAILURE.
EFFECT OF VENTILATORY PATTERN ON ALVEOLAR
AND DEAD-SPACE VENTILATION
VENTILATORY PATTERN, DEAD SPACE, AND VA
• FIGURE C, ILLUSTRATES SLOW (BRADYPNEA),
DEEP(HYPERPNEA) BREATHING, WHICH ALSO ACHIEVES A VE
OF 8000 ml/min . BECAUSE VDANAT IS CONSTANT, ALL THE
ADDITIONAL VT ENTERS ALVEOLI, INCREASING VA . VD IS ONLY
8 X 150, WHICH EQUALS 1200 ml/min, LEAVING 6800 ml/min FOR
VA .
• THE VD/VT IS 150/1000 OR EQUAL TO 15%, MEANING 85% OF
THE VE PARTICIPATES IN GAS EXCHANGE. SLOW, DEEP
BREATHING IS THUS THE MOST EFFICIENT VENTILATORY
PATTERN IN TERMS OF THE FRACTION OF VE RECEIVED BY
ALVEOLI.