1. VENTILATION CHAPTER 4 DR. CARLOS ORTIZ BIO-208

2. PARTIAL PRESSURES OF RESPIRATORY GASES AIR IS A GAS MIXTURE OF MOSTLY N 2 AND O 2. THIS TRACES OF ARGON, CARBON DIOXIDE, AND OTHER GASES. THE TOTAL COMBINED PRESSURE EXERTED BY THESE GASES, THE BAROMETRIC PRESSURE(P B ) CAN BE MEASURED BY A Hg BAROMETER. AT SEA LEVEL THE P B IS EQUIVALENT TO THE WEIGHT OF A MERCURY COLUMN OF 760 mmHg. THUS STANDARD P B 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 (PO 2 ) AT SEA LEVEL IS AS FOLLOWS: PO2= 0.2093 X760 =159 mm Hg

3. PARTIAL PRESSURES OF RESPIRATORY GASES IN PHYSIOLOGICAL CALCULATIONS THE P CO2 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 P B TO CALCULATE P GAS IN THE LUNG OR BLOOD. IN THE TRACHEA THE PO 2 IS CALCULATED AS FOLLOWS: P02= 0.2093 X ( 760 -47) = 149 mmHg.

4. CLASIFICATION OF VENTILATION MINUTE OR TOTAL VENTILATION MINUTE VENTILATION(V E ) IS USUALLY DEFINED AS THE VOLUME OF FRESH AIR ENTERING THE LUNG EACH MINUTE. IN CLINICAL PRACTICE, V E IS USUALLY MEASURED BY ADDING THE COLLECTIVE EXHALED V TS OBTAINED OVER 1 MINUTE. V E IS CALCULATED AS FOLLOWS: V E = V T x RR FOR EXAMPLE : V E = 500 mL x 12/ min = 6000mL OR 6.O L/min NOT ALL THE V E 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 V E VENTILATES ALVEOLI, ALVEOLAR VENTILATION(V A ). THE REMAINING PART VENTILATES CONDUCTING AIRWAYS, DEAD-SPACE VENTILTION(V D )

5. DEAD SPACE VENTILATION ANATOMICAL DEAD SPACE THE CONDUCTING AIRWAYS FROM THE MOUTH AND NOSE DOWN TO AND INCLUDING TERMINAL BRONCHIOLES CONSTITUTE ANATOMICAL DEAD SPACE(VD ANAT ). 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. VD ANAT 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, VD ANAT VOLUME IS CONSIDERED CONSTANT AT ANY TIME. MEASURING V DANAT VD ANAT IS RELATED TO LUNG SIZE; IN NORMAL ADULTS, ANATOMICAL DEAD SPACE IS APROXIMATELY 1mL PER POUND OF IDEAL BODY WEIGHT.

6. ALVEOLAR AND PHYSIOLOGICAL DEAD SPACE ALVEOLAR DEAD SPACE(V DA ) IS THE VOLUME CONTAINED IN NONPERFUSED ALVEOLI, OR ALVEOLI WITH NO BLOOD FLOW. V DA IS ABNORMAL. ANY FACTOR DECREASING PULMONARY BLOOD FLOW, SUCH AS EXTREMELY LOW CARDIAC OUTPUT OR A PULMONARY EMBOLUS, INCREASES V DA. PHYSIOLOGICAL DEAD SPACE IS THE SUM OF VD ANAT AND V DA. V D = VD ANAT + V DA V D 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 V T MOVES THROUGH THE VD ANAT, THUS DOUBLING THE VD ANAT.

7. ALVEOLAR VENTILATION V A IS THE AMOUNT OF GAS ENTERING OR LEAVING THE ALVEOLI PER MINUTE. V A = V E – V D. PRACTICALLY SPEAKING, ALL CO 2 IN EXHALED GAS COMES FROM VENTILATED, PERFUSED ALVEOLI. THE SOURCE OF THIS CO 2 IS TISSUE METABOLISM. NORMAL AEROBIC METABOLISM PRODUCES CO 2, WHICH IS CARRIED BY VENOUS BLOOD TO THE LUNGS. THE MIXED VENOUS PCO 2 (PvCO 2 ) APPROACHING THE ALVEOLI IS SEVERAL mmHg HIGHER THAN ALVEOLAR PCO 2 (PACO 2 ). THUS CO 2 DIFFUSES INTO THE ALVEOLI. THE BALANCE BETWEEN METABOLIC CO 2 PRODUCTION PER MINUTE (VCO 2 ) AND ITS RATE OF ELIMINATION (V A ) DETERMINES THE PCO 2 OF THE BLOOD LEAVING THE LUNG.

9. HYPERVENTILATION AND HYPOVENTILATION IF V A REMOVES MORE CO 2 PER MINUTE THAN IS METABOLICALLY PRODUCED, ALVEOLAR AND BLOOD PCO 2 DECREASE AND A STATE OF HYPERVENTILATION EXISTS. IF V A REMOVES LESS CO 2 THAN THE BODY PRODUCES, ALVEOLAR AND BLOOD PCO 2 RISE AND A STATE OF HYPOVENTILATION EXISTS. ARTERIAL BLOOD ARISING FROM THE LEFT VENTRICLE HAS THE SAME PCO 2 AS THE ALVEOLI (PACO 2 = PaCO 2 ) V A DETERMINES ARTERIAL PCO 2 BECAUSE IT CONTROLS ALVEOLAR PCO 2. THE PaCO 2 OBTAINED CLINICALLY THROUGH ABG ANALYSIS IS THE DEFINITIVE INDEX OF V A. HYPERVENTILATION AND HYPOVENTILATION ARE DEFINED BY V A RELATIVE TO CO 2 PRODUCTION, A RELATIONSHIP THAT CAN BE KNOWN ONLY BY MEASURING PaCO 2. IF PaCO 2 IS ABOVE NORMAL HYPERCAPNIA, HYPOVENTILATION EXISTS; IF PaCO 2 IS BELOW NORMAL HYPOCAPNIA, HYPERVENTILATION EXISTS.

10. V A AND PACO 2 IF V A IS INVERSELY RELATED TO P A CO 2 ; IF V A IS REDUCED BY HALF, P A CO 2 DOUBLES. IF V A DOUBLES, P A CO 2 ( AND PaCO 2 ) IS REDUCED BY HALF. RATIO OF DEAD SPACE TO V T V A CAN BE CALCULATED IF IT IS KNOWN WHAT FRACTION OF THE V T IS DEAD SPACE (V D /V T ). NORMALLY, ABOUT 20% TO 40% OF THE INSPIRED V T REMAINS IN CONDUCTING AIRWAYS, NEVER REACHING ALVEOLI. SHALLOW V TS INCREASE THE V D /V T RATIO BECAUSE CONDUCTING AIRWAY VOLUME REMAINS CONSTANT. DEEP BREATHS DECREASE THE V D /V T FOR THE SAME REASON, CAUSING A LARGER PERCENTAGE OF THE INSPIRED VOLUME TO REACH THE ALVEOLI. THE V D /V T 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 V D /V T TO BE CALCULATED.

11. CAPNOMETERS ARE USED IN THE CLINICAL SETTING TO ANALYZE EXHALED CO 2. CAPNOGRAPHY REFERS TO THE PCO 2 CHANGES OF EXHALED V TS GRAPHYCALLY DISPLAYED AS A WAVEFORM (CAPNOGRAM). CAPNOGRAMS ALLOW THE PCO 2 TO BE IDENTIFIED AT THE END OF A TIDAL EXHALATION (P ET CO 2 ), WHICH CORRESPONDS TO AVERAGE ALVEOLAR PCO 2 (P A CO 2 = P ET CO 2 ). THE V D /V T RATIO IS A MEASURE OF VENTILTORY EFFICIENCY. A HIGH V D /V T MEANS MUCH OF THE V E IS WASTED IN VENTILATING NONPERFUSED ALVEOLI, REQUIRING HIGH- ENERGY EXPENDITURE TO ACCOMPLISH A RELATIVELY SMALL AMOUNT OF V A.

12. VENTILATORY PATTERN, DEAD SPACE, AND V A THE RATE AND DEPTH OF VENTILATION AFFECT V A AND THE V D /V T RATIO. V E IS NOT A RELIABLE INDICATOR OF V A. IN A, B AND C V DANAT AND V E ARE IDENTICAL. (V E IS 8000 ml/min AND V DANAT IS 150 ml IN EACH INSTANCE).THE FIGURE B, REPRESENTS A NORMAL V T AND RESPIRATORY RATE. DEAD SPACE VENTILATION IS THE PRODUCT OF RESPIRATORY FREQUENCY AND DEAD SPACE VOLUME ( V D = V D X F). FIGURE B, V D EQUALS 16 MULTIPLIED BY 150, WHICH EQUALS 2400 ml/min. THE V A OF 5600 ml/min IS EQUAL TO V E MINUS V D (8000-2400=5600). FOR THE FOLLOWING DISCUSSION, IT IS ASSUMED THAT THIS V A MAINTAINS A NORMAL PaCO 2 OF 40 mmHg, REPRESENTING NEITHER HYPERVENTILATION NOR HYPOVENTILATION.

13. EFFECT OF VENTILATORY PATTERN ON ALVEOLAR AND DEAD-SPACE VENTILATION

14. VENTILATORY PATTERN, DEAD SPACE, AND V A FIGURE A, ILLUSTRATES THE INEFFICENCY OF RAPID(TACHYPNEA), SHALLOW (HYPOPNEA) BREATHING. THE LUNG STILL ACHIEVES A V E OF 8000 ml/min. HOWEVER, V D NECESSARILY INCREASES ( V D = 32 X 150 = 4800 ml/min, COMPARED WITH A V D OF 24OO ml/min IN FIGURE B. THIS LEAVES ONLY 3200 ml/min FOR V A, COMPARED WITH 5600 ml/min IN B. THE V D /V T INCREAES ALSO; IN B IT IS 150/500, WHICH EQUALS 30%, AND IN A IT IS 150/250=60%. THUS 70% OF THE V E 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.

15. EFFECT OF VENTILATORY PATTERN ON ALVEOLAR AND DEAD-SPACE VENTILATION

16. VENTILATORY PATTERN, DEAD SPACE, AND V A FIGURE C, ILLUSTRATES SLOW (BRADYPNEA), DEEP(HYPERPNEA) BREATHING, WHICH ALSO ACHIEVES A V E OF 8000 ml/min. BECAUSE V DANAT IS CONSTANT, ALL THE ADDITIONAL V T ENTERS ALVEOLI, INCREASING V A. V D IS ONLY 8 X 150, WHICH EQUALS 1200 ml/min, LEAVING 6800 ml/min FOR V A. THE V D /V T IS 150/1000 OR EQUAL TO 15%, MEANING 85% OF THE V E PARTICIPATES IN GAS EXCHANGE. SLOW, DEEP BREATHING IS THUS THE MOST EFFICIENT VENTILATORY PATTERN IN TERMS OF THE FRACTION OF V E RECEIVED BY ALVEOLI.