VENTILATION by lonyoo

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									VENTILATION
General Goal: To describe how air flow (ventilation) in to and out of the lung affects alveolar gas concentrations. Specific Objectives: The student should: 1. understand the concepts of anatomical dead space and physiological dead space. Know how the Bohr Equation is used to measure dead space and understand the principles involved in its use. 2. know how minute ventilation is related to tidal volume and frequency and how it differs from alveolar ventilation. 3. know the meaning of the terms “respiratory quotient” and “respiratory exchange ratio”, how they are related to oxygen uptake and carbon dioxide production and under what conditions they might change and/or differ from each other. 4. know what factors determine alveolar PCO 2 and how these factors are interrelated as described by the “alveolar ventilation equation.” 5. know what factors determine alveolar PO2 and how these factors are interrelated by the clinical version of the “alveolar gas equation.” 6. be able to differentiate between ventilation and volume. Memorize the clinically used ventilatory terms. Resources Lecture: Dr. Baer Reading: West, JB. Respiratory Physiology—The Essentials (4th Ed.). Williams & Wilkins, 1990. Chapter 2. Excellent Additional Reading: Forester, RE, AB Dubois, WA Briscoe, AB Fisher. The Lung—Physiological Basis of Pulmonary Function Tests (3rd Edition). Year Book Medical Publishers, 1986.

Page 30 Respiratory Physiology I. VENTILATION A.

 Minute Ventilation ( VE ) is the volume of air per unit time (i.e., a flow) moved into or out of the lungs. Measured by collecting expired volume for a fixed time. Typical value is 7.5 L/min (BTPS).  Ventilation is the product of tidal volume (VT) and respiratory frequency ( VE  VT  f ) .
Anatomic dead space. The volume of the lung (including the mouth, pharynx, larynx, trachea, and bronchi) that are not involved in gas exchange. Ventilation of these areas results in no gas exchange. 1. Anatomic dead space in ml may be estimated as numerically equal to the ideal body weight measured in pounds. Fowler’s Method of measuring anatomic dead space. Expired N2 concentration is analyzed following a single breath of 100% oxygen. Nonuniformity of ventilation makes analysis difficult during obstructive disease because no phase III plateau exists.

B. C.

2.

Figure 1--The N2 analyzer samples, analyzes, and records continuously the N2 concentration of gas being inspired or expired. During inhalation of air “(left) “the N2 analyzer records 79% to 80% N2 in inspired and expired gas. The subject is then requested to take a deep breath of O2 and breathe out slowly and evenly. During inspiration, the N2 analyzer records 0% N2. At the beginning of expiration, about 50 ml of pure O2 (0% N2) is expired “(phase I)”; this is followed by about 200 to 300 ml of gas of rapidly rising N2 concentration “(phase II)”, which represents the washout of the remainder of the dead space gas by alveolar gas, and then by pure alveolar gas “(phase III)”. The N2 concentration of the last part of the expiration “(phase IV)” rises because of the progressive closure of the small airways at the bases of the lungs. This is an idealized presentation of events that would follow inhalation of O2 if functional residual capacity (including dead space gas) were 2,000 ml, volume of inspired O2 2,150 ml, dead space 150 ml, and distribution of O2 to the alveoli perfectly uniform.

D.

Physiological dead space. Anatomical dead space plus alveolar dead space. 1. Gas exchange is only optimal when individual regions are ventilated in proportion to their capillary blood flow. Well ventilated regions ideally have high capillary blood flows. Poorly ventilated regions ideally have little capillary blood flow.

Ventilation Page 31 2. Ventilation and blood flow are not homogeneous in the lung. There are regions which are well ventilated and poorly perfused, and regions which are poorly ventilated and well perfused. Thus, gas exchange is less than optimal in portions of the lung. Alveolar dead space. Conceptually, the lung is treated as if only two types of alveoli exist: those with ideal gas exchange and those with no gas exchange at all. The theoretical or “as if” volume contained in the units without gas exchange is alveolar dead space. Physiological dead space is the total effective volume of the lung NOT involved in ideal gas exchange (anatomical dead space plus alveolar dead space). Physiological dead space is only slightly greater than anatomical dead space in healthy supine individuals. This is because ventilation and perfusion are relatively homogeneous under these conditions. Physiological dead space is greater when in an upright posture or when disease   states alter ventilation/perfusion ( V / Q) relationships.

3.

4. 5.

6.

E.

Bohr Equation. Used to measure physiological dead space knowing: 1. 2. 3. that all CO2 comes from alveolar gas not dead space; that arterial PCO 2 is almost always equal to alveolar PCO 2 ; that there is conservation of mass.

Vd Pa CO2  PECO2  VT Pa CO
2

F.

 Alveolar Ventilation ( VA ) . Minute ventilation is composed of two components: the  volume per min entering gas exchange surfaces ( VA ) and the volume per minute  entering dead space ( Vd ) .
f VT 500 250 500 250

 VE
7500 7500 7500 7500

Vd 150 150 200 200

 Vd

 VA

Vd/VT

Normal dead space

15 30

Increased dead space

15 30

1.

   VA  VE  Vd  (VT  Vd ) f = VT f - Vd f

Page 32 Respiratory Physiology 2. If tidal volume increases alveolar ventilation increases but dead space ventilation is unchanged. If respiratory frequency increases both alveolar ventilation and dead space ventilation increase. This is less efficient than a tidal volume change. When dead space is high as in chronic obstructive disease, it is even more efficient to increase ventilation by increasing tidal volume instead of respiratory frequency.

3. 4.

G.

Alveolar ventilation equation.

  Given, VCO2  VA  FACO
 Then, VA ( BTPS)  863 
II.

2

 VCO2 (STPD) PA CO2

VENTILATION AND ALVEOLAR GAS COMPOSITION A. Cyclical variation. The amount of air entering with each breath is small compared to the volume already there. Thus, cyclical variation in the alveolar partial pressures of oxygen and carbon dioxide PA O 2 and PA CO is small. 2 Mean steady state values. By definition steady state alveolar PO2 exists when the rate

B.

 at which oxygen enters the alveoli ( VO2 ) equals the rate at which it is taken up by the
blood (used by the body for metabolism). By definition steady state alveolar PCO 2 exists when the rate at which carbon dioxide enters the alveoli (metabolic production by the  body) equals the rate that it is expired ( VCO2 ) . C.

  Respiratory exchange ratio. R  VCO2 / VO2
1. Normal less than 1.0. 2. values ar e

 VCO2  200 ml / min (STPD)

a nd

 VO2  250 ml / min (STPD) . Thus, the respiratory exchange ratio is normally
 This means that expiratory minute ventilation ( VE ) is slightly (about 60 ml/min at BTPS) less than inspiratory minute ventilation.
Respiratory quotient (RQ) is the ratio of CO2 production  O2 utilization in metabolic reactions of the body cells. Its value changes with substrate utilization (carbohydrates = 1.0; fats = 0.70; proteins = 0.80; average mixed diet = 0.8). The respiratory exchange ratio (lungs) must equal the respiratory quotient (body cell metabolism) in steady state conditions.

3.

4.

Ventilation Page 33 D. Factors determining alveolar PCO 2 ( PA CO ) 2 1. 2. Inspired air contains no CO2. Increased carbon dioxide production will increase flow into the alveoli and thus increase alveolar PCO 2 .

3.

 Increased alveolar ventilation ( VA ) will increase the flow of fresh air into the alveoli, thus diluting alveolar gas, and alveolar PCO 2 ( PA CO ) . 2
Rearrangement of the alveolar ventilation equation reminds us of how alveolar PA CO2 is affected by carbon dioxide production and alveolar ventilation.

4.

PA CO2 
5.

 VCO2  863 mmHg  VA

Clinically, arterial PCO 2 ( Pa CO ) is used to estimate alveolar PCO 2 ( PA CO ) because 2 2 carbon dioxide is seldom diffusion limited. Values of Pa CO allow clinical 2 assessment of whether a patient’s alveolar ventilation is appropriate to metabolic activity.

6. E.

 Factors that increase VCO2 : exercise, fever, hyperthyroidism.

Factors determining alveolar PO 2 ( PA O ) 2 1. Inspired

PO2  .209(760 - 47) = 149 mmHg under normal conditions.

ai r

contains

20.9%

O2.

Therefore,

inspired

2.

 Increased metabolic activity increases oxygen uptake ( VO2 ) and decreases
alveolar PO2 .

3.

 Increased alveolar ventilation ( VA ) increases flow of fresh air through alveoli and increases PO2
Two factors complicate the determination of alveolar PO2 a) b) oxygen in inspired air; a respiratory exchange ratio that’s less than 1.0 means that inspired volume is greater than expired volume.

4.

F.

Ideal Alveolar Gas Equation. (Sometimes called the “Alveolar Air Equation”) Used to calculate the mean partial pressure of oxygen in the alveoli. Limiting values of alveolar gas equation:

Page 34 Respiratory Physiology

PA O  PI O 
2 2

PA CO

1 R    PA CO  FI O   2 2  R R 
2

1. 2.

. when R= 0.7 (metabolizing fats): PA O  PI O  (13) PA CO . 2 2 2
when R= 0.82 (normal value):

PA O  PI O  (12) PA CO .
2 2

2

3.

when R= 1.0 (metabolizing carbohydrates):

PA O2  PI O2  (10) PA CO2 .
4. G. When FI O  1.0 (breathing 100% O2): PA O  PI O  PA CO 2 2 2 2

Clinical form of ALVEOLAR GAS EQUATION. In general, changes in FI O have 2 minimal effect on the term in parenthesis for a given R. The equation is often expressed in a clinically useful form:

PA O  PI O  PA CO / R
2 2 2

This is the form you should remember. III. CLINICAL USE OF IDEAL ALVEOLAR GAS VALUES A. B. Used for comparison with a measured Pa O . 2 A-a difference. The PA O is normally 5-20 mmHg greater than the Pa O . This occurs 2 2 because of normal anatomical shunt and ventilation/perfusion mismatching. 1. 2. The A-a difference increases with pulmonary disease. The normal range for A-a difference changes when breathing 100% O2.

Figure 2

Ventilation Page 35 C. a/A PO2 ratio. The arterial/alveolar oxygen tension ratio ( PO 2 / PA O ) in normally 2

averages over just 0.8 (Am.Rev. Resp. Dis. 109: 142-145, 1974). 1. 2. The a/A PO2 ratio falls with pulmonary disease. The a/A PO2 ratio remains fairly constant during administration of supplemental oxygen (increasing FI O 2 3. Lower limit of normal in young subjects is 0.78 on room air and lower limit in older subjects is 0.74 on room air. Lower limit for both groups is 0.82 on 100% O2.

D.

The PA O 2 is also be used to estimate the end-capillary Pc O when calculating venous 2 admixture. (We will discuss this with pulmonary blood flow).

IV.

VENTILATORY TERMS THAT ARE OFTEN USED CLINICALLY A. Eupnea. Normal spontaneous breathing of which we are normally unaware. Ventilation is matched to metabolic demands. Hyperpnea. Increased ventilation which matches increased metabolic demands such as exercise. As intensity increases ventilation is increased mainly by increasing tidal volume initially; increased frequency is proportionately more important at high intensities. Hyperventilation. A ventilation rate which is inappropriately high for the metabolic demands. The resulting alveolar and arterial PCO 2 are decreased. Alveolar PO2 is increased. D. Hypoventilation. A ventilation rate which is inappropriately low for the metabolic demands. Alveolar and arterial PCO 2 are elevated. Arterial PO2 is decreased. Tachypnea. Increased frequency of breathing. Ventilation may or may not be changed depending on what happens to tidal volume. Dyspnea. Subjective sensation of difficult or labored breathing on the part of patient. May occur in the absence of physical hypoventilation. Often associated with abnormal pulmonary mechanics and not directly related to abnormal blood gases. Orthopnea is dyspnea which only occurs when lying down and is characteristically seen in LV insufficiency. Apnea. Temporary absence or cessation of breathing (usually at FRC) with the implication that breathing will resume spontaneously. Normally apnea occurs after hyperventilation or swallowing.

B.

C.

E.

F.

G.

Page 36 Respiratory Physiology SUMMARY OF KEY EQUATIONS 1. Bohr Equation for Physiological Dead Space

Vd Pa CO2  PECO2  VT Pa CO
2

2. Alveolar Ventilation Equation

 VA  863

 VCO 2 Pa CO2

3. Alveolar Gas Equation for determining ideal alveolar PO2 (approximate formula)

PA O  PI O  Pa CO / R
2 2 2

VENTILATION Study Questions The information. A healthy 200 lb man is producing 300 ml/min of carbon dioxide (STPD) at sea level  (Barometric pressure = 760 mmHg). His minute ventilation ( VE ) is 7.8 l/min at a respiratory rate of 12/min. Assume his RQ is 0.8. 1. Estimate his anatomic dead space. Are anatomic and physiologic dead space likely to be similar? 2. What is his alveolar ventilation? 3. What is his estimated dead space ventilation? What percentage of his ventilation is his wasted ventilation? 4. What is his mean alveolar PCO 2 ( PA CO ) ? His mean arterial PCO 2 ( Pa CO ) ? 2 2 5. Is the patient hypoventilating or hyperventilating? 6. Calculate his estimated alveolar PO 2 ( PA O ) . 2

 7. Calculate his estimated oxygen consumption ( VO2 ) .
8. If his arterial PO2 (Pa O ) is 83 mmHg what is his A-a gradient? His a/A ratio? What does this tell us 2 about gas exchange?


								
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