# PULMONARY PHYSIOLOGY

1. Lung Volumes and Capacities, and the distinction between Obstructive and Restrictive Lung Disease.

Respiratory minute volume = VT × respiratory rate, where VT is tidal volume.

Alveolar ventilation =

(VT – anatomical dead space) × respiratory rate

Anatomical dead space is roughly equal to body weight in pounds.

If VT = 500 ml and respiratory rate = 12 per minute, then respiratory minute volume = 6 liters

If the anatomical dead space = 150 ml, then alveolar ventilation = (500 – 150) × 12 = 4.2 liters/minute. Note that only alveolar ventilation contributes to gas exchange.

Each lung volume is an independent fraction of total lung capacity (TLC). Lung capacities are combinations of lung volumes. Values given below are for a healthy young adult male weighing 80 kg with a body surface area of about

1.8 m2. Values in females are about 10% lower. Note that lung volumes and capacities are greatly influenced by height, weight, body surface area.

Tidal volume is about 5–7 ml/kg body weight;

By definition, the reserve volumes are recruited with effort.

FRC is the resting lung volume or the volume of air present in the lungs at the end of a tidal expiration. It is the lung volume at which the inward elastic recoil of lung parenchyma is balanced by the natural tendency of chest wall to recoil outward.

Lung capacities in a healthy adult male weighing 70 kg:

The term expiratory capacity is not used. Unless otherwise stated, vital capacity (often called forced vital capacity) is the maximum amount of air that can be expelled after a forced inspiration. If measured during inspiration, it is specifically called inspiratory vital capacity.

The following 4 factors affect vital capacity:

1. Strength of muscles of inspiration
2. Lung compliance
3. Strength of muscles of expiration
4. Airways resistance

Evaluating airways resistance:

Air flow = transairway pressure / airway resistance

Transairway pressure = intrathoracic pressure – pressure at the mouth. The latter is zero mm Hg with reference to atmospheric pressure.

FEV1, the volume of air expelled during the first second of a forced vital capacity maneuver, varies directly with expiratory pressure and inversely with airways resistance. It is normally at least 80% of FVC; FEV1/FVC is > 0.8.

If vital capacity is reduced, FEV1 will be reduced, yet FEV1/FVC may be normal as in restrictive lung disease.

FEV1/FVC is a specific index of airways resistance and helps discriminate restrictive from obstructive lung disease. See Table OLD vs. RLD next page.

Peak expiratory flow rate (PEFR) is the highest flow rate during forced expiration (vital capacity maneuver). When vital capacity is reduced, flow rates are reduced as well. Thus, for example, the peak flow rate during tidal expiration is much

lower than that during forced expiration. Normally, PEFR is about 12 liters/second or 720 liters/minute (values are 10-15% lower in age matched females).

PEFR is dependent upon vital capacity. Thus, it does not make sense to use PEFR as an index of airways resistance in a patient with restrictive lung disease. (Note that FEV1/FVC is normalized for flow whereas PEFR is not.) Thus, monitoring PEFR as an index of airways resistance is appropriate only in individuals known to have obstructive airways disease or asthma (low FEV1/FVC).

Forced expiratory time: this is a useful bedside index of airways resistance. Auscultate the trachea during forced expiration, if expiratory sounds are heard for longer than 4 seconds, airways resistance is increased.

Maximum mid-expiratory flow rate (MMEFR): The first 25% of expired air comes mainly from the major airways; MMEFR is the highest rate at which the middle 50% of VC is expelled; it is also called forced expiratory flow rate (FEF 25–75), and it is more sensitive than PEFR in reflecting the resistance of the small airways that are narrowed in bronchial asthma.

“Air trapping” occurs whenever there is expiratory flow limitation. Since flow is driven by pressure and opposed by resistance, air trapping is usually a consequence of an increase in airways resistance. Air trapping occurs in chronic obstructive pulmonary disease. As a result of this, total lung capacity increases, however the vital capacity is subnormal; in other words, patients with obstructive lung disease breathe at a higher FRC compared to normal subjects. The fraction of FRC that increases is the residual volume.

Lung compliance is the change in lung volume for a given change in pressure.

Compliance = ΔV / ΔP

The normal compliance of human lungs and chest wall is about 0.2 L/cm H2O. Compliance is reduced in restrictive lung disease.

To summarize, vital capacity is always reduced in lung disease; however, total lung capacity may be increased or decreased depending on the cause.

Obstructive (OLD) vs. Restrictive Lung disease (RLD)

• Lung Zones:

PA = Alveolar pressure;

Pa = Pressure at the arterial end of the pulmonary capillary;

Pv = Pulmonary venous pressure; Pi = Pulmonary interstitial pressure.

Zone 1: above the heart; arterial pressure is lower and may be lower than alveolar pressure if the alveoli are well expanded. Flow may be minimal. V/Q approaches infinity.

Zone 2: pulmonary arterial pressure is greater than alveolar pressure and flow is determined by arterial – alveolar pressure difference; however, during inspiration when alveolar pressure becomes more negative, blood flows from the arteries into the pulmonary veins. This is called the ‘waterfall effect’.

Zone 3: flow is continuous and is driven by pulmonary arterial – venous pressure gradient.

Zone 4: it occurs in pulmonary edema (always abnormal). When pulmonary interstitial pressure is > than alveolar pressure, alveolar collapse (atelectasis) would result.

When a Swan Ganz catheter is wedged in the pulmonary capillary to estimate left ventricular end diastolic pressure (LVEDP) in a patient who is on a ventilator with positive end expiratory pressure (PEEP) added, the measured pressure would reflect alveolar pressure rather than LVEDP; thus, the catheter must be placed in Zone 3 conditions (perhaps by momentarily discontinuing PEEP) to reliably estimate LVEDP

• Gas Exchange:

Ventilation–perfusion ratio is the ratio of alveolar ventilation to pulmonary blood flow. For example, at rest, alveolar ventilation = 12 × (500-150) = 4.2 L/min;

Assuming VT = 500 ml, VD = 150 ml; If pulmonary blood flow = 5 L/min; Thus, whole lung V/Q ratio = 0.84;

In the lung apices, V/Q approaches infinity; In the lung bases, V/Q is lower than 1.

As a result of regional differences in intrapleural pressure, upper lung zones are already in a more expanded position at the start of inspiration. In contrast, the lower lung zones are less distended at the start of inspiration and therefore more compliant. Thus, alveolar ventilation is much higher at the lung bases than the apices

Shunt: Perfusion of unventilated alveoli results in shunting of deoxygenated blood across the lungs to the heart, i.e. a right-to-left shunt.

Dead space: Ventilation of unperfused alveoli is effectively an extension of anatomic dead space since it cannot contribute to gas exchange.

At rest, a healthy adult weighing 70 kg uses about 250 ml of oxygen per minute and 200 ml of CO2 is produced.

Respiratory exchange ratio (RER, sometimes abbreviated R) is the ratio of the volume of CO2 to O2 exchanged across the lungs per minute. At rest, it is normally 200 / 250 = 0.8. Respiratory exchange ratio reflects the average respiratory quotient (RQ) when gas exchange across lungs is normal.

RQ is different for different energy substrates.

Average RQ depends upon the metabolic state as well.

What factors determine the tension of oxygen in alveolar gas? This is summarized by the alveolar gas equation:

Alveolar oxygen tension PAO2

= [(PB-PH20) × FiO2] – [(PAC02)/R]

PB is barometric pressure (760 mm Hg at mean sea level);

PH20 is the pressure of water vapor at body temperature (it is 47 mm Hg);

FiO2 is the percentage of oxygen in inspired air; and PACO2 is the CO2 tension in alveolar gas (normally about 40 mm Hg). When ventilation- perfusion balance is optimal, it is equal to PaCO2 because CO2 is highly soluble and readily equilibrates across the alveolocapillary membrane, and PaCO2 can be substituted for for PACO2. RER (or R) may be assumed to be 0.8.

Substituting values for someone breathing room air at mean sea level, we get,

PAO2 = [(760-47) × 0.21] – [40/0.8]

= 150-50 = 100 mm Hg

The alveolar gas equation is used to calculate the expected alveolar PO2. The alveolar-arterial oxygen gradient normally is less than 10 mm Hg.

One can this calculate the expected PaO2 in various conditions and compare it to the actual PaO2 and assess gas exchange in various conditions.

Diffusion capacity of the lungs: The “single breath technique”: The subject inhales a mixture containing 0.01% CO.

Diffusion rate J = (PACO–PcCO) × DA/x

In a nonsmoker, PcCO = 0 mm Hg and PACO is constant.

Diffusion capacity is defined as DA/x

Normally, diffusion capacity of lungs for CO = 25 ml/min/mm Hg. The value for oxygen is similar. Since CO exchange is diffusion limited, it is used for assessing diffusion capacity of lungs.

The oxygen cascade: Factors that affect oxygen delivery to the tissues include the following (the oxygen cascade):

• Alveolar ventilation
• Pulmonary blood flow
• Ventilation / perfusion balance
• Diffusion capacity of lungs for oxygen
• Cardiac output
• Hb concentration of arterial blood
• Affinity of Hb for oxygen
• Blood flow to each tissue