Alveolar ventilation- Gas exchange and transport

Alveolar ventilation- Gas exchange and transport.

Alveolar ventilation. The total ventilation per minute, termed the minute ventilation, is equal to the tidal volume multiplied by the respiratory rate. For example, at rest, a normal person moves approximately 500 ml of air in and out of the lungs with each breath and takes 12 breaths each minute. The minute ventilation is there- fore 500 ml/breath × 12 breaths/minute = 6000 ml of air per minute..

‘’Dead Space” and Its Effect on Alveolar Ventilation.

Dead space. 1- The anatomic dead space: Is the volume of all the space of the respiratory system other than the alveoli and their other closely related gas exchange areas. The size of the anatVD in mL is approximately equal to a person’s weight in pounds . Thus a 150-lb individual has an anatomic dead space of 150 mL. 2- The alveolar dead space: Some fresh inspired air is not used for gas exchange with the blood even though it reaches the alveoli because some alveoli may have little or no blood supply. 3- The physiologic dead space: The sum of the anatomic and alveolar dead spaces. This is also known as wasted ventilation because it is air that is inspired but does not participate in gas exchange..

Alveolar ventilation. Alveolar ventilation per minute is the total volume of new air entering the alveoli and adjacent gas exchange areas each minute. It is equal to the respiratory rate times the amount of new air that enters these areas with each breath . with a normal tidal volume of 500 milliliters, a normal dead space of 150 milliliters, and a respiratory rate of 12 breaths per minute, alveolar ventilation equals 12 x (500 – 150 ) = 4200 ml/min..

Alveolar ventilation. Alveolar ventilation rather than minute ventilation, is the more important factor in the effectiveness of gas exchange..

Gas exchange – Partial pressure. Atmospheric air consists of approximately 79 percent nitrogen and approximately 21 percent oxygen, with very small quantities of water vapor, carbon dioxide, and inert gases . The sum of the partial pressures of all these gases is termed atmospheric pressure , or barometric pressure. At sea level atmospheric pressure is 760 mmHg. Because the partial pressure of any gas in a mixture is the fractional concentration of that gas times the total pressure of all the gases , (DALTON LAW) the PO2 of atmospheric air is 0.21 × 760 mmHg = 160 mmHg at sea level . PCO2 = 0.3 mmHg.

Oxygen and carbon dioxide partial pressures. P Air 160 mmHg = 0.3 mmHg Alveoli 105 mmHg 40 mmHg Poz 40 mmHg Pc:oz = 46 mmHg Pulmonary arteries Right Systemic Lung capi"aries Tissue capillaries 02 = 40 mmHg — 100 mm Pulmonary Left arteries PCOa = 46 mmHg 40 mmHg Poa — Cells < 40 mmHg (mitochondrial < 5 mmHg) •Pcoz > 46 mmHg.

1 TABLE 13-5 Factors That Influence the Rate of Gas Transfer Across the Alveolar Membrane Partial pressure gradients of 02 and C02 Surface area of the alveolar membrane Thickness of the barrier separating the air and blCH)d across the alveolar membrane Diffusion constant Influence on the Rate of Gas Transfer Across the Alveolar Membrane Rate of transfer t as partial pressure gradient t Rate of transfer t as surface area t Rate of transfer as thickness t Rate of transfer t as diffusion constant t Comments Major determinant of the rate of transfer Surface area remains constant umler resting conditions surface area T during exercise as more pulmonary capillanes open up 'Mien the cardiæ output increases ard the alveoli expand as breathing deecpr Surface area with pathological conditions such as emphysema and lung collapse Thickress normally remains constant Thickness t with pathological conditions such as pulmonary edema, pulmonary fibrosis, and pneumonia Diffusion constant for C02 is 20 times that of 02, offsetting the smaller partial pressure graclient for C02; therefore, approximately aqual amounts of C02 and 02 are transferred across the membrane.

Gas Exchange Between Alveoli and Blood. Table13-7 NomalGasPrcssutc VemusBl(KKl 40 mmHg Pill Arterial Bld 100 mmllgi 40mmHg 105 40 lillilllg 160 mmllg (13 mmHg.

Matching of Ventilation and Blood Flow in Alveoli.

Ventilation- prfuslon ratio 024 0.07 Top Perfusion (blood now) Ventilation (airflow) 3 2 R4ion ot lung in Ipright indive (a) Regional veltjlation and perfusion rata and ventilation-prfusion ratios in the lungs Ventilation (airflow) (Limn) ot 0.24 lung 0.82 ot lung Perfusion (tiood flow) (Umin) 0.07 1.29 Ventilation- perfusion ratio 3.40 0.0 (b) Ventilation and perfusion rates and Entilatjon- prfusion ratios at top and bottom of lungs ) Figure 13-20 Differences in ventilation, perfusion, and ventilation-Musion ratios at the top and t»ttom Of the lungs as a result Of graitational effEts tote that the Of the lungs recervæ less air and blCüj tran the of tre lungs, tut the tcp of the lurs retEiE rew tively me air bhan and the bottom ci the lings recewes relatNety les air blon.

ventilation-perfusion inequality.. In disease states, regional changes in lung compliance, airway resistance, and vascular resistance can cause marked ventilation-perfusion inequalities : ( 1) There may be ventilated alveoli with no blood supply at all (dead space or wasted ventilation ) due to a blood clot, for example, or ( 2) There may be blood flowing through areas of lung that have no ventilation (this is termed a shunt) due to collapsed alveoli, for example..

Decreased airflow to regon of P'*mmary Vasomnstrictiorl of pWn«1ary vessels Decteased match a decrease in •entil*ion Diversion of flow and airfw. away from lod area Of disease to areas the lung Deceased Nood flow to region of lung Oeaeaæd -adm to maeh a decrease in perfusion Figure 13.24 control of ventilation--vrrfusion matching..

Transport of Oxygen in the Blood Oxygen Content. Table 13—8 Oxygen Content of Systemic Arterial Blood at Sea Level I liter (L) arterial blood contains 3 ml 02 physically dissolved (1.5%) 197 ml 02 bound to hemoglobin (98.5%) Total 200ml 02 Cardiac outPUt - ; L/min 02 carried to tissues/min = ; L/min x 200 ml 02/ L - 1000 ml ()z/rnin.

Maximum Amount of Oxygen That Can Combine with the Hemoglobin of the Blood (Oxygen Carrying capacity).

Percent hemoglobin saturation. In a blood sample containing many hemoglobin molecules, the fraction of all the hemoglobin in the form of oxyhemoglobin is expressed as the percent hemoglobin saturation: Percent Hb saturation = O 2 bound to Hb Maximal capacity of Hb to bind O2.

Oxygen-Hemoglobin dissociation curve. 10 40 70 % Sat 13-5 57 75 927 945 975 02 (ml-&) 01B 0.12 0.15 0.18 021 024 027 03) o 10 20 30 40 60 70 90 1m 110 P02 (mm Hg).

Oxygen-Hemoglobin dissociation curve. 1- Shape The S-shaped (Why ?) oxyhemoglobin equilibrium curve enables oxygen to saturate hemoglobin under high partial pressures in the lungs and to give up large amounts of oxygen with small changes in PO2 at the tissue level. 2- Interpretation: A- between 60 and 10 mmHg PO2: unloading (Steepest part) B- between 70 and 100 mmHg PO2: loading (Plateau part) 3- P50 4- Effects of blood PCO2, [H ions], Temperature and DPG (or BPG). 5- Effect of carbon monoxide poisoning..

P 50. A convenient index for comparison of oxygen dissociation curve shifts is the P 50 , “P O2 at which 50% of the hemoglobin is saturated with O 2”. The higher the P 50 , the lower the affinity of hemoglobin for O 2. The normal P50 for arterial blood is 26 to 28 mm Hg..

No DPG Normal DPG Effect Of DPG concentration. Effect of temperature.

100 70 so 30 10 0.2 Gas pressure of carbon rnonoxide (rnrn Hg) 0.3 0.4.

CARBON DIOXIDE TRANSPORT IN BLOOD. Forms of CO2 in Blood 1- Dissolved CO2, 2- Carb- amino -hemoglobin (CO2 bound to hemoglobin ) 3- Bicarbonate (HCO3−), which is a chemically modified form of CO2 NB***HCO3− is quantitatively the most important of these forms..

1- Dissolved CO2. The concentration of CO2 in solution is given by Henry’s law , which states that: The concentration of CO2 in blood = partial pressure multiplied by the solubility of CO2 . The solubility of CO2 is 0.07 mL CO2/100 mL 40 mm Hg × 0.07 mL CO2/100 mL blood/mm Hg )= 2.8 ml CO2/100ml blood It represents approximately 5 % of the total CO2 content of blood..

2- Carbaminohemoglobin (Bohr and Haldane effects).

HCO3− (The chemically modified form). It accounts for more than 90% of the total CO2.

Continue. All of the reactions previously described occur in reverse in the lungs: 1- H + is released from its buffering sites on deoxyhemoglobin , 2- HCO3 − enters the red blood cells in exchange for Cl − , 3- H+ and HCO3− combine to form H2CO3, 4- H2CO3 dissociates into CO2 and H2O. 5- The regenerated CO2 and H2O are expired by the lungs..

Hypoxia. Hypoxia is O2 deficiency at the tissue level . There are four categories of hypoxia: (1) hypoxic hypoxia, in which the PO2 of the arterial blood is reduced ; ( 2) anemic hypoxia, in which the arterial PO2 is normal but the amount of hemoglobin available to carry O2 is reduced ; ( 3) stagnant or ischemic hypoxia, in which the blood flow to a tissue is so low that adequate O2 is not delivered to it despite a normal PO2 and hemoglobin concentration ; ( 4) histotoxic hypoxia, in which the amount of O2 delivered to a tissue is adequate but, because of the action of a toxic agent, the tissue cells cannot make use of the O2 supplied to them..

TABLE 127.1: Characteristic features of different types of hypoxia Features I P02 in arterial blood 2, Oxygen carryng capacity of blood 3. Velocity of blood flow 4. Utilization of oxygen by tissues 5. Eficacy of oxygen therapy Hypoxic hypoxia Anemic hypoxia Stagnant hypoxia Histotoxic hypoxia Reduced Normal Normal Normal 100% Normal Reduced Normal Normal Normal Normal Reduced Normal Normal Normal Normal Reduced Not useful.

Cyanosis. The term cyanosis means blueness of the skin and mucous membranes. The cause is excessive amounts of deoxygenated hemoglobin in the skin blood vessels, especially in the capillaries reaching more than 5 gm /dl . This deoxygenated hemoglobin has an intense dark blue-purple color that is transmitted through the skin..

Cyanosis. Cyanosis has one of two causes, which may act together: 1- Reduction of the arterial oxygen saturation 2- Increase in the arterio -venous oxygen content difference. A large oxygen extraction is seen in disorders with low blood flow. Its occurrence depends on: 1- the total amount of hemoglobin in the blood, 2- the degree of hemoglobin unsaturation, 3- and the state of the capillary circulation..

Types of Cyanosis. Cyanosis is divided into two main types: Central (around the core, lips, and tongue) and Peripheral (only the extremities or fingers ). Central cyanosis is often due to a circulatory or ventilatory problem that leads to poor blood oxygenation in the lungs. Peripheral cyanosis is the blue tint in fingers or extremities, due to inadequate circulation..

• Mini Glossary of Clinically portant Respiratory States Apnea -Transient of breathing Asphyxia 02 starvation Of tissues. a lack Of 02 i n air. or inability of the tissues to use 02 Cyanosis Blueness of skin resulting insufficiently oxygenated blood in arteries Dyspnea Difficult or labored i breathing Hypercapnia Excess C 02 i n arterial Hyper-pnea ventilation that roatches increased as in exercise Increased pulrnor-.ar—y• ventilation in Of rnetabolic resulting in decreased P respiratory alkalosis pr•ia C02 in the arterial blood Hypoventilation Under—ventilation in relation to bolic requirorner•ts. resulting in increased respiratory acidosis Hypoxia I at level hypoxia c of the blood Circulatory h y poxia little oxygenated blood delivered tissues: also as stagnant H Inability• Of cells to available to Hypoxic arterial blood by '-lb saturation rat or-y arrest cessation of broathing Cu r•loss corrected) Suffocation 02 deprivation as a result Of i r.ability to breathe oxygenated a ir.