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Ventilation perfusion relationships

Gas exchange between the alveoli and the pulmonary capillary blood occurs by diffusion, as will be discussed in the next chapter. Diffusion of oxygen and carbon dioxide occurs passively, according to their concentration differences across the alveolar-capillary barrier. These concentration differences must be maintained by ventilation of the alveoli and perfusion of the pulmonary capillaries.

Alveolar ventilation brings oxygen into the lung and removes carbon dioxide from it. Similarly, the mixed venous blood brings carbon dioxide into the lung and takes up alveolar oxygen. The alveolar Image not available. and Image not available. are thus determined by the relationship between alveolar ventilation and pulmonary capillary perfusion. Alterations in the ratio of ventilation to perfusion, called the Image not available., will result in changes in the alveolar Image not available. and Image not available., as well as in gas delivery to or removal from the lung.

Alveolar ventilation is normally about 4 to 6 L/min and pulmonary blood flow (which is equal to cardiac output) has a similar range, and so the Image not available. for the whole lung is in the range of 0.8 to 1.2. Image not available. However, ventilation and perfusion must be matched on the alveolar-capillary level, and the Image not available. for the whole lung is really of interest only as an approximation of the situation in all the alveolar-capillary units of the lung. For instance, suppose that all 5 L/min of the cardiac output went to the left lung and all 5 L/min of alveolar ventilation went to the right lung. The whole lung Image not available. would be 1.0, but there would be no gas exchange because there could be no gas diffusion between the ventilated alveoli and the perfused pulmonary capillaries.

Oxygen is delivered to the alveolus by alveolar ventilation, is removed from the alveolus as it diffuses into the pulmonary capillary blood, and is carried away by blood flow. Similarly, carbon dioxide is delivered to the alveolus in the mixed venous blood and diffuses into the alveolus in the pulmonary capillary. The carbon dioxide is removed from the alveolus by alveolar ventilation. As will be discussed in Chapter 6, at resting cardiac outputs the diffusion of both oxygen and carbon dioxide is normally limited by pulmonary perfusion. Thus, the alveolar partial pressures of both oxygen and carbon dioxide are determined by the Image not available. If the Image not available. in an alveolar-capillary unit increases, the delivery of oxygen relative to its removal will increase, as will the removal ...

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Ventilation perfusion relationships

  2. 2. VENTILATION- PERFUSION RELATIONSHIPS • Oxygen Transport from Air to Tissues • Causes of Hypoxemia • Effect of Altering the V/Q Ratio of a Lung Unit • Regional Gas Exchange in the Lung • Effect of Ventilation-Perfusion Inequality on Overall Gas Exchange • Distributions of V/Q Ratios
  3. 3. OXYGEN TRANSPORT FROM AIR TO TISSUES • The Po2 inspired air is (20.93/100) ×(760 − 47) =149 mm Hg. • At Alveoli Po2 has fallen to about 100 mmHg. • Po2 of alveolar gas is determined by: a) the removal of O2 by pulmonary capillary blood b) continual replenishment by alveolar ventilation. • The alveolar Po2 is largely determined by the level of alveolar ventilation. • When the systemic arterial blood reaches the tissue capillaries, O2 diffuses to the mitochondria, where the Po 2 is much lower.
  5. 5. CAUSES OF HYPOXEMIA Four principal potential mechanisms of failure of the O2 transport pathway can lead to a reduced arterial PO2: • Hypoventilation • Diffusion Limitation • Shunt • The Ventilation-Perfusion inequality
  6. 6. HYPOVENTILATION • The alveolar ventilation is abnormally low • Alveolar Po2 falls • Pco2 rises • Hypoventilation
  7. 7. ALVEOLAR GAS EQUATION - quantitatively relates PAO2 and PACO2, and is used to calculate how much PAO2 will change for a change in PACO2.
  8. 8. PATHOLOGICAL PROCESSES INVOLVED IN DISTURBANCES OF ALVEOLAR VENTILATION  Extrapulmonary causes: A. Central nervous system dysfunction • Drug induced inhibition of respiratory centres (morphine and barbiturates) • Infection processes (e.g. bulbar polio etc.) • Trauma • Idiopathic depression of the respiratory centre (Ondine’s curse)
  9. 9. B. Peripheral nervous system • Guillain - Barré syndrome • Poliomyelitis • Trauma (spinal cord, phrenic nervs damage etc.) C. Primary or secondary myopathy • Myasthenia gravis • Adverse reactions to curare • Other forms of myopathy (myositis, myalgia, respiratory muscles fatique)
  10. 10. D. Metabolic causes • Metabolic alkalosis • Hypothyroidism E. Chest wall • Kyphoscoliosis • Morbid Obesity • Trauma, surgery
  11. 11.  Pulmonary (airway) causes A. Obstruction of central airways – OSA B. Obstruction of peripheral airways • Inflammation of the airway mucosa • Contraction of smooth muscles - bronchospasm • Loss of elasticity of airway wall and lung tissue, airway remodelation
  12. 12. C. Lung parenchyma • Emphysema • Post – inflammatory (postinjury) fibrosis • Interstitial infiltration or fibrosis • Intra alveolar processes – pneumonia, alveolar edema.... D. Vascular • Pulmonary congestion • Pulmonary hypertension E. Pleural • Pleural effusions, inflammations • Pleural scaring • Pneumothorax, hydrothorax...
  13. 13. Relationship between alveolar ventilation and Pco2: VA- alveolar ventilation VCO2- CO2 production PACO2- partial pressure of CO2 in alveoli K- constant
  14. 14. • If alveolar ventilation increased ( by voluntary hyperventilation), it may take several minutes or the alveolar Po2 and Pco2 to assume their new steady-state values. • The CO2 stores are much greater than the O2 stores (in the form of bicarbonate) • Alveolar Pco2 takes longer to come to equilibrium.
  15. 15. DIFFUSION LIMITATION Po2 difference between alveolar gas and end-capillary blood resulting from incomplete diffusion is immeasurably small
  16. 16. Difference can become larger: • During exercise • When the blood-gas barrier is thickened • If a low O2 mixture is inhaled ( exercising at altitude) Diffusion limitation rarely causes hypoxemia at rest at sea level even when lung disease is present because the red blood cells spend enough time in the pulmonary capillary to allow nearly complete equilibration.
  17. 17. SHUNT • Shunt refers to blood that enters the arterial system without going through ventilated areas of the lung. Consequently, blood passes through a shunt maintaining a mixed venous blood composition. Anatomical: • Right to left shunt, admixture of blood occurs through the atrial and ventricular defect. • Also branch of pulmonary artery connecting directly to pulmonary vein. Physiological: • In bronchial circulation, deoxygenated bronchial venous blood drains directly into oxygenated blood of pulmonary veins.
  18. 18. Pathophysiological scenarios giving rise to shunts: (1) Pulmonary edema (alveoli with fluid) thereby abolishing their ventilation and any gas exchange. (2) Alveolar filling with cellular and micro-organismal debris as in pneumonia, with the same result as in edema. (3) Collapse of a region of lung due to pneumothorax, gas absorption distal to a fully obstructed airway, or to external compression. (4) Rarely, the presence of abnormal arteriovenous vascular channels in the lungs, that can occur in, for example, hepatic cirrhosis. (5) Direct right-to-left vascular communications at the level of the heart or great (extrapulmonary) blood vessels.
  21. 21. • The hypoxemia cannot be abolished by giving the subject 100% O2 to breathe. • This is because the shunted blood that bypasses ventilated alveoli is never exposed to the higher alveolar Po2 > depress the arterial Po2. • A shunt usually does not result in a raised Pco2 > chemoreceptors sense any elevation of arterial Pco2> hyperventilation. • In some patients with a shunt, the arterial Pco2 is low because the hypoxemia increases respiratory drive
  22. 22. VENTILATION AND PERFUSION VENTILATION The rate at which air enters or leaves the lungs. Types : i) Pulmonary Ventilation ii) Alveolar Ventilation 1)Pulmonary Ventilation (minute ventilation): Is the volume of air moving in and out of respiratory tract in a given unit of time during quiet breathing. Pulmonary Ventilation= Tidal volume X Respiratory Rate = 500 ml x 12/minute = 6000 ml/minute
  23. 23. 2) Alveolar ventilation: It is the amount of air utilized for gaseous exchange every minute. Alveolar ventilation = (Tidal volume – Dead space) X Respiratory Rate = ( 500 – 150 ) ml x 12/minute = 4200ml/minute PERFUSION: The movement of blood into the lungs through pulmonary capillaries.
  24. 24. VENTILATION- PERFUSION RATIO • It’s the ratio of alveolar ventilation to blood flow in lung. • In normal individual at rest alveolar ventilation (V) is 4L/min and pulmonary blood flow (Q) is 5lit/min. • The normal ventilation-perfusion ratio is 0.8.
  25. 25. EFFECT OF VENTILATION- PERFUSION INEQUALITY ON OVERALL GAS EXCHANGE  ZERO V/Q: Pulmonary shunt No ventilation but perfusion remains normal. Causes: • Alveolar flooding found in pneumonia and ARDS, • Complete obstruction of the airway • Extrinsic compression of alveoli present in compression, atelectasis due to hydrothorax or pneumothorax.
  26. 26.  LOW V/Q or V/Q<1 Low ventilation relative to its perfusion such as inpartial obstruction of the airways. Causes: • Low compliance such as in pulmonary fibrosis. • Lack of surfactant or due to high airway resistance found in asthma and COPD.
  27. 27. V/Q of Infinity- Dead space No perfusion but ventilation remains normal. Causes: • Embolism • Emphysema • Bronchiectasis
  28. 28. HIGH V/Q or V/Q>1 Low perfusion relative to its ventilation. Causes: Hypotensive states or a partial obstruction of pulmonary blood vessels present in pulmonary embolism may be responsible for a high V/Q.
  29. 29. PATTERN OF DISTRIBUTION OF RATIOS (A) COPD. The blood flow to units of very low ratio would cause arterial hypoxemia and simulate a shunt. (B) Asthma, with a more pronounced bimodal distribution of blood flow than the patient shown in (A).
  30. 30. (C) Bimodal distribution of ventilation in a 60-year-old patient with chronic obstructive pulmonary disease, predominantly emphysema. A similar pattern is seen after pulmonary embolism. (D) Pronounced bimodal distribution of perfusion after a bronchodilator was administered to the patient shown in (B).
  31. 31. REGIONAL GAS EXCHANGE IN THE LUNG • A normal lung has different V/Q ratios in its different regions. This may be attributed to the pull of gravity and the heart’s location relative to the lung. • Airflow and blood flow increase down the lung, but the differences in perfusion are greater than the differences in ventilation. • Blood flow is proportionately greater than ventilation at the base- lower V/Q ratio • Ventilation is proportionately greater than blood flow at the apex- higher V/Q ratio.
  32. 32. VENTILATION- PERFUSION INEQUALITY • V/Q ratio determines the gas exchange in any single lung unit. • Regional differences of V/Q in the upright human lung cause a pattern of regional gas exchange. • V/Q inequality impairs the uptake or elimination of all gases by the lung. • Although the elimination of CO2 is impaired by V/ Q inequality, this can be corrected by increasing the ventilation to the alveoli. • By contrast, the hypoxemia resulting rom V/ Q inequality cannot be eliminated by increases in ventilation.
  33. 33. SUMMARY ■ The magnitudes of ventilation and perfusion, as well as their distribution, are key factors determining pulmonary gas exchange. ■ Distribution of ventilation and perfusion is predominantly affected by gravity in the normal lung, but intrinsic lung structure also plays a role. ■ Distribution of ventilation-perfusion (V A/Q ) ratios is non uniform, the V A/Q ratio being generally higher in nondependent lung regions and lower in dependent lung regions. ■ Regional alveolar PO2 and PCO2 are determined principally by the V A/Q ratio of each region. Secondary factors are the PO2 and PCO2 of inspired gas and mixed venous blood and also the shape of the oxygen and carbon dioxide dissociation curves.
  34. 34. ■ There are four causes of hypoxemia: hypoventilation, alveolar- capillary diffusion limitation, shunt, and V A/Q inequality. ■ There are two principal causes of hypercapnia : hypoventilation and V A/Q inequality. ■ V A/Q inequality is the most important cause of gas exchange abnormalities in most lung diseases.
  35. 35. REFERENCE West respiratory physiology Fishman textbook of pulmonary disease and diorders Guyton physiology Thank You…!!!
  36. 36. In a German tale known as Sleep of Ondine, Ondine is a water nymph. She was very beautiful and, like all nymphs, immortal. However, should she fall in love with a mortal man and bear his child, she would lose her immortality. Ondine eventually falls in love with a handsome knight, Sir Lawrence, and they were married. When they exchange vows, Lawrence vows to forever love and be faithful to her. A year after their marriage, Ondine gives birth to his child. From that moment on she begins to age. As Ondine’s physical attractiveness diminishes, Lawrence loses interest in his wife. One afternoon, Ondine is walking near the stables when she hears the familiar snoring of her husband. When she enters the stable, she sees Lawrence lying in the arms of another woman. Ondine points her finger at him, which he feels as if kicked, waking him up with surprise. Ondine curses him, stating, "You swore faithfulness to me with every waking breath, and I accepted your oath. So be it. As long as you are awake, you shall have your breath, but should you ever fall asleep, then that breath will be taken from you and you will die!"