1 / 17

6. Mechanisms of Arterial Hypoxemia

jeanne
Download Presentation

6. Mechanisms of Arterial Hypoxemia

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


    1. 6. Mechanisms of Arterial Hypoxemia swood@trinityphysiology.org

    2. Types of Hypoxia Stagnant hypoxia Anemic hypoxia Histotoxic hypoxia Arterial hypoxia, or hypoxemia Methemoglobinemia portrait from Trost, C., The blue people of Troublesome Creek. Science 82, November, pp. 35-39, 1982. Methemoglobinemia portrait from Trost, C., The blue people of Troublesome Creek. Science 82, November, pp. 35-39, 1982.

    3. This slide illustrates the 5 causes of arterial hypoxemia. The A-a gradient is normal in the top two but widened in the other 3. You’ll learn how to differentiate the possible causes in this lecture.This slide illustrates the 5 causes of arterial hypoxemia. The A-a gradient is normal in the top two but widened in the other 3. You’ll learn how to differentiate the possible causes in this lecture.

    4. 1. Low Inspired O2 High altitude, mines (A – a)PO2 = normal

    5. In normal ventilation the A-a PO2 gradient is normal (10 in this example) and the arterial and alveolar PCO2 are normal (40 mmHg is normal for sea level; the normal value at higher altitude locations; e.g., Denver, is lower).In normal ventilation the A-a PO2 gradient is normal (10 in this example) and the arterial and alveolar PCO2 are normal (40 mmHg is normal for sea level; the normal value at higher altitude locations; e.g., Denver, is lower).

    6. The significance of the shape of the CO2 and O2 dissociation curves on V/Q problems is shown here. V/Q mismatch may not cause abnormal CO2 in blood because high V/Q areas of the lung can be compensated by low V/Q areas. This is not the case for O2.The significance of the shape of the CO2 and O2 dissociation curves on V/Q problems is shown here. V/Q mismatch may not cause abnormal CO2 in blood because high V/Q areas of the lung can be compensated by low V/Q areas. This is not the case for O2.

    7. Tetralogy of Fallot A ventricular septal defect Pulmonary stenosis Right ventricular hypertrophy An overriding aorta Draw v and q boxes conceptDraw v and q boxes concept

    8. An unlearned behavior in infants with congenital heart defects is to squat down when they get cyanotic. The squat results in increased peripheral vascular resistance. This reduces the magnitude of the right to left shunt; e.g., ventricular septal defect by elevating left ventricle pressure. Tetralogy Ventral septal defect Pulmonary stenosis Overriding aorta Rt. ventricle hypertrophyAn unlearned behavior in infants with congenital heart defects is to squat down when they get cyanotic. The squat results in increased peripheral vascular resistance. This reduces the magnitude of the right to left shunt; e.g., ventricular septal defect by elevating left ventricle pressure. Tetralogy Ventral septal defect Pulmonary stenosis Overriding aorta Rt. ventricle hypertrophy

    11. Shunt can be measured using a dilution technique illustrated here. It is important to understand that oxygen therapy can not fix a right to left shunt.Shunt can be measured using a dilution technique illustrated here. It is important to understand that oxygen therapy can not fix a right to left shunt.

    12. Diffusion Limitation Diffusion limitation can be “unmasked” by two techniques. Using low inspired oxygen; e.g., 12% O2 or using exercise. The patient with “abnormal” lungs has complete equilibration at sea level (see p. 201) but not with low inspired oxygen as shown above.Diffusion limitation can be “unmasked” by two techniques. Using low inspired oxygen; e.g., 12% O2 or using exercise. The patient with “abnormal” lungs has complete equilibration at sea level (see p. 201) but not with low inspired oxygen as shown above.

    13. Diffusion limitation can be “unmasked” by two techniques. Using low inspired oxygen; e.g., 12% O2 or using exercise. The patient with “abnormal” lungs has complete equilibration at sea level (see p. 201) but not with low inspired oxygen as shown above.Diffusion limitation can be “unmasked” by two techniques. Using low inspired oxygen; e.g., 12% O2 or using exercise. The patient with “abnormal” lungs has complete equilibration at sea level (see p. 201) but not with low inspired oxygen as shown above.

    14. Even though clubbing is a widely recognized symptom of many diseases the physiological mechanism that actually causes clubbing is not well understood. Current understanding is that these diseases cause vasodilation in the distal circulation which leads to hypertrophy of the tissue of the nailbeds and thus to the clubbed fingernails. Other factors that have been implicated are the local effects of growth factors (such as platelet-derived growth factor and hepatocyte growth factor) that are usually sequestrated in the pulmonary capillary bed. Many of the conditions associated with clubbing result in shunting across some of the capillary beds in the pulmonary circulation. Lung cancer, mainly large-cell (35% of all cases), not seen frequently in small cell lung cancer[3] Interstitial lung disease Tuberculosis Bronchiectasis Suppurative lung disease: lung abscess, empyema Cystic fibrosis Pulmonary hypertension Mesothelioma Heart disease: Any disease featuring chronic hypoxia Congenital cyanotic heart disease (most common cardiac cause) Subacute bacterial endocarditis Even though clubbing is a widely recognized symptom of many diseases the physiological mechanism that actually causes clubbing is not well understood. Current understanding is that these diseases cause vasodilation in the distal circulation which leads to hypertrophy of the tissue of the nailbeds and thus to the clubbed fingernails. Other factors that have been implicated are the local effects of growth factors (such as platelet-derived growth factor and hepatocyte growth factor) that are usually sequestrated in the pulmonary capillary bed. Many of the conditions associated with clubbing result in shunting across some of the capillary beds in the pulmonary circulation. Lung cancer, mainly large-cell (35% of all cases), not seen frequently in small cell lung cancer[3] Interstitial lung disease Tuberculosis Bronchiectasis Suppurative lung disease: lung abscess, empyema Cystic fibrosis Pulmonary hypertension Mesothelioma Heart disease: Any disease featuring chronic hypoxia Congenital cyanotic heart disease (most common cardiac cause) Subacute bacterial endocarditis

    15. Flow chart used in differential diagnosis of arterial hypoxemia.Flow chart used in differential diagnosis of arterial hypoxemia.

    16. After an unusually large meal of manioc root (cassava) a Ross student is diagnosed with cyanide poisoning. This type of hypoxia which prevents oxygen uptake by cells is called: A. anemic hypoxia B. stagnant hypoxia C. arterial hypoxia (hypoxemia) D. histotoxic hypoxia

    17. Chronic obstructive pulmonary disease (COPD) involves V/Q mismatch in the lungs. Mixing of the bloods from the below three V/Q units result in an increased (alveolar-arterial) difference for PO2 but not PCO2. One reason for this is: A. Because of the shapes of the O2 & CO2 dissociation curves. B. The Haldane effect compensates for CO2 but not for O2. C. Most low V/Q units are at the top of the lung where the total blood flow is small. D. CO2 is less soluble in blood than O2.

More Related