GAS TRANSFER
C02 and 02 are transported between the environment and the tissues by convection and diffusion (Fig. 17-5). In the blood, 02 combines with hemoglobin, and the resulting 02 saturation is determined by the oxyhemoglobin dissociation curve (Fig. 17-6A). More than 98 per cent of the 02 in the blood travels combined with hemoglobin; the remainder is dissolved in the plasma. Above a Pao2 of 150 mm Hg, hemoglobin is totally saturated and carries 1.34 ml 02/gm hemoglobin; further rises in Pao2 increase only the amount of 02 dissolved in the plasma at the rate of 0.003 ml O2/100 ml blood/mm Hg Po2. C02 is carried in the blood in three forms: bicarbonate (90 per cent), dissolved in plasma, or combined with protein, predominantly hemoglobin. The relationship between the Pco2 and the C02 content is represented by the carboxyhemoglobin dissociation curve (Fig. 17-6B), which is steeper and more linear than the oxyhemoglobin dissociation curve.
A number of factors influence the relationship between Po2 and Pco2 and their contents, which can be described as changes in the shape or position of the respective dissociation curves. Increased Pco2 and temperature and decreased pH shift the oxyhemoglobin dissociation curve to the right, decreasing affinity of hemoglobin for 02 and expediting its release to the tissues. Converse changes in the above factors have the opposite effect. Increased levels of 2,3-DPG, produced during chronic hypoxemia or anemia, also shift the curve to the right, while carbon monoxide shifts it to the left. The most important influence on the carboxy-hemoglobin dissociation curve is Po2; increased Po2 shifts the curve to the right, thus reducing the C02 content for any given Pco2 and assisting in the unloading of C02 in the lungs.
- CARDIOVASCULAR RESPONSE TO EXERCISE
- Lidocaine
- CHIP Perinatal Coverage
- HYPERKINETIC PULMONARY HYPERTENSION
- ARTERJAL BLOOD GASES
- Bleeding Diatheses
- VENTILATION
- CLINICAL MANIFESTATIONS OF MALABSORPTION
- GASTROESOPHAGEAL REFLUX DISEASE
- Liver Failure
- ORIGIN OF ABDOMINAL PAIN
- CARDIOMYOPATHY
- Other Cystic Diseases
- CLINICAL PRESENTATION
- DIAGNOSTIC TECHNIQUES AND THEIR INDICATIONS - IMAGING PROCEDURES
- Conjugated Hyperbilirubinemia
- CLINICAL SYMPTOMS OF ESOPHAGEAL DISEASE
- Vitamin Dresistant Rickets
- PHYSIOLOGY OF THE PULMONARY CIRCULATION
- ETIOLOGY
- Specific Etiologies
- VASCULAR DISEASE OF THE LIVER
- Urinary Tract Infection
- NORMAL ESOPHAGEAL PHYSIOLOGY
- Etiology and Pathogenesis
- CLINICAL PRESENTATION
- EMBOLIC DISEASE
- CARDIAC PACEMAKERS
- Pulmonary Vasculitis
- Pulmonary Infiltrates with Eosinophilia PIE
- DISEASES OF THE ESOPHAGUS
- Pathogenic Mechanisms - Mechanism of Injury
- PERIPHERAL VENOUS DISEASE
- Procainamide
- Mechanism of Proteinuria