4. Hypercapnic Respiratory Failure (PAO2 - PaO2) Alveolar Hypoventilation V/Q abnormality PI max increased normal Nl VCO2 PaCO2 >46mmHg Not compensation for metabolic alkalosis Central Hypoventilation Neuromuscular Problem VCO2 V/Q Abnormality Hypermetabolism Overfeeding
5.
6. Hypercapnic Respiratory Failure (PAO2 - PaO2) Alveolar Hypoventilation V/Q abnormality PI max increased normal Nl VCO2 PaCO2 >46mmHg Not compensation for metabolic alkalosis Central Hypoventilation Neuromuscular Problem VCO2 V/Q Abnormality Hypermetabolism Overfeeding
7. Hypercapnic Respiratory Failure Alveolar Hypoventilation Brainstem respiratory depression Drugs (opiates) Obesity-hypoventilation syndrome PI max Central Hypoventilation Neuromuscular Disorder nl PI max Critical illness polyneuropathy Critical illness myopathy Hypophosphatemia Magnesium depletion Myasthenia gravis Guillain-Barre syndrome
8. Hypercapnic Respiratory Failure (PAO2 - PaO2) Alveolar Hypoventilation V/Q abnormality PI max increased normal Nl VCO2 PaCO2 >46mmHg Not compensation for metabolic alkalosis Central Hypoventilation Neuromuscular Disorder VCO2 V/Q Abnormality Hypermetabolism Overfeeding
Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg. Furthermore, respiratory failure may be acute or chronic. While acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.
Alveolar hypoventilation can cause both hypoxemia and hypercapnia. In trauma, we see this acutely when pts splint from painful rib fxs - tire out, need intubation. Maximum inspiratory pressure.
VCO2 is rate of CO2 production. Nl is 90 to 130 L/min/m2, which is 80% of VO2.
VCO2 is rate of CO2 production. Nl is 90 to 130 L/min/m2, which is 80% of VO2.
VCO2 is rate of CO2 production. Nl is 90 to 130 L/min/m2, which is 80% of VO2.
This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.
This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.
DO2 oxygen delivery; VO2 oxygen uptake. Imbalance can aggravate hypoxemia caused by abnl gas exchange in lungs.
* pulmonary oedema * normal vascular pedicle * no cardiomegaly or upper lobe blood diversion * when pulmonary vessels can be distinguished they are often constricted * septal lines usually absent because capillary leak occurs directly into alveolar spaces (cf cardiogenic pulmonary oedema) * progressive lung destruction and transition from alveolar to interstitial opacities Chronic phase * fibrosis * focal emphysema
* pulmonary oedema * normal vascular pedicle * no cardiomegaly or upper lobe blood diversion * when pulmonary vessels can be distinguished they are often constricted * septal lines usually absent because capillary leak occurs directly into alveolar spaces (cf cardiogenic pulmonary oedema) * progressive lung destruction and transition from alveolar to interstitial opacities Chronic phase * fibrosis * focal emphysema
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
Direct Lung Injury : a) PNA and aspiration of gastric contents or other causes of chemical pneumonitis b) pulmonary contusion, penetrating lung injury c) fat emboli d) near drowning e) inhalation injury f) reperfusion pulm edema after lung transplant Indirect lung injury a) sepsis b) severe trauma w/ shock hypoperfusion c) drug over dose d) cardiopulmonary bypass e) acute pancreatitis f) transfusion of multp blood products
Indirect lung injury a) sepsis b) severe trauma w/ shock hypoperfusion c) drug over dose d) cardiopulmonary bypass e) acute pancreatitis f) transfusion of multp blood products
patients with ALI/ARDS at 10 centers, 861 patients Patients randomized to tidal volumes of 12 mL /kg or 6 ml/kg(volume control, assist control, plat Press = 30 cm H2O) 22% reduction in mortality in patients receiving smaller tidal volume Number-needed to treat: 12 patients
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