IN THE NAME OF GOD

Acute Respiratory Failure Dr.h-kayalha Anesthesiologist

Acute Respiratory Failure Failure in one or both gas exchange functions: oxygenation and carbon dioxide elimination In practice: PaO2<60mmHg or PaCO2>46mmHg Derangements in ABGs and acid-base status 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.

Acute Respiratory Failure Hypercapnic Hypoxemic Mixed ARDS and ALI

Hypercapnic Respiratory Failure PaCO2 >46mmHg Not compensation for metabolic alkalosis (PAO2 - PaO2) normal increased Alveolar Hypoventilation V/Q abnormality Nl VCO2 VCO2 PI max Central Hypoventilation Neuromuscular Problem V/Q Abnormality Hypermetabolism Overfeeding

Hypercapnic Respiratory Failure Alveolar Hypoventilation nlPI max PI max Central Hypoventilation Neuromuscular Disorder Brainstem respiratory depression Drugs (opiates) Obesity-hypoventilation syndrome Critical illness polyneuropathy Critical illness myopathy Hypophosphatemia Magnesium depletion Myasthenia gravis Guillain-Barre syndrome 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.

Hypercapnic Respiratory Failure V/Q abnormality Increased Aa gradient VCO2 Nl VCO2 Hypermetabolism Overfeeding V/Q Abnormality Increased dead space ventilation advanced emphysema PaCO2 when Vd/Vt >0.5 Late feature of shunt-type edema, infiltrates VCO2 is rate of CO2 production. Nl is 90 to 130 L/min/m2, which is 80% of VO2.

Hypercapnic Respiratory Failure V/Q abnormality Increased Aa gradient VCO2 Nl VCO2 Hypermetabolism Overfeeding V/Q Abnormality VCO2 only an issue in pts with limited ability to eliminate CO2 Overfeeding with carbohydrates generates more CO2 VCO2 is rate of CO2 production. Nl is 90 to 130 L/min/m2, which is 80% of VO2.

Hypoxemic Respiratory Failure Is PaCO2 increased? Yes No Hypoventilation (PAO2 - PaO2)? (PAO2 - PaO2) Yes No Hypovent plus another mechanism Is low PO2 correctable with O2? V/Q mismatch No Yes Inspired PO2 Hypoventilation alone High altitude FIO2 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. Respiratory drive Neuromuscular dz Shunt

Hypoxemic Respiratory Failure V/Q mismatch PvO2>40mmHg PvO2<40mmHg DO2/VO2 Imbalance V/Q mismatch DO2 oxygen delivery; VO2 oxygen uptake. Imbalance can aggravate hypoxemia caused by abnl gas exchange in lungs. DO2: anemia, low CO VO2: hypermetabolism

Hypoxemic Respiratory Failure V/Q mismatch Atelectasis Intraalveolar filling Pneumonia Pulmonary edema ARDS Interstitial lung dz Pulmonary contusion SHUNT V/Q = 0 DEAD SPACE V/Q = ∞ Pulmonary embolus Pulmonary vascular dz Airway dz (COPD, asthma) Intracardiac shunt Vascular shunt in lungs

Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome Severe ALI B/L radiographic infiltrates PaO2/FiO2 <200mmHg (ALI 201-300mmHg) * 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

Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome Develops ~4-48h Persists days-wks Diagnosis: Distinguish from cardiogenic edema History and risk factors * 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

Inflammatory Alveolar Injury 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

Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8) 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

Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8) Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium 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

Fluid in interstitium and alveoli Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8) Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium 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 Fluid in interstitium and alveoli

Fluid in interstitium and alveoli Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8) Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium 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 Fluid in interstitium and alveoli Impaired gas exchange  Compliance  PAP

Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome 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 Exudative phase Proliferative phase Fibrotic phase Diffuse alveolar damage

Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome Direct Lung Injury Infectious pneumonia Aspiration, chemical pneumonitis Pulmonary contusion, penetrating lung injury Fat emboli Near-drowning Inhalation injury Reperfusion pulmonary edema - 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

Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome Indirect Lung Injury Sepsis Severe trauma with shock/hypoperfusion Burns Massive blood transfusion Drug overdose: ASA, cocaine, opioids, phenothiazines, TCAs. Cardiopulmonary bypass Acute pancreatitis

Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome Complications Barotrauma Nosocomial pneumonia Sedation and paralysis  persistent MS depression and neuromuscular weakness