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RESPIRATORY FAILURE

RESPIRATORY FAILURE. Sevda Özdoğan MD, prof. Chest Diseases. Definition. If PaO2 <55 mmHg and/or PaCO2>45 mmHg in arterial blood gas values of a resting person who inhales room air on the sea level, the condition is called Respiratory Failure.

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RESPIRATORY FAILURE

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  1. RESPIRATORY FAILURE Sevda Özdoğan MD, prof. Chest Diseases

  2. Definition • If PaO2 <55 mmHg and/or PaCO2>45 mmHg in arterial blood gas values of a resting person who inhales room air on the sea level, the condition is called Respiratory Failure Respiratory failure is a condition in which the respiratory system fails in its gas exchanging functions.

  3. Normal ABG values pH 7.35 – 7.45 PCO2 35 – 45 mmHg PO2 80 – 100 mmHg HCO3 22 – 26 mmol/L BE -2 - +2 SaO2 >95%

  4. Acidosis Alkalosis pH > 7.45 PCO2 < 35 HCO3 > 26 pH < 7.35 PCO2 > 45 HCO3 < 22

  5. Respiratory Acidosis • Think of CO2 as an acid • failure of the lungs to exhale adequate CO2 • pH < 7.35 • PCO2 > 45 • CO2 + H2CO3  pH

  6. Metabolic Acidosis • failure of kidney function •  blood HCO3 which results in  availability of renal tubular HCO3 for H+ excretion • pH < 7.35 • HCO3 < 22

  7. Respiratory Alkalosis • too much CO2 exhaled (hyperventilation) •  PCO2, H2CO3 insufficiency =  pH • pH > 7.45 • PCO2 < 35

  8. Metabolic Alkalosis •  plasma bicarbonate • pH > 7.45 • HCO3 > 26

  9. Definition • If PaO2 <55 mmHg and/or PaCO2>45 mmHg in arterial blood gas values of a resting person who inhales room air on the sea level, the condition is called Respiratory Failure Respiratory failure is a condition in which the respiratory system fails in its gas exchanging functions.

  10. Acute Chronic Hypoxemic Hypercapnic (Mixed) Classification

  11. Acute Respiratory Failure (ARF) • Characterized by acute life-treatening (reversible) derangements in ABG and acid-base status • Usually the patients do not have an underlying pulmonary disease • As the CO2 values increases rapidly respiratory acidosis occurs • Kardiogenic pulmonary edema • Respiratory depressing drug intoxications

  12. Acute respiratory failure can occur in patients who already have chronic respiratory failure • Eg: Acute exacerbations in advanced COPD patients • 5 mm Hg or more increase in the stable PaCO2 value is diagnostic

  13. Chronic Respiratory Failure (CRF) • Develops over several days or longer and may be clinically inapparent • Patients have an underlying disease • Neuromusculer disease • Advanced interstitial lung disease etc • Chronic hypoxemia and/or hypercapnia is irreversible with slow progression • Hypercapnia is compansated by metabolic alkalosis so pH remains in normal limits

  14. Hypoxemic Respiratory Failure(Type I; Pulmonary Failure) • PaO2< 55 mmHg • PaCO2 normal or decreased • Acute and chronic forms of HRF can not be differentiated only by ABG analysis • Polystemia and corpulmonale is common in chronic hypoxemia • The initial signs of acute hypoxemia are usually confusion and neurologic signs due to cerebral edema (impaired tissue oxygenation)

  15. Tissue oxygenation is not only affected by PaO2 but also by cardiac output and hemoglobine concentration

  16. Three pathophysiologic mechanisms account for the hypoxemia • Ventilation/Perfusion (V/Q) mismatch • Decreased perfusion in the areas of good ventilation (dead space ventilation)seen in • pulmonary embolism, • pneumothorax • asthma • localised pneumonia,

  17. Right to left shunt • Perfusion of nonventilated areas of the lung causes right to left shunt • Massive pulmonary hemorragie, • drowning, • diffuse pneumonia, • pulmonary edema (ARDS or Cardiac) • Diffusion limitation • Thickening in the alveolocapillary membrane causes diffusion abnormalities • İnterstitial lung diseases

  18. Hypercapnic Respiratory Failure(Type II; Pump failure) • PaCO2>45 mmHg and pH<7.30 in acute form (Respiratory acidosis) Eg: • Drug overdose • Trauma • Cerebrovascular accident • Infections • Chronic hypercapnia is compansated by metabolic alkalosis so pH remains within normal limits • Neuromusculer diseases • Thorax deformities • Advanced COPD

  19. Hypercapnic Respiratory Failure • Two pathophysiologic mechanisms account for the hypercapnia • Alveolar hypoventilation • A decrease in minute ventilation without dead space ventilation cause hypercapnia (CNS, neuromusculer or chest wall diseases) PaO2 is also decreased but (PAO2-PaO2) is normal • V/Q mismatch • Dead space ventilation is increased with normal minute ventilation (airway diseases like COPD, asthma)

  20. Types of respiratory failure and and the frequent causes

  21. Alveoloarterial oxygen gradient (PAO2-PaO2) PAO2-PaO2=[PıO2-PaCO2/R]-PaO2 PıO2: inspired PO2 R: Respiratory exchange ratio=0.8

  22. PıO2=(PB-PH2O)(FiO2) (760-47)(21) = 149 PAO2-PaO2=[PıO2-PaCO2/R]-PaO2 =[149-PaCO2/0.8]-PaO2

  23. Acute Hypoxemic Respiratory Failure:Acute Respiratory Distress Syndrome (ARDS) • Acute severe alteration in lung structure and function due to several causes. It is characterized by acute dyspnea, severe hypoxemia, diffuse radiographic infiltrates. • It is a pulmonary edema due to increased vascular permeability

  24. Direct insult Pulmonary contusion* Toxic gas inhalation* Neardrowning Pulmonary infection* Gastric aspiration* Pulmonary embolism Thoracic radiation Radiologic Contrast Indirect insult Septisemia* Multisystem trauma* Hypertransfusion* Acute pancreatitis Drug overdose (Neurogenic) DIC Cardiyopulmonary by-pass High altitude Lung reexpansion Risk Factors for ARDS

  25. Insult direct/indirect Inflamation Cellular Neutrophyl Macrophage/monocyt Lymphocyt Humoral Compleman Coagulation, Fibrinolysis Mediators Cytokines Lipid mediators Oxygen radicales Proteases Nitric oxid Growth factors Neuropeptides

  26. Direct insult Pulmonary epithelium and alveoli are subjected to the initial injury Alveolar filling by edema, fibrin, collagen, neutrophlic aggregates and/or blood Pulmonary consolidation Indirect insult pulmonary endothelial cell is subjected to the initial injury by mediators released from extrapulmonary foci Microvessel congestion and interstitial edema Intra-alveolar spaces are relatively spared

  27. Pulmonary arterial pressure is increased in ARDS (>30 mmHg)

  28. Clinical manifestation • Acute dyspnea, hypoxia, bilateral diffuse infiltration occuring most often 12-48 hours of the predisposing event (up to 5 days) • Diagnosis: • Chest radiogram • ABG analysis • Risk factor evaluation

  29. Hypoxia is refractory to oxygen treatment • There are no signs of left atrial hypertension (Pulmonary wedge pressure <18 mm Hg) • ALI/ARDS

  30. Diagnostic criteria for ALI and ARDS

  31. Differential diagnosis • Cardiac pulmonary edema • Infectious causes that cause diffuse pulmonary infiltrates and acute respiratory failure • Non infectious causes

  32. Bacterial pneumonia (S aureus, streptococus, legionella, salmonella, tb, mycoplasma, chlamydia) Viral pneumonia (CMV, RSV, HSV, VZV, adenovirus, influensa) Fungi H capsulatum, coccidioides immitis, cryptococcus) Parasites (PCP, Toxoplasma, strongiloides stercoralis) Infectious causes of acute respiratory failure

  33. Cardiovascular Congestive heart failure Drugs Aspirin Heroin Toxic gas inhalation Tricyclic antidepressants Acute radiation Idiopathic Acute eosinophyl.pn Acute interstitial pn BOOP Idyopatic inters. Pn sarcoidosis Immunologic Acute lupus pneumonitis Goodpasture’s sydr İdy. Hemosiderosis Hypersensitivity pn Pulmonary vasculitis with hemorragia Metabolic Alveolar proteinosis Neoplastic Lymphangitic carsinomatosis Leukemic infiltration Lymhoma Miscellaneous Fat, amnion embolism High altitude edema Noninfectious causes of acute respiratory failure

  34. Treatment • Treatment of the predisposing factor • Cardiovascular supportive care • Mechanic ventilation • Fluid management • Pharmacological treatment

  35. Cardiogenic Pulmonary Edema • Radiology of cardiac edema with central alveolar consolidation (bat wing pattern) • Increased cardiothoracic index • Increased pulmonary wedge pressure (>18 mm Hg)

  36. Radiology of non cardiac pulmonary edema with the differences of cardiac edema

  37. Cardiogenic pulmonary edema

  38. Radiology of a casulty of 1999 Izmit earthquake (ARDS)

  39. 15.July 16.July 17.July 22.July ARDS due to Gr(-) sepsis

  40. 21. May 23. May 26. May 29 .May 21.May ARDS occured 24 hours after a traffic accident. Resolution due to MV on May 26 but progression on May 29

  41. Pulmonary edema

  42. Positional redistribution of the densities due to gravity

  43. Ground grass appearance and pneumotocel formation on CT

  44. Prognosis of respiratory failure • Morbidity and mortality depends on degree of respiratory failure and the underlying disease • Mortality is higher in old age with acute hypercapnic respiratory failure • In COPD patients with acute respiratory failure mortality is 10-20% • In ARDS patients mortality is around 50%

  45. THE END

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