Acute Respiratory Failure

1. Acute Respiratory Failure

2. Classification of respiratory insufficiency according to L. Usenko (1993): • A. Primary (caused by disorders of external respiration). Reasons: • airway patency disorders (obstruction with tongue, vomit, mucus, gastric contents, foreign bodies; laryngeal spasm, etc.) • central nervous system disorders (intoxication, brain injuries, haemorrhages, inflammations, etc.) • disorders of respiratory muscles activity (myasthenia, botulism, tetanus, muscle relaxants, etc.) • defects of chest structure or functional chest disorders ( chest injuries, limited diaphragm mobility – for example due to enteroparesis) • disorders of pulmonary compliance (pneumonia, bronchiolitis, atelectasis, “shock lung” syndrome, etc.) • disorders of ventilation-perfusion system (irregularity of ventilation and perfusion during artificial ventilation, pulmonary oedema, etc.)

3. B. Secondary (caused by inability of blood to contain enough oxygen for metabolic needs of tissues or disorders of transportation and cellular consumption). • Respiratory insufficiency is characterized with hypoxia (“lowering of the oxygen”). Hypoxia occurs in case of: • 1. Inability of external respiration to provide arterial blood with enough amount of oxygen (hypoxic hypoxia) • 2. Lowering of oxygen amount due to anaemia - decreased level of haemoglobin, red blood cells or appearance of their atypical forms (haemic hypoxia). • 3. Inability of cardiovascular system to provide systemic and pulmonary circulation enough for metabolic needs of the body (circulatory hypoxia). • 4. Disorders of oxidative phosphorylation on cellular level of different organs and systems (tissue hypoxia).

4. Symptoms of acute respiratory failure are really various. • Central nervous system. Conscious patients can complain of breathlessness (feeling of the air-lack), difficult inspiration or expiration. Due to development of hypoxia patients become restless, anxious, and sometimes euphoric; they can not evaluate critically their condition or environment. Terminal stages of insufficiency show total CNS inhibition – comatose state (hypoxic or hypercapnic). Quite often, especially in children, convulsions appear. • Skin and mucosa are mirror of respiratory insufficiency: their changes are quite illustrative. • In case of external respiration disorders the amount of oxygenated haemoglobin is decreased and thus quantity of reduced haemoglobin. Arterial blood becomes “venous” (dark): skin and mucosa become cyanotic (blue, purple). First of all their colour change lips, nail plates, earlobes, afterwards face and other body parts. In case of anaemic patients with haemoglobin level 60 grams per litre and lower skin stays pale even in terminal stages of respiratory insufficiency. In case of cyanic and carbon monoxide intoxication skin, nail plates and mucosa turn bright pink, although patients are greatly suffering from hypoxia. Hydrosis is quite significant feature of hypercapnia. Terminal respiratory insufficiency is characterized with dark-grey color cold skin covered with clammy sweat.

5. Disorders of external respiration are the most obvious symptoms of respiratory insufficiency. Clinically in case of those patients next symptoms might be observed: • complete breathing arrest (apnea); • low respiratory rate – less than 12 per minute (bradypnea); • high respiratory rate – more than 20 per minute (tachypnea); • shallow breathing (respiratory volume less than 5 ml per kilogram of body weight); • respiratory “anarchy” (irregular breathing with pauses and uneven amplitude of respiratory movements);

6. pathological types of respiration: • Cheyne-Stokes breathing (periods of apnea, which are followed with chaotic frequent breathing); • Biot’s breathing (periods of apnea which are followed with breathing of equal amplitude); • Difficult breathing (noticeable at a distance, correlation between inspiration and expiration is violated, with active participation of additional muscles): • 1.      inspiratory dyspnea (difficult inspiration) – inspiration is prolonged, intercostals spaces, jugular fossa and subclavian fossa are retracted; sometimes stridorous noise can be heard • 2.      expiratory dyspnea (difficult expiration) – patients should make a great physical effort in order to exhale; exhalation is prolonged, noisy, heard at a distance; chest is enlarged, becomes barrel shaped

7. 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

8. Acute Respiratory Failure • Hypercapnic v Hypoxemic respiratory failure • ARDS and ALI

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

10. The Case of Patient RV 71M s/p L AKA revision. PMH: CAD s/p CABG, COPD on home O2 and CPAP, DM, CVA, atrial fibrillation PACU: L pleural effusion, hypotension, altered mental status. Sent to ICU for monitoring. POD#1: RR overnight, intermittently hypoxic. BiPAP 40%: 7.34/65/63/35/+10 Preintubation: 7.28/91/81/43

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

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

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

15. Hypercapnic Respiratory Failure V/Q abnormality VCO2 Increased Aa gradient Nl VCO2 Hypermetabolism Overfeeding V/Q Abnormality

17. Hypercapnic Respiratory Failure V/Q abnormality VCO2 Increased Aa gradient 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

18. Hypercapnic Respiratory Failure V/Q abnormality VCO2 Increased Aa gradient Nl VCO2 Hypermetabolism Overfeeding V/Q Abnormality • VCO2 only an issue in pts with ltd ability to eliminate CO2 • Overfeeding with carbohydrates generates more CO2

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

20. The Case of Patient ES 77F s/p MVC. Injuries include multiple L rib fxs, L hemopneumothorax s/p chest tube placement, L iliac wing fx. PMH: atrial arrhythmia, on coumadin. INR>2 HD#1 RR 30s and shallow. Pain a/w breathing deeply. Placed on BiPAP overnight PID#1 BiPAP 80%: 7.45/48/66/32/+10

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

22. Hypoxemic Respiratory Failure V/Q mismatch PvO2<40mmHg PvO2>40mmHg DO2/VO2 Imbalance V/Q mismatch DO2: anemia, low CO VO2: hypermetabolism

23. 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

24. 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

26. Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome • Severe ALI • B/L radiographic infiltrates • PaO2/FiO2 <200mmHg (ALI 201-300mmHg) • No e/o L Atrial P; PCWP<18

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

29. Inflammatory Alveolar Injury

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

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

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

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

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

35. 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 s/p lung transplant

36. 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

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

38. Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome • 861 patients, 10 centers • Randomized • Tidal Vol 12mL/kg PDW, PlatP<50cmH2O • Tidal Vol 6mL/kg PDW, PlatP<30cmH2O • NNT 12 • 31% mortality v 39.8% • 65.7% breathing without assistance by day 28 v 55% • Significantly more ventilator-free days • Significantly more days without failure of nonpulmonary organs/systems