RESPIRATORY FAILURE

1. University of Medicine and Pharmacy, Iasi School of Medicine ANESTHESIA and INTENSIVE CARE Conf. Dr. Ioana Grigoras MEDICINE 4th year English Program Suport de curs RESPIRATORY FAILURE

2. RESPIRATORY FAILURE Respiration is a fundamental cellular process. Definition = respiratory failure is the incapacity of the body to maintain normal gas exchange at the cellular level as well as the incapacity of maintaining the aerobic metabolism.

3. RESPIRATORY FAILURE Mechanisms of respiratory failure: - the incapacity of the thoracic-pulmonary system to achieve a normal gas exchange at the pulmonary level (pulmonary respiratory failure); - the incapacity of the cardio-vascular system to maintain an optimal tissue perfusion (e.g. referring to the shock states); • the incapacity of tissues to use the oxygen brought by the arterial blood at the cellular level (e.g. septic shock, cyanide poisoning);

4. RESPIRATORY FAILURE Respiration is a function of the respiratory system Definition = the incapacity of the lung to maintain normal levels of oxygen and carbon dioxide in arterial blood.

5. RESPIRATORY FAILURE - partial pressure of oxygen in arterial blood PaO2< 60 mmHg Hypoxemia is the mandatory consequence of respiratory failure. • partial pressure of CO2 in arterial blood PaCO2> 44 mmHg While respiratory failure always means the decrease of PaO2, the alteration of PaCO2 is not the rule.

6. RESPIRATORY FAILURE PaO2 • 60 mm Hg - threshold of hypoxemia is a relative value. • PaO2 which defines respiratory failure is specific to each patient. • It depends on: • the inspiratory fraction of O2 – FiO2 • the patient age • the chronic level of the blood gases

7. RESPIRATORY FAILURE PaO2 Inspiratory fraction of O2: • FiO2 = 0,21 → PaO2= 100mm Hg • FiO2 = 0,4 → PaO2= 200mm Hg • FiO2 = 0,6 → PaO2= 300mm Hg • FiO2 = 1 → PaO2= 500mm Hg respiratory dysfunction / respiratory failure

8. CLASSIFICATION OF RESPIRATORY FAILURE = pathophysiological classification: - hypoxemic RF PaO2< 60mmHg PaCO2</= 40mmHg Synonyms: Type I RF Partial RF Nonventilatory RF - hypoxemic-hypercapnic RF PaO2 < 60mmHg PaCO2> 45 mmHg Synonyms: Type II RF Global RF Ventilatory failure

9. CLASSIFICATION OF RESPIRATORY FAILURE • classification according to the duration of the evolution: - acute RF - chronic RF

10. RESPIRATORY FAILURE Common features of acute RF: - appears within minutes, hours or days; • is associated with • hypoxemia • imbalance of the acid-base status (acidemia or alkalemia); - is a immediate life threatening condition.

11. RESPIRATORY FAILURE Common features of chronic RF: - appears after months/years of evolution; • is associated with • hypoxemia • hypercapnia; - is a potential life threatening condition; - results after a chronic disease or a sequel of an acute/chronic process.

12. RESPIRATORY FAILURE Clinical classification -manifest RF - hypoxemia and hypercapnia at rest - compensated RF a low level of exercise is possible, but results in homeostatic alterations: hypoxemia and respiratory acidosis with metabolic compensation - decompensated RF severe alterations of blood gases, accompanied by alterations of the normal functions of the different tissues (e.g. the brain - respiratory encefalopathy). - latent RF - no signs of RF at rest; - RF is manifest in case of different levels of exercise.

13. RESPIRATORY FAILURE Mechanisms of hypoxemia (RF): • decreased FiO2 • alveolar hypoventilation - ventilation-perfusion mismatch - diffusion alteration - intrapulmonary shunt In clinical practice RF is rarely the result of a single pathophysiological mechanism (e.g. acute obstruction of upper airways). Usually more than one mechanism are associated and are responsible for RF generation.

14. RESPIRATORY FAILURE Decreased oxygen inspiratory concentration: • high altitude • closed spaces • combustion in closed spaces, etc. rare The pulmonary system is normal. RF is a result of external factors. Treatment - removal from the abnormal environment

15. RESPIRATORY FAILURE Alveolar hypoventilation The normal pulmonary gas exchange requires a constant, normal composition of the alveolar gas. The aim of the external ventilation is to preserve this normal composition of the alveolar gas. Alveolar hypoventilation (AH) is the result of alterations in external ventilation (abnormal composition or abnormal volume of the air at the alveolar level) AH concerns evenly all the alveolar spaces. Type II RF (hypoxemia + hypercapnia)

16. ALVEOLAR HYPOVENTILATION Mechanisms of the AH: -restriction of the movements of the thoracic-pulmonary system (amplitude and/or frequency); -obstruction of the airways; -coexistence of the restrictive and obstructive mechanisms.

17. RESTRICTIVE ALVEOLAR HYPOVENTILATION CAUSES: 1.disorders envolving the respiratory center 2. disorders envolving the respiratory neural pathways 3. muscle disorders 4. alteration of the thoracic cage 5. alterations of the thoracic cage content 6. extensive lung tissue diseases, which alter gas exchange

18. RESTRICTIVE ALVEOLAR HYPOVENTILATION 1.disorders envolving the respiratory center • drug overdose • opioids, anaethetics, CO, barbiturates, benzodiazepines, tricyclic antidepresives, etc.; • endogenous or exogenous coma • infections (meningitis, encephalitis); • tumors; • head trauma and increased intracranial pressure • stroke All these conditions may alter the respiratory drive initiated by the respiratory center and cause RF.

19. RESTRICTIVE ALVEOLAR HYPOVENTILATION 2. disorders envolving the respiratory neural pathways: • medullar disorders (trauma, bulbar polio) • intercostal/phrenic nerves damages (trauma, polio) • neuro-muscular junction alterations (myasthenia gravis, neuro-muscular relaxants) All these conditions may alter the transmission of the neural command (stimulus) to the respiratory muscles and cause failure of the external ventilation.

20. RESTRICTIVE ALVEOLAR HYPOVENTILATION 3. muscle disorders • respiratory muscles atrophy ( decreased mass of respiratory muscle) • starvation, cachexia • congenital or acquired muscle dystrophies, miopathies • respiratory muscles weakness ( steady decreased force of contraction) • congenital or acquired muscle dystrophies, • miopathies, hypoKmia, steroid therapy, chronic renal failure • respiratory muscles fatigue ( decreasing force of contraction due to persistent increased respiratory work overload) • the final pathway of any type of RF All patients who die due to RF, die due to type II RF, no matter the initial form (type I or type II) RF

21. RESTRICTIVE ALVEOLAR HYPOVENTILATION 4. alteration of the thoracic cage • thoracic trauma (flail chest) • thoracic cage deformities (scoliosis, kyphosis)

22. RESTRICTIVE ALVEOLAR HYPOVENTILATION 5. alterations of the thoracic cage content • pleural interposition (pneumothorax, massive pleural effusion, tumors) • intrathoracic tumors • elevated diaphragms (massive ascitis, intestinal occlusion, large abdominal tumors ...)

23. RESTRICTIVE ALVEOLAR HYPOVENTILATION 6. extensive lung tissue diseases, which alter gas exchange pulmonary edema pneumonia,etc. Only late stage or severe parenchimal diseases may result in AH

24. OBSTRUCTIVE VENTILATORY FAILURE CAUSES: • upper airway obstruction (nasopharinx, larynx, trachea) • airway obstruction by the tongue • coma, anaesthesia, head trauma, etc. • foreign bodies, fluids • blood, aspirated gastric content, drowning • neck and facial trauma • laryngeal or tracheal tumors • infections • laryngitis, epiglotytis • obstruction of bronchi • aspiration of gastric content, drowning

25. OBSTRUCTIVE VENTILATORY FAILURE The obstruction of the most distal airways does not result in alveolar hypoventilation, but in ventilation-perfusion mismatch because of uneven obstruction of the very numerous small airways. Type II RF (hypoxemia + hypercapnia)

26. ALVEOLAR HYPOVENTILATION Principles of treatment in ventilatory failure: • oxygen therapy • combined with endotracheal intubation and ventilatory support, whenneeded • airways management • mandatory treatment in case of obstructive ventilatory failure • often the procedures are life-saving; • mechanical ventilatory support • substitute of spontaneous respiratory mechanical activity until restauration of normal alveolar ventilation.

27. VENTILATION-PERFUSSION MISMATCH Normal status of the lung is defined by a matching of ventilation and perfusion. Uneven intrapulmonary distibution of the inspired air and/or of the pulmonary blood Zones of hypo/hyperventilation are uneven coupled with zones of hypo/hyperperfusion. The consequence of this imbalance is the impairment of gas exchange.

28. VENTILATION-PERFUSSION MISMATCH Consequences of ventilation-perfusion mismatch: - hypoxemia + normocapnia (CO2 has a great diffusibility; the normally ventilated areas compensate for CO2 elimination in hypoventilated zones). - hypoxemia + hypocapnia (hypoxemia results in hyperventilation with an increased elimination of CO2) - hypoxemia + hypercapnia (highly severe ventilation-perfusion mismatch; may be accompanied by alveolar hypoventilation).

29. VENTILATION-PERFUSSION MISMATCH CAUSES: - pulmonary diseases which affect the airways leading to an uneven distribution of the inspiratory air into the lungs; e.g. chronic bronchitis. - pulmonary diseases with functional or organic impairment of pulmonary vasculature (vasospasm, vascular thrombosis, pulmonary capillary bed distruction, etc.) e.g.: pulmonary embolism, emphysema. In COPD the bronchial and vascular impairment coexist.

30. VENTILATION-PERFUSSION MISMATCH PRINCIPLES OF TREATMENT: - oxygen therapy is efficient. The increased FiO2 leads to improvement of the gas exchange in the hypoventilated areas and to the partial or total correction of hypoxemia. In the chronic RF O2 therapy can withdraw the hypoxic stimulus of ventilation and can cause the worsening of hypoxemia and hypercapnia. - the establishment of airways pattency can contribute to a more even distribution of the inspired flow (aerosols, nebulization, bronhodilators, etc;) • the improvement of the pulmonary blood flow distribution is difficult to achieve; alleviation of pulmonary hypertension, prophylaxis and treatment of pulmonary embolism, etc. • ventilatory support should be initiated in type II RF

31. DIFFUSION IMPAIRMENT Mechanism: The concentration of the O2 in the alveolar air is normal. The hypoxemia is a consequence of an increased oxygen alveolo-arterial gradient. This increased gradient is caused by the impairment of the oxygen diffusion through the alveolo-capillar membrane.

32. DIFFUSION IMPAIRMENT CAUSES: • alterations of the structure and/or thickness of the alveolo-capillary membrane (interstitial edema, alveolar edema, pulmonary fibrosis) - the decrease of the contact time of the arterial blood with the alveolar air (e.g. in pneumonectomy the contact time is decreased because the whole cardiac output passes through the single lung per time unit)

33. DIFFUSION IMPAIRMENT Consequences: • hypoxemia + hypo/normocapnia • CO2 has a 20 fold greater diffusibility compared to O2; • CO2 elimination remains normal even in cases with severe alterations of O2 diffusion

34. DIFFUSION IMPAIRMENT Principles of treatment : - O2 therapy may ameliorate hypoxemia (increased alveolar O2 partial pressure, but the O2 alveolo-arterial gradient remains the same) - the causative treatment is the most important -whenever possible (e.g. the treatment of the pulmonary edema, etc.)

35. INTRAPULMONARY SHUNT Normally there is a small amount of venous blood which contaminates the arterial blood through extrapulmonary pathways (e.g. Tebesius vein) or through intrapulmonary pathways (anastomosis between bronchial and pulmonary circulations) (1% of the cardiac output) The increased shunt fraction is generated by the presence of numerous areas of nonventilated but perfused alveoli. The shunt fraction is measured as percents of cardiac output. When it is more than 15% the hypoxemia is highly severe, even if the pulmonary gas exchange is normal.

36. INTRAPULMONARY SHUNT Acute respiratory distress syndrome (ARDS) acute lung injury (ALI) ARDS severity of intrapulmonary shunt: PaO2/ FiO2: 500 normal < 300 ALI < 200 ARDS

37. INTRAPULMONARY SHUNT Acute respiratory distress syndrome (ARDS) CAUSES: • pulmonary causes: • aspiration of gastric content • smoke or toxic gases inhalation • pulmonary contusion • atelectasis • bacterial or viral pneumonia • systemic causes: • all types of shock • massive transfusion TRALI • acute pancreatitis • polytrauma • extracorporeal circulation

38. Acute respiratory distress syndrome (ARDS) PATHOPHISYOLOGY noncardiogenic pulmonary edema permeability edema • pulmonary or systemic aggresion → ↑permeability of alveolo-capilary membrane (“pulmonary capillary leak syndrome”) • ↑ extravascular lung water (interstitial and alveolar space) (“wet lung”) •  alveoli volume → alveolar collaps (perfused, but unventilated alveoli) →↑ intrapulmonar shunt •  lung volumes (“baby lung”) •  lung compliance • ↑ pulmonary vascular pressure • hypoxemia + hypocapnia (type I RF) – ventilated alveoli compensate for the CO2 removal

39. Acute respiratory distress syndrome (ARDS)

40. Acute respiratory distress syndrome (ARDS) DIAGNOSIS: American European Consesus Conference on ARDS (1994): • acute onset; • pulmonary or systemic conditionassociated with ARDS; • PaO2/FiO2 <200 at any PEEP level; • bilateral infiltrates on chest X-ray; • pulmonary capillary wedge pressure ≤ 18mmHg or absence of clinical/radiological signs of increased left atrial pressure.

41. Acute respiratory distress syndrome (ARDS)

42. Acute respiratory distress syndrome (ARDS) TREATMENT: • treatment of the causative disease • supportive treatment • ventilatory support • PEEP (positive end expiratory pressure) • “open lung strategy” • pressure or volume support • tidal volume 5-6ml/kg • peak airway pressure < 30-35 cmH2O; • respiratory rate 20-22/min; • permisive hypercapnia; • PEEP to correct hypoxemia (usually 10-15 cmH2O); • low FiO2 (preferable <0,6) to maintain SpO2 > 90%; • prone position ventilation; • nonventilatory therapy

43. Acute respiratory distress syndrome (ARDS) PEEP (positive end expiratory pressure) Advantages • Prevention of end-expiratory alveolar colapse • Opening of distal airways • Increase of lung volumes (mainly FRC) • Reduction of intrapulmonary shunt • Facilitation of FiO2 decrease • Prevention of biotrauma Disadvantages • Risk of barotrauma • Hemodynamic instability (increased intrathoracic pressure decreases venous return and decreases cardiac output) • Increased dead space by distension of normal alveoli

44. CLINICAL SIGNS OF RESPIRATORY FAILURE • clinical signs of hypoxemia and hypoxia • clinical signs of hypo/hypercapnia Clinical signs of hypoxemia and hypoxia Simptoms depend on: • rapidity of hypoxemia development, • the degree of hypoxia, • the duration of hypoxia, • the associated alterations of PaCO2.

45. Clinical signs of hypoxemia and hypoxia • respiratory signs: • hyperventilation with tachypnea • hyperventilation may lead to hypocapnia • cardio-circulatory signs: • ↑ adrenergic response: • ↑ cardiac output + tachycardia • cold extremities + profuse diaphoresis • the arterial pressure increases (initially) • cyanosis • cardio-circulatory deterioration: • bradycardia , decreased cardiac output, decreased arterial pressure and cardiac arrest. • central nervous system signs: • fatigue and decreased mental capacity • impressive restlessness, then stupor and coma

46. Clinical signs of hypercapnia • Respiratory signs: • hypoventilation – low breathing rate/volume • Cardio-circulatory signs: • Adrenergic response: tachycardia, increased myocardial contractility • Peripheral vasodilation • Pulmonary vasoconstriction • Acidemia may result in decreased myocardial contractility • CNS signs: • Progresive loss of conciousness (hypercapnic coma) • Cerebral vasodilation

47. DIAGNOSIS OF RF 1.clinical examination may be difficult to be performed at the critically ill patient because: • the patient can be restless, stuporous or comatous • it may be difficult to take the history of the disease when the patient is dyspneic • physical examination may be tiresome to the patient • physical examination may be difficult because of monitoring devices, i.v. lines, etc. Clinical examination is of the main importance in the RF diagnosis because: • can be performed at once during the first contact with the patient • a presumptive diagn. may be evoked before laboratory • it allows the assessment of other organs and systems, producing important keys to final diagnosis • it allows to start emergency treatment

48. DIAGNOSIS OF RF 2. blood gas analysis It allows the measurement of PaO2, PaCO2, pH and other parameters useful in the interpretation of the acid-base status. Blood gas analysis is very important in the RF diagnosis because • proves the existence of hypoxemia • differentiates the forms of RF(type I and II) • assessment of the severity degree of hypoxemia • assessment of the presence of the metabolic compensations, • allowing to differentiate between acute and chronic RF • it allows the assessment of evolving RF before the moment of • time when the clinical signs are diagnostic.

49. DIAGNOSIS OF RF 3. radiology and laboratory • Radiological methods of examination offer data on the morphology and not on functional status of the respiratory system. Are contributive to the etiologic diagnosis, but are irrelevant in the diagnosis of RF. • Laboratory is orientative for the etiologic diagnosis and for the assessment of functional and organic involvement of other organs.

50. PULMONARY EMBOLISM