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Pathophysiology of Respiratory Failure

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Pathophysiology of Respiratory Failure

  1. 1. Pathophysiology of Respiratory Failure Gamal Rabie Agmy ,MD ,FCCP Professor of Chest Diseases, Assiut University
  2. 2. Non Respiratory Functions Biologically Active Molecules: *Vasoactive peptides *Vasoactive amines *Neuropeptides *Hormones *Lipoprotein complexes *Eicosanoids
  3. 3. Non Respiratory Functions Haemostatic Functions Lung defense : *Complement activation *Leucocyte recruitment *Cytokines and growth factors Protection Vocal communication Blood volume/ pressure and pH regulation
  4. 4. Respiratory Functions *Oxygenation *CO2 Elimination
  5. 5. Definition *Failure in one or both gas exchange functions: oxygenation and carbon dioxide elimination *In practice: PaO2<60mmHg or PaCO2>50mmHg *Derangements in ABGs and acid-base status
  6. 6. Definition Respiratory failure is a syndrome of inadequate gas exchange due to dysfunction of one or more essential components of the respiratory system
  7. 7. Types of Respiratory Failure Type 1 (Hypoxemic ): * PO2 < 60 mmHg on room air. Type 2 (Hypercapnic / Ventilatory): *PCO2 > 50 mmHg Type 3 (Peri-operative): *This is generally a subset of type 1 failure but is sometimes considered separately because it is so common. Type 4 (Shock): * secondary to cardiovascular instability.
  8. 8. The respiratory System Lungs Respiratory pump Pulmonary Failure Ventilatory Failure • PaO2 • PaO2 • PaCO2 N/ • PaCO2 Hypoxic Respiratory Failure Hypercapnic Respiratory Failure
  9. 9. Cardiogenic pulmonary edema Post surgery changes Hypoxic Pneumonia pulmonary ARDS Atelectasis Respiratory Failure extra pulmonary ARDS Infiltrates in immunsuppression Trauma Pulmonary fibrosis Aspiration
  10. 10. Brainstem Airway Lung Spinal cord Nerve root Nerve Pleura Chest wall Neuromuscular junction Respiratory muscle Sites at which disease may cause ventilatory disturbance
  11. 11. Type 3 (Peri-operative) Respiratory Failure Residual anesthesia effects, postoperative pain, and abnormal abdominal mechanics contribute to decreasing FRC and progressive collapse of dependant lung units.
  12. 12. Type 3 (Peri-operative) Respiratory Failure Causes of post-operative atelectasis include; *Decreased FRC *Supine/ obese/ ascites *Anesthesia *Upper abdominal incision *Airway secretions
  13. 13. Type 4 (Shock) Type IV describes patients who are intubated and ventilated in the process of resuscitation for shock • Goal of ventilation is to stabilize gas exchange and to unload the respiratory muscles, lowering their oxygen consumption *cardiogenic *hypovolemic *septic
  14. 14. Hypoxemic Respiratory Failure (Type 1) Causes of Hypoxemia 1. 2. 3. 4. 5. 6. Low FiO2 (high altitude) Hypoventilation V/Q mismatch (low V/Q) Shunt (Qs/Qt) Diffusion abnormality low mixed venous oxygen due to cardiac desaturation with one of above mentioned factors.
  15. 15. Hypoxemic Respiratory Failure (Type 1) Physiologic Causes of Hypoxemia Low FiO2 is the primary cause of ARF at high altitude and toxic gas inhalation
  16. 16. Hypoxemic Respiratory Failure (Type 1) Physiologic Causes of Hypoxemia However, the two most common causes of hypoxemic respiratory failure in the ICU are V/Q mismatch and shunt. These can be distinguished from each other by their response to oxygen. V/Q mismatch responds very readily to oxygen whereas shunt is very oxygen insensitive.
  17. 17. V/Q: possibilities ∞ 0 1 V/Q =1 is “normal” or “ideal” V/Q =0 defines “shunt” V/Q =∞ defines “dead space” or “wasted ventilation”
  18. 18. Hypoxemic Respiratory Failure (Type 1) V/Q Mismatch V/Q>1 V/Q<1 V/Q=o V/Q=∞
  19. 19. Optimal V/Q matching
  20. 20. Dead Space
  21. 21. Shunt
  22. 22. Why does “V/Q mismatch” cause hypoxemia? • Low V/Q units contribute to hypoxemia • High V/Q units cannot compensate for the low V/Q units • Reason being the shape of the oxygen dissociation curve which is not linear
  23. 23. Hypoxic respiratory failure • Gas exchange failure • Respiratory drive responds • Increased drive to breathe – Increased respiratory rate – Altered Vd /Vt (increased dead space etc) – Often stiff lungs (oedema, pneumonia etc) Increased load on the respiratory pump which can push it into fatigue and precipitate secondary pump failure and hypercapnia
  24. 24. Hypoxemic Respiratory Failure (Type 1) Types of Shunt 1. Anatomical shunt 2. Pulmonary vascular shunt 3. Pulmonary parenchymal shunt
  25. 25. Hypoxemic Respiratory Failure (Type 1) Common Causes for Shunt 1. Cardiogenic pulmonary edema 2. Non-cardiogenic pulmonary edema (ARDS) 3. Pneumonia 4. Lung hemorrhage 5. Alveolar proteinosis 6. Alveolar cell carcinoma 7. Atelectasis
  26. 26. Causes of increased dead space ventilation *Pulmonary embolism *Hypovolemia *Poor cardiac output, and *Alveolar over distension.
  27. 27. Ventilatory Capacity versus Demand Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue. Ventilatory demand is the spontaneous minute ventilation that results in a stable PaCO 2. Normally, ventilatory capacity greatly exceeds ventilatory demand.
  28. 28. Ventilatory Capacity versus Demand Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller. Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing.
  29. 29. Components of Respiratory System *CNS or Brain Stem *Nerves *Chest wall (including pleura, diaphragm) * Airways * Alveolar–capillary units *Pulmonary circulation
  30. 30. Type 2 ( Ventilatory /Hypercapnic Respiratory Failure) Causes of Hypercapnia 1. Increased CO2 production (fever, sepsis, burns, overfeeding) 2. Decreased alveolar ventilation • decreased RR • decreased tidal volume (Vt) • increased dead space (Vd)
  31. 31. Hypercapnic Respiratory Failure • Depressed drive: Drugs, Myxoedema,Brain stem lesions and sleep disordered breathing • Impaired neuromuscular transmision: phrenic nerve injury, cord lesions, neuromuscular blokers, aminoglycosides, Gallian Barre syndrome, myasthenia gravis, amyotrophic lateral sclerosis, botulism • Muscle weakness: fatigue, electrolyte Derangement ,malnutrition , hypoperfusion, myopathy, hypoxaemia • Resistive loads; bronchospasm, airway edema ,secretions scarring ,upper airway obstruction, obstructive sleep apnea • Lung elastic loads:PEEPi, alveolar edema, infection, atelectasis • Chest wall elastic loads:pleural effusion, pneumothorax, flail chest, obesity,ascites,abdominal distension
  32. 32. Hypercapnic Respiratory Failure PaCO2 >50mmHg Not compensation for metabolic alkalosis (PAO2 - PaO2) normal Alveolar Hypoventilation NPI max Central Hypoventilation PI max Neuromuscular Disorder increased V/Q abnormality Nl VCO2 V/Q Abnormality VCO2 Hypermetabolism Overfeeding
  33. 33. Hypercapnic Respiratory Failure V/Q abnormality Increased Aa gradient VCO2 Nl VCO2 V/Q Abnormality Hypermetabolism Overfeeding
  34. 34. Hypercapnic Respiratory Failure V/Q abnormality Increased Aa gradient VCO2 Nl VCO2 V/Q Abnormality • Increased dead space ventilation • advanced emphysema • PaCO2 when Vd/Vt >0.5 • Late feature of shunt-type • edema, infiltrates Hypermetabolism Overfeeding
  35. 35. Hypercapnic Respiratory Failure V/Q abnormality Increased Aa gradient VCO2 Nl VCO2 V/Q Abnormality Hypermetabolism Overfeeding • VCO2 only an issue in pts with ltd ability to eliminate CO2 • Overfeeding with carbohydrates generates more CO2
  36. 36. Hypoxemic Respiratory Failure Yes Is PaCO2 increased? (PAO2 - PaO2)? Hypoventilation (PAO2 - PaO2) Hypoventilation alone No Yes Hypovent plus another mechanism Respiratory drive Neuromuscular dz Is low PO2 correctable with O2? No Shunt Yes No Inspired PO2 High altitude FIO2 V/Q mismatch
  37. 37. Hypercapnic Respiratory Failure PaCO2 >50 mmHg Not compensation for metabolic alkalosis (PAO2 - PaO2) normal Alveolar Hypoventilation PI max Central Hypoventilation NPI max Neuromuscular Problem increased V/Q abnormality N VCO2 V/Q Abnormality VCO2 Hypermetabolism Overfeeding
  38. 38. Hypercapnic Respiratory Failure Alveolar Hypoventilation PI max Central Hypoventilation Brainstem respiratory depression Drugs (opiates) Obesity-hypoventilation syndrome N PI max Neuromuscular Disorder Critical illness polyneuropathy Critical illness myopathy Hypophosphatemia Magnesium depletion Myasthenia gravis Guillain-Barre syndrome
  39. 39. Evaluation of Hypercapnia NIF (negative inspiratory force). This is a measure of the patient's respiratory system muscle strength. It is obtained by having the patient fully exhale. Occluding the patient's airway or endotracheal tube for 20 seconds, then measuring the maximal pressure the patient can generate upon inspiration. NIF's less than -20 to -25 cm H2O suggest that the patient does not have adequate respiratory muscle strength to support ventilation on his own.
  40. 40. Evaluation of Hypercapnia P0.1 max. is an estimate of the patient's respiratory drive. This measurement of the degree of pressure drop during the first 100 milliseconds of a patient initiated breath. A low P0.1 max suggests that the patient has a low drive and a central hypoventilation syndrome. Central hypoventilation vs. Neuromuscular weakness central = low P0.1 with normal NIF Neuromuscular weakness = normal P0.1 with low NIF
  41. 41. A-a Gradient n The P (A—a)O2 ranges from 10 mm Hg in young patients to approximately 25mm Hg in the elderly while breathing room air. n P (A-a)O2 Shunt • if greater than >300 < 300 = V/Q mismatch on 100% = RULE OF THUMB The mean alveolar-to-arterial difference [P(A—a)o2] increases slightly with age and can be estimated ~ by the following equation: Mean age-specific P(A—a)O2 age/4 + 4
  42. 42. Increased Work of Breathing Work of breathing is due to physiological work and imposed work. Physiological work involves overcoming the elastic forces during inspiration and overcoming the resistance of the airways and lung tissue Imposed Work of Breathing In intubated patients, sources of imposed work of breathing include: n n n the endotracheal tube, ventilator Circuit auto-PEEP due to dynamic hyperinflation with airflow obstruction, as is commonly seen in the patient with COPD. Increased Work of Breathing n Tachypnea is the cardinal sign of increased work of breathing n Overall workload is reflected in the minute volume needed to maintain normocapnia.
  43. 43. Pediatric considerations The frequency of acute respiratory failure is higher in infants and young children than in adults for several reasons.
  44. 44. Pediatric considerations Neonates are obligate nose breathers. This nose breathing occurs until the age of 2-6 months because of the close proximity of the epiglottis to the nasopharynx. Nasal congestion can lead to significant distress in this age group.
  45. 45. Pediatric considerations The airway size is smaller. Size is one of the primary differences in infants and children younger than 8 years when compared with older patients.
  46. 46. Pediatric Consideration The epiglottis is larger and more horizontal to the pharyngeal wall. The cephalad larynx and large epiglottis makes laryngoscopy more challenging.
  47. 47. Pediatric Consideration Infants and young children have a narrow subglottic area. In children, the subglottic area is cone shaped, with the narrowest area at the cricoid ring. A small amount of subglottic edema can lead to significant narrowing, increased airway resistance, and increased work of breathing. Older patients and adults have a cylindrical airway that is narrowest at the glottic opening.
  48. 48. Pediatric considerations In slightly older children, adenoidal and tonsillar lymphoid tissue is prominent and can contribute to airway obstruction. The intrathoracic airways and lung include the conducting airways and alveoli, the interstitia, the pleura, lung lymphatics, and the pulmonary circulation.
  49. 49. Pediatric considerations Infants and young children have fewer alveoli. The number dramatically increases during childhood, from approximately 20 million after birth to 300 million by 8 years of age. Therefore, infants and young children have less area for gas exchange. The alveolus is smaller. Alveolar size increases from 150-180 mcm to 250-300 mcm during childhood.
  50. 50. Pediatric considerations Collateral ventilation is less developed, making atelectasis more common. During childhood, anatomic channels form to provide collateral ventilation to alveoli. These pathways exist between adjacent alveoli (pores of Kohn), bronchiole and alveoli (Lambert channel), and adjacent bronchioles. This important feature allows alveoli to participate in gas exchange in the presence of an obstructed distal airway. Smaller intrathoracic airways are more easily obstructed. With age, the airways enlarge in diameter and length.
  51. 51. Pediatric considerations Infants and young children have less cartilaginous support of the airways. As cartilaginous support increases, dynamic compression during high expiratory flow rates is prevented. The respiratory pump includes the nervous system with central control (ie, cerebrum, brain stem, spinal cord, peripheral nerves), respiratory muscles, and chest wall. The respiratory center is immature in infants and young children, which leads to irregular respirations and the risk of apnea.
  52. 52. Pediatric considerations The ribs are horizontally oriented. During inspiration, less volume is displaced, and the capacity to increase tidal volume is limited when compared with that in older patients. The surface area for the interaction between the diaphragm and thorax is small, which limits displacing volume in the vertical direction.
  53. 53. Pediatric considerations The musculature is less developed. The slow-twitch fatigue-resistant muscle fibers in the infant are underdeveloped. The soft compliant chest wall provides little opposition to the deflating tendency of the lungs. This leads to a lower functional residual capacity than in adults
  54. 54. Acute Type 1 RF • • • • Cardiogenic pulmonary edema Non cardiogenic pulmonary edema Pneumonia Acute pulmonary thromboembolic disease • Acute allergic alveolitis • Severe bronchial asthma without diaphragmatic fatigue • Acute milliary TB and lymphagitis tuberculosa reticularis
  55. 55. ChronicType 1 RF • • • • Fibrosing alveolitis Other causes of IPF Chronic allergic alveolitis Thromboembolic pulmonary hypertension • Chronic pulmonary edema • Lymphangitis carcinomatosis
  56. 56. Acute Type 2 RF • Upper airway obstruction • Acute severe asthma diaphragmatic fatigue • Acute CNS disorder • Myathenia gravis • polyneuritis • AE of COPD • Pneumothorax with
  57. 57. Chronic Type 2 RF • • • • • • Chronic bronchitis Emphysema Pickwikian syndrome kyphoscoliosis Chronic neuromuscular diseases Progressive respiratory diseases preterminally
  58. 58. Clinically • Clinical picture of causative disease • Manifestations of hypoxaemia. 1-Central cyanosis if reduced hemoglobin is >5gram%. 2- Restlessness, irritability,, impaired intellectual functions. Acute severe hypoxaemia may cause convulsions, coma and death. 3- Hyperventilation and tachypnae through stimulation of chemoreceptors
  59. 59. Clinically • 4-Tachycardia,arrythmias,increased COP and dilatation of peripheral vessels • 5-Pulmonary vasoconstriction with pulmonary hypertension • 6-Secondary polycythaemia with predisposition to DVT and pulmonary embolism
  60. 60. Clinically Manifestations of hypercapnia: • 1-Drowsines,flapping tremors, coma(CO2 narcosis) and papillodema due to increased CSF formation secondary to cerebral vasodilatation and increased cerebral blood flow. • 2-Paradoxical action on peripheral blood vessels: Vasodilatation through direct action and vasoconstriction through sympathetic stimulation and the predominant action is the local one. • 3-Tachycardia,sweating and generalized vasodilatation with hypotension due to sympathetic stimulation. • 4-Gastric dilatation and may be paralytic ileus.
  61. 61. Investigations • for the cause • arterial blood gas analysis. • non-invasive methods
  62. 62. Investigations
  63. 63. • Treatment of the underlying cause • Correction of hypoxaemia • Treatment of complications
  64. 64. Complications of RF: • 1-Cardiac arrythmias due to severe hypoxaemia and acidaemia secondary to CO2 retention. • 2-Pulmonary hypertension and cor pulmonale due to pulmonary vasoconstriction as aresult of hypoxaemia and acidaemia. • 3-DVT and pulmonary embolism due to polycythaemia secondary to chronic hypoxaemia. • 4-Complications of oxygen therapy and mechanical ventilation.
  65. 65. Oxygen Therapy • Controlled O2 therapy • Uncontrolled O2 therapy
  66. 66. Oxygen Therapy
  67. 67. Different equipments of oxygen supply:: A) Central oxygen in hospitals. B) Home oxygen, includes : 1. Compressed gas cylinders. 2. Liquid oxygen cylinders. 3. Oxygen concentrators. 4. Small devices.
  68. 68. Compressed gas cylinders
  69. 69. Liquid oxygen cylinders easier to refill, but of higher cost
  70. 70. An oxygen concentrator works by taking in room air which has an oxygen concentration of around 21% and passing it through a series of molecular, bacterial and dust filters to remove any dust particles and unwanted gases. Purified oxygen with a concentration of up to 95% is then delivered to the patient via a flowmeter, with mask or nasal cannulae.
  71. 71. Aquagen Opure O2 Oxyshot These three forms of oxygen in small devices applied by ingestion in Aquagen, inhalation in Opure O2, and spray in Oxyshot.
  72. 72. Indications for acute oxygen therapy • Respiratory failure(PaO2<60 mmHg; SaO2<90%). • Cardio-respiratory arrest. • Hypotension and low cardiac output. • Metabolic acidosis(HCO3<18 mmol/L). • Respiratory distress. • Myocardial infarction. • Sickle cell crises.
  73. 73. Nasal cannula: The most commonly used. Simple inexpensive, easy. The FiO2 from 24%-44% increasing the flow more than 6L/min doesn't raise FiO2 than 44 %, and may result in drying of mucous secretions.
  74. 74. Simple face mask
  75. 75. Face mask with reservoir bag and one way valve.
  76. 76. Venturi mask Ideal for type II respiratory failure (hypercapnia) as in COPD
  77. 77. Different colors of venturi control parts adjusted to certain O2 flow to deliver different concentrations of O2.
  78. 78. Treanstracheal oxygen catheter: •Bypass the anatomical dead space of upper airway,using it as an oxygen reservoir during respiration. •Lack of nasal or facial irritation due to oxygen flow. •Infrequency of catheter displacement during sleep.
  79. 79. Invasive ventilator Endotracheal tube Invasive ventilator with endotreacheal tube: •Give up to 100% oxygen under positive pressure. •Used in sever cases when there is deterioration of spontaneous breathing with decreased pH, raised CO2, and persistent hypoxaemia.
  80. 80. Non invasive ventilator with face mask
  81. 81. Hyperparic Oxygen A medical treatment in which the patient is entirely enclosed in a pressure chamber breathing 100% O2 at > 1.4 times atmospheric pressure. Hyperbaric oxygen (HBO) therapy uses a monoplace (single-person) chamber pressurized with pure O2 or a larger multiplace chamber pressurized with compressed air in which the patient receives pure O2 by mask, head tent, or endotracheal tube.
  82. 82. Indications • CARBON MONOXIDE POISONING . •ARTERIAL GAS EMBOLISM DECOMPRESSION SICKNESS. AND •Gas gangrene. •Crush injury. •Compromized skin grafts and flaps. •Mixed aerobic anerobic soft tissue infections. •Nonhealing ischaemic wounds. •Burns. •Smoke ionhalation.
  83. 83. Rationale for ventilatory assistance Abnormal ventilatory drive  Respiratory load Alveolar hypoventilation  PaO2 and  PaCO2  Respiratory muscles capacity
  84. 84. Mechanical ventilation unloads the respiratory muscles Respiratory load Mechanical ventilation Respiratory muscles

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