Pathophysiology of respiratory failure
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Pathophysiology of respiratory failure

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Pathophysiology of respiratory failure Pathophysiology of respiratory failure Presentation Transcript

  • Pathophysiology of Respiratory Failure Gamal Rabie Agmy ,MD ,FCCP Professor of Chest Diseases, Assiut University ERS National Delegate of Egypt
  • Non Respiratory Functions Biologically Active Molecules: *Vasoactive peptides *Vasoactive amines *Neuropeptides *Hormones *Lipoprotein complexes *Eicosanoids
  • Non Respiratory Functions Haemostatic Functions Lung defense : *Complement activation *Leucocyte recruitment *Cytokines and growth factors Protection Vocal communication Blood volume/ pressure and pH regulation
  • Respiratory Functions *Oxygenation *CO2 Elimination
  • 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
  • Definition Respiratory failure is a syndrome of inadequate gas exchange due to dysfunction of one or more essential components of the respiratory system
  • 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.
  • The respiratory System Lungs Respiratory pump Pulmonary Failure • PaO2 • PaCO2 N/ Ventilatory Failure • PaO2 • PaCO2 Hypoxic Respiratory Failure Hypercapnic Respiratory Failure
  • Cardiogenic pulmonary edema Pneumonia pulmonary ARDS extra pulmonary ARDS Atelectasis Post surgery changes Aspiration Trauma Infiltrates in immunsuppression Hypoxic Respiratory Failure Pulmonary fibrosis
  • Type 3 (Peri-operative) Respiratory Failure Residual anesthesia effects, post- operative pain, and abnormal abdominal mechanics contribute to decreasing FRC and progressive collapse of dependant lung units.
  • Type 3 (Peri-operative) Respiratory Failure Causes of post-operative atelectasis include; *Decreased FRC *Supine/ obese/ ascites *Anesthesia *Upper abdominal incision *Airway secretions
  • 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
  • Hypoxemic Respiratory Failure (Type 1) Causes of Hypoxemia 1. Low FiO2 (high altitude) 2. Hypoventilation 3. V/Q mismatch (low V/Q) 4. Shunt (Qs/Qt) 5. Diffusion abnormality 6. low mixed venous oxygen due to cardiac desaturation with one of above mentioned factors.
  • Physiologic Causes of Hypoxemia Low FiO2 is the primary cause of ARF at high altitude and toxic gas inhalation 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. Hypoxemic Respiratory Failure (Type 1)
  • 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”
  • Hypoxemic Respiratory Failure (Type 1) V/Q Mismatch V/Q>1 V/Q<1 V/Q=o V/Q=∞
  • 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
  • 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
  • Hypoxemic Respiratory Failure (Type 1) Types of Shunt 1. Anatomical shunt 2. Pulmonary vascular shunt 3. Pulmonary parenchymal shunt
  • 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
  • Causes of increased dead space ventilation *Pulmonary embolism *Hypovolemia *Poor cardiac output, and *Alveolar over distension.
  • 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 PaCO2. Normally, ventilatory capacity greatly exceeds ventilatory demand.
  • 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.
  • Components of Respiratory System *CNS or Brain Stem *Nerves *Chest wall (including pleura, diaphragm) * Airways * Alveolar–capillary units *Pulmonary circulation
  • 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)
  • 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
  • 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
  • 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
  • Hypoxemic Respiratory Failure (Type 1) Types of Shunt 1. Anatomical shunt 2. Pulmonary vascular shunt 3. Pulmonary parenchymal shunt
  • 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
  • Causes of increased dead space ventilation *Pulmonary embolism *Hypovolemia *Poor cardiac output, and *Alveolar over distension.
  • 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 PaCO2. Normally, ventilatory capacity greatly exceeds ventilatory demand.
  • 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.
  • Components of Respiratory System *CNS or Brain Stem *Nerves *Chest wall (including pleura, diaphragm) * Airways * Alveolar–capillary units *Pulmonary circulation
  • 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)
  • 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
  • Hypercapnic Respiratory Failure (PAO2 - PaO2) Alveolar Hypoventilation V/Q abnormality NIF N P0.1 increasednormal N VCO2 PaCO2 >50 mmHg Not compensation for metabolic alkalosis Central Hypoventilation Neuromuscular Problem VCO2 V/Q Abnormality Hypermetabolism Overfeeding NNIF  P0.1
  • Hypercapnic Respiratory Failure Alveolar Hypoventilation Brainstemrespiratorydepression Drugs (opiates) Obesity-hypoventilation syndrome NIF Central Hypoventilation Neuromuscular Disorder N NIF Critical illness polyneuropathy Critical illness myopathy Hypophosphatemia Magnesium depletion Myasthenia gravis Guillain-Barre syndrome
  • 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. 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. Neuro- muscular weakness central = low P0.1 with normal NIF Neuromuscular weakness = normal P0.1 with low NIF Evaluation of Hypercapnia
  • 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 if greater than >300 on 100% = Shunt < 300 = V/Q mismatch • 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 A-a Gradient
  • 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 the endotracheal tube, n ventilator Circuit n 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.
  • Rationale for ventilatory assistance  Respiratoryload  Respiratorymuscles capacity Alveolar hypoventilation  PaO2 and  PaCO2 Abnormal ventilatorydrive
  • Mechanical ventilation unloads the respiratory muscles Respiratory load Respiratory muscles Mechanical ventilation