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Chronic respiratory failure 1



Respiratory failure

I.C.U ReSiDeNt

Respiratory failure

  1. 1. Respiratory Failure
  2. 2. By Dr.SoliMaN ELKADY I.C.U ReSiDeNt
  3. 3. Introduction Most common reason for admission to ICU is to protect airway and ventilator care to critically ill patients
  4. 4. Primary functions of lung and thorax is to oxygenate arterial blood and to eliminate CO2.
  5. 5. Dysfunction may occur in oxygenation (intrapulmonary gas exchange) or in ventilation (the movement of gases between the environment and the lungs)
  7. 7. Gas Exchange Unit
  8. 8. Respiratory system includes: CNS (medulla) Peripheral nervous system (phrenic nerve) Respiratory muscles Chest wall Lung Upper airway Bronchial tree Alveoli Pulmonary vasculature
  10. 10. Respiratory insufficiency The condition in which the lungs can not take in sufficient oxygen or expel sufficient carbon dioxide to meet the needs of the cells of the body..
  11. 11. Respiratory failure Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination.
  12. 12. In practice : respiratory failure defiend as Pao2 value less than 60 mm Hg or PaCO2 value more than 50 mm Hg.
  13. 13. classification (1)according to PaCO2 ■ hypoxemic (Group Ⅰ) respiratory failure PaO2 of less than 60 mm Hg with a normal or low PaCO2. Cause of: Edema, Vascular disease, Chest Wall. ■ hypercapnic (Group Ⅱ ) respiratory failure PaO2 low 60 mm Hg and PaCO2 of more than 50 mm Hg. Cause of: Airway obstruction, Neuromuscular disease.
  14. 14. (2)according to pathogenic mechanism ■ ventilatory disorders 1-obstructive ventilatory disorders asthma, emphysema, chronic bronchitis, and bronchiectasis 2-restrictive ventilatory disorders deformity of thorax , fracture of several ribs, tension pneumothorax diffuse interstitial fibrosis ■ gas exchange disorders 1-diffusion disorders 2-ventilation-perfusion mismatching
  15. 15. (3)according to primary site ■ central respiratory failure ■ peripheral respiratory failure airway obstruction between the glottis and the carina ■Obstruction is located in the airway outside the thorax: inspiratory dysnea ■Obstruction is located in the airway inside the thorax: expiratory dysnea expire inspire
  16. 16. ■ peripheral respiratory failure Peripheral airway obstruction may be caused by: specific chemical mediators (such as histamine, leukotrienes, prostaglandins ), other substances released during inflammatory and allergic responses (4)according to duration ■ acute respiratory failure minute to hours ■ chronic respiratory failure several dayes or longer
  17. 17. clinical
  18. 18. The most important practical classification
  19. 19. HYPOXIC RESPIRATORY FAILURE (TYPE 1) Most common form of respiratory failure Lung disease is severe to interfere with pulmonary O2 exchange, but over all ventilation is maintained
  20. 20. Causes of Hypoxic Respiratory failure 1- FiO2 high altitude 2- Ventilation-perfusion (V/Q) mismatch 3- Shunt 4- Diffusion limitation 5- Alveolar hypoventilation
  21. 21. V/Q mismatch Normal ventilation of alveoli is comparable to amount of perfusion Normal V/Q ratio is 0.8 (more perfusion than ventilation) V/Q Mismatch : Inadequate ventilation Poor perfusion VA Q VA/ Q Top 1.2L/min 0.4L/min 3.0 Middle 1.8L/min 2.0L/min 0.9 Bottom 2.1L/min 3.4L/min 0.6
  22. 22. Causes COPD Pneumonia Asthma Atelectasis Pulmonary embolus
  23. 23. Shunt An extreme V/Q mismatch ((Perfusion without ventilation)) Shunting is the most common cause for hypoxaemic respiratory failure in ICU patients. The deoxygenated blood bypasses the ventilated alveoli and mixes with oxygenated blood → hypoxemia Persistent of hypoxemia despite 100% O2 inhalation Hypercapnia occur when shunt is excessive > 60%
  24. 24. Causes I- Anatomic shunt Blood passes through parts of respiratory system that receives no ventilation II- Intracardiac Right to left shunt Fallot’s tetralogy Eisenmenger’s syndrome III- IntraPulmonary A/V malformation Pneumonia Pulmonary edema Atelectasis/collapse Pulmonary Hge Pulmonary contusion
  25. 25. Diffusion limitation Distance between alveoli and pulmonary capillary is one- two cells thick With diffusion abnormalities: there is an increased distance between alveoli and pulmonary capillary. causes A.R.D.S Sever emphysema Recurrent pulmonary emboli Pulmonary fibrosis
  26. 26. Alveolar hypoventilation Is a generalized decrease in ventilation of lungs and resultant buildup of CO2 Causes Restrictive lung disease CNS disease Chest wall dysfunction Neuromuscular disease
  27. 27. Hypercapnic Respiratory Failure (Type II) This occurs in patients with chronic CO2 retention who worsen and have rising CO2 and low pH. Mechanism: respiratory muscle fatigue
  28. 28. Causes of Hypercapnic Respiratory failure Respiratory centre (medulla) dysfunction Drug over dose, CVA hypothyroidism Neuromuscular disease Guillain-Barre, Myasthenia Gravis, polio, spinal injuries Chest wall/Pleural diseases kyphoscoliosis, pneumothorax, massive pleural effusion Upper airways obstruction tumor, foreign body, laryngeal edema Peripheral airway disorder asthma, COPD
  29. 29. Common causes Hypoxemic RF • Hypercapnic RF • Chronic bronchitis, emphysema Chronic bronchitis,emphysema Pneumonia, pulmonary edema Severe asthma, drug overdose Pulmonary fibrosis Poisonings, Myasthenia gravis Asthma, pneumothorax Polyneuropathy, Poliomyelitis Pulmonary embolism, Primary ms disorders Pulmonary hypertension 1ry alveolar hypoventilation Bronchiectasis, ARDS Obesity hypoventilation synd. Fat embolism, KS, Obesity Pulmonary edema, ARDS Cyanotic congenital heart disease Myxedema, head and cervical Granulomatous lung disease cord injury
  30. 30. Effects of respiratory failure 1- Acid-base disturbances & disorders of electrolyte balance 2- Alteration of the respiratory system peripheral chemoreceptor ■ PaO2↓ <60mmHg respiratory center(+) respiratory movement↑ <30mmHg respiratory center (-) respiratory movement ↓ ■ PaCO2↑ central chemoreceptor <80mmHg respiratory center (+) respiratory movement↑ >80mmHg respiratory center (-) respiratory movement ↓
  31. 31. 3. Alteration of the cardiovascular system ■ compensatory reaction PaO2<60 mmHg,PaCO2 increase cardiovascular center(+) increase in cardiac output : increase in stroke volume and heart rate redistribution of blood flow ■ injurious changes PaO2< 40 mmHg,PaCO2> 80 mmHg cardiovascular center(-) rate slow, decreased blood pressure cardiac output decrease pulmonary hypertension
  32. 32. 4. Alteration of the nervous system (1) Hypoxia: the nervous system is very sensible to oxygen lack. < 40~50 mmHg, serious but reversible deterioration in cerebral function ( orientation, arithmetic tasks, memory) occurs, and restlessness and confusion are common. < 30 mmHg, loss of consciousness results. < 20 mmHg, irreversible damage of neural cells. (2) Hypercapnia: CO2 nacosis. condition of confusion, tremors, convulsions, and possible coma that may occur if blood levels of carbon dioxide increase to 80mm Hg or higher
  33. 33. 5. Alteration of the renal function 6. Alteration of the digestive system
  34. 34. Respiratory Failure Symptoms When compensatory mechanisms fail, respiratory failure occurs CNS: Headache Visual Disturbances Anxiety Confusion Memory Loss Weakness Decreased Functional Performance
  35. 35. Pulmonary: Cough Chest pains Sputum production Stridor Dyspnea Cardiac: Orthopnea Chest pain Other: Fever, Abdominal pain, Anemia, Bleeding
  36. 36. Clinical diagnosis Respiratory compensation Tachypnoea RR > 35 Breath /min Accessory muscl Retraction intercostal ms Nasal flaring Sympathetic stimulation HR BP Tissue hypoxia sweating Altered mental state Haemoglobin desaturation HR and BP (late) Low spo2 Cyanosis (late)
  37. 37. Causes of error Pulse oximetry Poor peripheral perfusion Dark skin False nails or nail PAINTING Bright ambient light Poorly adherent probe Excessive motion Carboxyhaemoglobin or methaemoglobin
  38. 38. ASSESSMENT OF PATIENT 1-Careful history 2-Physical Examination 3-Investigations I- ABG analysis : PaO2 PaCO2 pH Alveolar-Arterial PO2 Gradient P(A-a)02 = (PiO2 - PaCO2) – PaO2 R
  39. 39. where PiO2 = partial pressure of inspired air, R = 0.8 i.e, at sea level, breathing air; PAO2 = 20 - PaCO2/0.8 A-a Gradient = 20 - PaCO2/0.8 -PaO2 Normal P(A-a)O2 gradient: 5-10 mm of Hg A sensitive indicator of disturbance of gas exchange. Useful in differentiating extrapulmonary and pulmonary causes of resp. failure.
  40. 40. II-Chest x-ray III-CBC, IV- sputum/blood cultures, V- Serum electrolytes VI- ECG VII- Urinalysis VIII-V/Q lung scan IX- Pulmonary artery catheter (severe cases)
  41. 41. Management of Respiratory Failure Principles Hypoxemia may cause death in RF Primary objective is to reverse and prevent hypoxemia Secondary objective is to control PaCO2 and respiratory acidosis Treatment of underlying disease Patient’s CNS and CVS must be monitored and treated
  42. 42. Management Correction of hypoxemia Supplemental O2 therapy essential Titration based on SaO2, PaO2 levels and PaCO2 Goal is to prevent tissue hypoxia Tissue hypoxia occurs (normal Hb & C.O.) - venous PaO2 < 20 mmHg or SaO2 < 40% - arterial PaO2 < 38 mmHg or SaO2 < 70% Increase arterial PaO2 > 60 mmHg(SaO2 > 90%) or venous SaO2 > 60% Correction of hypercapnia Control the underlying cause Controlled O2 supply 1 -3 lit/min, titrate according O2 saturation O2 supply to keep the O2 saturation >90% but <93 to avoid inducing hypercapnia
  43. 43. Mobilization of secretions Encourage pt 4 Effective coughing Positioning Semisetting
  44. 44. Hydration and humidification Chest Physiotherapy Chest percussion to loosen secretion Airway suctioning
  45. 45. Drug Therapy Relief of bronchospasm Bronchodilators Reduction of airway inflammation Corticosteroids Reduction of pulmonary congestion IV diuretics Treatment of pulmonary infections IV antibiotics Nutritional Therapy Maintain protein and energy stores Enteral or parenteral nutrition Supplements
  46. 46. Noninvasive Ventilatory support (IPPV) BiPAP CPAP Mild to moderate RF NIPPV INDICATED In Acute exacerbation of COPD WITH Respiratory acidosis pH 7.25 Or less Cardiogenic pulmonary edema Asthma Type II R.F secondary to chest wall deformity or neuro muscular diseases Weaning off mechanical ventilation
  47. 47. Benefits NIPPV of Improved alveolar ventilation Reduced work of breathing Rest of the respiratory musculature Increased intrathoracic pressure decreases preload and afterload
  48. 48. should not be considered for NPPV? Contraindications Cardiac or respiratory arrest Nonrespiratory organ failure Hemodynamic instability Severe encephalopathy Severe UGI bleed Facial or neurosurgery, trauma Upper airway obstruction Inability to cooperate or protect airway High risk for aspiration
  49. 49. Mechanical ventilation Indications PaO2< 55 mm Hg or PaCO2 > 60 mm Hg despite 100% oxygen therapy. Deteriorating respiratory status despite oxygen and Nebulization therapy Anxious, with deteriorating mental status. Respiratory fatigue: for relief of metabolic stress of the work of breathing
  50. 50. Mechanical Ventilation: Strategies 1-SIMV, A/C with PEEP PEEP (positive End-Expiratory pressure) Increase intrathoracic pressure Keeps the alveoli open Decrease shunting Improve gas exchange
  51. 51. 2-High frequency ventilation (HFV) Very small tidal volumes are used (<1ml/kg), very rapid rates and lower mean airway pressures are used 3-Lung Recruitment To open the collapsed alveoli A sustained inflation of the lungs to higher airway pressure and volumes 4-Permissive Hypercapnia Allows the PaCO2 to rise into the 60-70 mm of Hg range, as long as the patient is adequately oxygenated (SaO2> 92%), and able to tolerate the acidosis. This strategy is used to limit the amount of barotrauma and volutrauma to the patient
  52. 52. 5-Prone positioning Improve oxygenation in about 2/3 of all treated patients No improvement on survival, time on ventilation, or time in ICU Might be useful to treat refractory hypoxemia Routine use is not recommended
  53. 53. Respiratory failure common in old age due to ↓ Ventilatory capacity Alveolar dilation Larger air spaces Loss of surface area Diminished elastic recoil Decreased respiratory muscle strength ↓ Chest wall compliance
  54. 54. Thanks for attention
  55. 55. Direct Lung Injury Infectious pneumonia Aspiration, chemical pneumonitis Acute Respiratory Distress Syndrome Pulmonary contusion, penetrating lung injury Fat emboli Near-drowning Inhalation injury Reperfusion pulmonary edema s/p lung transplant Indirect Lung Injury Sepsis Severe trauma with shock/hypoperfusion Burns Massive blood transfusion Drug overdose: ASA, cocaine, opioids, phenothiazines, TCAs. Cardiopulmonary bypass Acute pancreatitis
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