Respiratory failure &ards منتدى تمريض مستشفى غزة الاوروبي

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  • Effect of prone position on ventilation distribution. In the supine position, the distribution of ventilation is preferentially distributed to the ventral regions. When the patient is prone, the stiffness of the dorsal chest wall favors the distribution of ventilation to the dorsal regions, facilitating reinflation in this area.
  • Respiratory failure &ards منتدى تمريض مستشفى غزة الاوروبي

    1. 1. Hala Ayyash EGH-NSG.ForumPalestine.com
    2. 2. <ul><li>Respiratory Failure (RF) </li></ul><ul><li>& </li></ul><ul><li>ARDS </li></ul><ul><li>10/12/2011 </li></ul><ul><li>Hala Ayyash </li></ul>Hala Ayyash
    3. 3. (1) Respiratory Failure (RF) Hala Ayyash
    4. 4. Respiratory Failure (RF) <ul><li>Definition </li></ul><ul><li>Classification of RF </li></ul><ul><li>Distinction between Acute and Chronic RF </li></ul><ul><li>Diagnosis of RF </li></ul><ul><li>Causes </li></ul><ul><li>Clinical presentation </li></ul><ul><li>Investigations </li></ul><ul><li>Management of RF </li></ul><ul><li>Complications of ARF </li></ul>
    5. 5. Definitions RF <ul><li>Definition </li></ul><ul><li>Respiration is gas exchange between the organism and its environment. Function of respiratory system is to transfer O 2 from atmosphere to blood and remove CO 2 from blood. </li></ul><ul><li>Clinically </li></ul><ul><li>Respiratory failure is defined as PaO 2 <60 mmHg while breathing air, or a PaCO 2 >50 mmHg. </li></ul><ul><ul><li>-Acute and chronic </li></ul></ul>Hala Ayyash
    6. 6. Classification of RF Hala Ayyash
    7. 7. Classification of RF <ul><ul><li>Type 1 </li></ul></ul><ul><li>Hypoxemic RF ** </li></ul><ul><li>PaO2 < 60 mmHg with normal or ↓ PaCO2 </li></ul><ul><li>Associated with acute diseases of the lung </li></ul><ul><li>Pulmonary edema (Cardiogenic, noncardiogenic (ARDS), pneumonia, pulmonary hemorrhage, and collapse </li></ul><ul><ul><li>Type 2 </li></ul></ul><ul><li>Hypercapnic RF </li></ul><ul><li>PaCO2 > 45 mmHg </li></ul><ul><li>Hypoxemia is common </li></ul><ul><li>Drug overdose, neuromuscular disease, chest wall deformity, COPD, and Bronchial asthma </li></ul>Hala Ayyash
    8. 8. Distinction between Acute and Chronic RF <ul><li>Acute RF </li></ul><ul><li>Develops over minutes to hours </li></ul><ul><li>↓ pH quickly to <7.2 </li></ul><ul><li>Example; Pneumonia </li></ul><ul><li>Chronic RF </li></ul><ul><li>Develops over days </li></ul><ul><li>↑ in HCO3 </li></ul><ul><li>↓ pH slightly </li></ul><ul><li>Polycythemia, Corpulmonale </li></ul><ul><li>Example; COPD </li></ul>Hala Ayyash
    9. 9. Diagnosis of RF 1 – Clinical (symptoms, signs) <ul><li>Hypoxemia </li></ul><ul><li>Dyspnea, Cyanosis </li></ul><ul><li>Confusion, somnolence, fits </li></ul><ul><li>Tachycardia, arrhythmia </li></ul><ul><li>Tachypnea (good sign) </li></ul><ul><li>Use of accessory ms </li></ul><ul><li>Nasal flaring </li></ul><ul><li>Recession of intercostal ms </li></ul><ul><li>Polycythemia </li></ul><ul><li>Pulmonary HTN, Corpulmonale, Rt. HF </li></ul><ul><li>Hypercapnia </li></ul><ul><li>↑ Cerebral blood flow, and CSF Pressure </li></ul><ul><li>Headache </li></ul><ul><li>Asterixis </li></ul><ul><li>Papilloedema </li></ul><ul><li>Warm extremities, collapsing pulse </li></ul><ul><li>Acidosis (respiratory, and metabolic) </li></ul><ul><li>↓ pH, ↑ lactic acid </li></ul>Hala Ayyash
    10. 11. Diagnosis of RF 2 – Causes <ul><li>1 – CNS </li></ul><ul><li>Depression of the neural </li></ul><ul><ul><li>drive to breath </li></ul></ul><ul><li>Brain stem tumors or vascular abnormality </li></ul><ul><li>Overdose of a narcotic, sedative </li></ul><ul><ul><li>Myxedema, chronic metabolic </li></ul></ul><ul><ul><li>alkalosis </li></ul></ul><ul><li>Acute or chronic hypoventilation </li></ul><ul><ul><li>and hypercapnia </li></ul></ul>Hala Ayyash
    11. 12. Diagnosis of RF 2 – Causes <ul><li>2 - Disorders of peripheral </li></ul><ul><li>nervous system, Respiratory ms, and Chest wall </li></ul><ul><li>Inability to maintain a level of minute ventilation appropriate for the rate of CO2 production </li></ul><ul><li>Guillian-Barre syndrome, muscular dystrophy, myasthenia gravis, morbid obesity </li></ul><ul><li>Hypoxemia and hypercapnia </li></ul>Hala Ayyash
    12. 13. Diagnosis of RF 2 – Causes <ul><li>3 - Abnormities of the airways </li></ul><ul><li>Upper airways </li></ul><ul><ul><li>Acute epiglotitis </li></ul></ul><ul><ul><li>Tracheal tumors </li></ul></ul><ul><li>Lower airway </li></ul><ul><ul><li>COPD, Asthma, cystic fibrosis </li></ul></ul><ul><li>Acute and chronic hypercapnia </li></ul>Hala Ayyash
    13. 15. Diagnosis of RF 2 – Causes <ul><li>4 - Abnormities of the alveoli </li></ul><ul><li>Diffuse alveolar filling </li></ul><ul><li>hypoxemic RF </li></ul><ul><ul><li>Cardiogenic and noncardiogenic pulmonary edema </li></ul></ul><ul><ul><li>Aspiration pneumonia </li></ul></ul><ul><ul><li>Pulmonary hemorrhage </li></ul></ul><ul><li>Associate with Intrapulmonary shunt and increase work of breathing </li></ul>Hala Ayyash
    14. 16. Diagnosis of RF 3 – Common causes <ul><li>Hypoxemic RF </li></ul><ul><li>Chronic bronchitis, emphysema </li></ul><ul><li>Pneumonia, pulmonary edema </li></ul><ul><li>Pulmonary fibrosis </li></ul><ul><li>Asthma, pneumothorax </li></ul><ul><li>Pulmonary embolism, </li></ul><ul><li>Pulmonary hypertension </li></ul><ul><li>Bronchiectasis, ARDS </li></ul><ul><li>Fat embolism, Obesity </li></ul><ul><li>Cyanotic congenital heart disease </li></ul><ul><li>Granulomatous lung disease </li></ul><ul><li>Hypercapnic RF </li></ul><ul><li>Chronic bronchitis,emphysema </li></ul><ul><li>Severe asthma , drug overdose </li></ul><ul><li>Poisonings, Myasthenia gravis </li></ul><ul><li>Polyneuropathy, Poliomyelitis </li></ul><ul><li>Primary ms disorders </li></ul><ul><li>1ry alveolar hypoventilation </li></ul><ul><li>Obesity hypoventilation synd. </li></ul><ul><li>Pulmonary edema , ARDS </li></ul><ul><li>Myxedema, head and cervical cord injury </li></ul>Hala Ayyash
    15. 18. Diagnosis of RF 3 - Investigations <ul><li>ABG </li></ul><ul><li>CBC, Hb </li></ul><ul><ul><li>Anemia -> tissue hypoxemia </li></ul></ul><ul><ul><li>Polycythemia -> chronic RF </li></ul></ul><ul><li>Urea, Creatinine </li></ul><ul><li>LFT -> clues to RF or its complications </li></ul><ul><li>Electrolytes (K, Mg, Ph) -> Aggravate RF </li></ul><ul><li>↑ CPK, ↑ Troponin 1 -> MI </li></ul><ul><li>↑ CPK, normal Troponin 1 -> Myositis </li></ul><ul><li>TSH -> Hypothyroidism </li></ul>Hala Ayyash
    16. 19. Diagnosis of RF 3 - Investigations <ul><li>Chest x ray -> Pulmonary edema -> ARDS </li></ul><ul><li>Echocardiography -> Cardiogenic pulmonary edema </li></ul><ul><li> -> ARDS </li></ul><ul><li> -> PAP, Rt ventricular hypertrophy in CRF </li></ul>Hala Ayyash
    17. 20. Diagnosis of RF 3 - Investigations <ul><li>ECG -> cardiac cause of RF </li></ul><ul><li>-> Arrhythmia due to hypoxemia and severe acidosis </li></ul><ul><li>■ Right heart catheterization to measure </li></ul><ul><li> ● Pulmonary capillary wedge pressure (PCWP) </li></ul><ul><li> ● Normal -> ARDS (<18 mmHg) </li></ul><ul><li> ● Increased -> Cardiogenic pulmonary edema </li></ul>Hala Ayyash
    18. 22. Management of ARF <ul><li>ICU admition </li></ul><ul><li>1 -Airway management </li></ul><ul><ul><li>Endotracheal intubation: </li></ul></ul><ul><ul><ul><li>Indications </li></ul></ul></ul><ul><ul><ul><ul><li>Severe Hypoxemia </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Altered mental status </li></ul></ul></ul></ul><ul><ul><li>Importance </li></ul></ul><ul><ul><ul><li>precise O2 delivery to the lungs </li></ul></ul></ul><ul><ul><ul><li>remove secretion </li></ul></ul></ul><ul><ul><ul><li>ensures adequate ventilation </li></ul></ul></ul>Hala Ayyash
    19. 23. Management of ARF <ul><li>2 -Correction of hypoxemia </li></ul><ul><ul><li>O2 administration via nasal prongs, face mask, intubation and Mechanical ventilation </li></ul></ul><ul><ul><li>Goal: Adequate O2 delivery to tissues </li></ul></ul><ul><ul><li>PaO2 = > 60 mmHg </li></ul></ul><ul><ul><li>Arterial O2 saturation >90% </li></ul></ul>Hala Ayyash
    20. 24. Management of ARF <ul><li>3- Correction of hypercapnia </li></ul><ul><li>Control the underlying cause </li></ul><ul><li>Controlled O2 supply </li></ul><ul><li>1 -3 lit/min, titrate according O2 saturation </li></ul><ul><li>O2 supply to keep the O2 saturation >90% but <93 to avoid inducing hypercapnia </li></ul><ul><li>COPD-chronic bronchitis, emphysema </li></ul>Hala Ayyash
    21. 25. Management of ARF <ul><li>4 – Mechanical ventilation </li></ul><ul><li>Indications </li></ul><ul><ul><li>Persistence hypoxemia despite O2supply </li></ul></ul><ul><ul><li>Decreased level of consciousness </li></ul></ul><ul><ul><li>Hypercapnia with severe acidosis (pH< 7.2) </li></ul></ul>Hala Ayyash
    22. 26. Management of AR <ul><li>4 - Mechanical ventilation </li></ul><ul><ul><li>Increase PaO2 </li></ul></ul><ul><ul><li>Lower PaCO2 </li></ul></ul><ul><ul><li>Rest respiratory ms (respiratory ms fatigue) </li></ul></ul><ul><ul><li>Ventilator </li></ul></ul><ul><ul><ul><li>Assists or controls the patient breathing </li></ul></ul></ul><ul><ul><li>The lowest FIO2 that produces SaO2 >90% and PO2 >60 mmHg should be given to avoid O2 toxicity </li></ul></ul>Hala Ayyash
    23. 27. Management of ARF <ul><li>5 -PEEP (positive End-Expiratory pressure </li></ul><ul><li>Used with mechanical ventilation </li></ul><ul><ul><li>Increase intrathoracic pressure </li></ul></ul><ul><ul><li>Keeps the alveoli open </li></ul></ul><ul><ul><li>Decrease shunting </li></ul></ul><ul><ul><li>Improve gas exchange </li></ul></ul><ul><li>Hypoxemic RF (type 1) </li></ul><ul><ul><li>ARDS </li></ul></ul><ul><ul><li>Pneumonias </li></ul></ul>Hala Ayyash
    24. 28. Management of ARF <ul><li>6 - Noninvasive Ventilatory support (IPPV) </li></ul><ul><li>Mild to moderate RF </li></ul><ul><li>Patient should have </li></ul><ul><ul><li>Intact airway, </li></ul></ul><ul><ul><li>Alert, normal airway protective reflexes </li></ul></ul><ul><li>Nasal or full face mask </li></ul><ul><ul><li>Improve oxygenation, </li></ul></ul><ul><ul><li>Reduce work of breathing </li></ul></ul><ul><ul><li>Increase cardiac output </li></ul></ul><ul><li>COPD, asthma, CHF </li></ul>Hala Ayyash
    25. 29. Management of ARF <ul><li>7 - Treatment of the underlying causes </li></ul><ul><li>After correction of hypoxemia, hemodynamic stability </li></ul><ul><li>Antibiotics </li></ul><ul><ul><li>Pneumonia </li></ul></ul><ul><ul><li>Infection </li></ul></ul><ul><li>Bronchodilators (COPD, BA) </li></ul><ul><ul><li>Salbutamol </li></ul></ul><ul><ul><ul><li>reduce bronchospasm </li></ul></ul></ul><ul><ul><ul><li>airway resistance </li></ul></ul></ul>Hala Ayyash
    26. 30. Management of ARF <ul><li>7 - Treatment of the underlying causes </li></ul><ul><li>Anticholinergics (COPD,BA) </li></ul><ul><ul><li>Ibratropium bromide </li></ul></ul><ul><ul><ul><li>inhibit vagal tone </li></ul></ul></ul><ul><ul><ul><li>relax smooth ms </li></ul></ul></ul><ul><li>Theophylline (COPD, BA) </li></ul><ul><ul><li>improve diaphragmatic contraction </li></ul></ul><ul><ul><li>relax smooth ms </li></ul></ul><ul><li>Diuretics (pulmonary edema) </li></ul><ul><ul><li>Frusemide, Metalzone </li></ul></ul>Hala Ayyash
    27. 31. Management of ARF <ul><li>7 - Treatment of the underlying causes </li></ul><ul><li>Methyl prednisone (COPD, BA, acute esinophilic pn) </li></ul><ul><ul><li>Reverse bronchospasm, inflammation </li></ul></ul><ul><li>Fluids and electrolytes </li></ul><ul><ul><li>Maintain fluid balance and avoid fluid overload </li></ul></ul><ul><li>IV nutritional support </li></ul><ul><ul><li>To restore strength, loss of ms mass </li></ul></ul><ul><ul><li>Fat, carbohydrate, protein </li></ul></ul>Hala Ayyash
    28. 32. Management of ARF <ul><li>7 - Treatment of the underlying causes </li></ul><ul><li>Physiotherapy </li></ul><ul><ul><li>Chest percussion to loosen secretion </li></ul></ul><ul><ul><li>Suction of airways </li></ul></ul><ul><ul><li>Help to drain secretion </li></ul></ul><ul><ul><li>Maintain alveolar inflation </li></ul></ul><ul><ul><li>Prevent atelectasis, help lung expansion </li></ul></ul>Hala Ayyash
    29. 33. Complications of ARF <ul><li>Pulmonary </li></ul><ul><ul><li>Pulmonary embolism </li></ul></ul><ul><ul><li>barotrauma </li></ul></ul><ul><ul><li>pulmonary fibrosis (ARDS) </li></ul></ul><ul><ul><li>Nosocomial pneumonia </li></ul></ul><ul><li>Cardiovascular </li></ul><ul><ul><li>Hypotension, </li></ul></ul><ul><ul><li>Arrhythmia </li></ul></ul><ul><ul><li>MI, pericarditis </li></ul></ul><ul><li>GIT </li></ul><ul><ul><li>Stress ulcer, ileus, diarrhea, hemorrhage </li></ul></ul><ul><li>Infections </li></ul><ul><ul><li>Nosocomial infection </li></ul></ul><ul><ul><li>Pneumonia, UTI, catheter related sepsis </li></ul></ul><ul><li>Renal </li></ul><ul><ul><li>ARF (hypoperfusion, nephrotoxic drugs) </li></ul></ul><ul><ul><li>Poor prognosis </li></ul></ul><ul><li>Nutritional </li></ul><ul><ul><li>Malnutrition, diarrhea hypoglycemia, electrolyte disturbances </li></ul></ul>Hala Ayyash
    30. 35. (2) ARDS
    31. 36. ARDS Also known as DAD (diffuse alveolar disease) or ALI (acute lung injury) a variety of acute and diffuse infiltrative lesions which cause severe refractory arterial hypoxemia and life-threatening arrhythmias
    32. 37. Memory Jogger <ul><li>A ssault to the pulmonary system </li></ul><ul><li>R espiratory distress </li></ul><ul><li>D ecreased lung compliance </li></ul><ul><li>S evere respiratory failure </li></ul>
    33. 38. Direct Causes (Inflammatory process is involved in all) <ul><li>Pneumonia* </li></ul><ul><li>Aspiration of gastric contents* </li></ul><ul><li>Pulmonary contusion </li></ul><ul><li>Near drowning </li></ul><ul><li>Inhalation injury </li></ul>
    34. 39. Indirect Causes ( Inflammatory process is involved) <ul><li>Sepsis* (most common) gm - </li></ul><ul><li>Severe trauma with shock state that requires multiple blood transfusions* </li></ul><ul><li>Drug overdose </li></ul><ul><li>Acute pancreatitis </li></ul>
    35. 41. Pathophysiology of ARDS <ul><li>Damage to alveolar-capillary membrane </li></ul><ul><li>Increased capillary hydrostatic pressure </li></ul><ul><li>Decreased colloidal osmotic pressure </li></ul><ul><li>Interstitial edema </li></ul><ul><li>Alveolar edema or pulmonary edema </li></ul><ul><li>Loss of surfactant </li></ul>
    36. 42. Pathophysiologic Stages in ARDS <ul><li>Injury or Exudative- 1-7 days </li></ul><ul><ul><li>Interstitial and alveolar edema and atelectasis </li></ul></ul><ul><ul><li>Refractory hypoxemia and stiff lungs </li></ul></ul><ul><li>Reparative or Proliferative-1-2 weeks after </li></ul><ul><ul><li>Dense fibrous tissue, increased pulmonary hypertension occurs </li></ul></ul><ul><li>Fibrotic-2-3 week after </li></ul><ul><ul><li>Diffuse scarring and fibrosis, decreased surface area, decreased compliance and pulmonary hypertension </li></ul></ul>
    37. 43. The essential disturbances of ARDS **interstitial and alveolar edema and atelectasis
    38. 44. Clinical Manifestations: Early <ul><li>Dyspnea-(almost always present), tachypnea, cough, restlessness </li></ul><ul><li>Chest auscultation may be normal or reveal fine, scattered crackles </li></ul><ul><li>ABGs </li></ul><ul><ul><li>**Mild hypoxemia and respiratory alkalosis caused by hyperventilation </li></ul></ul>
    39. 45. Clinical Manifestations: Early <ul><li>Chest x-ray may be normal or show minimal scattered interstitial infiltrates </li></ul><ul><ul><li>Edema may not show until 30% increase in lung fluid content </li></ul></ul>
    40. 46. Clinical Manifestations: Late <ul><li>Symptoms worsen with progression of fluid accumulation and decreased lung compliance </li></ul><ul><li>Pulmonary function tests reveal decreased compliance and lung volume </li></ul><ul><li>Evident discomfort and increased WOB </li></ul>
    41. 47. Clinical Manifestations: Late <ul><li>Suprasternal retractions </li></ul><ul><li>Tachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis, and pallor </li></ul><ul><li>Hypoxemia and a PaO 2 /FIO 2 ratio <200 despite increased FIO 2 ( ex: 80/.8=100) </li></ul>
    42. 48. Clinical Manifestations <ul><li>As ARDS progresses, profound respiratory distress requires endotracheal intubation and positive pressure ventilation </li></ul><ul><li>Chest x-ray termed whiteout or white lung because of consolidation and widespread infiltrates throughout lungs </li></ul>
    43. 49. Chest X-Ray of ARDS
    44. 50. Clinical Manifestations <ul><li>If prompt therapy not initiated, severe hypoxemia, hypercapnia, and metabolic acidosis may ensue </li></ul>
    45. 51. Nursing Diagnoses <ul><li>Ineffective airway clearance </li></ul><ul><li>Ineffective breathing pattern </li></ul><ul><li>Risk for fluid volume imbalance </li></ul><ul><li>Anxiety </li></ul><ul><li>Impaired gas exchange </li></ul><ul><li>Imbalanced nutrition: Less than body requirements </li></ul>
    46. 52. Planning <ul><li>Following recovery </li></ul><ul><ul><li>PaO 2 within normal limits or at baseline </li></ul></ul><ul><ul><li>SaO 2 > 90% </li></ul></ul><ul><ul><li>Patent airway </li></ul></ul><ul><ul><li>Clear lungs or auscultation </li></ul></ul>
    47. 53. Dyspnea and Tachypnea The Auscultation Assistant - Breath Sounds
    48. 54. Nursing Assessment <ul><li>Lung sounds </li></ul><ul><li>ABG’s </li></ul><ul><li>CXR </li></ul><ul><li>Capillary refill </li></ul><ul><li>Neuro assessment </li></ul><ul><li>Vital signs </li></ul><ul><li>O2 sats </li></ul><ul><li>Hemodynamic monitoring values </li></ul>
    49. 55. Diagnostic Tests <ul><li>ABG-review </li></ul><ul><li>CXR </li></ul><ul><li>Pulmonary Function Tests- dec. compliance and dec vital capacity - (max exhaled after max inhale) </li></ul><ul><li>Hemodynamic Monitoring- (Pulmonary artery pressures) to rule out pulmonary edema </li></ul>
    50. 56. Severe ARDS
    51. 57. *Goal of Treatment for ARDS Maintain adequate ventilation and respirations. Prevent injury Manage anxiety
    52. 58. Treatment <ul><li>Mechanical Ventilation-goal PO2>60 and 02 sat 90% with FIO2 < 50 </li></ul><ul><li>PEEP- can cause dec. CO, B/P and barotrauma </li></ul><ul><li>Positioning- prone, continuous lateral rotation therapy </li></ul><ul><li>Hemodynamic Monitoring- fluid replacement or diuretics </li></ul><ul><li>Enteral or Parenteral Feeding- high calorie, high fat. Research shows that formulas enriched with omega -3 fatty acids may improve the outcomes of those with ARDS </li></ul>
    53. 59. Cont. <ul><li>Crystalloids versus colloids </li></ul><ul><li>Mild fluid restriction and diuretics </li></ul>
    54. 60. Proning <ul><li>Proning typically reserved for refractory hypoxemia not responding to other therapies </li></ul><ul><ul><li>Plan for immediate repositioning for cardiopulmonary resuscitation </li></ul></ul>
    55. 61. Proning-Principles <ul><li>Positioning strategies </li></ul><ul><ul><li>Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone </li></ul></ul><ul><ul><ul><li>Predisposes to atelectasis </li></ul></ul></ul><ul><ul><li>Turn from supine to prone position </li></ul></ul><ul><ul><ul><li>May be sufficient to reduce inspired O 2 or PEEP </li></ul></ul></ul><ul><ul><li>Fluid pools in dependent regions of lung </li></ul></ul>
    56. 62. Effect of prone position on ventilation distribution. In the supine position, the distribution of ventilation is preferentially distributed to the ventral regions. When the patient is prone, the stiffness of the dorsal chest wall favors the distribution of ventilation to the dorsal regions, facilitating reinflation in this area.
    57. 63. Prone Device <ul><li>*Prone positioning </li></ul><ul><ul><li>With position change to prone, previously nondependent air-filled alveoli become dependent, perfusion becomes greater to air-filled alveoli opposed to previously fluid-filled dependent alveoli, thereby improving ventilation-perfusion matching. </li></ul></ul>No benefit in mortality
    58. 64. Benefits to Proning Before proning After proning
    59. 65. Positioning <ul><li>Other positioning strategies </li></ul><ul><ul><li>Continuous lateral rotation therapy </li></ul></ul>
    60. 66. Continuous Lateral Rotation
    61. 67. Oxygen Therapy <ul><li>Oxygen </li></ul><ul><ul><li>High flow systems used to maximize O 2 delivery </li></ul></ul><ul><ul><li>SaO 2 continuously monitored, Usually have arterial line for frequent ABG’s </li></ul></ul><ul><ul><li>Give lowest concentration that results in PaO 2 60 mm Hg or greater </li></ul></ul>
    62. 68. Respiratory Therapy <ul><li>Risk for O 2 toxicity increases when FIO 2 exceeds 60% for more than 48 hours </li></ul><ul><ul><li>Patients will commonly need intubation with mechanical ventilation because PaO 2 cannot be maintained at acceptable levels </li></ul></ul>
    63. 69. Mechanical ventilation <ul><li>PEEP </li></ul><ul><ul><li>Higher levels of PEEP are often needed to maintain PaO 2 at 60 mm Hg or greater </li></ul></ul><ul><ul><li>**High levels of PEEP can compromise venous return </li></ul></ul><ul><ul><ul><li>↓ Preload, CO, and BP </li></ul></ul></ul>
    64. 70. Medical Supportive Therapy <ul><li>Maintenance of cardiac output and tissue perfusion </li></ul><ul><ul><li>Continuous hemodynamic monitoring </li></ul></ul><ul><ul><li>Continuous BP measurement via arterial catheter </li></ul></ul>
    65. 71. Medical Supportive Therapy <ul><li>Pulmonary artery catheter to monitor pulmonary artery pressure, pulmonary artery wedge pressures, and CO </li></ul><ul><ul><li>Administration of crystalloid fluids or colloid fluids, or lower PEEP if CO falls </li></ul></ul>
    66. 72. Medical Supportive Therapy <ul><li>Use of inotropic drugs may be necessary </li></ul><ul><li>Hemoglobin usually kept at levels greater than 9 or 10 with SaO 2 ≥90% </li></ul><ul><li>Packed RBCs </li></ul><ul><li>Maintenance of fluid balance </li></ul>
    67. 73. Medical Supportive Therapy <ul><li>May be volume depleted and prone to hypotension and decreased CO from mechanical ventilation and PEEP </li></ul><ul><li>Monitor PAWP, daily weights, and I and O’s to assess fluid status </li></ul>
    68. 74. Medications <ul><li>Inhaled Nitric Oxide </li></ul><ul><li>Surfactant therapy </li></ul><ul><li>corticosteroids </li></ul>
    69. 75. Questions?? Hala Ayyash
    70. 76. THANK YOU

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