IPPR

INDICATIONS: The need to improve lung expansion The presence of clinically significant pulmonary atelectasis when other forms of therapy have been unsuccessful Inability to clear secretions adequately because of pathology that severely limits the ability to ventilate or cough effectively and failure to respond to other modes of treatment In patients with severe hyperinflation, IPPB may decrease dyspnea and discomfort during nebulized therapy The need for short-term ventilatory support for patients who are hypoventilating IPPB may be used to deliver aerosol medications to patients with fatigue as a result of ventilatory muscle weakness CONTRAINDICATIONS: Tension pneumothorax (untreated) Intracranial pressure (ICP) > 15 mm Hg Hemodynamic instability Recent facial, oral, or skull surgery Tracheoesophageal fistula Recent esophageal surgery Active hemoptysis Active untreated tuberculosis Radiographic evidence of bleb Recent lobectomy/pneumonectomy Physiological changes during IPPR, hypoventilation, and hyperventilation Respiratory o Altered V/P ratio Increased physiological dead space Blood flow continues to dependent part o Volutrauma due to rapid collapse and reexpansion of alveoli

IPPR
Barotrauma Increase in airway pressure is not transmitted to alveolar pressure in healthy patient but in noncomplaint lung, it is transmitted and may cause pressure induced injury Gas trapping occurs if there is insufficient time for alveoli to empty before the next breath more likely to occur: o in patients with asthma or COPD o when inspiratory time is long (and therefore expiratory time short) o when respiratory rate is high (absolute expiratory time is short) o results in progressive hyperinflation of alveoli and progressive rise in end-expiratory pressure (known as intrinsic PEEP) o Mechanical bronchodilation o Decreased atelectasis o Improve breathing pattern o Decrease work of breathing o Increase mobilization of secretions o Increased airway resistance Cardiovascular o If non complaint lung, PPV transmitted to heart and blood vessels o Increase in intrathorasic pressure along with compression of heart cause decrease in venous return o Preload of lt. ventricle increases as blood is squeezed from pulmonary vessels into lt. atrium o Increase in rt ventricular afterload o Decrease in lt. ventricular afterload caused by the compression effect of hyperinflated lungs o Interventricular septum is pushed towards lt ventricle 9ventricular interdependence o If intravascular volume is normal, CO increased & viceversa o Myocardial oxygen consumption is decreased Systolic pressure variation o Difference in maximal and minimal SBP during respiratory cycle o Delta up segment difference between maximal SBP and SBP during apnoa period Indicate inspiratory augmentation of COP o Delta down segment difference between minimal SBP and SBP during apnoa period Indicate decrease in venous return Decrease in blood flow to liver and kidney o

IPPR
GI ulceration may be there due to decrease blood flow Increase in ICT

Criteria for discontinuing mechanical support of ventilation 1. Vital capacity>15ml/kg 2. A-aDO2<350mmhg 3. PaO2>60mmhg while maintaining fio2<50% 4. Maximal inspiratory pressure>-20mmhg after kinking tube 5. Maintain normal art ph 6. Spontaneous breathing rate<20/min 7. Dead space/TV<0.6 Criteria for tracheal extubation 1. Vital capacity>15ml/kg 2. PaO2>60mmhg while maintaining fio2<50% 3. PaCO2<50mmhg 4. Maintain normal art ph 5. Spontaneous breathing rate <30/min 6. Active laryngeal reflex 7. Patient able to tolerate spont breathing for 2hrs on T piece/or SIMV rate<2/min Removal of ventillatory support 1. T-piece 2. SIMV mode and gradually decreasing rate 3. Decreasing level of pressure support ventilation Complications of mechanical ventilation 1. Infection 2. Barotraumas 3. Atelectasis 4. Critical illness myopathy Treatment of acute respiratory failure 1. Supplemental oxygen 2. Mechanical ventilation(TV 6-8ML/Kg ) 3. PEEP 4. Inverse ratio ventilation(kept <40mmhg) 5. Diuresis 6. Inotropic support 7. Glucocorticoid ? 8. Infection control 9. Nutritional support 10. Inhaled b2 agonist 11. Removal of secretions PEEP benefit 1. Prevent alveolar collapse at end expiration 2. Increase FRC

IPPR
3. Improve VP match 4. Prevent intrapulmonary left to right shunt PEEP hazard 1. Barotraumas 2. Decrease cardiac output PEEP 1. It should be kept <15mmhg n increased at 2.5-5cmhg of h2o till pao2>60mmhg 2. It does not decrease extravascular lung water neither decrease its formation but shift the water from alveoli to interstitial space thus improving oxygenation