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Page 11. Define IPPB and discuss the physiological bases for this therapy · IPPB stands for Intermittent Positive Pressure Breathing · IPPB is the application of positive pressure breaths as a short-term therapy for hyper-expansion therapy. A SMI [sustained maximal inspiration] is created by running pressurized gas into a mouthpiece or mask. The breath ends when a pre-selected peak pressure is reached. This pressure is called the PIP. A person with healthy lungs will require much less pressure than a person with decreased lung compliance. In fact, the definition of compliance is the change in volume/change in pressure. · IPPB is generally accompanied by nebulization of a sterile saline or a bronchodilator so that the air is humidified for the 10-15 minutes of the treatment. This involves placing a small volume pneumatic jet [SVN] in line with the pressurized gas.
How the machine works: · In IPPB we set a driving pressure on the machine, and when the patient triggers the machine by decreasing the pressure in the line, gas starts to move down the tube into the mouth and airways. When the preset PIP is reached, the gas flow shuts down immediately. The inspiratory phase has cycled off. · During the inspiratory phase, while gas is moving down the mainline, gas is sent down the exhalation valve line to shut the exhalation port by inflating a mushroom valve. · At the same time, gas is sent down the nebulizer drive line to power the inline SVN. · The result is a deeper breath with only minimal work from the patient [-2 cmH20] This deeper breath tends to move to the periphery first so that the basal posterior lung gets the benefit of the SMI. · Unfortunately this breath also transmits positive pressure into the thorax. That is responsible for a lot of side effects. · In both IPPB and normal breathing, exhalation is passive and takes a bit longer. · Because this is a SMI, we will limit the respiratory rate of IPPB to 6-8 bpm
2. The role of normal breathing in the regulation of the blood pressure in the heart and brain. · In normal breathing, one creates negative [subatmospheric] intrathoracic pressure by increasing the chest volume. In a normal deep breath, one holds this negative pressure for a longer time so that more air moves down the airway into the lung. Generally, these pressures are tiny. [-5 to –10 cmH20] because the normal lung had good compliance and the driving pressures required to move a volume into the lungs are low [normal lung C =100-150 ml/cmH20]. A normal –5 creates a driving pressure of 5 cmH20 that moves 500-750 ml Vt. · When one breathes normally, there is negative pressure created in the thorax. This suction helps move blood into the right side of the heart. Just as coughing or sneezing will decrease this venous return. IPPB with its high thoracic pressures will hamper venous return to the right side of the heart. · Just as with a cough, blood from the head will back up due to these positive pressures. If there is high pressure in the head, this pressure will only increase 3. Indications for IPPB. · Clinically diagnosed atelectasis not responsive to other therapies [cough deep breath, and IS] · Inability to clear airways due to inability to take deep breaths · Short-term non-invasive ventilatory support for hypercapnic patients [IPPB has been replaced by BiPap these days—but if you don't have a BiPap machine handy, it still works] · Delivery of aerosolized drugs when SVN has failed · Delivery of aerosolized drugs when patient cannot take a deep breath [less than 10 ml/cmH20]
4. Goals of IPPB: · Improve the Vt by 25%--- which should increase the IC [hopefully the patient's respiratory rate returns to normal after the treatment] · increased PEFR & FEV1 [medication portion of the treatment.] · Improve cough by accomplishing the first two · Improve chest film. Reduce atelectasis · Improve breath sounds: increased BBS in the basal areas · Improve oxygenation: check pulse oximeter before and after TX · Favorable patient response. [subjective]
5. Contraindications for IPPB: · Tension pneumothorax. Any untreated pneumothorax can become a tension pneumothorax as positive pressure pushes more air into the chest wall from the airway. Conditions that predispose a patient to pneumothorax · Air trapping/ asthma, COPD, emphysema · Excessive pressure set on the control which will deliver excessive Vt. [max 45 mL/kg IBW] Please note, setting the Vt at 15 ml/kg should be enough to increase the IC so that the patient can cough. · ICP over 15 mmHg. High intercranial pressure can be made worse by positive pressure in the chest that will hamper drainage from blood from the head. · Hemodynamic instability. Because the positive pressure in the chest hampers return of venous blood to the heart, it will decrease the stroke volume of the heart. To compensate the patients heart rate may have to increase · Active hemoptysis: application of positive pressure on the airways can make bleeding worse, so if the patient is already coughing up blood, stop IPPB. Report to the doctor. Suggest SVN to deliver drugs, or IS to expand the chest. Conditions that predispose a patient to hemoptysis: · Active untreated TB: Tuberculosis is a necrotic infection that can lead to holes in the lung thus bleeding and pneumothorax · Lung cancer: cancer can lead to delicate [friable] tissues · Cystic fibrosis: air-trapping. Bleeding is common with these kids--- particularly those with blebs on their X-rays · Recent surgery to the lung such as a lobectomy, wedge section or a lung reduction · Tracheo-esophageal fistula: hole between the esophagus and the tracheal. In a newborn this can be congenital, in an adult it can be the result of trauma to the chest. Air will leave the airway and go into the chest or into the esophagus. · Recent esophageal surgery: Because so many folks on IPPB swallow a lot of air this can hamper healing of the esophagus and can lead to bleeding · Recent facial, oral or skull surgery: see the problems with ICP · Singulation: hiccups. This is a spasm of the diaphragm and will trigger breaths so that the patient will get frustrated. [Although this isn't in the literature, my personal experience hints that IPPB triggers hiccups in some folks] · Nausea: because of swallowing air, this can rapidly inflate the belly and cause vomiting. Pressures over 20 cmH20 are particularly associated with gastric distension · Wheezing: give IPPB with bronchodilator if patient is wheezing or has history. IPPB with normal saline can trigger wheezing
6. Hazards of IPPB: · Increased RAW in persons who are sensitive to cooling airways · Barotrauma: in persons who are getting excessive volumes and pressures or who air trap. The IPPB forces in more air than they can exhale. If they have blebs, these weak spots can burst · Nosocomial infection: just as it sends medication deep into the lungs, it sends bacteria deep into the lung. Use filters on the mainline and on the nebulizer driveline. · Hyperventilation: because the VT is increased, if the patient breathes fast, he can blow off his C02 and suffers finger tingling and lightheadedness as intracranial blood vessels constrict. The blood pH becomes alkalotic. Worst case: the increased pH of the blood can trigger cardiac arrhythmias. · Respiratory depression in the chronic hypercapnic patient. Because the Air/mix mode has an Fi02 of 40-60%, this can depress ventilation in a person with chronic hypercapnia. You can offer the IPPB to the patient with compressed air. · Psychological dependence: this can happen to folks with long term lung disease. They might need to be weaned from the IPPB to SVN or one might considered BiPap [maybe they really need extra help all the time] 7. Discuss the assessment of the patient on IPPB. How do we assess for safe effective therapy? · Pre-IPPB · Assess need for therapy/ expected outcomes determined 1. outcomes should be measurable 2. consider alternative means of hyperinflation such as IS, or SMI or ez-PAP · read chart: look for contraindications in history or X-ray report · Assess baseline vital signs: 1. HR can increase from the baseline due to the pressure. If the HR increases and returns to normal within a few minutes, it is pressure not medication increasing the heart…slow down the IPPB and wait more between each breath 2. respiratory rate should decrease after Tx if all is well. If it triggered bronchospasm or barotrauma, increased rapid shallow breathing might result. During Tx the patient's retractions should be diminished as WOB has decreased 3. check sensorium. If patient has chronic hypercapnia, this additional Fi02 will cause him to get sleepy & confused. Suggest monitoring the patient with a pulse-ox to watch for Sp02 rising as Pa02 rise.
· Assess breath sounds & breathing pattern 1. As WOB decreases during the Tx, the patient should respond favorably by decreasing retractions, flaring and other S/S of respiratory distress 2. Hopefully this will persist for a while after the treatment is over 3. measure the return Vt [see below] to make sure the IC is between 15 ml/kg and 45 ml/Kg · After 5 minutes: repeat VS to make sure the HR hasn’t increased. If it has, wait for a minute or two & recheck. If the HR increased 20 over the baseline give it a few minutes to return to normal. If it does, it is positive pressure, if it doesn't the tachycardia was due to the medication. · Re-check sensorium · Recheck the return Vt · Post Tx: recheck the return Vt · after getting the patient to cough, repeat breath sounds, VS and breathing pattern to assess safety & effectiveness of the therapy
8. How do we measure exhaled volumes using: · Wright's Spirometer: place the spirometer on the exhalation valve and read the volume · Venti-comp bag: place the bag on the exhalation valve and count the number of breaths it takes to inflate the bag, remove it and read the volume.
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