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Clinical Indications and Goals for IPPB
Hemoptysis. Bronchial bleeding sometimes accompanies the improvement of a patient's cough during or after IPPB therapy. If the RCP observes blood in the patient's sputum, the treatment should be terminated and the attending physician notified.

Hypocapnia and respiratory alkalosis. Patients often have a tendency to breathe more rapidly than desired during IPPB therapy. When tidal volumes are also being augmented, a large increase in minute ventilation can occur, causing respiratory alkalosis. Keeping the patient's respiratory rate between 6 to 8/min helps avoid this problem. RCPs need to stay with these patients throughout their therapy, remaining vigilant for signs and symptoms of hypocapnia: dizziness and numbness or tingling of the extremities.

Hypoventilation, hyperoxia, and respiratory acidosis.
Worsened V/Q imbalance and hypoxemia also occur during IPPB therapy when air is the source gas. This is probably due to the maldistribution of ventilation and perfusion caused by positive pressure ventilation. In some patients with chronic hypercapnia, abrupt lowering of the PaC02 during IPPB therapy may result in a period of post-treatment hypoventilation and respiratory acidosis, and hyperoxia may decrease ventilation in sensitive patients. In either situation, the rising C02 levels after therapy may cause any pre-existing hypoxemia to worsen.

Gastric distension.
Poor patient instruction or lack of patient cooperation may result in gastric distension. When positive pressure is applied to the pharynx, the esophagus can open and gas can pass directly into the stomach. The pressure at which this occurs is called the esophageal opening pressure. The esophageal opening pressure is somewhere between 20 to 25 cm H2O. Pharyngeal pressures exceeding this range may cause gastric distension.

It is rare for cooperative patients to experience gastric distension during IPPB therapy. Normally, this reaction is limited to the neurologically obtunded or comatose patients receiving IPPB via a mask. The higher pressures and higher flows often used with these patients can drive the gas down the esophagus and into the stomach, resulting in gastric distention.

While the gastric distension by itself is merely a minor inconvenience, the real danger with excess air in the stomach is the potential for vomiting and aspiration. This hazard can generally be avoided with proper instruction and supervision of cooperative patients, and avoidance of pressures higher than needed to achieve the desired goal.

RCPs are alerted to the presence of this complication when they observe: an increase in the size of the abdomen, rising ventilatory pressure, and evidence of abdominal pain on the part of the patient. The problem can be avoided by starting the therapy at low pressures, volumes, flows, and by increasing them gradually to the point where the lungs are adequately ventilated.

Air trapping, auto-PEEP, overdistension.
Air trapping exists when the pressure remaining in the alveoli at end-expiration is greater than zero. When caused by mechanical ventilation like IPPB, air trapping is often referred to as auto-PEEP or intrinsic PEEP (positive end-expiratory pressure). In some patients, especially those with COPD, IPPB can cause or worsen air trapping, causing overdistension of lung tissue and increasing the incidence of pulmonary barotrauma. Air trapping can also:

  • directly impair cardiovascular performance

  • compress pulmonary blood vessels

  • increase pulmonary vascular resistance

  • impair inspiratory muscle action

  • increase the work of breathing

Air trapping generally occurs when insufficient time is provided for exhalation during therapy. This can sometimes be prevented by mechanically retarding exhalation, thereby lengthening the expiratory phase and preventing early small airway closure. Expiratory retard raises pleural pressures, increasing the possibility of detrimental cardiovascular effects and pulmonary barotrauma. Allowing sufficient time for exhalation is the best way to avoid air trapping during IPPB. This can generally be achieved by using low rates (6 to 8/min) and long expiratory times (at least 4 to 5 seconds).

Psychological dependence.
It is certainly understandable that many patients come to rely on the perceived benefits of IPPB, even in the absence of proven physiologic effects. Patients with chronic lung disease often experience significant feelings of relief with IPPB therapy. While patients who have been using IPPB for years could clearly receive the same benefits from simpler and less costly therapeutic modalities, habit and psychological attachment preclude their changing treatment regimen without considerable resistance. RCPs need to show patience and understanding in dealing with these patients.

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