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<< Ventilator Management And Troubleshooting In The Emergency Department

Clinical Course In The Emergency Department

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Clinical Course In The Emergency Department

Clinical Course In The Emergency Department

Determining Stability

Stabilizing the patient with acute respiratory failure in the ED should focus on 2 questions: (1) Is gas exchange sufficient to meet the patient’s metabolic needs? and (2) Is the ventilator adjusted in a way to prevent further injury or decompensation? With regard to gas exchange, emergency physicians should keep in mind that oxygenation is the first priority. A normal PaO2 is 90 to 100 mm Hg while breathing room air, with an SaO2 of 98% to 100%. In critically ill patients, however, it is acceptable in most cases to maintain a PaO2 of 55 to 80 mm Hg and an SpO2 of 88% to 95%.5,13 It has been established that breathing 100% oxygen can cause an acute tracheobronchitis.20 It has not been clearly established that higher concentrations of inspired oxygen are associated with worse clinical outcomes, but the potential for adverse effects still exists.21 A multicenter cohort study of patients resuscitated from cardiac arrest found that an initial PaO2 > 300 mm Hg was independently associated with higher in-hospital mortality.22 It seems prudent to treat oxygen as any other drug and only use the amount necessary to meet the patient’s needs.

Ventilation should be focused on maintaining a pH of at least 7.15. Most often, the rate on the ventilator can be adjusted safely to keep the PaCO2 in the normal range of 35 to 45 mm Hg and the pH in the range of 7.35 to 7.45. In certain cases, however, it may not be possible to have normal CO2 clearance. For instance, in status asthmaticus, a higher respiratory rate may lead to more dynamic hyperinflation, and higher tidal volumes may cause excessive alveolar stretch and result in lung injury.23 In many cases, it is better to accept some degree of respiratory acidosis rather than risk further injury to the patient. Hypercapnia can increase intracranial pressure, however, and a respiratory acidosis should be avoided in patients with traumatic brain injury, intracranial bleeding, or other conditions associated with intracranial hypertension. Severe alkalemia (pH > 7.60) can also have adverse effects. Cerebral and myocardial arteriolar constriction can occur. Additionally, alkalemia can lead to ionized hypocalcemia, seizures, tetany, and stupor.24 Respiratory alkalosis should also be avoided.

Obtaining an arterial blood gas after the initial ventilator settings are applied and after any major changes in the settings is prudent. Continuous cardiac monitoring and pulse oximetry are also recommended for all ventilated patients in the ED. Continuous waveform capnography, while not universally available, is very helpful in monitoring proper ETT placement and in following ventilation. The end-tidal CO2 does not correlate exactly with the PaCO2, but significant changes in the end-tidal CO2 level should prompt the emergency physician to reassess the patient. An in-depth discussion of the use of waveform capnography is beyond the scope of this review, but interested readers are recommended to the excellent review by Kodali,25 or refer to the Pediatric Emergency Medicine Practice issue titled “Capnography In The Pediatric Emergency Department: Clinical Applications,” available at www.ebmedicine.net/capnography.

Identifying And Managing Deterioration

Whenever a critically ill patient deteriorates in the ED, the emergency physician must perform a rapid primary survey. In ventilated patients, this includes ensuring that the ETT is still in the trachea (confirming aeration of both lungs) and assessing the patient’s perfusion.

Emergency physicians should always go back to the primary survey when something goes wrong. An agitated patient on the ventilator should never be sedated before the physician checks the tube, sounds, and SpO2. Following are some specific targets to consider, based on the alarm or diagnostic testing, once the primary survey is completed.

Problem: High Airway Pressure
This is the alarm in VCV. If PCV is being used, the alarm will be for low tidal volume; however, the approach is the same. This alarm indicates that there is a reduction in the compliance of the respiratory system. The first step is to determine whether this is a lung problem or an airway problem (See Table 3):

  • Perform an inspiratory hold maneuver to determine the PPLAT. If there is high PAP and low PPLAT, then the problem is high airway resistance. If there is high PAP and high PPLAT, then the problem is in the lungs or compression of the lungs, leading to decreased lung compliance.
  • Bedside ultrasound is an effective way to evaluate for pneumothorax, pleural effusion, and pulmonary edema.
  • Chest x-ray can confirm proper position of the ETT and will show atelectasis, infiltrates, pneumothorax, or pulmonary edema.

Problem: Hypoxemia
New or worsening hypoxemia is always serious. The first step is to exclude mechanical problems or tube dislodgement. Disconnect the patient from the ventilator, and connect a bag-valve mask with 100% oxygen. Confirm ETT placement with capnography and auscultation. Consider direct visualization. Once it is confirmed that the ventilator and the ETT are functioning properly, consider the following workup for hypoxemia:

  • Bedside lung ultrasound is a rapid way to diagnose pneumothorax, pleural effusion, or pulmonary edema.26
  • Chest x-ray will also demonstrate worsening infiltrates, pneumothorax, pulmonary edema, atelectasis, or new effusions. Increase the PEEP if the problem is in the lung parenchyma.
  • Always consider pulmonary embolism as a cause for new hypoxemia in a critically ill patient. Bedside ultrasonography to assess for right ventricular strain or noncompressible femoral veins can aid in the diagnosis. Computed tomography pulmonary angiography is considered to be the gold standard for diagnosis of a pulmonary embolism.
  • If there are absent breath sounds on one side, pull the ETT back a few centimeters if it is entering the mainstem bronchus on the chest x-ray. Direct visualization of tube placement with bronchoscopy is another alternative.
  • If there are absent breath sounds on one side, even with the tube in the correct place, consider pneumothorax or mucus plugging with complete atelectasis of the lung.
  • Tension pneumothorax should be suspected if breath sounds are absent on one side and if the patient is hypotensive, tachycardic, and hypoxic. Unilateral absent breath sounds are not sensitive to diagnose this condition, and a deviated trachea is a late sign.

Problem: Dynamic Hyperinflation
Dynamic hyperinflation is usually due to inadequate time for exhalation. High airway resistance only makes it worse. On the ventilator, the expiratory flow will not return to baseline before the next breath begins, and there will be measurable autoPEEP. On physical examination, the patient will appear uncomfortable. The patient’s abdominal muscles will contract during forced exhalation, and there may be jugular venous distension. Due to the increasing amount of dead space, the PaCO2 will actually go up as the ventilator rate is increased. Below are some steps to correct dynamic hyperinflation:

  • If the patient is hemodynamically unstable, disconnecting the ventilator is a rapid way to allow trapped air to escape. Ventilation with a bagvalve mask can be performed until the patient’s condition has stabilized, after which the ventilator can be adjusted.
  • Lower the ventilator rate, usually between 10 and 14 breaths/min. This is the easiest and quickest way to improve expiratory flow.
  • Shorten the inspiratory time to keep the inspiratory time to expiration time (I:E) ratio in the 1:3 to 1:5 range.
  • Keep the tidal volume in the 6 to 8 mL/kg range. A higher tidal volume will often slow the patient’s spontaneous respirations, but a tidal volume > 8 mL/kg predicted body weight may cause lung injury.16,17
  • Increase the inspiratory flow to 60 to 80 L/min to permit more time for exhalation.
  • Adequate sedation with opioids will help blunt tachypnea, but can also lead to CO2 retention and respiratory acidosis. This may be harmful in patients with increased intracranial pressure.
  • Treat bronchospasm with inhaled bronchodilators and systemic steroids.
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