What bedside monitoring parameters are used to assess for adequacy of oxygenation and ventilation

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In the United States, we care for more than four million patients in an ICU each year; and at any given time, approximately 40% are receiving invasive mechanical ventilation.1,2 When considering monitoring mechanically ventilated patients, we must contemplate three questions:

• Why are we monitoring?
• How good are the tools we use to monitor?
• Does monitoring lead to a change in management that impacts outcomes?

With any patient monitoring system or parameter, our general goal is to identify early warning signs that allow us to reduce or prevent patient harm. This goal is crucial during mechanical ventilation, as almost everything we do can cause patient harm.

Respiratory therapists are the front-line care providers for patients requiring mechanical ventilation, especially those in intensive care units or other chronic ventilator units. We will focus on the rationale, accuracy, and effectiveness of preventing harm for each of these monitoring modalities. Monitoring includes both non-ventilator-specific parameters as well as ventilator monitoring.

Non-ventilator Monitoring

Vital signs, mental status, and respiratory effort

With all the advanced monitoring equipment we use, we must not overlook the importance of a focused clinical exam performed by a skilled respiratory therapist. Depending on the patient care setting and patient acuity, we may perform this almost continuously or as infrequently as once per shift.

We must take care not to perform each assessment in isolation but rather to evaluate whether the patient’s status has changed over the last several minutes, hours, or even days. For example, a therapist detecting a change in mental status with a slight increase in respiratory rate may be a critical early clue to a patient deteriorating. Both of these abnormalities are criteria for early detection of sepsis.

In addition to vital signs and mental status, we must closely monitor the patient’s respiratory effort or work of breathing. An increase in respiratory effort could be a clue to patient-ventilator dyssynchrony, acidemia, pneumothorax, or other pulmonary or non-pulmonary abnormality. While not immediately apparent as to what is causing the problem, recognizing when something is not quite right is essential and allows for earlier evaluation and treatment.

Pulse oximetry

Pulse oximetry allows us to continuously and noninvasively monitor the arterial hemoglobin saturation [SpO2] in patients who may have rapidly changing clinical conditions due to respiratory failure. It identifies early warning signs of changes in respiratory status and ensures hypoxemic patients receive appropriate supplemental oxygen.

We want to ensure we provide adequate supplemental oxygen to prevent hypoxemia and reduce the risk for long-term neuropsychological impairment.3 On the other end, if we provide patients with excess supplemental oxygen and maintain high SpO2 levels, they may have significant hyperoxia that goes unrecognized without arterial sampling of the PaO2. This is important to recognize because providing supplemental oxygen to maintain an SpO2 of 98-100% also can worsen outcomes, even when only maintained for short periods of time.4,5 Therefore, targeting an SpO2 of 94-98% in most patients requiring mechanical ventilation best balances the risks of both hypoxia and hyperoxia.6

End-tidal CO2

If we do not provide adequate ventilation to patients, they can develop hypercarbia, leading to respiratory acidosis and cardiovascular collapse. Significant hypercarbia may not cause desaturation on pulse oximetry until very late in a patient receiving supplemental oxygen or manifest as a change in mental status if the patient receives sedative medications. End-tidal CO2 [EtCO2], which provides a measurement of CO2 concentration in exhaled gas, can help us monitor the adequacy of perfusion and ventilation. We commonly use EtCO2 to confirm proper endotracheal tube placement, assess the quality and effectiveness of cardiopulmonary resuscitation, and monitor for ventilation changes.

We can generally expect EtCO2 to be an acceptable estimate of alveolar PCO2 [PACO2] in normal subjects; however, the difference between the EtCO2 and PACO2 can be quite large in patients with diseased lungs. Since many of the patients we care for on mechanical ventilators have diseases that affect either the pulmonary parenchyma or the pulmonary vasculature, they often have significantly increased alveolar dead space, which leads to a greater difference between PACO2 and EtCO2. In this case, the trend of the EtCO2 may be more useful that the absolute value and a blood gas may be required periodically to assess the difference between EtCO2 and PCO2 in the blood.

EtCO2 can be useful in weaning mechanical ventilation and initiation of trials off the ventilator in patients with tracheostomies. EtCO2 can serve as one additional safety monitor to warn when a patient is failing liberation or weaning from mechanical ventilation. Finally, volumetric capnography, which plots the partial pressure of exhaled CO2 against exhaled tidal volume allows for more accurate calculation of dead space and CO2 production, but it is not readily available in most settings.7

Airway cuff pressure

We monitor the airway cuff pressure on an endotracheal or tracheostomy tube for two main reasons: maintain airway pressure during mechanical ventilation and prevent leakage of secretions into the lungs. If we overinflate the cuff, then we may be applying focal pressure on the tracheal mucosa that impedes capillary blood flow, leading to ischemia of the tissue. This injury can cause long-term complications, such as vocal cord paralysis and tracheal stenosis. Unfortunately, even modern airway cuffs that use a larger volume to distribute the pressure more evenly across the airway mucosa and achieve a seal with a much lower pressure do not eliminate this risk.8

Maintaining the upper range of airway cuff pressures less than 30 cm H2O does not exceed the capillary perfusion pressure and can help reduce pressure-related ischemia and injury to the trachea. Therefore, we cannot wholly prevent secretion drainage solely by increasing airway cuff pressures. We do, however, see an apparent increase in leakage of fluid around the cuff and ventilator-associated pneumonia at a cuff pressure of