7 Integrated Respiratory Care Practice
A practical guide to recognizing respiratory deterioration, interpreting oxygenation and ventilation findings, and responding to airway and ventilator emergencies.
Recognize and respond to deterioration
Begin with the patient, not a test result or device alarm. Assess airway patency, work of breathing, mental status, skin color, vital signs, oxygen saturation, and breath sounds. A concerning trend or a patient who is exhausted, confused, or poorly responsive requires urgent escalation; do not wait for an ABG before acting.
Reassess after each intervention. Check mental status, breathing effort, SpO₂, hemodynamics, and response to oxygen or ventilatory support. Escalate promptly if the patient worsens.
For many acutely or critically ill adults, the suggested SpO₂ target is . For patients with COPD or CO₂ retention, a target of is often used. Individualize targets to the clinical situation and orders, and titrate oxygen to the target rather than assuming that more oxygen is always better.
Separate from
is assessed with PaO₂ and SpO₂, while is reflected in PaCO₂ and pH. Supplemental oxygen may improve hypoxemia, but it does not by itself correct inadequate . Interpret both processes alongside the patient's overall condition.
An can help clarify the pattern, but its values must be considered with the patient's baseline and clinical picture. Read it systematically:
Check pH: acidemia is below , and alkalemia is above .
Identify whether PaCO₂ or HCO₃⁻ explains the pH change.
Assess compensation and . Compensation that is not expected may indicate a mixed disorder.
Relate the results to the patient's condition and baseline, and act on clinical deterioration without waiting for another ABG.
In acute , a low pH with high PaCO₂ identifies the respiratory disorder. An elevated HCO₃⁻ may suggest chronic or prior renal compensation, while acidemia may indicate an acute worsening superimposed on CO₂ retention. When a baseline is known, compare the current results with it; in chronic CO₂ retention, the degree of acidemia can be more informative than PaCO₂ alone.
Respond to worsening COPD
A patient with COPD has worsening breathlessness, respiratory rate breaths per minute, SpO₂ on room air, accessory muscle use, and increasing drowsiness after initially being alert. The ABG is pH , PaCO₂ , HCO₃⁻ , and PaO₂ .
This pattern is acute with elevated bicarbonate suggesting pre-existing renal compensation. The low pH and high PaCO₂ identify ; the elevated bicarbonate suggests chronic or prior compensation, but the acidemia indicates that acute worsening may be superimposed. Compare with the patient's baseline if known.
Drowsiness, significant work of breathing, tachypnea, and hypoxemia are urgent warning signs. Drowsiness may signal worsening hypercapnia, fatigue, or loss of airway protection. Notify the responsible clinician or rapid-response team promptly according to local policy; do not delay escalation to obtain another ABG.
Prioritize airway, breathing, and close reassessment. Position the patient to support breathing, apply and titrate prescribed oxygen, continuously monitor , assess mental status and respiratory effort, and prepare for escalation. For COPD or CO₂ retention, an SpO₂ target of is often used, individualized to the patient.
may be considered if the patient can cooperate and protect their airway, with close monitoring and a clear plan to escalate. Worsening consciousness, inability to protect the airway, hemodynamic instability, or failure to improve requires urgent reassessment for invasive airway support.
Respond to severe hypoxemia
A patient with pneumonia has increasing oxygen needs despite supplemental oxygen, respiratory rate breaths per minute, SpO₂ while receiving FiO₂ , anxiety, and signs of tiring. The ABG is pH , PaCO₂ , HCO₃⁻ , and PaO₂ .
The elevated pH and low PaCO₂ indicate , consistent with rapid breathing. PaO₂ of despite FiO₂ of indicates serious impairment. A low PaCO₂ does not rule out respiratory failure.
High oxygen requirement, low SpO₂, rapid breathing, and fatigue indicate possible impending respiratory failure. Anxiety and tachypnea may precede exhaustion, so reassess frequently and escalate support without waiting for the patient to become obtunded.
If intubation and mechanical are required, use if ARDS is present or suspected. For adults with ARDS, the recommended tidal volume range is predicted body weight, with plateau pressure below . Monitor , ventilator pressures, delivered tidal volume, hemodynamics, and patient–ventilator synchrony; report deterioration promptly.
Respond to ventilator alarms
A mechanically ventilated patient suddenly desaturates, becomes hypotensive, and triggers a high-pressure alarm. Breath sounds are markedly decreased on the left, while the endotracheal tube appears secured.
Assess the patient immediately rather than simply silencing the alarm or changing settings without identifying the cause. Check , chest movement, airway and tube position, breath sounds, and hemodynamics while calling for urgent assistance.
Consider as an emergency. Sudden hypoxemia, hypotension, and markedly reduced breath sounds on one side in a ventilated patient are concerning. Other causes of a high-pressure alarm include secretions or a kinked or obstructed tube, biting, bronchospasm, coughing, or reduced lung compliance. A low-pressure alarm can suggest a disconnection or leak. Mechanical can cause barotrauma and pneumothorax, so sudden deterioration needs immediate evaluation.
Stay with the patient, summon the airway or critical-care team, and follow emergency protocol. Check accessible tubing and connections, verify that the airway is secure, and prepare suction and emergency airway equipment. If is ineffective or equipment failure is suspected, act under local emergency procedures and qualified direction; do not delay help while troubleshooting. If secretions or other clinical signs indicate suction, preoxygenate as appropriate and use the recommended technique.
Integrate assessment and escalation
Recognize respiratory deterioration from the whole clinical picture, not from an ABG or oxygen saturation alone. Interpret pH, PaCO₂, HCO₃⁻, and PaO₂ in context; distinguish failure from ventilatory failure; and escalate early when work of breathing, mental status, oxygen needs, or hemodynamics worsen. For ventilated patients, assess the patient before reacting to alarms, look for reversible causes, and monitor lung-protective targets when ARDS is present.