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Obtain a medical order for the administration of sodium bicarbonate: Sodium bicarbonate is used to treat metabolic acidosis, not respiratory acidosis. In this case, the elevated PaCO₂ indicates hypoventilation and respiratory acidosis, so bicarbonate would not address the underlying problem and could worsen acid-base imbalance.

Prepare for intubation: Intubation may be necessary if the client cannot maintain adequate ventilation or oxygenation. However, this client is showing mild respiratory acidosis with only slightly decreased oxygenation, and less invasive interventions like deep breathing and coughing should be attempted first.

Have the client breathe into a rebreather bag at a slow rate: Rebreathing into a bag increases CO₂ levels and would worsen respiratory acidosis. This intervention is inappropriate for a client already retaining CO₂ and could further compromise acid-base balance and oxygenation.

Increase the PEEP: Positive end-expiratory pressure helps keep alveoli open and improve oxygenation but does not directly increase CO₂ elimination. While beneficial for hypoxemia, adjusting PEEP alone will not correct respiratory acidosis caused by hypoventilation.

Sedate and paralyze the client: Sedation and paralysis may be used to facilitate ventilator synchrony in specific situations, but they do not directly correct CO₂ retention. These interventions are not the first-line approach for managing respiratory acidosis and could worsen hypoventilation if not carefully managed.

Increase the FiO2 and/or PEEP: Increasing FiO₂ and PEEP improves oxygenation but does not enhance CO₂ removal. Respiratory acidosis requires interventions that increase alveolar ventilation rather than just oxygen delivery.

pH 7.50; PaCO2 28 mmHg; PaO2 100 mmHg; HCO3 24 mEq/L: While respiratory alkalosis is present, the PaO2 is normal, which is not consistent with early ARDS. Early ARDS typically shows hypoxemia with low PaO2 despite supplemental oxygen, reflecting impaired gas exchange.

pH 7.34; PaCO2 60 mmHg; PaO2 68 mmHg; HCO3 30 mEq/L: Elevated PaCO2 and normal pH with mild hypoxemia suggest respiratory acidosis, which is more characteristic of late or severe ventilatory failure, not early ARDS. Early ARDS usually presents with hypoxemia and compensatory hyperventilation.

pH 7.34; PaCO2 25 mmHg; PaO2 80 mmHg; HCO3 19 mEq/L: While PaCO2 is low, the PaO2 is normal, indicating adequate oxygenation. Early ARDS usually presents with significant hypoxemia despite initial compensation, so this ABG does not match early ARDS.

Carbonic acid: Carbonic acid would increase acid load in the body and worsen acidosis. Administering it in the setting of metabolic acidosis is contraindicated and would exacerbate the acid-base imbalance.

Calcium carbonate: Calcium carbonate is an antacid used primarily to neutralize gastric acid or treat calcium deficiency, not to correct systemic metabolic acidosis. It has minimal effect on serum bicarbonate levels in acute metabolic disturbances.

Acetazolamide: Acetazolamide is a carbonic anhydrase inhibitor that promotes renal bicarbonate excretion and is used to correct metabolic alkalosis, not acidosis. Its administration in metabolic acidosis would further lower bicarbonate and worsen the condition.

Normal ABG results: The ABG shows a pH of 7.50 (alkalemia) and PaCO₂ of 30 mmHg (hypocapnia), indicating respiratory alkalosis, which is not normal. PaO₂ is slightly low at 76 mmHg, and SaO₂ is decreased at 90%, further confirming abnormal gas exchange.

Acute ventilatory failure: Acute ventilatory failure usually presents with respiratory acidosis (elevated PaCO₂) and hypoxemia, indicating insufficient ventilation. This client has low PaCO₂, which indicates hyperventilation rather than ventilatory failure.

Late acute respiratory distress syndrome: Late ARDS is marked by worsening hypoxemia, hypercapnia, and respiratory acidosis due to alveolar collapse and decreased lung compliance. This client’s ABG shows alkalosis and mild hypoxemia, consistent with early, not late, ARDS.

Administration of IV antibiotics routinely: Routine prophylactic antibiotics are not recommended because they do not prevent VAP and may promote antibiotic resistance. Antibiotics should be reserved for treatment of confirmed infections, not routine prevention.

Changing ventilator circuit tubing every 72 hours: Frequent scheduled changes of ventilator circuits have not been shown to reduce VAP incidence and may increase the risk of contamination. Tubing should only be changed if visibly soiled or malfunctioning.

Routine prone positioning: Prone positioning is used selectively for clients with severe ARDS to improve oxygenation, not as a routine VAP prevention strategy. While beneficial for gas exchange, it does not specifically reduce the risk of ventilator-associated pneumonia.

The client displays zero twitch responses: Zero twitches indicate complete neuromuscular blockade, which is usually excessive and can lead to complications such as prolonged paralysis or respiratory compromise. This level is not desired for most ventilated patients receiving titrated paralytics.

The client displays three out of four twitch responses: Three twitches suggest a light blockade. This may not provide sufficient muscle relaxation for optimal ventilator synchrony or procedural requirements and may require an increase in paralytic dose.

The client can blink their eyes on command: The ability to follow commands indicates minimal or no neuromuscular blockade, which is inadequate for clients requiring paralysis for mechanical ventilation or other critical interventions.

The arterial line shows a blood pressure of 108/60: This blood pressure is within an acceptable range and does not immediately indicate the need to adjust ventilator settings. Hemodynamic monitoring must consider overall trends, not a single reading within normal limits.

The pulmonary artery wedge pressure (PAWP) is increased: An elevated PAWP indicates increased left ventricular preload or fluid overload, which may require fluid management but does not directly necessitate changing PEEP unless it is contributing to cardiac compromise.

The pulmonary artery pressure (PAP) is decreased: A decrease in PAP is generally not concerning in isolation and may reflect effective oxygenation or reduced pulmonary vascular resistance. It does not typically signal the need to change ventilator settings.

Bradycardia: Bradycardia is a late sign of hypoxia, often occurring after prolonged oxygen deprivation when compensatory mechanisms fail. Relying on bradycardia as an early warning could delay life-saving interventions, making it less useful for early detection.

Hypotension: Hypotension is also a late manifestation of inadequate oxygenation or shock. It typically occurs after hypoxemia has caused significant tissue hypoperfusion and is not an early clinical indicator of oxygen deprivation.

Cyanosis: Cyanosis reflects severe or prolonged hypoxia and is considered a late sign. By the time cyanosis is visible, the client may already be experiencing critical oxygen deficit, making early recognition and intervention more difficult.

Turn off ventilator alarms when suctioning client: Ventilator alarms are safety features that alert the nurse to changes in airway pressure or ventilation status. Turning them off can prevent timely detection of serious complications such as disconnection or obstruction, so this action is unsafe and not recommended.

Suction the client every hour: Routine suctioning on a fixed schedule can cause mucosal trauma, hypoxia, and infection. Suctioning should be performed only as needed, based on clinical assessment such as increased secretions, rhonchi, or decreased oxygen saturation.

Keep the client's hands restrained: Restraints may sometimes be necessary to prevent accidental extubation, but they are not an essential intervention for all ventilated clients. Use of restraints should be minimized and based on individual risk assessment rather than applied routinely.