A client is in septic shock, has ARDS and is intubated on a ventilator.

Cardiac output (CO) = 7.5 L/min

Pulmonary artery wedge pressure (PAWP) 15 mmHg

Systemic vascular resistance (SVR) - 500 dynes/second/cm-5

BP-70/46 mmHg

In order to improve the client's hemodynamic status the nurse would expect to

A. Notify the client's health care provider: Contacting the provider will be necessary, but the nurse must first verify the potassium level because the ECG changes—widened QRS and peaked T waves—strongly suggest life-threatening hyperkalemia. Having the value ready allows immediate, precise communication and intervention.

B. Look at the client's current blood urea nitrogen (BUN) and creatinine levels: These levels confirm AKI severity but do not directly explain the dangerous conduction changes. Hyperkalemia poses an immediate risk of cardiac arrest, so potassium assessment takes priority for rapid correction.

C. Document the QRS interval: Documentation is routine but not urgent when ECG changes indicate an unstable electrolyte imbalance. Delaying assessment of potassium prolongs exposure to a potentially fatal arrhythmia and does not address the underlying cause.

D. Check the chart for the most recent blood potassium level: Peaked T waves and a widened QRS are hallmark findings of severe hyperkalemia. Verifying the potassium level is the most immediate step because it confirms the cause and guides emergent therapy such as calcium gluconate, insulin, or dialysis.

A. 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.

B. 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.

C. pH 7.50; PaCO2 28 mmHg; PaO2 58 mmHg; HCO3 24 mEq/L: This ABG demonstrates hypoxemia (PaO2 < 60 mmHg) and respiratory alkalosis due to hyperventilation, which is typical in the early stages of ARDS as the patient attempts to compensate for impaired oxygenation. This pattern aligns with early ARDS pathophysiology.

D. 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.