Based on this rhythm strip, which interpretation should the nurse make?

A. Low PaO2. Clients with DKA do not typically have significant hypoxemia unless there is concurrent respiratory compromise. The primary issue in DKA is metabolic acidosis rather than oxygenation.
B. Low lactic acid. Lactic acidosis is not a hallmark of DKA. Instead, DKA is characterized by ketone production from fatty acid metabolism. Elevated lactic acid is more common in conditions like sepsis or tissue hypoxia.
C. Low pH. Diabetic ketoacidosis (DKA) causes metabolic acidosis due to the accumulation of ketone bodies, leading to a pH below 7.35. The absence of insulin results in unregulated lipolysis and ketogenesis, significantly lowering blood pH.
D. Low bicarbonate (HCO3-). In metabolic acidosis, bicarbonate acts as a buffer and gets depleted while neutralizing excess acids. Clients with DKA typically have a bicarbonate level below 18 mEq/L (18 mmol/L), confirming metabolic acidosis.
E. High PaCO2. In metabolic acidosis, respiratory compensation leads to hyperventilation (Kussmaul respirations), causing PaCO2 to decrease as the body attempts to blow off excess CO2 to normalize pH.

A. Promote oxygenation to tissues. Oxygenation is not a primary goal in DKA management unless there is a coexisting condition causing hypoxia. DKA primarily leads to metabolic acidosis and dehydration rather than respiratory failure, and oxygenation is typically maintained unless complications such as pneumonia or severe shock develop.
B. Reverse dehydration. Severe dehydration occurs in DKA due to osmotic diuresis caused by hyperglycemia. The priority is to restore intravascular volume with isotonic IV fluids such as 0.9% normal saline to improve circulation, support kidney function, and prevent shock. Fluid replacement is essential for stabilizing blood pressure and promoting glucose clearance.
C. Replace insulin. The lack of insulin is the primary cause of DKA, leading to unchecked lipolysis and ketone production. IV insulin therapy is necessary to suppress ketogenesis, lower blood glucose levels, and allow cells to use glucose for energy. Insulin must be administered cautiously with continuous monitoring to prevent hypoglycemia and electrolyte imbalances.
D. Correct electrolytes that are out of normal range. Electrolyte imbalances, particularly potassium depletion, are common in DKA due to osmotic losses and shifting caused by insulin therapy. Potassium replacement is required even if levels appear normal initially, as insulin will drive potassium into cells, leading to hypokalemia. Sodium and bicarbonate levels should also be monitored and corrected as needed.
E. Provide respiratory support. Respiratory support is not typically required unless the client experiences severe respiratory distress or altered mental status. Kussmaul respirations are a natural compensatory mechanism that helps the body exhale CO₂ and correct acidosis. Supplemental oxygen is only necessary if there is an underlying pulmonary condition or respiratory failure.
F. Prevent hyperventilation. Hyperventilation in the form of Kussmaul respirations is the body's way of compensating for metabolic acidosis. It should not be suppressed, as it plays a crucial role in reducing acid buildup. Treating the underlying cause of DKA with fluids, insulin, and electrolyte replacement will allow respiratory function to normalize.