The nurse assesses the telemetry monitor of a client who is 24 hours postoperative from having a permanent pacemaker insertion. The nurse observes that a pacemaker spike is present before each QRS complex in lead II of the electrocardiogram (ECG). Which intervention should the nurse implement?

Answer:

Potential Condition:

Acute Adrenal Crisis

• The client has a history of Addison’s disease (chronic steroid use) and recent illness with vomiting, leading to decreased oral intake and medication noncompliance.
• Symptoms such as hypotension (80/50 mmHg), tachycardia (115 bpm), confusion, nausea, vomiting, and abdominal pain are classic signs of acute adrenal insufficiency.

Actions to Take:

Bolus Intravenous Fluids

• Fluid resuscitation with 0.9% normal saline is critical to restore intravascular volume and correct hypotension due to adrenal insufficiency.

Check Blood Glucose

• Hypoglycemia is a common complication of adrenal crisis due to cortisol deficiency, requiring close monitoring and possible glucose administration.

Parameters to Monitor:

Blood Pressure

• Hypotension is a hallmark of adrenal crisis and must be monitored closely to assess response to fluid resuscitation and steroid therapy.

Electrolytes

• Clients with adrenal crisis often have hyponatremia and hyperkalemia due to aldosterone deficiency, requiring frequent electrolyte monitoring.

Incorrect Choices:

Potential Conditions:

• Ketoacidosis: More common in diabetes, presents with high blood glucose and ketonuria.
• Diabetes Insipidus: Causes polyuria and dehydration but lacks hypotension and hyperkalemia.
• Myxedema: Linked to hypothyroidism, causing bradycardia and hypothermia, not hypotension and hyperkalemia.

Actions to Take:

• Hold hydrocortisone dose: Steroid replacement is necessary, not withholding it.
• Collect urine for a urinalysis: Not a priority; adrenal crisis is diagnosed via history, symptoms, and labs.
• Change intravenous fluids to 0.45%: Hypotension requires 0.9% normal saline, not hypotonic fluids.

Parameters to Monitor:

• Urine output: Useful but less critical than blood pressure and electrolytes in adrenal crisis.
• Thyroid stimulating hormone: Relevant for hypothyroidism, not adrenal insufficiency.
• Heart rate: Tachycardia is expected but is not the most critical indicator of improvement.

• Compensated respiratory acidosis occurs when the lungs retain CO₂, causing acidosis, but the kidneys compensate by increasing bicarbonate (HCO₃⁻) levels. In this case, the pH is low, and the PaCO₂ is within normal limits, which does not indicate a respiratory issue or compensation. Compensation would require an elevated HCO₃⁻, which is not provided in the lab results.
• Compensated metabolic acidosis would require a low pH with a decreased PaCO₂, as the respiratory system compensates by increasing ventilation (hyperventilation) to "blow off" CO₂. Since the PaCO₂ in this case is within normal limits, no significant respiratory compensation has occurred yet, making this uncompensated metabolic acidosis instead.
• Uncompensated respiratory acidosis would present with a low pH and an elevated PaCO₂ (>45 mmHg) due to inadequate ventilation and CO₂ retention. Since the PaCO₂ here is 37 mmHg (within normal range), respiratory acidosis is unlikely. The metabolic component, rather than a respiratory problem, is driving the acidosis.
• Uncompensated metabolic acidosis is characterized by a low pH (7.23) and a normal PaCO₂ (37 mmHg), indicating a primary metabolic problem without sufficient respiratory compensation. In diabetic ketoacidosis (DKA), the lack of insulin results in fat breakdown and ketone production, leading to a drop in pH and metabolic acidosis. This client likely has DKA due to their history of type 1 diabetes and the lack of insulin administration.
• Kussmaul respirations are a compensatory response to metabolic acidosis, seen in conditions like DKA. However, they do not cause acidosis; instead, they are the body's attempt to correct it by exhaling CO₂. Since the ABG shows normal PaCO₂, there is no strong evidence of hyperventilation, suggesting compensation has not yet occurred.
• Starvation can lead to ketoacidosis due to prolonged fasting and fat metabolism, producing ketones. However, in type 1 diabetes, the primary issue is no insulin production, not caloric deprivation. The severity of metabolic acidosis in this client is more likely due to insulin deficiency rather than starvation.
• Tissue hypoxia leads to lactic acidosis, which results from anaerobic metabolism. This can be seen in conditions like sepsis or shock. However, in this case, the client has type 1 diabetes, and the more likely cause of acidosis is ketoacidosis due to insulin deficiency rather than hypoxia.
• A lack of insulin in type 1 diabetes prevents glucose uptake, forcing the body to break down fat, leading to ketone formation and metabolic acidosis. This matches the clinical scenario of a patient with a history of type 1 diabetes, hyperglycemia >500 mg/dL, and metabolic acidosis.