What is the next line of management for a 63-year-old male with elevated blood glucose, moderate dehydration, metabolic acidosis (pH 7.34, PaCO₂ 41 mm Hg, bicarbonate 22 mmol/L, anion gap 14.7), left ventricular ejection fraction 19% and severe pulmonary arterial hypertension?

Management of Hyperglycemic Crisis with Severe Cardiac Dysfunction

This patient requires immediate fluid resuscitation with isotonic saline, cautious insulin therapy after confirming potassium >3.3 mEq/L, and intensive cardiopulmonary monitoring given the severe left ventricular dysfunction and pulmonary hypertension.

Initial Assessment and Diagnosis

This clinical presentation suggests hyperglycemic hyperosmolar state (HHS) or mild diabetic ketoacidosis (DKA) based on the elevated blood glucose, moderate dehydration, and borderline metabolic acidosis (pH 7.34, bicarbonate 22.1 mEq/L, anion gap 14.7 mEq/L). 1, 2

• The pH of 7.34 with bicarbonate 22.1 mEq/L places this patient in a borderline category—just above the DKA threshold (pH <7.3, bicarbonate <15 mEq/L) but with metabolic acidosis and an elevated anion gap suggesting ketoacid accumulation. 1
• The anion gap of 14.7 mEq/L is elevated (normal <10-12 mEq/L), indicating organic acid accumulation rather than simple hyperchloremic acidosis. 1, 3
• Calculate corrected serum sodium by adding 1.6 mEq for each 100 mg/dL glucose above 100 mg/dL to assess true volume status and osmolality. 2

Critical Considerations for Cardiac Dysfunction

The severe left ventricular systolic dysfunction (LVEF 19%) and severe pulmonary arterial hypertension fundamentally alter the management approach, requiring extreme caution with fluid administration and close hemodynamic monitoring. 4

• Avoid excessive fluid administration which may precipitate pulmonary edema and worsen pleural effusions in the setting of severe cardiac dysfunction. 4
• Position the patient upright if hemodynamically stable to improve lung expansion and reduce work of breathing. 4
• Provide supplemental oxygen to maintain saturation >92% to improve tissue oxygenation and reduce respiratory drive. 4

Fluid Resuscitation Strategy

Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/h during the first hour, but reduce this rate significantly given the severe cardiac dysfunction—consider starting at 7-10 mL/kg/h with close monitoring of respiratory status, oxygen saturation, and jugular venous pressure. 1, 4, 2

• Monitor fluid input/output, hemodynamic parameters (blood pressure, heart rate, central venous pressure if available), and clinical examination (lung auscultation, peripheral edema) every 1-2 hours to assess tolerance of fluid replacement. 4, 2
• After the initial hour, switch to 0.45% NaCl if corrected serum sodium is elevated, or continue 0.9% NaCl if corrected sodium is normal or low, but maintain conservative rates (250-500 mL/h maximum) given cardiac limitations. 1, 2
• The typical total body water deficit in HHS is 9 liters (100-200 mL/kg), but in this patient, aim to correct deficits more gradually over 36-48 hours rather than 24 hours to avoid cardiac decompensation. 1, 2

Insulin Therapy

Do not initiate insulin until serum potassium is confirmed to be >3.3 mEq/L, as insulin drives potassium intracellularly and can precipitate life-threatening cardiac arrhythmias, particularly dangerous in this patient with severe cardiac dysfunction. 1, 4, 5

• Once potassium is adequate, administer intravenous regular insulin without an initial bolus (given cardiac compromise) at a continuous infusion rate of 0.1 units/kg/h. 4, 5
• Target a gradual reduction in blood glucose by 50-75 mg/dL per hour—avoid more rapid correction which increases risk of cerebral edema and osmotic shifts. 4, 2
• If plasma glucose does not fall by 50 mg/dL in the first hour, double the insulin infusion rate hourly until achieving steady glucose decline. 2, 6
• When blood glucose reaches 250 mg/dL, add dextrose (5% dextrose in 0.45% NaCl) to IV fluids while continuing insulin infusion at a reduced rate (0.05-0.1 units/kg/h) to clear ketones and prevent hypoglycemia. 4, 2

Electrolyte Management

Potassium replacement is critical as total body potassium deficits are common (4-6 mEq/kg) despite potentially normal or elevated initial serum levels due to acidosis and insulin deficiency causing transcellular shifts. 1, 2, 6

• Once urine output is confirmed and serum potassium falls below 5.5 mEq/L, add 20-40 mEq/L potassium chloride to each liter of IV fluid. 1, 2
• If initial potassium is <3.3 mEq/L, hold insulin and aggressively replace potassium before starting insulin therapy. 1, 4
• Consider phosphate replacement (20-30 mEq/L as potassium phosphate) given the cardiac dysfunction, as hypophosphatemia can worsen cardiac contractility and respiratory muscle weakness—particularly relevant with LVEF 19%. 1, 2

Monitoring Protocol

Draw blood every 2-4 hours for serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH (arterial blood gases are unnecessary for ongoing monitoring). 1, 4, 2, 6

• Monitor blood glucose every 1-2 hours until stable, then every 4 hours. 4, 6
• Calculate effective serum osmolality: 2[measured Na (mEq/L)] + glucose (mg/dL)/18, and ensure the induced change does not exceed 3 mOsm/kg/h to prevent cerebral edema. 1, 2
• Watch for signs of cerebral edema (lethargy, behavioral changes, seizures, bradycardia, respiratory arrest), though this is more common in younger patients. 4, 2
• Monitor for signs of fluid overload (worsening dyspnea, crackles, declining oxygen saturation, increasing jugular venous pressure) given the severe cardiac dysfunction. 4

Management of CO2 Retention

The PaCO2 of 41.4 mmHg is inappropriately normal for the degree of metabolic acidosis present—expected compensatory PaCO2 should be approximately 35-37 mmHg (using Winter's formula: expected PaCO2 = 1.5 × HCO3 + 8 ± 2). 7, 3

• This relative CO2 retention suggests impaired respiratory compensation, likely due to the combination of severe pulmonary arterial hypertension, cardiac dysfunction, and possible pleural effusions. 4, 7
• Consider chest imaging to evaluate for pleural effusions and pulmonary edema. 4
• If significant bilateral pleural effusions are present and contributing to respiratory compromise, therapeutic thoracentesis may be necessary, but coordinate with cardiology given the severe PAH. 4
• Avoid sedatives and narcotics that may further suppress respiratory drive. 7

Resolution Criteria and Transition

DKA is resolved when: glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, and venous pH >7.3. 1, 4

HHS is resolved when: mental status improves and hyperosmolarity resolves (effective osmolality <320 mOsm/kg). 2, 6

• Administer subcutaneous basal insulin (long-acting insulin such as glargine or detemir) 2-4 hours before discontinuing IV insulin infusion to prevent rebound hyperglycemia and recurrent metabolic decompensation. 4, 2, 6
• Continue IV insulin for 1-2 hours after subcutaneous insulin is given to ensure adequate overlap and plasma insulin levels. 1, 4

Identification of Precipitating Causes

Obtain bacterial cultures (blood, urine, other sites as indicated) and chest X-ray, as infection is the most common precipitating factor for hyperglycemic crises. 2, 6

• Evaluate for acute coronary syndrome with serial troponins and ECG, as myocardial infarction can precipitate hyperglycemic crisis and is more likely in patients with severe cardiac dysfunction. 2, 6
• Review medication compliance and recent changes, particularly diuretics which may have precipitated volume depletion. 1, 2

Critical Pitfalls to Avoid

• Never start insulin before confirming potassium >3.3 mEq/L—this can precipitate fatal arrhythmias, especially in a patient with LVEF 19%. 4, 5
• Avoid overly aggressive fluid resuscitation—the standard 15-20 mL/kg/h may precipitate acute pulmonary edema in this patient with severe LV dysfunction and PAH. 4
• Do not correct hyperglycemia and osmolality too rapidly—limit osmolality change to <3 mOsm/kg/h to prevent cerebral edema. 4, 2
• Do not discontinue IV insulin prematurely—ketosis may persist even after glucose normalization, and abrupt discontinuation without subcutaneous insulin overlap causes rebound hyperglycemia. 1, 4
• Bicarbonate administration is not indicated at this pH (7.34) and does not improve outcomes; it may worsen intracellular acidosis and cause hypocalcemia. 1, 8

Admission and Multidisciplinary Care

Admit to the cardiac care unit or intensive care unit for at least 24-48 hours of continuous monitoring given the severe cardiac dysfunction and pulmonary hypertension. 1

• Assemble a multidisciplinary team including endocrinology, cardiology, and critical care to coordinate management of the complex interplay between hyperglycemic crisis and severe cardiopulmonary disease. 1
• Consider early cardiology consultation regarding optimization of heart failure therapy and PAH-specific medications once metabolic stabilization is achieved. 1