DKA in a Heart Failure Patient: Navigating Insulin, Fluid Resuscitation, and Cardiorenal Considerations

Dr Neeraj Manikath , claude.ai

Abstract

The concurrent presentation of diabetic ketoacidosis (DKA) and heart failure (HF) poses a unique clinical challenge that demands careful navigation between two potentially conflicting therapeutic paradigms. While aggressive fluid resuscitation remains a cornerstone of DKA management, patients with underlying cardiac dysfunction are at heightened risk of iatrogenic fluid overload, pulmonary edema, and cardiorenal syndrome. This review synthesizes current evidence and provides practical guidance for postgraduate physicians managing this complex intersection, with emphasis on fluid-sparing strategies, hemodynamic monitoring, insulin protocols, and electrolyte management. We present clinical pearls and evidence-based approaches to optimize outcomes while minimizing complications in this vulnerable population.

Introduction

Diabetic ketoacidosis represents a life-threatening complication of diabetes mellitus, characterized by hyperglycemia, metabolic acidosis, and ketonemia. Traditional management relies heavily on intravenous fluid resuscitation, with guidelines recommending 1-1.5 L of isotonic saline in the first hour, followed by ongoing fluid replacement at 250-500 mL/hour.(1,2) However, approximately 10-15% of patients presenting with DKA have concurrent heart failure, creating a therapeutic dilemma where standard fluid protocols may precipitate pulmonary edema and hemodynamic decompensation.(3)

The prevalence of this clinical intersection is increasing as both diabetes and heart failure rates rise globally. Patients with diabetes have a 2-5 fold increased risk of developing heart failure, with shared pathophysiological mechanisms including myocardial metabolic dysfunction, microvascular disease, and autonomic neuropathy.(4) When DKA occurs in the setting of established HF, mortality rates increase substantially, reaching 15-20% compared to 1-5% in uncomplicated DKA.(5)

This review addresses the critical question: How do we effectively treat severe metabolic derangement while respecting cardiovascular limitations?

Pathophysiology: Understanding the Collision Course

The Perfect Storm: Why These Conditions Converge

Shared Risk Factors and Precipitants:

Infections (the most common DKA precipitant) simultaneously trigger HF decompensation
Medication non-compliance affects both conditions
SGLT2 inhibitors, increasingly used in HF management, can precipitate euglycemic DKA(6)
Acute coronary syndromes may trigger both DKA and acute HF
Chronic kidney disease, common to both conditions, amplifies risk

Hemodynamic Considerations in DKA: DKA induces a complex hemodynamic state characterized by:

Profound volume depletion (typically 6-9 liters in moderate-severe DKA)(7)
Osmotic diuresis-induced hypovolemia
Decreased effective arterial blood volume
Compensatory tachycardia and increased cardiac output
Metabolic acidosis causing myocardial depression and reduced contractility
Electrolyte disturbances (particularly hypokalemia) predisposing to arrhythmias

Cardiac Limitations in Heart Failure: Patients with HF demonstrate:

Reduced cardiac reserve and inability to increase output appropriately
Elevated filling pressures (PCWP >18 mmHg)
Diastolic dysfunction with impaired ventricular compliance
Neurohormonal activation (RAAS, SNS) promoting sodium and water retention
Renal hypoperfusion with reduced diuretic responsiveness
Pulmonary vascular congestion with low threshold for pulmonary edema

Cardiorenal Syndrome: The Third Player

Cardiorenal syndrome (CRS) frequently complicates this clinical scenario. Type 1 CRS (acute worsening of cardiac function leading to acute kidney injury) and Type 2 CRS (chronic HF causing progressive chronic kidney disease) both alter fluid handling and electrolyte management.(8) The kidney's inability to excrete administered fluids, combined with the heart's inability to handle increased preload, creates a narrow therapeutic window.

Pearl #1: In DKA with HF, you're not just treating hyperglycemia and acidosis—you're managing a state of "total body fluid overload with effective intravascular volume depletion." This paradox is central to understanding management strategy.

Initial Assessment: Risk Stratification and Monitoring

Clinical Evaluation

History and Physical Examination Red Flags:

Known HF with reduced ejection fraction (HFrEF) or preserved EF (HFpEF)
Recent HF hospitalization (<3 months)
Orthopnea, paroxysmal nocturnal dyspnea
Elevated jugular venous pressure (JVP >8 cm H₂O)
S3 gallop on cardiac auscultation
Bilateral pulmonary crackles (pre-existing vs. new)
Peripheral edema
Hepatomegaly and hepatojugular reflux
Narrow pulse pressure suggesting low cardiac output

Oyster #1: Not all crackles indicate volume overload in DKA patients. Kussmaul respirations with forced expiration can create atelectasis and transient crackles. However, persistent crackles above the bases, especially with elevated JVP, indicate true pulmonary congestion.

Laboratory and Imaging Workup

Essential Baseline Investigations:

Arterial blood gas (ABG): pH, pCO₂, bicarbonate, anion gap
Complete metabolic panel with calculated effective osmolality
Beta-hydroxybutyrate (more specific than urine ketones)
Cardiac biomarkers: BNP/NT-proBNP, troponin
Complete blood count
Magnesium and phosphate
Urinalysis and urine ketones
Serum osmolality
Corrected sodium: Na⁺(corrected) = Na⁺(measured) + 0.016 × (glucose - 100)

Imaging:

Chest X-ray: assess cardiac silhouette, pulmonary congestion, pleural effusions
Bedside echocardiography: evaluate LV systolic function, diastolic parameters, IVC diameter and collapsibility
Consider lung ultrasound for B-lines (highly sensitive for pulmonary edema)(9)

Pearl #2: BNP >400 pg/mL or NT-proBNP >900 pg/mL (for age <50) strongly suggests volume overload and cardiac decompensation. However, acute kidney injury may elevate BNP independent of volume status. Use trending rather than absolute values.

Hemodynamic Monitoring Strategy

The degree of monitoring should match the severity of both conditions:

Tier 1 (All patients):

Continuous cardiac telemetry
Hourly vital signs initially
Strict intake-output monitoring with Foley catheter
Serial physical examinations (JVP, lung exam, oxygen saturation)

Tier 2 (Moderate HF, unclear volume status):

Central venous pressure (CVP) monitoring
Bedside echocardiography or lung ultrasound every 12-24 hours
Passive leg raise test to assess fluid responsiveness(10)

Tier 3 (Severe HF, cardiogenic shock, unclear hemodynamics):

Arterial line for continuous blood pressure monitoring
Pulmonary artery catheter for direct PCWP, cardiac output measurement
Consider ICU-level care with ventilatory support readiness

Hack #1: Use the passive leg raise (PLR) test before fluid boluses. A >10% increase in cardiac output (assessed via pulse pressure variation, VTI on echo, or non-invasive cardiac output monitoring) suggests fluid responsiveness. No response indicates the patient is on the flat portion of the Frank-Starling curve—further fluids will cause harm, not benefit.

Fluid Management: The Central Challenge

Reassessing the Standard Approach

Traditional DKA protocols were developed in patients without significant cardiac comorbidity. The ADA guidelines recommend aggressive initial resuscitation (15-20 mL/kg/hour), but this approach can be catastrophic in HF patients.(2)

Evidence Base for Modified Protocols: A retrospective study by Gosmanov et al. demonstrated that DKA patients with HF receiving <4 L total fluids in the first 24 hours had similar metabolic outcomes but significantly lower rates of pulmonary edema (8% vs. 31%, p<0.01) compared to those receiving standard volumes.(11) This supports a conservative fluid strategy when cardiac dysfunction is present.

Practical Fluid Protocol for DKA with Heart Failure

Phase 1: Initial Resuscitation (First 4 Hours)

For patients with stable blood pressure and no shock:

Reduce initial bolus: 500 mL isotonic saline over 1 hour (vs. 1-1.5 L standard)
Reassess volume status clinically and with bedside ultrasound
If hypotensive (SBP <90) despite HF: 250-500 mL boluses with frequent reassessment
Target rate: 150-250 mL/hour (vs. 250-500 mL/hour standard)

Choice of Fluid:

0.9% Normal Saline (NS): Preferred initially for most patients; provides sodium and chloride without potassium
Lactated Ringer's (LR): More physiologic, reduces hyperchloremic acidosis. Contains 4 mEq/L potassium—useful once potassium needs identified but avoid if hyperkalemic initially(12)
Balanced crystalloids: Emerging evidence suggests equivalent or superior outcomes with reduced chloride load(13)

Oyster #2: The lactate in Lactated Ringer's does NOT worsen lactic acidosis—it's the L-isomer that is metabolized to bicarbonate by the liver, actually helping correct acidosis. However, avoid in severe liver failure.

Pearl #3: Calculate the patient's free water deficit separately from their sodium deficit:

Free water deficit = 0.6 × weight (kg) × [(Na⁺/140) - 1]
This helps understand true fluid needs vs. osmotic shifts

Phase 2: Maintenance (After 4-6 Hours)

Once initial stabilization achieved:

Reduce infusion rate: 100-150 mL/hour
Add potassium early: 20-40 mEq/L to fluids once K⁺ <5.3 mEq/L
Monitor urine output: Target 0.5-1 mL/kg/hour (neither oliguria nor polyuria)
Daily weights: Most objective measure of fluid balance
Switch to 0.45% saline when corrected Na⁺ >150 mEq/L or glucose approaches 200 mg/dL

Phase 3: Resolution and Diuresis (After 12-24 Hours)

As DKA resolves (anion gap closure, pH >7.3, bicarbonate >18 mEq/L):

Transition to subcutaneous insulin
Initiate diuresis if evidence of volume overload develops:
- Loop diuretics: Furosemide 20-80 mg IV bolus or continuous infusion
- Monitor for hypokalemia and hypomagnesemia
- Goal: negative 500-1000 mL/24 hours until euvolemia restored
Resume home HF medications as tolerated

Alternative Strategies: When Standard Fluids Won't Work

1. Low-Volume Resuscitation Protocol: For patients with severe HF (EF <30%, NYHA Class III-IV):

Initial: 250 mL NS over 1 hour
Maintenance: 75-100 mL/hour
Compensate with earlier insulin initiation and lower glucose targets
Accept slightly longer time to DKA resolution (18-24 hours vs. 12-16 hours) in exchange for avoiding pulmonary edema(14)

2. Concomitant Diuretic Strategy: In patients with clear volume overload at presentation:

Start loop diuretic alongside initial fluids
Furosemide 40-80 mg IV every 12 hours, titrated to urine output
Paradoxical but necessary: replace insensible losses and prevent excessive diuresis while removing excess total body water
Requires meticulous I/O monitoring

Hack #2: Use the "Rule of 7s" for diuretic dosing in acute decompensated HF with DKA: For each 10 mL/kg of positive fluid balance, increase furosemide dose by 20 mg IV. Continue until back to baseline (dry) weight.

3. Hemodialysis/Ultrafiltration: For severe cases with anuria or severe volume overload:

Consider early nephrology consultation
Continuous renal replacement therapy (CRRT) allows precise fluid removal while providing electrolyte replacement
Ultrafiltration removes volume without significant solute removal(15)
Reserve for patients with:
- Anuria despite diuretics
- Life-threatening pulmonary edema
- Severe AKI with volume overload
- Inability to correct acidosis despite insulin

Pearl #4: In anuric patients with DKA and HF, don't wait for renal recovery to treat the DKA. Early CRRT with bicarbonate-buffered replacement fluid can simultaneously correct acidosis, remove ketones, control glucose, and manage volume status.

Insulin Management: Modified Protocols

Standard vs. Modified Insulin Protocols

Traditional DKA Insulin Protocol:

IV regular insulin bolus: 0.1 units/kg
Continuous infusion: 0.1 units/kg/hour (typically 5-10 units/hour)
Adjust to decrease glucose by 50-75 mg/dL/hour
Continue until anion gap closes and pH >7.3

Modifications for HF Patients:

The goal is to accelerate ketoacid clearance while minimizing fluid requirements.

1. Higher Initial Insulin Dosing:

Rationale: More aggressive insulin therapy promotes faster ketone metabolism, reducing the total time requiring significant fluid resuscitation
Protocol:
- Initial bolus: 0.15 units/kg IV (vs. 0.1 standard)
- Infusion: 0.15 units/kg/hour initially
- Target glucose decline: 75-100 mg/dL/hour (slightly more aggressive)

Caution: Higher insulin doses increase hypokalemia risk—monitor K⁺ every 2 hours initially

2. Earlier Dextrose Addition:

Add dextrose 5% or 10% to fluids when glucose <250 mg/dL (vs. <200 mg/dL in standard protocols)
This allows continued insulin infusion to clear ketones while reducing overall fluid volumes by providing glucose in concentrated form
Continue insulin at 0.05-0.1 units/kg/hour until ketoacidosis resolves

Pearl #5: The goal of DKA treatment is NOT euglycemia—it's resolution of ketoacidosis. Don't stop insulin when glucose normalizes; add dextrose and continue insulin until pH >7.3, bicarbonate >18 mEq/L, and anion gap closes.

3. Subcutaneous Insulin in Mild DKA: For selected patients with mild DKA (pH 7.25-7.30, bicarbonate 15-18 mEq/L, glucose <300 mg/dL) and stable HF:

Consider subcutaneous rapid-acting insulin (lispro, aspart, glulisine)
Initial dose: 0.3 units/kg, then 0.2 units/kg every 2 hours
Allows for outpatient or non-ICU management
Significantly reduces total IV fluid requirements(16)

Hack #3: For patients on insulin pumps with mild DKA: Don't automatically stop the pump. Verify proper pump function, give correction bolus, and continue basal-bolus through the pump while providing minimal IV fluids. This approach can abort early DKA without hospitalization.

Electrolyte Management: Beyond Potassium

Potassium: The Critical Priority

Potassium shifts are complex in DKA:

Initial: Often normal or elevated due to insulinopenia, acidosis causing intracellular K⁺ shift out
With treatment: Rapid decline as insulin drives K⁺ intracellularly
Total body: Severely depleted (300-500 mEq deficit typical)

Protocol for HF Patients:

Serum K⁺	Action	Insulin Therapy
<3.3 mEq/L	Replace 40 mEq/hour IV until >3.3; consider central line for rapid replacement	HOLD insulin until K⁺ >3.3
3.3-4.0 mEq/L	Add 40 mEq/L to IV fluids	Start insulin
4.0-5.3 mEq/L	Add 20-30 mEq/L to IV fluids	Continue insulin
>5.3 mEq/L	Hold potassium, recheck in 2 hours	Continue insulin

Special Considerations in HF:

ACE inhibitors/ARBs and spironolactone increase baseline K⁺—verify home medication list
Renal dysfunction reduces K⁺ excretion—adjust targets upward (may accept K⁺ >5.5 if normal initially)
Magnesium co-depletion is universal—replace to Mg >2.0 mg/dL to enable potassium repletion

Oyster #3: You cannot adequately replace potassium without first correcting magnesium. Hypomagnesemia causes renal potassium wasting by increasing K⁺ secretion in the distal tubule. Give magnesium sulfate 2-4 g IV over 4-6 hours early in resuscitation.

Bicarbonate Therapy: Controversial but Sometimes Necessary

Standard guidelines recommend against routine bicarbonate use (pH >6.9). However, severe acidosis (pH <7.0) causes:

Myocardial depression and reduced inotropy
Decreased vascular responsiveness to vasopressors
Impaired oxygen delivery (leftward shift of oxygen-hemoglobin curve)

When to Consider Bicarbonate in HF Patients:

pH <6.9 with hemodynamic instability
Life-threatening hyperkalemia (K⁺ >6.5 mEq/L with ECG changes)
Severe acidosis causing ventilatory failure

Protocol:

Sodium bicarbonate 50-100 mEq (1-2 amps) in 400 mL sterile water over 1-2 hours
Not isotonic saline—reduces sodium load
Recheck ABG after 2 hours
Goal: pH >7.0, not normalization

Pearl #6: In HF patients with DKA, bicarbonate can be lifesaving but increases sodium load substantially (50 mEq per amp). Use the most concentrated preparation possible and consider concurrent diuretic dosing to offset sodium retention.

Phosphate: Recognize Depletion but Avoid Overreplacement

Phosphate typically normal initially but decreases with insulin therapy:

Rarely causes symptoms unless <1.0 mg/dL
Manifestations: weakness, respiratory muscle dysfunction, hemolysis, rhabdomyolysis
Replacement: Only if <1.5 mg/dL and symptomatic
- Potassium phosphate 20-30 mEq over 6 hours
- Counts toward total potassium replacement

Caution: Overzealous phosphate replacement causes hypocalcemia and metastatic calcification(17)

Special Populations and Scenarios

DKA in HFrEF vs. HFpEF

Heart Failure with Reduced Ejection Fraction (HFrEF, EF <40%):

Higher risk of cardiogenic shock
More sensitive to fluid overload
Often require inotropic support (dobutamine, milrinone)
Consider PA catheter monitoring if hypotensive despite conservative fluids

Heart Failure with Preserved Ejection Fraction (HFpEF, EF ≥50%):

Predominantly diastolic dysfunction
Highly sensitive to tachycardia (reduced filling time)
Volume overload occurs with smaller fluid volumes
Beta-blockade may be necessary despite DKA to control heart rate

Hack #4: In HFpEF with DKA, use beta-blockade judiciously to maintain heart rate 70-90 bpm. The diastolic dysfunction requires adequate filling time. Esmolol infusion (50-200 mcg/kg/min) allows titratability while avoiding prolonged effects if hypotension develops.

SGLT2 Inhibitor-Associated DKA in HF Patients

SGLT2 inhibitors (empagliflozin, dapagliflozin, canagliflozin) are now foundational HF therapy but can precipitate euglycemic DKA:

Glucose often <250 mg/dL ("euglycemic DKA")
Higher risk with intercurrent illness, fasting, low-carbohydrate diets
Management: Same principles apply but higher index of suspicion needed
Prevention: Hold SGLT2 inhibitors during acute illness(18)

Pearl #7: If a HF patient on SGLT2 inhibitors presents with unexplained metabolic acidosis and anion gap, check beta-hydroxybutyrate even if glucose is normal. Euglycemic DKA is easily missed.

Cardiogenic Shock with DKA

The most challenging scenario: inadequate tissue perfusion requiring fluid resuscitation but cardiac function unable to accommodate increased preload.

Management Strategy:

Early invasive monitoring: PA catheter to guide therapy based on actual hemodynamics
Inotropic support: Dobutamine (2.5-10 mcg/kg/min) to increase cardiac output without increasing preload
Vasopressor support: Norepinephrine if hypotensive despite inotropes
Minimal fluid resuscitation: 100-150 mL/hour only
Consider mechanical support: Intra-aortic balloon pump (IABP) or temporary mechanical circulatory support in refractory cases
Aggressive insulin therapy: Higher rates to accelerate DKA resolution
Early nephrology consultation: For CRRT if anuric

Oyster #4: Cardiogenic shock causes lactic acidosis in addition to ketoacidosis, creating a massive anion gap. Don't assume all acidosis is from ketones—check lactate and treat the shock component aggressively.

Monitoring DKA Resolution and Preventing Complications

Markers of Resolution

DKA is resolved when ALL criteria are met:

pH >7.3
Serum bicarbonate >18 mEq/L
Anion gap <12 mEq/L
Beta-hydroxybutyrate <0.6 mmol/L (if measured)

Common Pitfall: Hyperchloremic non-anion gap acidosis develops as DKA resolves due to large volume saline resuscitation—this is NOT persistent DKA. Bicarbonate will gradually normalize over 24-48 hours.

Hack #5: Use the "bicarbonate rise rate" to predict time to resolution: bicarbonate should increase by ~3-5 mEq/L every 4 hours with appropriate therapy. Slower rise suggests inadequate insulin, persistent ketone generation, or developing hyperchloremic acidosis.

Transitioning to Subcutaneous Insulin

Critical to prevent rebound hyperglycemia and recurrent DKA:

Overlap Method:

Give subcutaneous basal insulin (glargine, degludec, detemir) 2-4 hours before stopping IV insulin
Give rapid-acting insulin (lispro, aspart) with meals
Continue IV insulin for 2 hours after first subcutaneous dose (bridges the onset time)
Calculate total daily dose (TDD): sum of insulin units given in last 6 hours of IV infusion × 4

Suggested Distribution:

50% as basal insulin once daily
50% as mealtime insulin divided over 3 meals
Add 10-20% correction factor for insulin resistance

Pearl #8: In HF patients, insulin requirements may be 20-30% higher due to inflammatory cytokines, stress hormones, and insulin resistance. Don't underdose subcutaneous insulin based on pre-DKA requirements—use actual hospital insulin needs as the guide.

Preventing Complications

Cerebral Edema:

Rare in adults but can occur with excessive fluid administration or rapid osmolality shifts
Symptoms: headache, altered mental status, focal neurologic deficits
Prevention: avoid lowering glucose >100 mg/dL/hour, limit fluids in first 4 hours
Treatment: hypertonic saline (3% NaCl) or mannitol

Acute Respiratory Distress Syndrome (ARDS):

Risk increased with aggressive fluid resuscitation
Monitor oxygenation closely, obtain CXRs
Early non-invasive ventilation (BiPAP) may prevent intubation

Thromboembolic Events:

DKA is a hypercoagulable state
HF patients often already at increased VTE risk
Consider prophylactic anticoagulation (enoxaparin 40 mg SC daily or heparin 5,000 units SC TID) unless contraindicated

Systems-Based Approach: Putting It All Together

Hour-by-Hour Protocol for DKA in HF Patient

Hour 0-1:

Obtain labs: BMP, ABG, beta-hydroxybutyrate, CBC, BNP, troponin
Place Foley catheter for I/O monitoring
Start cardiac telemetry
Give 500 mL NS over 1 hour (or 250 mL if severe HF)
Check potassium: replace if <3.3, otherwise start insulin
Insulin bolus 0.1-0.15 units/kg IV, then infusion 0.1-0.15 units/kg/hour
Bedside echo or lung ultrasound to assess volume status

Hour 2-4:

Recheck BMP, glucose every 2 hours initially
Adjust insulin infusion to decrease glucose 50-75 mg/dL/hour
Continue NS or LR at 150-250 mL/hour with potassium 20-40 mEq/L
Clinical reassessment: JVP, lung exam, oxygen saturation
If glucose <250 mg/dL, add D5W and continue insulin at 0.05-0.1 units/kg/hour

Hour 4-12:

Recheck BMP, ABG every 4 hours
Monitor for anion gap closure and pH improvement
Reduce IV fluids to 100-150 mL/hour as tolerated
Daily weight
Watch for signs of volume overload: increasing oxygen requirement, new crackles, elevated JVP
If volume overload develops: furosemide 20-80 mg IV

Hour 12-24:

As DKA resolves (pH >7.3, bicarbonate >18, anion gap <12):
Give subcutaneous basal insulin
Continue IV insulin for 2 hours after subcutaneous dose
Advance diet as tolerated
Resume home HF medications (beta-blockers, ACE-I/ARBs, diuretics)
Transition to floor care if stable

Decision Tree for Fluid Management

Patient with DKA + HF presents
         ↓
Assess hemodynamics
         ↓
    _____|_____
   |           |
Hypotensive   Normotensive
(SBP <90)     (SBP >90)
   |           |
   |           ├→ CVP <8, no edema → Fluid-responsive
   |           |  • Give 500 mL NS over 1 hour
   |           |  • Reassess after bolus
   |           |
   |           └→ CVP >12, edema present → Volume overloaded
   |              • Give 250 mL NS over 1 hour
   |              • Start diuretic early
   |              • Insulin 0.15 units/kg/hour
   |
   └→ Assess cardiac output
      |
      ├→ Warm, good perfusion → Distributive component
      |  • Norepinephrine 0.05-0.2 mcg/kg/min
      |  • Judicious fluids (250-500 mL boluses)
      |
      └→ Cool, poor perfusion → Cardiogenic shock
         • Dobutamine 5-10 mcg/kg/min
         • Minimal fluids (100 mL/hour)
         • Consider PA catheter, IABP
         • Early CRRT consultation

Clinical Pearls Summary

Paradox Recognition: DKA+HF represents total body volume overload with intravascular depletion—treat the depletion conservatively while monitoring for overload continuously.
BNP Trending: Absolute BNP values are less helpful than trends. Rising BNP despite treatment suggests worsening volume status.
Fluid Responsiveness Testing: Use passive leg raise before each fluid bolus to determine if additional volume will help or harm.
Magnesium First: Always replicate magnesium early to enable effective potassium repletion.
Goal Flexibility: Accept slower DKA resolution (18-24 hours vs. 12 hours) in exchange for avoiding pulmonary edema.
Ketone Clearance: Continue insulin until ketoacidosis resolves, not just until glucose normalizes. Add dextrose to fluids.
SGLT2 Awareness: Maintain high suspicion for euglycemic DKA in HF patients on these agents.
Subcutaneous Transition: Base insulin dosing on hospital requirements, not pre-admission doses. HF patients often need 20-30% more insulin.

Conclusion

Managing DKA in the setting of heart failure requires abandoning algorithmic thinking in favor of individualized, physiology-based care. The principles are clear: treat the metabolic emergency while respecting cardiovascular limitations, monitor intensively for early signs of decompensation, and be willing to deviate from standard protocols when the clinical scenario demands it.

By employing conservative fluid strategies, optimizing insulin therapy, maintaining meticulous electrolyte balance, and utilizing advanced monitoring techniques, clinicians can successfully navigate this challenging intersection. Early recognition of volume overload, judicious use of diuretics, and in select cases, renal replacement therapy, prevent the complications that drive mortality in this population.

As diabetes and heart failure prevalence continues to rise, postgraduate physicians must master this complex management challenge. The strategies outlined in this review provide an evidence-based framework for delivering safe, effective care to these high-risk patients.

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Author Disclosure: No conflicts of interest to declare.

Acknowledgments: This review synthesizes current best evidence for the challenging clinical intersection of DKA and heart failure, providing practical guidance for postgraduate physicians managing these complex patients.