Immediate Management of Bradycardia with Anemia and Renal Dysfunction in an Elderly Patient
This patient requires immediate evaluation for BRASH syndrome (Bradycardia, Renal failure, AV-nodal blockade, Shock, and Hyperkalemia), with urgent assessment of potassium levels, medication review for AV-nodal blocking agents, and consideration of temporary pacing if symptomatic bradycardia persists. 1
Critical Initial Assessment
Obtain immediate 12-lead ECG and continuous cardiac monitoring to document the bradycardia, assess for AV block, and identify the specific rhythm disturbance (sinus bradycardia vs. AV nodal block vs. infranodal conduction disease). 2
Essential Laboratory Workup
- Check serum potassium immediately - hyperkalemia is a critical component of BRASH syndrome and can synergize with renal dysfunction to cause profound bradycardia resistant to atropine. 1
- Repeat comprehensive metabolic panel focusing on BUN/creatinine ratio (currently 48/1.07 = 45:1, suggesting prerenal azotemia or dehydration). 2
- Obtain troponin levels to exclude acute myocardial infarction as a cause of transient AV block, which would require different management. 2
- Check thyroid function (TSH) as hypothyroidism can cause bradycardia and is common in elderly females. 2
Medication Review - Critical Priority
Immediately review and hold all AV-nodal blocking agents (beta-blockers, calcium channel blockers, digoxin, clonidine) and renin-angiotensin system inhibitors that may be contributing to hyperkalemia and renal dysfunction. 1 The combination of these medications with acute kidney injury creates the perfect storm for BRASH syndrome, where bradycardia becomes resistant to standard interventions like atropine. 1
Hemodynamic Assessment
Determine if the patient is hemodynamically stable or unstable:
If Unstable (Hypotension, Altered Mental Status, Chest Pain, Heart Failure)
- Initiate transcutaneous pacing immediately if available, though recognize this is a temporizing measure only. 2
- Administer atropine 0.5-1 mg IV (may repeat up to 3 mg total), but recognize that atropine may be ineffective in BRASH syndrome or infranodal block. 3, 4
- Consider dopamine infusion (2-10 mcg/kg/min) for symptomatic bradycardia with hypotension, as used successfully in documented BRASH cases. 1
- Prepare for transvenous temporary pacing if pharmacologic measures fail and the patient remains symptomatic. 2
If Stable
- Continue continuous cardiac monitoring for at least 24-48 hours to observe for recurrent episodes and assess for transient vs. persistent conduction abnormalities. 2
- Observe for at least 72 hours before considering permanent pacing, as conduction abnormalities may be reversible once metabolic derangements and medication effects resolve. 2
Address Underlying Metabolic Derangements
Hyperkalemia Management (If Present)
If potassium >5.5 mEq/L with ECG changes or >6.0 mEq/L:
- Calcium gluconate 1-2 grams IV for cardiac membrane stabilization. 1
- Insulin 10 units IV with dextrose 50 grams (D50W). 1
- Consider urgent hemodialysis for resistant hyperkalemia, especially given the BUN of 48 and creatinine 1.07 suggesting acute-on-chronic kidney disease. 1
Anemia Management
The hemoglobin of 9.7 g/dL requires investigation but not immediate transfusion unless the patient is hemodynamically unstable or has active ischemia. 2 Routine transfusion in hemodynamically stable patients with hemoglobin >8 g/dL provides no benefit and may cause harm. 2
- Evaluate for source of anemia: Check iron studies, B12, folate, reticulocyte count, and stool guaiac. 2
- Consider anemia of chronic disease given the multiple comorbidities (chronic kidney disease, recurrent infections, inflammatory conditions). 2
Volume Status and Renal Function
The BUN:creatinine ratio of 45:1 with albumin 3.3 suggests prerenal azotemia:
- Administer cautious IV fluid resuscitation with isotonic crystalloid (250-500 mL boluses) while monitoring for fluid overload, given the history of heart failure risk factors. 2
- Avoid nephrotoxic agents including NSAIDs and contrast dye unless absolutely necessary. 2
- Adjust all renally-cleared medications based on estimated creatinine clearance. 2
Determine Need for Permanent Pacing
Permanent pacemaker implantation is NOT indicated at this time because: 2
- The bradycardia may be entirely reversible once medications are adjusted and metabolic abnormalities corrected. 2
- Transient bradycardia in the setting of acute illness does not constitute an indication for permanent pacing. 2
- A minimum observation period of 72 hours is recommended to allow for recovery of AV conduction. 2
Permanent pacing WOULD be indicated if: 2
- Symptomatic bradycardia persists after correction of reversible causes
- Third-degree AV block is documented (especially if infranodal)
- Second-degree Mobitz II AV block is present
- Symptomatic sinus node dysfunction persists despite medication adjustment
Evaluate for Cardiac Ischemia
Given the history of CVA/TIA, consider cardiac ischemia as a potential cause:
- Inferior MI can cause transient AV block due to increased vagal tone or decreased blood supply to the AV node. 2
- If troponin is elevated, this represents acute MI with conduction disturbance requiring urgent cardiology consultation and possible cardiac catheterization. 2
- Temporary pacing may be needed, but permanent pacing should be deferred until adequate observation period has passed. 2
Additional Diagnostic Considerations
Screen for atrial fibrillation with Holter monitoring once the acute bradycardia resolves, given the patient's age >65 years, diabetes, hypertension, and history of CVA/TIA. 5 Paroxysmal atrial fibrillation may be completely absent on resting ECG but still cause thromboembolic events. 5
If atrial fibrillation is detected:
- Calculate CHA₂DS₂-VASc score (will be ≥2 with age, diabetes, hypertension, and prior stroke). 5
- Initiate oral anticoagulation with a NOAC (apixaban, rivaroxaban, dabigatran, or edoxaban) to prevent recurrent thromboembolic events. 5
Common Pitfalls to Avoid
- Do not implant a permanent pacemaker within 72 hours of presentation, as this may result in unnecessary device implantation when the conduction abnormality is reversible. 2
- Do not give atropine in the setting of suspected infranodal block (wide QRS escape rhythm), as it may worsen the situation by increasing AV nodal conduction while the His-Purkinje system remains blocked. 2
- Do not transfuse blood routinely for hemoglobin >8 g/dL in stable patients, as this provides no benefit. 2
- Do not restart AV-nodal blocking agents until the bradycardia has completely resolved and the patient is hemodynamically stable for at least 48-72 hours. 1
- Do not overlook hyperkalemia as a reversible cause of bradycardia, especially in patients with renal dysfunction on ACE inhibitors or ARBs. 1