Relaxin-2 (Serelaxin)

Best for

Consider alternatives if

Covers reconstitution · step-by-step technique · storage · a sample daily schedule.

Common side effects · experienced by some users

• Hypotension (low blood pressure) - most common

  Vasodilation induced by relaxin-2 activation of RXFP1/RXFP2 receptors on vascular endothelium predictably reduces systemic vascular resistance and blood pressure. [6][7][11] This is dose-dependent and most pronounced in the first 24 hours of IV infusion, with systolic BP typically dropping 10-20 mmHg.

  Management: Establish baseline blood pressure before infusion. Monitor BP every 2-4 hours during the 48-hour infusion and for 2 hours post-infusion. Position patient semi-recumbent or upright to promote venous return. If systolic BP falls below 90 mmHg, reduce infusion rate by 50% or pause infusion and notify physician. Ensure adequate hydration. Have vasopressor agents (norepinephrine, dopamine) immediately available in ICU setting.

• Tachycardia (increased heart rate)

  Compensatory tachycardia occurs as the heart responds to vasodilation and reduced peripheral resistance. [2][7][11] Heart rate typically increases 5-15 bpm and reflects normal baroreceptor reflex activation, though some patients experience reflex tachycardia exceeding 100 bpm.

  Management: Monitor heart rate continuously during infusion. Document baseline and post-infusion rates. Tachycardia typically resolves as blood pressure stabilizes. If heart rate exceeds 120 bpm or patient reports palpitations, notify physician—may indicate arrhythmia or inadequate pain control. Ensure adequate hydration and avoid sudden position changes.

• Headache

  Cerebral vasodilation from relaxin's endothelial effects combined with hemodynamic changes can trigger or exacerbate headaches. [8][11] Occurs in approximately 5-10% of infusion recipients, typically mild to moderate severity.

  Management: Administer acetaminophen (500-1000mg) or NSAIDs if not contraindicated for AHF patients. Ensure dark, quiet environment. Apply cool compresses to temples. Assess BP—hypotension-induced headaches resolve when BP normalizes. Maintain hydration. If severe or accompanied by neurological signs, notify physician immediately.

• Nausea

  Nausea can result from acute hemodynamic changes, IV administration discomfort, or medication interactions. [11] Generally mild and transient, occurring during initial hours of infusion.

  Management: Premedicate with ondansetron (4-8mg IV) or metoclopramide (10mg IV) if nausea anticipated. Avoid food 1-2 hours before and during infusion. Maintain NPO status per institutional protocol. Monitor hydration status. Most nausea resolves within first 12 hours. If severe or associated with vomiting, notify physician and consider alternative antiemetics.

• Dizziness

  Dizziness or lightheadedness results from acute blood pressure reduction and changes in cerebral perfusion. [11] Risk increases with rapid infusion rate or inadequate hydration. More common in elderly or volume-depleted patients.

  Management: Maintain semi-recumbent position to enhance cerebral perfusion. Move slowly when changing positions. Ensure adequate hydration per heart failure protocol. Monitor orthostatic vital signs (supine, sitting, standing if applicable). Reduce infusion rate if dizziness severe. Assess for concurrent medication effects (narcotics, sedatives). Notify physician if accompanied by syncope risk.

• Peripheral edema (swelling)

  Relaxin-mediated vascular permeability increases and sodium/fluid retention in acute HF can cause or exacerbate peripheral edema, particularly in dependent areas (ankles, sacrum in bed-bound patients). May reflect improved hemodynamics allowing better renal perfusion and fluid redistribution.

  Management: Monitor daily weights pre- and post-infusion. Assess pedal edema severity and location. Elevate lower extremities above heart when resting. Apply compression stockings if ordered. Diuretic regimen continuation per cardiology. Check for signs of cellulitis or skin breakdown from chronic edema. Notify physician if edema worsens despite appropriate diuresis.

• Increased creatinine levels

  Serum creatinine may transiently rise during infusion due to reduced renal perfusion pressure from hypotension or intrinsic glomerular effects. [1][11] Typically reversible post-infusion as hemodynamics normalize. Can reflect acute tubular necrosis risk in pre-existing renal disease.

  Management: Draw baseline creatinine and BUN before infusion start. Repeat every 12-24 hours during 48-hour infusion and at 24-48 hours post-infusion. Calculate eGFR to assess glomerular filtration rate trend. If creatinine increases >0.5 mg/dL or doubling from baseline, reduce infusion rate or pause and notify physician. Ensure adequate hydration. Monitor urine output for oliguria. Hold ACE-I/ARB per institutional protocol during infusion.

• Hyperkalemia (high potassium)

  Acute kidney injury risk and potential aldosterone suppression from improved renal hemodynamics can elevate serum potassium. [11] Risk increases in patients with baseline renal impairment (eGFR <30) or on ACE-I/ARB therapy.

  Management: Draw baseline potassium before infusion. Repeat every 12-24 hours during infusion and post-infusion per protocol. If K+ exceeds 5.5 mEq/L, notify physician immediately. Restrict potassium intake during hospitalization. Hold potassium supplements and potassium-sparing agents. Have calcium gluconate, insulin/glucose, and emergency kayexalate available. Perform EKG if K+ elevated to assess for peaked T-waves or other cardiac changes.

• Syncope (fainting)

  Profound hypotension combined with positive chronotropic effects can precipitate vasovagal syncope or hypotensive episodes, particularly with sudden position changes or straining. [11] Risk highest in first 24 hours of infusion.

  Management: Maintain patient on continuous cardiac telemetry. Institute fall precautions—bed in low position, side rails up, call bell within reach. Assist with all position changes and ambulation. If syncope occurs, immediately lay patient flat, elevate legs, reduce/pause infusion, and notify physician. Assess for injuries from fall. May require vasopressor support or infusion rate reduction. Hold patient in ICU setting post-syncope.

• Atrial fibrillation

  Acute hemodynamic changes, atrial dilation from HF, or catecholamine surges can trigger atrial fibrillation de novo or exacerbate pre-existing AF. [11] Occurs in 2-5% of infusion recipients, particularly those with structural heart disease or elevated filling pressures.

  Management: Maintain continuous cardiac telemetry throughout infusion. Obtain baseline 12-lead EKG before infusion. If AF develops, notify physician immediately. Do not delay intervention. Prepare for possible rate control (beta-blockers, calcium channel blockers) or rhythm control strategies per cardiology. Ensure adequate anticoagulation if not already on anticoagulant. Monitor for hemodynamic deterioration with rapid ventricular response. Have emergency equipment available.

• Blood pressure checks every 2-4 hours during infusion

  Continuous hemodynamic monitoring is essential to assess the critical vasodilatory effects of relaxin-2 and catch hypotension early. [6] Invasive (arterial line) or non-invasive BP monitoring every 1-4 hours captures BP trend and infusion tolerance.

  Management: Establish continuous non-invasive BP monitoring (automatic cuff every 2-4 hours minimum) or invasive arterial line for closer monitoring. Position BP cuff at heart level for accuracy. Document systolic, diastolic, and mean arterial pressures. Plot trend on chart to visualize hemodynamic response. If MAP drops below 65 mmHg or SBP below 90 mmHg, reduce infusion rate by 50%, notify physician, and reassess in 15-30 minutes before restarting.

• Kidney function (creatinine and eGFR)

  Acute kidney function assessment is critical because hypotension and intrinsic renal effects from relaxin can precipitate acute kidney injury. [11] Baseline renal function predicts risk—patients with eGFR <30 are at higher risk for worsening function.

  Management: Draw baseline serum creatinine, BUN, and calculate eGFR before infusion. Repeat creatinine every 12-24 hours during 48-hour infusion. Monitor 24-hour urine creatinine and urine electrolytes per protocol. Assess urine output hourly (target >0.5 mL/kg/hr). If creatinine rises >0.5 mg/dL acutely, reduce infusion rate and ensure adequate hydration. Hold nephrotoxic agents. Consider contrast avoidance for any imaging during treatment window.

• Electrolytes, particularly potassium

  Acute shifts in serum electrolytes (sodium, potassium, magnesium) occur from hemodynamic changes, diuretic therapy, and altered renal handling. [10] Hyponatremia and hyperkalemia represent the primary electrolyte concerns during relaxin infusion.

  Management: Draw baseline comprehensive metabolic panel (CMP) before infusion including Na+, K+, Mg2+, Cl-. Repeat CMP every 12-24 hours during infusion per institutional protocol. Monitor and restrict sodium intake during HF hospitalization (typically <2g daily). Supplement potassium only if serum K+ <3.5 mEq/L. Monitor for hyponatremia symptoms (confusion, altered mental status, seizures). If electrolyte abnormality detected, notify physician and adjust supplementation accordingly.

• Heart rate and cardiac rhythm

  Continuous cardiac monitoring captures the heart rate response to hemodynamic changes and detects arrhythmias. [11] Telemetry surveillance is mandatory during 48-hour infusion given the potent hemodynamic effects of relaxin.

  Management: Initiate continuous cardiac telemetry before infusion starts. Monitor QRS rate, rhythm, PR interval, and QT interval. Obtain baseline 12-lead EKG before infusion. Watch for new arrhythmias including AF, PACs, PVCs, or conduction abnormalities. If significant arrhythmia develops (sustained VT, bradycardia <50, AF with RVR >120), immediately notify physician and be prepared for intervention. Continue telemetry for 2+ hours post-infusion.

• Urine output

  Diuresis or oliguria responses to relaxin infusion depend on baseline renal function and hemodynamics. Expected response is improved urine output (>1-1.5 L/24hr in most) as renal perfusion improves. [10][17] Oliguria (<400-500 mL/24hr) signals acute kidney injury.

  Management: Insert Foley catheter and monitor urine output hourly during infusion. Document color, clarity, and specific gravity. Target urine output >0.5 mL/kg/hr (approximately 30-40 mL/hr for average adult). If output <0.3 mL/kg/hr, assess fluid status, reduce infusion rate if hypotensive, and notify physician—may indicate acute kidney injury. Maintain accurate I/O records. Send urine for urinalysis and electrolytes if oliguria develops.