Integrative Care for Improved Health from Cardiorenal Syndrome

Understand the principles of integrative care for cardiorenal syndrome and its impact on patient wellness and recovery.

Abstract

I am Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. In this educational post, I guide you through a clear, evidence-based understanding of the heart–kidney relationship known as cardiorenal syndrome. We will explore how decreased cardiac output, increased preload, and chronic neurohormonal activation—especially the renin–angiotensin–aldosterone system (RAAS) and sympathetic nervous system (SNS)—drive congestion, inflammation, and progressive organ dysfunction. I discuss why venous congestion and right ventricular (RV) mechanics are pivotal, what natriuretic peptides signal, and how splanchnic venous reservoir dynamics and renal tubular injury shape decisions.
You will also see how our multidisciplinary team at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic) in El Paso, Texas integrates chiropractic care, functional medicine, personal injury care, rehabilitation, and medical oversight to deliver safe, modern cardiorenal care. Our Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine; NPI #1164426749; Texas MD License #J2933), provides medical direction as I implement integrative chiropractic and functional strategies. I present practical frameworks for loop diuretic regimens, sequential nephron blockade, guideline-directed medical therapy (GDMT), and when to consider inotropes, ultrafiltration, or mechanical circulatory support. Throughout, I explain how integrative chiropractic fits—via thoracic and diaphragmatic mechanics, autonomic modulation, and postural optimization—to complement medical therapy.

Integrative Cardiorenal Care in El Paso: Our Collaborative Model

Practice within a multidisciplinary structure common to modern integrative and injury care clinics. At Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), I work alongside Dr. Maria Guadalupe Cardenas, MD, our Medical Director and Collaborative Physician, who is board-certified in Internal Medicine with over 40 years of experience (NPI #1164426749; Texas MD License #J2933). Dr. Cardenas provides comprehensive medical oversight, directing our cardiometabolic and internal medicine pathways and ensuring our care aligns with current standards and safety protocols.
My integrated role combines:

• Chiropractic and rehabilitative biomechanics to improve mobility, breathing mechanics, and venous return
• Autonomic and pain modulation techniques to temper sympathetic drive
• Functional medicine frameworks for inflammation, nutrition, and mitochondrial health
• Personal injury care and graded rehabilitation for safe return to function
• Close medical coordination for diagnostics, pharmacology, and escalation pathways

This coordinated model allows us to deliver evidence-based care for complex syndromes like cardiorenal syndrome, chronic kidney disease (CKD), and heart failure, while integrating spine-focused biomechanics and lifestyle interventions under medical supervision.

The Cardiorenal Connection: Heart–Kidney Crosstalk

Cardiorenal syndrome describes the bidirectional relationship in which heart dysfunction worsens kidney injury and kidney dysfunction exacerbates heart failure. To act precisely, we must understand the crosstalk:

• Natriuretic peptides (ANP, BNP/NT-proBNP, CNP): They promote vasodilation, natriuresis, and reduced preload, signaling the heart’s attempt to counter congestion.
• RAAS: Renin, angiotensin II, and aldosterone drive vasoconstriction and sodium/water retention—powerful mechanisms that often dominate in chronic heart failure.
• SNS activation: Increases heart rate and contractility to compensate for low stroke volume; chronically, it amplifies inflammation and oxidative stress.

Why this matters: Chronic low cardiac output and elevated filling pressures tip the endocrine tug-of-war toward RAAS dominance, promoting fluid retention, vascular stiffness, and fibrosis. Over time, this neurohormonal imbalance becomes maladaptive, feeding back into both cardiac and renal decline (American College of Cardiology, n.d.; American Heart Association, n.d.; European Society of Cardiology, n.d.).

Decreased Cardiac Output, Increased Preload, and Maladaptive Responses

Early in heart failure, two key changes dominate:

• Decreased cardiac output from reduced stroke volume, adverse remodeling, and increased LV wall stress
• Increased preload with elevated left atrial and central venous pressures

Compensatory responses:

• RAAS activation stabilizes blood pressure but increases sodium and water retention
• SNS activation maintains cardiac output (CO = HR × SV) but increases oxidative stress and inflammatory signaling

Short-term benefits can lead to long-term harm: persistent vasoconstriction strains the myocardium; aldosterone drives interstitial fibrosis in the heart and kidney; sustained SNS activity increases reactive oxygen species (ROS), worsening myocardial and tubulointerstitial injury (American College of Cardiology, n.d.; American Heart Association, n.d.).

Renal Pathophysiology: Tubular Injury, Fibrosis, and RAAS Amplification

At the nephron level, chronic inflammation and catecholamine exposure create:

• Glomerular and interstitial damage leading to sclerosis
• Renal tubular injury with vacuolization and reduced effective surface area, impairing natriuresis and diuresis
• Apoptosis and fibrosis that diminish renal reserve
• Local RAAS amplification from injured renal tissue, compounding systemic signals

Clinical implications:

• Worsening CKD is both a consequence and driver of advanced heart failure
• NT-proBNP rises as a counter-regulatory endocrine signal; yet in chronic disease, it is overwhelmed
• Progressive dysfunction narrows the therapeutic windows for ACEi/ARBs/ARNIs, MRAs, SGLT2 inhibitors, and diuretics, thereby demanding careful dosing and monitoring (European Society of Cardiology, n.d.; Natriuretic peptides and heart failure outcomes, n.d.; RAAS inhibition and cardiorenal protection, n.d.).

Venous Congestion and the Splanchnic Reservoir: Abdominal Physiology in Focus

A frequently under-recognized driver is abdominal (splanchnic) congestion. The liver, spleen, omentum, and mesenteric vasculature form a large venous reservoir. In heart failure:

• Fluid redistributes early to splanchnic beds, preceding peripheral edema
• Elevated portal and mesenteric pressures impair gut perfusion and barrier function, contributing to intestinal edema, malabsorption, dysbiosis, and systemic inflammation.
• Hepatic congestion elevates liver enzymes, lowers albumin, and alters drug metabolism—crucial for dosing loop diuretics and other GDMT agents.

Clinically, splanchnic congestion explains early satiety, bloating, nausea, RUQ discomfort, and variable diuretic responses. Effective care must reduce central venous pressure and consider RV dynamics, not just peripheral edema.

Right Ventricular Hemodynamics: The Hidden Driver of Renal Outcomes

The right ventricle (RV) primes venous return and pulmonary flow. Elevated RV afterload (e.g., pulmonary hypertension) or intrinsic RV dysfunction raises central venous pressure, compressing renal perfusion pressure (mean arterial pressure minus renal venous pressure). Even with preserved systemic BP, renal venous hypertension narrows the filtration gradient, impairing GFR and accelerating tubulointerstitial injury.
Therapeutic implications:

• RV unloading through oxygenation, judicious pulmonary vasodilators, and careful fluid offloading can improve renal perfusion and diuretic responsiveness
• Thoracic mobility, diaphragmatic mechanics, and postural optimization—core chiropractic strategies—support venous return and respiratory efficiency, synergizing with cardiology care

Forward Versus Backward Flow: A Modern Hemodynamic Framework

Four decades of hemodynamics reframed heart failure from contractility-centric to congestion-centric:

• Forward flow is arterial delivery—cardiac output reaching organs
• Backward flow is venous pressure burden—congestion impeding organ drainage

High venous pressures collapse the transglomerular filtration gradient. The kidney depends on strong arteriolar inflow against low venous outflow. When venous pressures rise, filtration falls—creating cardiorenal and veno-renal states. Effective therapy must preserve forward arterial perfusion while reducing venous congestion (Stevenson, 1999).

The Veno-Renal State: Why Decongestion Restores Filtration

Elevated renal vein pressure increases interstitial and capsular pressures, diminishing net filtration pressure. Renal congestion triggers inflammatory pathways, worsens tubular oxygen demand, and perpetuates sympathetic tone. Decongestion widens renal gradients, improves filtration, and reduces neurohormonal stress. This is why diuretics, volume redistribution, and venous pressure relief can yield renal recovery, even without dramatic increases in forward cardiac output.

Clinical Assessment: How We Characterize Congestion and Risk

Under Dr. Cardenas’s medical direction, we integrate physical exam and testing:

• Jugular venous pressure (JVP) and hepatojugular reflux
• Lung auscultation for rales and airflow changes
• Hepatic size/tenderness, ascites signs, and abdominal wall tension
• Peripheral edema grading
• Bioimpedance and segmental composition when available
• Functional measures: orthopnea, bendopnea, exercise tolerance, and heart rate recovery
• BNP/NT-proBNP, CMP, urinalysis, albumin–creatinine ratio
• Echocardiography for LV/RV function and pulmonary pressures
• IVC ultrasound for collapsibility as a central venous pressure surrogate
• POCUS for lung B-lines and portal flow; renal Doppler for resistive index when indicated

These findings guide diuretic regimens, fluid targets, and GDMT adjustments, defining whether pulmonary, splanchnic, or peripheral compartments dominate.

Beating the Odds: “Conquering Congestive Heart Failure”- Video

Diuretic Therapy: Thresholds, Ceilings, and Precision Offloading

Loop diuretics are cornerstone therapies for decongestion. Our approach emphasizes pharmacokinetics and physiology:

• Agent selection:
  • Furosemide: Widely used; variable oral bioavailability; IV preferred in acute decompensation; SQ options in supervised settings
  • Torsemide: High, consistent bioavailability; favorable half-life; potential antifibrotic aldosterone-modulating effects; often preferred in gut edema
  • Bumetanide: Potent, reliable absorption; useful in intestinal edema or furosemide resistance
• Dosing strategy:
  • Start weight-adjusted doses; escalate based on urine output targets (e.g., 150–200 mL/hour acutely) and daily weight trends
  • Sequential nephron blockade: Add thiazide-like diuretics (e.g., metolazone) or acetazolamide when resistance occurs
  • Consider IV or subcutaneous routes when oral absorption is limited
• Safety checks:
  • Monitor electrolytes, renal function, blood pressure; anticipate hypokalemia, hyponatremia, metabolic alkalosis
  • Use IVC ultrasound and lung B-lines to avoid over-diuresis and renal hypoperfusion

Physiologic rationale: Targeting nephron segments reduces venous pressures, improves renal perfusion by lowering renal venous hypertension, and reduces splanchnic reservoir volume—improving symptoms and organ function (Felker et al., 2011; Mullens et al., 2022).

Managing Diuretic Resistance: Push vs Drip and Sequential Blockade

When resistance appears, we reassess dose, bioavailability, timing, and add-ons:

• Bolus vs infusion: Adequate bolus dosing can be comparable to continuous infusion; continuous infusion may aid severe resistance by sustaining tubular drug levels (Felker et al., 2011)
• Sequential nephron blockade:
  • Add a thiazide (e.g., metolazone) to increase distal blockade
  • Layer MRAs for neurohormonal modulation and sodium balance
  • Consider acetazolamide to augment proximal diuresis in alkalotic patients (Mullens et al., 2022)

Cardiorenal nuance: Patients often have higher thresholds due to renal venous congestion and interstitial edema; higher initial doses of loop diuretics may be required. A modest early rise in creatinine can reflect hemodynamic shifts rather than intrinsic injury—context matters.

Guideline-Directed Medical Therapy: Renal-Safe Sequencing

We tailor GDMT to renal function:

• ACE inhibitors/ARBs/ARNI: Reduce afterload and RAAS activity; monitor creatinine and potassium, especially in CKD
• Mineralocorticoid receptor antagonists (MRAs): Counter aldosterone-mediated fibrosis and retention; monitor for hyperkalemia
• SGLT2 inhibitors: Provide osmotic diuresis, modulate tubuloglomerular feedback, and deliver cardio-renal protection; initiation feasible down to eGFR ≥20 mL/min/1.73 m² in many protocols
• Beta-blockers: Temper SNS overactivation; we typically initiate after decongestion to avoid acute hemodynamic compromise

Why it works: GDMT attenuates maladaptive RAAS/SNS cascades, reduces fibrosis, improves hemodynamics, and stabilizes renal function when combined with congestion management and lifestyle support (Yancy et al., 2017; McDonagh et al., 2021; McMurray et al., 2019; Heerspink et al., 2020).

Inotropes and Escalation: Milrinone, Dobutamine, Ultrafiltration, and MCS

In refractory oliguria or low-output states:

• Milrinone: PDE-3 inhibition improves calcium handling, reduces systemic and pulmonary vascular resistance, and unloads the RV—lowering venous pressures and improving renal gradients; renally cleared, so dose cautiously
• Dobutamine: Beta-1 agonism increases contractility; beta-2 effects can vasodilate; monitor for tachyarrhythmias and ischemia; useful when faster augmentation of output is needed, including RV responsiveness

If diuretics fail:

• Ultrafiltration/CRRT/hemodialysis: Remove fluid without RAAS activation associated with loops; decompress venous beds to restore renal output; modality choice depends on blood pressure and setting
• Mechanical circulatory support (MCS):
  • Impella platforms for LV unloading; Impella RP for RV support
  • Protek Duo RVAD systems for right-sided failure
  • VA-ECMO for biventricular support and oxygenation

Early referral to advanced heart failure teams prevents prolonged renal congestion and organ compromise (McDonagh et al., 2021; Yancy et al., 2017).

Integrative Chiropractic Care: Mechanobiology Meets Hemodynamics

Chiropractic care must be thoughtfully integrated into cardiorenal frameworks to support mobility, autonomic balance, and venous return safely. My priorities include:

• Thoracic spine mobility and rib cage mechanics: Enhancing diaphragmatic excursion improves the respiratory pump, supporting venous return and lymphatic drainage
• Diaphragmatic training and myofascial release: Reducing abdominal wall tension aids interstitial fluid movement and improves GI motility affected by splanchnic congestion
• Cervical and upper thoracic autonomic modulation: Gentle techniques that reduce sympathetic tone may improve heart rate variability and sleep quality
• Postural optimization: Correcting kyphosis and forward head posture improves intrathoracic pressure dynamics and may reduce venous congestion in splanchnic and hepatic beds
• Safe exercise prescription: Low-intensity, interval-based activity focusing on calf-muscle pump activation mobilizes peripheral venous blood without hemodynamic instability

Clinical guardrails:

• Coordinate with Dr. Cardenas for patients on high-dose diuretics, vasodilators, or with orthostatic risk
• Avoid aggressive manipulations in decompensated states; prioritize gentle mobilization, breathing mechanics, and isometrics tailored to stability.
• Monitor for signs of worsening congestion: new orthopnea, weight gain, increased abdominal girth, escalating fatigue.

Physiologic rationale: Improving respiratory mechanics increases negative intrathoracic pressure and IVC collapsibility, supporting RV preload management. Autonomic balancing reduces catecholamine burden, which otherwise constricts venous capacitance and impairs renal perfusion (Shaffer & Ginsberg, 2017).

Functional Medicine Foundations: Inflammation, Oxidative Stress, and Nutrition

Functional medicine complements GDMT by addressing systemic drivers:

• Anti-inflammatory nutrition: Emphasize omega-3s, polyphenol-rich plants, and sodium-aware choices tailored to renal function
• Mitochondrial support: Consider medically supervised supplementation (e.g., CoQ10 in select cases) with lab-guided oversight
• Gut barrier integrity: Address dysbiosis with dietary fiber, fermented foods when tolerated, and targeted probiotics; splanchnic congestion can impair gut function, heightening systemic inflammation
• Sleep and stress modulation: Screen for sleep apnea and apply stress-reduction practices to lower SNS activity

Why it helps: Reducing ROS and inflammatory cytokines alleviates endothelial and tubular stress, potentially slowing fibrosis and improving responsiveness to GDMT and diuretics (Heerspink et al., 2020; McMurray et al., 2019; Yancy et al., 2017).

Personal Injury Care and Rehabilitation: Cardiorenal-Aware Protocols

Many patients with heart failure or CKD present with musculoskeletal pain or injuries that limit activity:

• Tailor rehabilitation to avoid preload spikes and excessive intrathoracic pressure
• Use graded activity while monitoring heart rate, blood pressure, oxygen saturation, and perceived exertion
• Emphasize non-opioid pain management and mechanically informed approaches compatible with cardiovascular safety

In trauma-related cases, thoracoabdominal mechanics may be impaired. Post-injury diaphragm dysfunction and altered posture can exacerbate venous congestion. Our protocols restore:

• Respiratory mechanics via diaphragm training and rib mobility drills
• Core stability with low-load exercises to improve abdominal wall tone without excessive pressure
• Graded activity to enhance skeletal muscle pump and lymph flow

Team-Based Care: Medical Oversight and Integrated Delivery

Under Dr.Cardenas’ss direction:

• We define congestion targets and diuretic protocols with lab and ultrasound monitoring
• Chiropractic and rehab schedules are synchronized with medical therapy
• Functional medicine plans are reviewed for renal safety (e.g., potassium and magnesium loads) and medication interactions
• Fast-track escalation pathways are in place for decompensation—cardiology, nephrology, advanced heart failure programs, or transplant centers when indicated

This structure ensures precision, safety, and continuity across disciplines.

Clinical Observations From My Practice

In my hands-on experience and professional insights:

• Patients with pronounced abdominal congestion respond better when we combine respiratory mechanics and gentle thoracic mobility with diuretic therapy
• Torsemide often outperforms oral furosemide in gut edema due to consistent bioavailability; bumetanide is reliable and potent when absorption is uncertain
• Adjusting diuretic timing (morning and early afternoon) reduces nocturia and fall risk, improving adherence
• Pairing loops with metolazone for short, closely monitored bursts can break resistance effectively
• Low-dose milrinone for RV congestion improves urine output within hours by lowering venous backflow
• Integrative chiropractic rib mobilization and diaphragmatic retraining lessen dyspnea, enhance exercise tolerance, and reduce perceived fatigue

For deeper insight into my approach and clinical perspectives, see my professional pages:

• Injury Medical Clinic: https://chiromed.com/
• Professional profile: https://www.linkedin.com/in/dralexjimenez/

Putting It All Together: A Practical, Stepwise Pathway

• Assess congestion comprehensively
  • JVP, hepatojugular reflux, IVC ultrasound, lung B-lines, abdominal exam
  • Determine whether pulmonary, splanchnic, or peripheral compartments dominate
• Initiate or adjust diuretics
  • Choose loop based on bioavailability and potency; set a dosing schedule that minimizes nocturia.
  • Use sequential nephron blockade when necessary; monitor electrolytes and renal function closely.y
• Implement GDMT with renal consideratio.ns
  • ACEi/ARB/ARNI, MRA, SGLT2 inhibitor, beta-blocker—tailored to ejection fraction and kidney function
  • Sequence therapies to avoid acute hemodynamic compromise
• Layer integrative chiropractic and rehabilitation
  • Thoracic and rib mobility, diaphragmatic training, postural optimization, autonomic modulation, calf-pump-centric activity
• Apply functional medicine strategies.
  • Nutrition, sleep optimization, stress reduction, and microbiome support to reduce inflammation and oxidative stress
• Coordinate under medical oversight
  • Align therapy changes, monitor safety, and escalate promptly when needed

Why this works: Cardiorenal syndrome is a systemic problem in which hemodynamics, endocrine signals, inflammation, and structural changes interlock. Our model reduces maladaptive neurohormonal activation, safely offloads venous congestion, supports autonomic balance and respiratory mechanics, and ensures medical oversight for complex decisions—bridging chiropractic practice with internal medicine standards.

The Initial Workup and Differentiation: Practical Details

When a patient presents with acute decompensation, we assemble the full physiological picture:

• CBC to assess infection and anemia, which can mimic refractory dyspnea
• Comprehensive Metabolic Panel (CMP) for electrolytes, BUN/creatinine, and liver enzymes to gauge hepatic congestion
• NT-proBNP/BNP to quantify cardiac strain and congestion
• Urinalysis and urinary sodium to evaluate tubular function and diuretic responsiveness
• Echocardiogram for ejection fraction, RV function, pulmonary pressures, and IVC size/collapsibility
• Renal ultrasound to rule out post-obstructive processes (e.g., hydronephrosis); neurogenic bladder and strictures can masquerade as intrinsic AKI
• 12-lead EKG to evaluate ischemia or arrhythmia triggers (e.g., atrial fibrillation)
• Lactate for perfusion assessment—elevated levels suggest malperfusion, guiding escalation beyond simple diuresis

This workup helps answer whether heart failure drove renal dysfunction or vice versa (Ronco et al., 2008; Stevenson, 1999).

Hemodynamic Profiles and Cardiorenal Types: Guiding Strategy

Categorizing hemodynamic profiles:

• Warm and wet: Good perfusion, congested—focus on diuresis
• Cold and wet: Poor perfusion and congested—combine diuretics with inotropic/perfusion support
• Warm and dry: Stable and compensated
• Cold and dry: Low output without congestion—consider volume or inotropes, not diuretics

Cardiorenal syndrome types:

• Type 1: Acute heart failure → acute kidney injury
• Type 2: Chronic heart failure → progressive CKD
• Type 3: Acute kidney injury → acute heart dysfunction
• Type 4: Chronic kidney disease → cardiac hypertrophy and diastolic dysfunction
• Type 5: Systemic condition (e.g., sepsis, lupus) → both heart and kidney dysfunction (Ronco et al., 2008)

These frameworks refine therapy and escalation plans.

Patient-Centered Communication: Functional Signs That Matter

I listen for specific functional clues:

• Orthopnea: Difficulty lying flat; ask how many pillows or whether the patient sleeps in a recliner
• Paroxysmal nocturnal dyspnea (PND): Sudden nighttime dyspnea often described as a panic episode
• Bendopnea: Shortness of breath when bending; a specific sign pointing to increased intracardiac pressures
• Dyspnea on exertion (DOE): Probe real-world activities (parking lot walk, vacuuming) rather than abstract distances
• Early satiety, bloating, weight gain, peripheral edema: Indicators of splanchnic and systemic congestion
• Fatigue, confusion, low urine output: Signs of malperfusion, corroborated by lactate

These narratives connect laboratory and imaging data to lived physiology, guiding personalized care.

Conclusion: A Modern, Multidisciplinary Path to Cardiorenal Stability

Cardiorenal syndromes require precision medicine anchored in physiology and delivered through integrated care. Diuretics, used with a clear grasp of thresholds, ceilings, and pharmacokinetics, remain foundational for decongestion. Thoughtful GDMT sequencing stabilizes neurohormonal networks. When needed, inotropes, ultrafiltration, and mechanical support provide timely escalation. In our El Paso practice, the co-led model—Dr. Maria Guadalupe Cardenas, M.D., providing internal medicine oversight, and I integrating chiropractic and functional medicine—help patients breathe easier, move better, and regain confidence in daily life.
For more about my clinical observations and approach, visit:

• Injury Medical Clinic: https://chiromed.com/
• Professional profile: https://www.linkedin.com/in/dralexjimenez/

References

• American College of Cardiology. (n.d.). Contemporary management of heart failure.
• American Heart Association. (n.d.). Heart failure guidelines.
• European Society of Cardiology. (n.d.). Heart failure.
• Felker, G. M., Lee, K. L., Bull, D. A., et al. (2011). Diuretic strategies in patients with acute decompensated heart failure (DOSE). New England Journal of Medicine.
• Heerspink, H. J. L., Stefansson, B. V., Correa-Rotter, R., et al. (2020). SGLT2 inhibitors in patients with kidney disease. New England Journal of Medicine.
• McDonagh, T. A., Metra, M., Adamo, M., et al. (2021). 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. European Heart Journal.
• McMurray, J. J. V., Solomon, S. D., Inzucchi, S. E., et al. (2019). Dapagliflozin in patients with heart failure and reduced ejection fraction. New England Journal of Medicine.
• Mullens, W., Dauw, J., Martens, P., et al. (2022). Acetazolamide in decompensated heart failure with volume overload. New England Journal of Medicine.
• Natriuretic peptides and heart failure outcomes. (n.d.). Review article.
• RAAS inhibition and cardiorenal protection. (n.d.). Review article.
• Ronco, C., McCullough, P., Anker, S. D., et al. (2008). Cardio-renal syndromes: Report from the Consensus Conference of the ADQI. Journal of the American College of Cardiology.
• Shaffer, F., & Ginsberg, J. P. (2017). An overview of heart rate variability metrics and norms. Frontiers in Public Health.
• Stevenson, L. W. (1999). The management of refractory heart failure. Circulation.
• Yancy, C. W., Jessup, M., Bozkurt, B., et al. (2017). 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure. Circulation.

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