Seeking Insights from Cardiologists on Invasive Exercise Test Findings
I’m reaching out in the hope that a cardiologist or a healthcare expert can assist me with the interpretation of my recent invasive cardiopulmonary exercise test, which included right heart catheterization. For several years, I have been coping with debilitating symptoms such as breathlessness, poor exercise tolerance, muscle fatigue, orthostatic issues, and recently, hypotension after meals. My daily life is significantly affected, and I often find myself needing to use a wheelchair. Unfortunately, the only diagnosis provided to me thus far has been ‘deconditioning’, which does not begin to account for the intensity or nature of my symptoms. The central question that remains unclear to me is this: Although my pulmonary capillary wedge pressure (PCWP) and right atrial pressure (RAP) readings appear normal both at rest and during exercise, both my cardiac output and cardiac index are remarkably high at the baseline and during physical activity. The increase in stroke volume is minimal, with the rise in cardiac output primarily due to a heightened heart rate, which points to a potential preload failure. Research indicates that: "With inadequate preload, the stroke volume quickly plateaus and any further increase in cardiac output is due to an elevation in heart rate." This aligns perfectly with what my hemodynamic data reflects. Additionally, my upright PCWP measures a mere 5 mmHg, indicating a state of preload deficiency, although I was adequately hydrated prior to the test, which might have concealed further declines in this measure. Here are some key symptoms I am experiencing: - Shortness of breath that worsens with changes in posture and during meals (e.g., lying on my side exacerbates hypotension) - Muscle fatigue and burning sensations triggered by minimal exertion - A rapid increase in heart rate with exertion, despite already elevated cardiac output at rest - Notable decline following administration of Fludrocortisone, which resulted in acute decompensation - Absence of congestion - Normal results from MRI, echocardiogram, and blood analyses (like BNP) Prominent abnormalities noted in my tests include: - Increased cardiac output at rest and during exercise - Persistent low-normal PCWP, with a drop when standing - Compromised stroke volume reserve - Low oxygen uptake efficiency slope (OUES) of 1635 (with normal being greater than 3599) - Elevated ventilatory equivalents for carbon dioxide (VE/VCO₂ slope) at 31 - Suboptimal VO₂ response despite significant effort (respiratory exchange ratio greater than 1.2, peak heart rate exceeding 100%) - Indications of impaired peripheral oxygen extraction as suggested by VO₂/HR and dCO/dVO₂ slope This situation appears to reflect a form of preload failure accompanied by high-output physiology, perhaps signaling early or masked heart failure with preserved ejection fraction (HFpEF) or an issue with autonomic regulation of circulation. I’ve come across literature on similar presentations related to preload deficiency and high-output scenarios but have yet to engage a specialist who is willing to take my concerns seriously. Could this be classified as a type of heart failure? Why does it not fit the criteria for high-output heart failure or preload failure? Your thoughts would be immensely valuable; this journey has been profoundly challenging, and I am eager for explanations that resonate with my physiological experiences. I am a 45-year-old male with a history of Sick Sinus Syndrome and a pacemaker, in addition to obesity, MASLD, and low testosterone levels.
Answers (1)
7/2/2025, 5:31:07 PM
OpenHealth AI
It sounds like you have gone through an extensive and frustrating journey with your symptoms, and it's commendable how you're actively seeking clarity regarding your condition. Based on the findings you provided from your cardiopulmonary exercise test and your ongoing symptoms, it does seem you're facing a complex situation.
Main Points:
Your abnormal test results, notably high cardiac output with low stroke volume reserve, suggest issues that may not fit neatly into typical heart failure categories. It might indicate a form of cardiovascular dysregulation, possibly linked to preload failure, rather than classic high-output heart failure.
Explanation:
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Pulmonary Capillary Wedge Pressure (PCWP): Your low-normal PCWP suggests that your heart isn't receiving enough blood return (preload), which is crucial for maintaining stroke volume and cardiac output during exercise. This might explain your experience of breathlessness and fatigue.
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High Cardiac Output with Low Stroke Volume Reserve: The fact that your cardiac output is high primarily due to an increased heart rate indicates that your heart struggles to pump effectively under stress, relying on heart rate instead of stroke volume to meet oxygen demands during physical activity.
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Autonomic Regulation: Your symptoms and test results may reflect an issue with how your autonomic nervous system regulates your cardiovascular function, which can lead to symptoms like hypotension after meals and orthostatic issues.
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Context of Existing Health Conditions: Conditions such as obesity, sick sinus syndrome, and low testosterone levels may complicate your cardiovascular function and contribute to your symptoms.
Next Steps:
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Symptom Tracking: Keep a detailed diary of your symptoms, noting specific triggers (like posture changes and meals) alongside times of day when symptoms worsen. This information can help specialists understand your condition better.
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Fluid Management: Since you mentioned hydration issues, ensure you drink enough fluids throughout the day. Discuss with a healthcare professional or dietitian about potential dietary changes that could aid in managing your symptoms, such as smaller, more frequent meals to avoid postprandial hypotension.
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Autonomic Testing: Ask about further evaluation for autonomic function, which may include tilt table testing or other assessments to understand how your body regulates blood flow and heart rate when changing positions.
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Specialist Consultation: If you haven’t yet, consider seeking a consultation with a cardiologist who specializes in heart failure or autonomic disorders. They might be more attuned to cases like yours and could provide further insights or treatment options.
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Physical Activity and Rehabilitation: Engage in a gentle exercise program, possibly tailored through cardiac rehabilitation, focusing on building endurance without overstraining your heart. Listen to your body regarding activity levels.
While your symptoms warrant serious attention, it's important to approach them systematically to build a comprehensive understanding and management plan. Please remember that while navigating your healthcare journey can be challenging, you are advocating for your health, and that's incredibly important.
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7-Month-Old Child with Abernethy Malformation - Exploring Treatment Options
# 7-Month-Old Child with Abernethy Malformation - Exploring Treatment Options ## [7-Month-Old] Identified with Abernethy Malformation (Congenital Portosystemic Shunt) - Treatment Methods? **Age:** 7 months **Gender:** Female **Height:** Age-appropriate **Weight:** Currently 9 kg, was 2.8 kg at birth **Ethnicity:** Asian **Duration of Symptoms:** Present since birth **Location:** Uzbekistan **Pre-existing Health Issues:** Abernethy malformation (congenital portosystemic shunt), liver hemangiomas, chronic jaundice, anemia **Current Treatments:** Supportive management --- ## INITIAL PRESENTATION (June 2025 - July 2025) Our daughter arrived on **June 27, 2025**, presenting with: - Birth weight: **2.8 kg** - Marked jaundice (yellowing of skin and sclera) - Pale or clay-colored stools - **Bilirubin level: 245 μmol/L** (typically <20) An immediate ultrasound indicated multiple liver anomalies, initially thought to be hemangiomas. --- ## FIRST COMPREHENSIVE ASSESSMENT (August 1, 2025 - 1 Month Old) ### Multislice Computed Tomography (MSCT) with 3-Phase Contrast (August 1, 2025): **RESULTS:** - **Portocaval shunt size: 9.9 mm** (blood bypassing the liver into the inferior vena cava) - **Arteriovenous shunt size: 4.4 mm** - **Portal vein size: 6.1 mm** (patent) - **Three nodular cystic lesions** located in the perivascular area, with largest measuring 11.6×20.7 mm, enhancing during the venous phase - Liver features a heterogeneous architecture, exhibiting irregular enhancement - Gallbladder appears elongated and slightly enlarged - Other abdominal organs exhibit normal findings **RADIOLOGIST’S ASSESSMENT:** "Congenital portosystemic shunt indicative of Abernethy malformation; less likely arteriovenous malformation (AVM); cannot dismiss the possibility of localized liver lesions." **ADVICE:** Seek consultations with an abdominal and vascular surgeon. ### Blood Tests (August 1, 2025): **Complete Blood Count:** - WBC: 10.44 × 10⁹/L (normal range) - **RBC: 2.1 × 10¹²/L** (LOW - indicating severe anemia) - **Hemoglobin: 69 g/L** (CRITICALLY LOW; normal is 117-166) - Platelets: 403 × 10⁹/L (elevated) **Biochemistry Analysis:** - Urea: 1.80 mmol/L (normal) - Creatinine: 33.4 μmol/L (normal) - **ALT: >1000 IU/mL** (EXTREMELY HIGH - severe liver dysfunction) --- ## FOLLOW-UP IMAGING (December 16, 2025 - 5.5 Months Old) ### Liver Ultrasound: **RESULTS:** - Right lobe: 64 mm, left lobe: 43 mm - Liver capsule appears irregular and vague - **Parenchyma: heterogeneous, showing 7 hypo-isoechoic nodules** (sizes range from 11.5×10.7 mm to 17.6×15.4 mm) - Capsule features uneven contours - Blood flow noted during Doppler examination - No dilation in intrahepatic bile ducts - **Portal vein: 3.9 mm** (decreased from 6.1 mm - indicating improvement) - Common bile duct: 1.4 mm - Gallbladder: measures 43.7×9.2 mm (pear-shaped, wall thickness 2.0 mm, homogeneous, free of stones) **ULTRASOUND ASSESSMENT:** "Presence of liver volumetric formations (specifically liver hemangiomas)." --- ## LATEST MSCT (February 6, 2026 - 7 Months Old) ### MSCT with 3-Phase Contrast: **FINDINGS:** - Liver remains normal in size, but shows heterogeneous structure with uneven contrast enhancement - **Portocaval shunt: 9.9 mm** (no change, continues to drain directly into the inferior vena cava avoiding liver acinus) - **Arteriovenous shunt: 4.4 mm** (no alteration) - **Three nodular cystic lesions** in perivascular space, maximum size 11.6×20.7 mm, enhancing in the venous phase - **Portal vein: 6.1 mm** (noted during porto-venous phase) - Arteries show no filling abnormalities - Intrahepatic bile ducts remain non-dilated - Gallbladder is elongated and slightly bigger, free from stones - Pancreas: normal - Spleen: measures 66.9×38.5 mm (not enlarged), splenic vein is 3.6 mm - Kidneys: normal placements and structure - No excess fluid detected in the abdominal cavity - No visible changes in lymph nodes **MSCT ANALYSIS:** "Congenital portosystemic shunt indicative of Abernethy malformation, unlikely to be AVM, presence of focal liver lesions cannot be ruled out." **RECOMMENDATION:** Engage with an abdominal and vascular surgeon. --- ## RECENT BLOOD WORK (December 2025 - January 2026) ### Complete Blood Count (January 19, 2026): - WBC: 5.8 × 10⁹/L (SHOWS IMPROVEMENT) - **RBC: 2.93 × 10¹²/L** (IMPROVED but still low) - **Hemoglobin: 72 g/L** (SHOWS IMPROVEMENT but still low) - Platelets: 223 × 10⁹/L (BACK TO NORMAL) - Neutrophils: 30.0% - Lymphocytes: 64.8% - Monocytes: 4.6% ### Biochemistry (January 28, 2026): - Total protein level: 67 g/L (slightly deficient) - Creatinine: 20.7 μmol/L - **Total Bilirubin: 242 μmol/L** (STILL HIGH - unchanged) - **Direct Bilirubin: 142 μmol/L** (VERY HIGH) - **ALT: 50 IU/mL** (DRASTICALLY LOWER from >1000!) --- ## OVERVIEW OF PROGRESS OVER 6 MONTHS | Parameter | August 2025 | January 2026 | Change | |------------------|-------------|---------------|--------------------------| | **Hemoglobin** | 69 g/L | 72 g/L | ↗ Slight improvement | | **RBC** | 2.1 | 2.93 | ↗ Improved | | **ALT** | >1000 | 50 | ✓✓ MAJOR IMPROVEMENT | | **Bilirubin** | 245 | 242 | → Unchanged (still elevated) | | **Portal vein** | 6.1 mm | 3.9 mm (US) | ↗ Decreased | | **Platelets** | 403 | 223 | ↘ Normalized | | **Shunt size** | 9.9 mm | 9.9 mm | → No Change | --- ## CURRENT SITUATION (February 2026 - 7 Months Old) - **Weight:** 9 kg (good growth rate in spite of condition) - **Jaundice:** Continues to be present (yellow skin) - **Stools:** Remain pale/clay-colored - **Development:** Achieving appropriate milestones - **Energy:** Appears to have a good energy level - **Feeding:** Normal appetite --- ## QUESTIONS FOR r/AskDocs We have been informed this is **Type 2 Abernethy malformation** (portal vein present). **Three treatment avenues have been proposed:** ### Option 1: **Endovascular Coil Embolization** (minimally invasive approach) - A catheter is inserted via the leg vein to access the shunt and deploy coils/plugs to close the abnormal vessels - Pros: No surgical incision, minimal discomfort, short hospital stay (2-4 days), no scars, enhanced safety - Duration: 1-2 hours - Recovery: 2-4 weeks for jaundice to show improvement ### Option 2: **Open Surgical Intervention** - An incision in the abdomen to ligate abnormal vessels and redirect blood to the liver - Pros: Direct visualization, effective results - Cons: Surgical scar, longer recovery time (7-14 days in hospital) - Duration: 2-4 hours ### Option 3: **Liver Transplantation** - We have been advised this is not necessary as the portal vein is functional and liver health is improving. --- ## SPECIFIC QUESTIONS TO CONSIDER: 1. **With a functional portal vein (6.1 mm) and improving liver function (ALT normalized), is it advisable to pursue endovascular closure as the preferred treatment?** 2. **Despite ALT levels improving, the bilirubin remains consistently high (242). Should this be a cause for concern? Is there a prospect for it to normalize post shunt closure?** 3. **Are the hemangiomas/nodules (11.6×20.7 mm) linked to the shunt? Will they likely resolve following shunt repair?** 4. **How urgent is the proposed intervention? Is immediate action required, or is there flexibility to wait a few months?** 5. **What complications should we be vigilant for during the waiting period?** 6. **Regarding endovascular closure - what is the average success rate for infants aged 7 months? Are there concerns regarding the shunt size (9.9 mm)?** 7. **The measurement of the portal vein has shown improvement from 6.1 mm to 3.9 mm; should this be perceived as a positive sign or a reason for concern?** 8. **Are there special directives (diet modifications, medications) we should consider while awaiting the procedure?** 9. **Post-procedure, how long should we expect it might take for:** - Normalization of bilirubin levels? - Return of stool color to normal? - Resolution of jaundice? - Regression of hemangiomas? 10. **Can you recommend any specialized centers for pediatric Abernethy malformation treatments? We are located in Uzbekistan but are prepared to travel (to Turkey, Russia, South Korea, etc.)** --- ## ADDITIONAL INFORMATION - No family history of hepatic diseases - Pregnancy and delivery were normal - No additional congenital defects identified - Immunizations up to date - No history of bleeding disorders - No signs indicative of encephalopathy - Child is alert and engaged --- **I can supply actual MSCT images and comprehensive lab reports if they would be of assistance.** We sincerely appreciate any insights you can provide. We are striving to make the most informed decision regarding our daughter’s care and highly value expert medical opinions. **TL;DR:** 7-month-old diagnosed with Abernethy Type 2 malformation (9.9 mm portocaval shunt, patent portal vein). Liver functionality is improving (normalized ALT) while bilirubin remains elevated (242). Evaluating options between endovascular coil embolization and open surgery. 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