ProJR Viral Fever Heart Failure in Metabolic Syndromes Presenting with Consolidation and Clinical Complexity
Thursday , August 14, 2025
Project Title:
*Loculated Pulmonary Edema: Revisiting Phantom Tumors and Diagnostic Challenges in Viral fever-Precipitated Heart Failure*
Summary:
This study investigates the phenomenon of loculated pulmonary edema, often misdiagnosed as pneumonia, in patient's with viral fever-induced heart failure. Drawing from clinical observations, imaging findings, and literature, the study explores how atypical radiological patterns-such as consolidation resembling pneumonia- are manifestations of pulmonary edema.
The research aims to elucidate the pathophysiological mechanisms behind loculated fluid accumulation, its prevalence, and diagnostic implications while highlighting the need for refined imaging interpretation and clinical correlation. The thematic analysis underscores the gap between textbook descriptions and real-world clinical presentations, emphasizing the importance of interdisciplinary approaches to improve diagnostic accuracy.
----
Keywords:
- Loculated Pulmonary Edema
- Phantom Tumor
- Viral Fever-Precipitated Heart Failure
- Pneumonia vs. Pulmonary Edema
- Diagnostic Imaging
- Pathophysiology
- Consolidation Patterns
- Clinical Complexity
Pilot case data links:
IMRaD Format Plan:
Introduction:
- *Background*: Discuss heart failure precipitated by viral fever and the diagnostic challenges posed by atypical imaging findings. Introduce "phantom tumors" and loculated pulmonary edema as phenomena requiring deeper investigation.
- *Objective*: To analyze the prevalence, imaging characteristics, and pathophysiological basis of loculated pulmonary edema in heart failure patients, distinguishing it from pneumonia.
Methods:
- *Clinical Case Review*: Analyze serial chest X-rays and HRCTs of patients presenting with fever, alveolar opacities, and heart failure. Include cases like the "Narketpally syndrome" and others with loculated pleural effusion patterns.
- *Imaging Studies*: Compare radiological findings (X-rays, CT scans) between heart failure pulmonary edema and pneumonia using published literature and case-specific data.
- *Literature Review*: Include thematic analysis of relevant papers, such as Stark and Leung’s study on pleural effusion distribution and recent studies differentiating cardiogenic and infectious edema.
Results:
- *Imaging Findings*: Present patterns such as sharp fissural margins, unilateral or loculated consolidation, and rapid resolution with diuresis. Highlight discrepancies between textbook descriptions and observed cases.
- *Pathophysiological Insights*: Discuss mechanisms like negative intrapleural pressure (suction effect) and systemic factors influencing localized fluid patterns.
- *Comparative Analysis*: Detail similarities and differences between heart failure pulmonary edema and pneumonia radiologically and clinically.
Discussion:
- *Diagnostic Challenges*: Explore why loculated pulmonary edema mimics pneumonia and its implications for misdiagnosis.
- *Clinical Significance*: Highlight the importance of serial imaging and clinical correlation in distinguishing between pulmonary edema and infectious processes.
- *Future Directions*: Suggest the need for pathophysiological models to explain loculated patterns and a narrative review to synthesize findings across cases and studies.
Conclusion:
-Summarize key learning points: the prevalence of loculated pulmonary edema, diagnostic criteria, and the importance of interdisciplinary approaches.
- Emphasize the need for awareness and updated clinical frameworks to address atypical presentations of heart failure pulmonary edema.
---
Thematic Analysis:
Themes Identified:
1. *Diagnostic Complexity*:
- Loculated pulmonary edema often presents as consolidation indistinguishable from pneumonia on imaging.
- Rapid resolution of opacities with diuresis is key to recognizing pulmonary edema rather than infection.
2. *Pathophysiological Mechanisms*:
- Negative intrapleural pressure and localized factors like atelectasis may contribute to fluid loculations.
- Systemic factors like heart failure drive pulmonary edema, but local variations in fluid distribution require further elucidation.
3. *Clinical Implications*:
- Misdiagnosis can delay appropriate treatment for heart failure pulmonary edema.
- Serial imaging and clinical correlation are essential for accurate diagnosis.
4. *Textbook vs. Practice Gap*:
- Textbooks fail to comprehensively describe loculated pulmonary edema patterns, leading to diagnostic challenges.
- Real-world clinical observations suggest this phenomenon is far more common than traditionally believed.
5. *Interdisciplinary Learning*:
- Collaboration between clinicians, radiologists, and researchers is critical to understanding and addressing these atypical presentations.
- Integrating imaging findings with clinical history and pathophysiology can improve diagnostic accuracy.
---
This project plan provides a structured approach to investigate loculated pulmonary edema, bridging gaps in understanding and refining diagnostic practices.
[14/08, 17:07] Meta AI: References for the Project:
1. *Severe Localized Re-Expansion Pulmonary Edema*
Gowrinath K, Reddy SP, Jyothi P. _Severe localized re-expansion pulmonary oedema: An unusual instance._
Natl Med J India. 2023;36:310–11. DOI: [10.25259/NMJI_838_20]((link unavailable))
This case report sheds light on the phenomenon of localized pulmonary edema, specifically after pleural drainage procedures, and discusses predisposing factors like atelectasis and pleural fluid dynamics.¹
2. *Differentiating Heart Failure and Pneumonia via Imaging*
MedRxiv preprint: _There was no difference of ground glass opacity (GGO), consolidation, crazy paving pattern, lobes affected, and septal thickening between heart failure and pneumonia. However, features like peribronchovascular thickening and fissural thickening were more common in heart failure._
DOI: [10.1101/2020.03.04.
This study highlights the radiological overlap and subtle differences between cardiogenic pulmonary edema and infectious pneumonia.
3. *Pulmonary Pseudotumors*
(link unavailable) _A pulmonary pseudotumor is often caused by loculated pleural effusions trapped in pulmonary fissures, mimicking a solid mass._
[Pulmonary pseudotumor | Radiology Reference Article]((link unavailable))
This resource provides insights into how pleural effusions can mimic tumors, emphasizing loculated effusions as a diagnostic challenge.²
4. *Pleural Effusion Management*
Folch E et al. _Principles and Practice of Pleural Diseases._
This comprehensive guide discusses loculated effusions, their imaging characteristics, and management strategies, including diuresis and thoracentesis.³
5. *Effects of Lobar Atelectasis on Pleural Effusion Distribution*
Stark P, Leung A. _Effects of Lobar Atelectasis on the Distribution of Pleural Effusion and Pneumothorax._
Chest. 1989;95:1170. DOI: [10.1016/j.chest.1989.1170]((
This older yet foundational paper provides a theoretical basis for localized fluid accumulation due to atelectatic forces, offering potential explanations for the phenomenon of loculated pulmonary edema.
6. *British Thoracic Society Guideline for Pleural Disease*
Roberts ME, Rahman NM, et al. _British Thoracic Society Guideline for pleural disease._
Thorax. 2023;78(Suppl 3):s1-s42. DOI: [10.1136/thorax-2022-219784]((
This guideline discusses pleural effusions, including loculated presentations, diagnostic challenges, and treatment options.⁴
These references provide a strong foundation for the study, addressing both clinical observations and literature-based insights into loculated pulmonary edema and its diagnostic complexities. Let me know if you'd like more detailed explanations or additional references!
Conversational Transcripts:
[18/05, 07:19]cm: Our current heart failure clinical complexity projects are picking up a lot of viral fever precipitated heart failures manifesting with fever and alveolar opacities in the chest X-ray, initially interpreted as pneumonia because of fever and consolidation signs in the chest X-ray (very similar to what we saw during the covid period) and finally after a few days when it all resolves dramatically we realise that the consolidation opacities were all due to heart failure pulmonary edema precipitated by a viral fever in people with a metabolic syn phenotype and not due to pneumonia as one initially misinterpreted them as!
The recent most example we published is the Narketpally syndrome sample patient!
[03/06, 14:48] Dhu1 Pulmonary Edema: Good afternoon sir,
I had been busy with exams recently sir so I am going through some of these messages a little late.
I wanted to ask whether these opacities you mentioned were significantly indistinguishable as pneumonia vs edema on the imaging itself?
[03/06, 17:00] cm: No in imaging they would simply be labelled as consolidation
[03/06, 17:13] cm: Take a look at this patient's serial chest x-rays and one HRCT showing his loculated pleural effusion and consolidation that eventually vanished one day after few days of admission and recovery from heart failure which is when we became sure that it wasn't pneumonia but pulmonary edema👇
[03/06, 18:04] Dhu1 Pulmonary Edema: Quite interesting sir, this xray from the case most certainly does not seem like it could be pulmonary edema.
[03/06, 18:06] Dhu1 Pulmonary Edema: But why would pulmonary edema due to heart failure be restricted to the right upper lobe as it appears to be, instead of being more uniformly bilateral?
[03/06, 19:43] cm: Exactly! These kind of loculations due to pulmonary edema are far more common than text books know!
Text books may teach about phantom tumor as a short note, which is what this phenomenon is and we used to think it's relatively rare when we started gradually seeing it in practice till it's become so very common as to make us believe that it's much more common than pneumonia!
So learning points here are:
1) (Known previously) Phantom tumor is a pulmonary edema with loculated pleural effusion that is known to disappear rapidly in chest X-ray with diuresis
2) It's actually much more common than pneumonia if one has a high index of suspicion for all patients with rapidly resolving pneumonias
3) Why pulmonary edema gets sometimes (and for us often) in this peculiar loculated manner is what needs more elucidation with pathophysiological models
[03/06, 19:51] cm: Yes but a pneumonia can't vanish overnight!
The sharp margin of the displaced pleural fissure that you may notice in this and the other serial chest x-rays is the one indicative of the loculated pleural effusion.
Again in the past Phantom tumors were probably termed for loculated pleural effusions due to heart failure although it's logical that they would also have had alveolar edema? @Meta AI
[03/06, 19:51] Meta AI: You're right, pneumonia typically doesn't resolve that quickly. The sharp margin of the displaced pleural fissure is indeed indicative of a loculated pleural effusion. And yeah, "phantom tumors" was a term used to describe loculated pleural effusions in heart failure patients, which likely had accompanying alveolar edema. It's interesting how terminology and understanding of these conditions have evolved over time. Are you looking into the specifics of how heart failure can manifest in chest x-rays?
[03/06, 19:51]cm: @Meta AI alright share the specifics
[03/06, 19:51] Meta AI: Heart failure can manifest in chest x-rays in several ways, including:
1. Cardiomegaly (enlarged cardiac silhouette)
2. Pulmonary venous hypertension (distension of upper lobe veins)
3. Kerley B lines (short, horizontal lines at lung periphery)
4. Perihilar batwing opacities (alveolar edema)
5. Pleural effusions (often bilateral and loculated)
Loculated pleural effusions, like the one you mentioned, can mimic masses or "phantom tumors" on x-ray. Serial chest x-rays can help track changes and response to treatment.
Would you like more details on these findings or their implications?
[03/06, 19:52]cm: @Meta AI strange that text books never make this mention about their being manifest as consolidation!
[03/06, 19:52] Meta AI: Textbooks often focus on classic presentations, but heart failure can indeed manifest in various ways, including consolidation-like patterns on chest x-rays. This can be due to pulmonary edema or hemorrhage. Some cases might show atypical patterns, making diagnosis more challenging.
In clinical practice, radiologists and clinicians consider the entire clinical picture, including patient history, symptoms, and lab results, to interpret x-ray findings accurately.
Are you finding that your clinical experience is diverging from textbook descriptions, or are you preparing for exams and wanting to bridge that gap?
[03/06, 20:25]cm: @Meta AI here's something interesting around this, although not representative of a single chest X-ray for single patient findings but rather findings from a study utilising many chest X-rays for a single patient from different directions inside a tubular body shaped electro mechanical contraption aka CT scan and I quote from that paper 👇
"There was no difference of ground glass opacity (GGO), consolidation, crazy paving pattern, lobes affected and septal thickening between heart failure and pneumonia. However, less rounded morphology (8.3% vs. 67%, p=0.003), more peribronchovascular thickening (75% vs. 33%, p=0.041) and fissural thickening (33% vs. 0%, p=0.028), less peripheral distribution (33% vs. 92%, p=0.003) were found in heart failure group than that in pneumonia."
[03/06, 20:25] Meta AI: That's fascinating! The study you mentioned highlights the complexities of differentiating between heart failure and pneumonia using CT scans. The findings suggest that certain radiological features, such as peribronchovascular thickening and fissural thickening, are more common in heart failure, while rounded morphology and peripheral distribution are more characteristic of pneumonia.
The overlap in features like ground glass opacity, consolidation, and crazy paving pattern between the two conditions underscores the importance of clinical correlation and careful interpretation of imaging findings.
Did you find any other interesting studies or insights that might help in distinguishing between cardiogenic and infectious pulmonary edema?
[03/06, 21:19] Dhu1 Pulmonary Edema: Precisely sir, the sharp demarcation at the right horizontal fissure is very suggestive of localized consolidation.
[03/06, 21:23] Dhu1 Pulmonary Edema: As for point 3 I do indeed think it's very curious how something like this might come to occur.
How common would this be? Perhaps something that could warrant a narrative/literature review sir? I will read up and think about what could be causing this.
[03/06, 21:45]cm: More sharper due to a loculated pleural effusion
[03/06, 21:47]cm: To answer the commonality question I had shared the quote from the link earlier which I am pasting here again 👇
@Meta AI here's something interesting around this, although not representative of a single chest X-ray for single patient findings but rather findings from a study utilising many chest X-rays for a single patient from different directions inside a tubular body shaped electro mechanical contraption aka CT scan and I quote from that paper 👇
"There was no difference of ground glass opacity (GGO), consolidation, crazy paving pattern, lobes affected and septal thickening between heart failure and pneumonia. However, less rounded morphology (8.3% vs. 67%, p=0.003), more peribronchovascular thickening (75% vs. 33%, p=0.041) and fissural thickening (33% vs. 0%, p=0.028), less peripheral distribution (33% vs. 92%, p=0.003) were found in heart failure group than that in pneumonia."
[05/06, 00:30] Dhu1 Pulmonary Edema: I went through this paper which led me to go through some of the literature I could get my hands on for this topic after my duty hours. I found this which you might find interesting:
[05/06, 00:31] Dhu1 Pulmonary Edema: An atelectatic lobe can develop a recoil equivalent of 50 mm Hg; normal lung has aretractile pull of only 5 mm Hg (4). When a lobe develops a greater retractile tendency than the rest of the lung, local variations in pleural pressure ensue. This variation results in greater negative intrapleural pressure surrounding the atelectatic lobe and produces a suction cup effect. Thus, when a buffer medium such as liquid or gas is present in the
pleural space, it will preferentially be attracted by the atelectatic lobe (Figs. 1-5).
Therefore, any atypical configuration of pleural effusion or pneumothorax should direct attention to the underlying lung parenchyma (5). An atypical arrangement of pleural effusion caused by focal alteration of intrapleural pressure can be readily differentiated from loculation due to adhesions by positional maneuvers that test the mobility of the effusion. Obstructive atelectasis develops the largest retractile forces and attracts a disproportionate amount of pleural effusion. An increased atelectatic
tendency in the lower lobes may explain large subpulmonic effusions (6).
~ Effects of Lobar Atelectasis on the Distribution of Pleural
Effusion and Pneumothorax (Paul Stark, M.D., and Ann Leung, M.D.)
[05/06, 00:34] Dhu1 Pulmonary Edema: It is a rather old paper but I believe it provides a theory for this phenomenon that is something along the lines of what I was thinking, since I have a strong feeling there is localized factor at play to explain the specific pattern of fluid accumulation, either by itself or in addition to a systemic factor like heart failure.
[06/06, 12:39] cm: Excellent! 👏👏
Please share the URL to it
[07/06, 17:47] Dhu1 Pulmonary Edema: https://pubmed.ncbi.nlm.nih.
This is the paper sir, I had to figure out a way to access it.
[13/06, 17:09] cm: Afternoon session:
The incidence of rheumatic valvular heart disease has remarkably decreased and this afternoon we found both mitral and aortic badly affected in this 33M
@ Pg please share his chest X-ray PA view
[13/06, 17:09]cm: A lot of pleural effusion on the right with consolidation likely due to heart failure pulmonary edema @huai1
[13/06, 17:27] Dhu1 Pulmonary Edema: Interesting sir, specifically since we have a CT available in this case. Should we then expect the consolidation to clear up with management appropriate to pulmonary edema soon?
[13/06, 17:27] Dhu1 Pulmonary Edema: Is this restricted only to the right lower lobe?
[13/06, 17:31]cm: Yes we should
But Hrcts can't be repeated to check that!
[13/06, 17:36] Dhu1 Pulmonary Edema: Yes quite certainly not. I will keep an eye out for more cases like these, but in this case given the distinct cardiac dysfunction pulmonary edema seems like the major culprit, leaving me confused again about why it isn't seen in both lungs.
[13/06, 19:24]cm: 👆 here's the reason perhaps
[13/06, 20:52] Dhu1 Pulmonary Edema: Not in this case I believe because there are no atelectatic factors present or local factors present.
[13/06, 21:38]cm: We don't know if they are
[19-08-2025 12.15] cm: @56M for the viral fever in metabolic syn heart failure pulmonary edema consolidation ProJR
[25-09-2025 16.37] cm: For that ProJR here's another similar patient PaJR
[25-09-2025 16.38] cm: Echocardiography: https://youtu.be/Xe18pe2efn4?feature=shared
75F with fever and shortness of breath, sepsis.
While not all our patients may have viral fever precipitating their heart failure, heart failure due to any cause is equally likely to produce this diagnostic uncertainty in most health professionals!
[29-09-2025 19.35] cm: More details about this patient in the below link. 👇
[09-10-2025 21.34] cm: https://youtube.com/shorts/UdBs7tlct74?si=pNk14NjNFjw_by_R
More about this patient in the below link. 👇
https://pajrcasereporter.blogspot.com/2025/10/55f-dengue-thrombocytopenia.html[01/12/2025 22.09] cm: From this to the last one gradual progression of the failure is evident
More details of this patient available in the below link. 👇
[8:52 pm, 07/12/2025] cm: @hu8 this patient is one of the patients of your pulmonary edema project detailed here👇
[10:37 pm, 07/12/2025] hu8: Sir do we know the patient's TSH?
[10:38 pm, 07/12/2025] hu8: Same progression of lung infiltrates resembling consolidation which resolved in 2-3 days sir?
[10:53 pm, 07/12/2025] cm: Yes although it hasn't resolved yet. Resolution would also depend on the severity of the heart failure and the patient's capacity for recovery.
[10.53 pm, 07/12/2025] cm: More details of the patient available in the below link👇
[11.55 am, 20/02/2026] cm:
Now seeing this patient of @hu9 who is a young 31 year old man, with a metabolic syn phenotype and recent viral fever with pain abdomen for which he approached his local doctor who promptly got a CT abdomen where some incidentaloma was diagnosed following which he had a syncope while going home and after reaching home, he also developed low backache and myalgia due to his viral fever for which another local doctor did MRI that thankfully didn't show another incidentaloma (or maybe it did but I didn't see the report) and then finally he developed shortness of breath that appeared to be cardiogenic pulmonary edema (one Hrct frame attached) fitting into our viral fever heart failure ProJR: https://pajrcasereporter.blogspot.com/2025/08/projr-viral-fever-heart-failure.html?m=1 but similar to @hu10's previous patient with LVF here: https://pajrcasereporter.blogspot.com/2026/02/75m-recent-breathlessness-metabolic-syn.html?m=1, this current patient's CTPA too showed pulmonary embolism, which is becoming a frequent incidentaloma here especially with one radiologist although again one can't contest it much seeing that it's a classic mimicker.
Let's add the above to our viral fever LVF ProJR although these cross sectional snippets without the rigor of a PaJR @hu1 can at best be termed anecdotal.
[10.12 am, 25/06/2026] cm: Conversational citations around another potentially similar patient:
Today's dyadic conversational data around another patient with probable viral fever , heart failure pulmonary edema
[24/06, 19:05]hu1: One dilemma
[24/06, 19:07]hu1: ... came back home on Saturday and upon return, and after being febrile for 15 days, and suspected to be TB (even though all tests were negative including met genome) was put on ATT- after taking one dose he became afebrile …
[24/06, 19:07]hu1: Should he continue ATT
[24/06, 20:17]hu2: How was TB suspected?
What symptoms other than fever? Chest X-ray?
[24/06, 20:21]hu1: Fever
[24/06, 20:21]hu1: They tapped pleural effusion which was T cell reactive but negative for AFb, ada and genexpert, repeated twice
[24/06, 20:22]hu1: Echo was okay, afb continued
Instead of apaxiben, out him on injectable heparin SC
[24/06, 21:48]hu1: Does it tell anything significant-father wore my Apple Watch for ECG
[25/06, 08:27]hu2: It shows his old atrial fibrillation. Since when is he having the atrial fibrillation?
[25/06, 08:28]hu1: We detected it a month back and since he is on ACs
[25/06, 08:28]hu1: Question about TB needs discussion and your decision
[25/06, 08:29]hu2: We have a project on this where we find a lot of these apparent consolidations are finally proven to be pulmonary edema due to heart failure but they end up getting treated unnecessarily for pneumonia and sometimes rarely TB as in your case 👇
[25/06, 08:30]hu2: We need to see his serial chest X-rays to rule out heart failure where the shadows will keep changing rapidly and disappear with reduction in failure
[25/06, 08:31]hu2 : 👆this chest X-ray is 11/6/26
Need to see the subsequent chest x-rays
[25/06, 08:32]hu1: But there was no pulmonary edema …only pleural effusion…I will read this
It’s great you almost document everything
[25/06, 08:35]hu2: Pleural effusion can be a result of pulmonary edema. Pleural effusion is aka pleural edema that like all other edemas can be either inflammatory (as in pneumonia) or non inflammatory as in heart failure
[25/06, 08:35]hu1: Got it thanks
[25/06, 08:36]hu1: So what should be the plan of action
Basically his problems are as below
Extremely lethargic
Feeling suffocated although spo2 and ecg seems okay as per cardiologist as long as it’s heartbeat isn’t too low or high
[25/06, 08:38]hu2: Sounds like heart failure
Does he also have pedal edema?
He needs good rest, diuretics as long as there is substantial pedal edema to reduce preload and ARBs to reduce afterload
[25/06, 08:39]hu1: Yes he has pedal edema
[25/06, 08:39]hu1: Will do
[25/06, 08:39]hu1: But I want him to be off ATT
[25/06, 08:39]hu1: Should I do it on our own without consulting chest people as they might not endorse this
[25/06, 08:41]hu2: We need to see his serial chest X-rays to rule in heart failure and rule out TB as the shadows of
11/6/26 is expected to keep changing rapidly and disappear with reduction in failure by now
[25/06, 08:42]hu3 (forwarded by hu1): Serial x ray?
[25/06, 08:49]hu3 (forwarded by hu1) : No CHF . We can repeat echo after a week or so for possible RV thrombus?
There was a tiny spec in RV
[25/06, 08:53]hu2: Serial chest X-ray would show lung changes of pulmonary edema recovery or worsening.
Echo may not help in this regard
[25/06, 08:54]hu2: Let's get a repeat chest X-ray now before that. I guess we.are going only by one single chest X-ray till now?
[25/06, 08:59]hu1: Yes that’s correct
Will try one today
[3.15 pm, 01/09/2026] cm: All the below images including chest X-rays are date 1/8/26
[3.15 pm, 01/09/2026] cm: Viral fever heart failure ProJR patient conversational update from 29/6/26
[29/06/26, 18:21]hu1 : Just an update - his breathlessness continues
[29/06, 18:21]hu1: Yet to get his x ray - he doesn’t want to do it - but will soon prevail
[03/07/26, 09:15]hu1: Is it worth experimenting to infuse my (younger) Plasma to him?
[03/07, 09:15]hu2: No
[03/07, 09:16]hu2: It will cause further cardiac overload
[03/07, 09:28]hu1: If done 10 mL a day for 30 days?
[03/07, 09:30]hu2: This experiment needs IEC clearance
[03/07, 09:31]hu1: Have such case to case clearances been taken earlier in medical practice other than our grant and RCT trials
[03/07, 09:33]hu2: Yes off course
One published in Lancet I had shared with you earlier
[03/07, 09:36]hu2: https://pubmed.ncbi.nlm.nih.gov/8093748/
[05/07, 05:39]hu1: What can I do to get him to move around - he feels immensely weak, even though his symptoms of breathlessness and cough seem to have receded…ATT?…we gave him multi vitamin drink-
he seems to have given up on living any more…sleeps the whole day and night …
[05/07, 07:16]hu2: Breathlessness and cough were part of the short term viral that precipitated his recent heart failure?
How is his wife? What does she feel about his depression?
[05/07, 07:25]hu1: Thanks-makes sense
Asked her-she doest feel so-he was depressed earlier and not any more
[15/07, 11:02]hu1: Ventilator is good for him?
[15/07, 11:02]hu1: His spo2 dipped to 85 today and increasingly feeling suffocated
[15/07, 11:03]hu1: He doesn’t want echo and x ray done ..but when I change his catheter I will try
[15/07, 11:03]hu1: Extremely weak and lethargic
[15/07, 11:03]hu2: Will need it if his hypoxia doesn't respond to oxygen but for that he'll need to be evaluated sos
[15/07, 11:05] hu2 : Home healthcare is best but these services are still not well established in India as of now.
Perhaps your team could be mobilized to work on this at a national scale
[15/07/26, 11:08]hu1: By an anesthesia or medicine consultant?
[04/08/26, 13:32]hu1: Before and after the patient’s pleural tap
Cardiologist ruled out any CHF
[04/08, 16:59]hu2: It can't be ruled out.
[04/08, 13:32]hu1: Breathlessness continues after temporary relief
[04/08, 14:36]hu2: Can I give him 10 mg dytor in addition to below
[04/08, 16:57]hu2: 👆Date?
[04/08, 16:57]hu2: 👆Date?
[04/08, 16:58]hu2: Lasilactone contains frusemide and dytor is similar action aka torsemide
Can take additional lasix if necessary
Any pedal edema?
[04/08, 16:58]hu1: 4 days back
[04/08, 16:59]hu1: Same day after tap
[04/08, 17:00]hu1: Yes he has pedal edema
[04/08, 19:17]hu2: This is most likely to be heart failure
[04/08, 19:17]hu2: Can add tablet lasix also separately other than the lasilactone
[04/08, 19:21]hu2: Tablet lasix 40 mg at 12 PM if lasilactone is taken at 8:00AM
Can stop tablet lasix once pedal edema and breathlessness subsides
[04/08, 19:34]hu1: Why do cardiologist refuse to accept it asked so many times
[04/08, 19:35]hu1: For heart failure nothing is to be done? …perhaps nothing can be done
Anything we can do to reduce the risk or delay
[04/08, 20:51]hu2: Yes we are reducing the load on the heart with lasix and lasilactone (aka preload) and the afterload can be reduced with vasodilators
[04/08, 20:52]hu2: The idea behind heart failure treatment is to give rest to the heart and reduce it's pre and afterload
[04/08, 21:24]hu1: Ok
[04/08, 21:24]hu1: Thanks
[05/08, 04:18]hu1: What is pre and after load
[05/08, 04:38]hu1: Does it also mean that I don’t walk him to the dining table? He feels extremely exhausted and his heart beat reaches 110-115 when we make him walk
[05/08, 04:38]hu1: Saturation is maintained
[05/08, 04:39]hu1: Heparin injections are continuing
[05/08, 04:39]hu1: AFs accelerate CHF?
[05/08, 05:17]hu2: Yes
[05/08, 04:38]hu1: His average daily resting heart rate is around 90 or so
[05/08, 05:17]hu2: 70-80 would be better
Is he on any heart rate reducing agents?
[05/08, 05:18]hu1: Cardiologists say untill 130-150, we don’t treat
[05/08, 05:18]hu2: Tell them it's likely to be Hfpef
[05/08, 05:18]hu1: Should I take second opinion
[05/08, 05:19]hu2: You are already 🙂🙏
[05/08, 05:21]hu1: Cardiologist says nothing from my side as heart is fine
[05/08, 05:21]hu2ai: Low dose beta blockers to begin with and then if dose is uptitrated would help especially also for AF rate control
Low-dose beta-blockers provide initial, partial clinical benefits in heart failure with reduced ejection fraction (HFrEF), but maximum target doses established in clinical trials offer superior reductions in mortality and hospitalizations. [1, 2]
Disclaimer: This information is for general knowledge and should not be taken as medical advice. Always consult a local healthcare professional for diagnosis and treatment.
Efficacy and Dosing Dynamics •
Starting Point:
Therapy is initiated at a low dose to prevent potential initial worsening of heart failure symptoms as the body adjusts, minimizing risks of reduced adrenergic drive.
• Dose-Dependent Benefit: Clinical data consistently show that the reduction in all-cause mortality and heart failure readmissions is dose-dependent, with superior outcomes achieved when patients reach guideline-directed target doses.
• Titration Goal: Providers systematically increase the dose over time as tolerated, aiming for established target levels rather than maintaining a low dose. Low doses are considered a necessary, temporary phase for safe initiation, not the final therapeutic target. [2, 4, 5, 6]
AI responses may include mistakes.
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC3396733/
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC12147320/
[3] https://www.youtube.com/watch?v=hf3j3TtDwYw
[4] https://innovationaljournals.com/index.php/ip/article/download/973/803
[5] https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.120.052926
[6] https://www.sciencedirect.com/science/article/pii/S1071916410001740
[05/08, 05:24]hu2ai: Why does the heart appear fine in hfpef and how can a cardiologist be convinced to treat heart failure symptoms for such patients?
In Heart Failure with Preserved Ejection Fraction (HFpEF), the heart appears fine on a standard routine ultrasound (echocardiogram) because the ejection fraction (EF)—the percentage of blood pumped out of the main pumping chamber with each beat—is normal (usually 50% or higher). [1, 2, 3, 4, 5]
Why the Heart Appears "Fine"
• Normal Squeezing (Systole): The heart muscle squeezes and ejects blood normally, which tricks standard tests into looking healthy.
• Stiff Pumping Chambers (Diastole): The problem isn't the squeeze; it's the relaxation. The heart muscle has become stiff or scarred.
• High Pressures: Because it cannot relax properly to fill with blood easily, pressure backs up into the lungs and body, causing severe shortness of breath and fluid retention, even though the pump itself looks strong on the outside. [1, 6, 7, 8, 9]
How to Convince a Cardiologist to Treat HFpEF
Many cardiologists historically hesitated to treat HFpEF aggressively because older traditional heart failure drugs did not change survival rates. Today, modern guidelines have shifted. You can guide a productive discussion with a cardiologist by focusing on concrete evidence and modern therapies:
• Highlight Current Guidelines: Mention that modern clinical trials (such as those for SGLT2 inhibitors like empagliflozin or dapagliflozin) prove that targeted therapy reduces hospitalizations and improves symptoms in HFpEF.
• Use Clinical Scoring: Bring up validated tools like the H2FPEF score, which combines clinical features (obesity, age, hypertension, atrial fibrillation) with simple echocardiogram markers to calculate the mathematical probability of HFpEF.
• Ask for Advanced Testing: If resting echocardiograms are inconclusive, request specialized evaluations such as natriuretic peptide blood tests (BNP or NT-proBNP) or an exercise stress echocardiography / invasive hemodynamic test to expose elevated heart filling pressures during physical stress.
• Focus on Comorbidities: Emphasize aggressive management of the underlying drivers of the disease, including high blood pressure, obesity, diabetes, and sleep apnea. [19, 20]
To help tailor this advice, could you tell me:What specific symptoms (like shortness of breath or swelling) are most bothersome? What test results or feedback has the cardiologist provided so far?
AI responses may include mistakes.
[1] https://www.youtube.com/watch?v=3NlC7jlPL04
[2] https://www.aafp.org/afp/2017/1101/p582
[3] https://www.mayoclinic.org/medical-professionals/cardiovascular-diseases/news/heart-failure-with-preserved-ejection-fraction-hfpef-more-than-diastolic-dysfunction/mac-20430055
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC6334030/
[5] https://www.heartfailurematters.org/understanding-heart-failure/what-is-ejection-fraction-hfref-and-hfpef/
[6] https://cvrti.utah.edu/whats-the-difference-between-hfref-and-hfpef-understanding-two-types-of-heart-failure/
[7] https://heart.bmj.com/content/109/11/874
[8] https://heartmatters.com/hfref-and-hfpef-understanding-the-two-types-of-heart-failure/
[9] https://cdn.ymaws.com/www.aahfn.org/resource/resmgr/docs/f139_passport_3c__1_.pdf
[10] https://www.acc.org/latest-in-cardiology/articles/2022/03/08/18/51/pharmacologic-treatment-for-hfpef
[11] https://pmc.ncbi.nlm.nih.gov/articles/PMC3821938/
[12] https://upcommons.upc.edu/bitstreams/85035a99-4057-433c-aad9-e6989dfedb81/download
[13] https://www.ajmc.com/view/rethinking-heart-failure-patient-classification-and-treatment
[14] https://www.touchcardio.com/cme/multidisciplinary-team-insights-on-the-promise-of-new-and-emerging-treatment-options-for-patients-with-hfref/
[15] https://www.thecardiologyadvisor.com/ddi/hfpef-heart-failure-with-preserved-ejection-fraction/
[16] https://www.youtube.com/watch?v=KngG_lCTNkg
[17] https://www.youtube.com/watch?v=Q2ZR6fx0FOI
[18] https://www.mayoclinic.org/medical-professionals/cardiovascular-diseases/news/heart-failure-with-preserved-ejection-fraction-hfpef-more-than-diastolic-dysfunction/mac-20430055
[19] https://www.youtube.com/watch?v=tBlYrpqRSmU
[20] https://www.ncbi.nlm.nih.gov/books/NBK599960/
[05/08, 05:25]hu1: This is the patient's video on a wheel chair
[05/08, 05:25]hu2: 👏nice so you managed to get that wheelchair you needed
[05/08, 05:26]hu1: Also got him roof display projector to watch movies which he watches as a duty, lying down
[05/08, 05:27]hu1: Would all of this help
[05/08, 05:27]hu2: All of?
[05/08, 05:28]hu1: Distractions
[05/08, 05:28]hu1: Diuretic you prescribed
[05/08, 05:29]hu1: Yes to be taken as long as there is visible pedal edema
What is his serum albumin?
[05/08, 05:32]hu1: Today we are repeating CBC and LFT as he is on empirical ATT
[05/08, 05:32] hu 1: Do you want to add a test like pro BNP or something
[05/08, 05:40]hu2: I'm fairly convinced about the heart failure and wouldn't need a pro BNP.
Also if it comes negative, the cardiologist will not be convinced in his her lifetime.
Approximately 20% to 33% of patients with confirmed heart failure with preserved ejection fraction (HFpEF) have a negative or normal NT-proBNP level (below standard rule-out thresholds like 125 pg/mL). [1, 2, 3]
Factors Increasing False-Negative NT-proBNP in HFpEF
• Obesity (BMI ≥ 30 kg/m²): Adipose tissue clears and suppresses natriuretic peptides, increasing false-negative rates significantly.
• Early or Mild Disease: Less myocardial wall stretch results in lower peptide release.
• Non-sinus rhythms or specific architectural variants: Preserved or unique ventricular-atrial remodeling can present with disproportionately low values. [1, 2, 4, 5]
Clinical Implication
A normal or negative NT-proBNP cannot safely rule out HFpEF if clinical suspicion remains high. Diagnosis typically requires correlation with echocardiography demonstrating diastolic dysfunction or elevated filling pressures. [2, 6, 7]
If you'd like, let me know:The patient's BMI / weight categoryWhether they are experiencing acute dyspnea or chronic symptomsAny other available echocardiogram findingsI can help outline further diagnostic steps or scoring tools used to evaluate suspected HFpEF.
AI responses may include mistakes.
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC11277408/
[2] https://emedicine.medscape.com/article/761722-overview
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC12089450/
[4] https://cardiophoenix.com/nt-probnp-in-hfpef-diagnosis/
[5] https://impactfactor.org/PDF/IJDDT/16/IJDDT,Vol16,Issue53s,Article132.pdf
[6] https://www.tctmd.com/news/nt-probnp-cutoffs-hfpef-diagnosis-may-need-tweaking
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC3432159/
[05/08, 05:44]hu1: Ok
[05/08, 05:45]hu1: BTW, His pro BNP levels were raised last time
[05/08, 05:48]hu2: Again clinical diagnosis in the head of the physician (aka medical cognition) reigns supreme and investigations may sway the physician if they are connected to a team based learning network where collective cognition plays a vital role in clinical decision making. Currently most physicians (cardiologists are also physicians albeit with less time to think) have barely time to think individually let alone collectively hence I wouldn't expect them to be convinced on the patient's advocate's persistence
[05/08, 05:49]hu1: His latest pleural tap results attached
[05/08, 05:49]hu1: Completely agree and aware of this
[05/08, 05:50]hu2: Very much suggestive of heart failure by Light's criteria of whatever information is available
Need serum and pleural fluid protein and LDH at the same time
[05/08, 05:51]hu1: And latest echo report
[05/08, 05:52]hu2: Very much Hfpef
LA dilatation even if just relative to the aortic root would have further sealed it
[05/08, 05:52]hu1: Ok
[05/08, 05:54]hu1: Pre load is the load on the heart before it contracts
Essentially the blood volume in the circuit and amenable to volume reduction with diuretics
Afterload is the aortic resistance offered to the heart after it contracts logically amenable to aortic vasodilators like ARBs like telmisartan etc
[05/08, 05:55]hu1: Got it thanks
[05/08, 05:58]hu1: To this at 8 am, we will add below at 12 pm
[05/08, 06:00]hu1: Hope it isn’t harmful to let him use oxygen concentrator set to 2 Units, as and when he feels breathlessness
So his suffocation comes from heart failure?
[05/08, 06:21]hu2: Yes
If his SpO2 is normal then oxygen may not be necessary and can be harmful
[05/08, 06:36]hu1: Ok
[05/08, 06:37]hu1: Then how to answer his call for “Ghutan ho rahi hai”
[05/08, 06:40]hu2: If SpO2 is normal then lasix or even NIV
[05/08, 06:41]hu2: Also one needs to check the respiratory rate first before taking any decision for intervention
[05/08, 06:45] hu 1: Spo2 is always above 90
[05/08, 06:48]hu1: respiratory rate is 18/20 as noted now
[05/08, 06:53]hu1: NIV will have to be recommended by cardiologist or pulmonary consultants?
[05/08, 07:25]hu1: It has to be above 92
[05/08, 07:26]hu2: So this is his baseline and it will be useful to check the rate when he complains of shortness of breath
[05/08, 07:27]hu2: Connecting to NIV is a complex decision to be handled by critical care physician and or pulmonology
[05/08, 18:47]hu1: He is feeling better Today
[06/08, 20:06]hu1: He is even better today ..less breathless
However, felt exhausted momentarily when I scored his RR which was 24, with above spo2 /heart rate, bp 112/74
[06/08, 20:07]hu1: 98/88
[06/08, 20:07]hu2: This would be expected with his heart failure
[06/08, 20:08]hu1: Momentarily his heart rate fell to 48 and in 3 secs rose to 88
[06/08, 21:42]hu2: That could sometimes be due to the sensor. Better verify with manual counting of the pulse in such situations
[07/08, 08:07]hu1: His bp fell to 105/67,!yesterday 112/74
[07/08, 08:08]hu1: It falls whenever we put him on double dose
Any change in Regimen
Pedal edema still there
[07/08, 08:13]hu2: That's expected. It means the medicine is working
Should be okay till it doesn't fall below 90/60
[07/08, 08:13]hu2: Pedal edema may take a few days to subside after which we can stop the second dose of the 13 PM lasix
[08/08, 09:49]hu1: Can nothing be done regarding his fatigue and exhaustion-can’t even walk to toilet
[08/08, 09:49]hu1: His Hb is 8.5
IV?
[08/08, 09:58]hu1: This is further precipitating his heart failure.
It's probably driven by his underlying CLL although one needs to rule out iron deficiency, although again his RBC indices do not suggest that except his RDW which is slightly raised.
A careful packed RBC transfusion could provide some symptomatic relief by taking care of cellular oxygenation that may reduce the current fatigue
[08/08, 09:59]hu1: Ok
[08/08, 09:59]hu2: IV only very slow prbc. Anything else will simply further load his heart and worsen his current symptoms.
[08/08, 09:59]hu1: Will discuss transfusion
[08/08, 10:00]hu2: Only slow prbc
[08/08, 11:44]hu1: Hematology say, "Yes, I can consider that after examining him. You may plan accordingly"
[08/08, 11:45]hu1: Does it require admission
[08/08, 11:47]hu1: Yes
[08/08, 11:48]hu1: Ok-does it carry risk?
[08/08, 16:05]hu2: Off course.
Mismatched blood transfusions can be fatal
[10/08, 12:02]hu1: Just sharing his pro BNP
[10/08, 12:08]hu2: I would not have changed my diagnosis even if it was normal
[10/08/26, 12:09]hu1: Ok
[01/09/26, 10:09]hu1: Which medicine you had prescribed at 12 pm?
[01/09, 10:09]hu1: Unable to dig out
[01/09, 10:09]hu1: As diuretic
[01/09, 10:49]hu2: Tablet Frusemide 20 mg
No comments:
Post a Comment