THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DEIDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[4:37 pm, 31/01/2026] PPM 1: 66M Currently admitted with @PPM3 @PPM4
[4:40 pm, 31/01/2026] PPM 1: This patient inspired a new project where we look into the factors in terms of event details as to what makes certain patients survive CPR well and some patients not survive at all vs some patients survive with persistent vegetative state or currently better known as Unresponsive wakefulness syndrome.
Handwritten notes during first admission with left ventricular failure and a diagnosis of CKD since three months. Patient was taken up for dialysis soon after admission by PPM5
[4:46 pm, 31/01/2026] PPM 3: He was previously admitted under us and was discharged sir, now he was again admitted for maintenance hemodialysis sir
[4:47 pm, 31/01/2026] PPM 5: That’s my handwritten notes.
[4:49 pm, 31/01/2026] PPM 1: From admission on 5/1/26 followed by discharge and then readmission on 26/1/26 he had a few dialysis sessions but had a sudden event during dialysis on 26/1/26 which was a republic day holiday. There is no note about the events before the intubation while the intubation note does mention that the patient was drowsy.
Can @PPM5 @PPM3 @PPM4 tell us more about that particular event which led to the intubation?
[4:51 pm, 31/01/2026] PPM 3: Morning till he was connected to hemodialyzer he was fine sir, 2 mins after that he complained of pain at the IJV Catheter site, and after that he suddenly became unresponsive and was in gasping state sir.
[5.00 pm, 31/01/2026] PPM 1: Well done CPR documented at 6:40AM by PPM3
Patient progress with ABG rtc on handwritten notes this republic day
[5.08 pm, 31/01/2026] PPM 1: @PPM3 can you clarify on why the CPR has been labelled as two cycles?
Further notes on 27/1/26 @PPM6 @PPM7 note the mnemonic fast hugs bid handwritten by @PPM3 and share it's significance in this patient if possible
[5:11 pm, 31/01/2026] PPM 3: Return of spontaneous circulation was achieved after 2 cycles sir
[5.11 pm, 31/01/2026] PPM 1: On 29/1/26 our team of local doctors started planning extubation
@PPM6 @PPM7 check the extubation criteria noted by @~Poreddy Jahnavi and comment in relation to this patient's supplied data if possible
https://youtu.be/zd6bmRYk8Rk?si=tM5vRKWCv14i7WQfThe patient is walking today
[5:16 pm, 31/01/2026] PPM 1: While gasping what did you notice about his pulse, heart rate?
[5.17 pm, 31/01/2026] PPM 1: His metabolic syn phenotype
[1.53 pm, 01/02/2026] PPM 1: 👆@PPM3 please answer the question above. I'm not sure who actually witnessed the patient just before CPR and intubation but I'm assuming it's you. The events before the CPR is not documented in the file and hence we are trying to at least document it here.
Was the monitor showing a flat line while he was gasping? Was he in the dialysis room when he was gasping and perhaps he was not connected to a cardiac monitor there? Was he shifted to the ICU from the dialysis room before CPR was started? If not cardiac monitor what about carotid pulse? Apical impulses? Heart sounds?
How much CPR time did rosc (return of spontaneous circulation) take? 40 seconds?
[2:55 pm, 01/02/2026] PPM 4: Patient was shifted to ICU from the dialysis before cpr was started
There was no carotid pulse before cpr or any pulse on cardiac monitor
[3:35 pm, 01/02/2026] PPM 6: Album
Found it sir
This is a daily ICU care mnemonic, not a diagnosis or treatment, but a checklist to prevent ICU-related complications.
🧠 FAST HUGS BID expanded:
Letter
Meaning
F
Feeding
A
Analgesia
S
Sedation
T
Thromboembolism prophylaxis
H
Head-up elevation
U
Ulcer (stress ulcer) prophylaxis
G
Glycemic control
S
Spontaneous breathing trial
B
Bowel care
I
Indwelling catheter review
D
De-escalation of drugs / Delirium
📌 It ensures holistic ICU care, not just survival.
[3:36 pm, 01/02/2026] PPM 8: Sudden event = sudden cardiac arrest?
[3:44 pm, 01/02/2026] PPM 1: Wish we could see the microscopic events before the macroscopic cardiac arrest
[7:55 pm, 01/02/2026] PPM 1: @PPM6 @PPM9 @PaJR Health how common is it to have cardiac arrest during dialysis and what are the prior identified factors and associations with this phenomenon that may also influence those patient outcomes in terms of recovery after CPR after a cardiac arrest during dialysis?
[7:55 pm, 01/02/2026] PaJR Health: *CARDIAC ARREST DURING DIALYSIS: INCIDENCE, RISK FACTORS, AND OUTCOMES*
💡 Patients undergoing hemodialysis face a significantly elevated risk of sudden cardiac arrest (SCA), with an incidence 10 to 20 times higher than that of the general population. While sudden cardiac death is a rare event during individual dialysis sessions (approximately 1 event per 10,000 sessions), it carries a very high mortality rate [1].
*PRIOR IDENTIFIED FACTORS AND ASSOCIATIONS*
💡 Several factors have been identified that predispose dialysis patients to cardiac arrest:
📍 *Cardiovascular Conditions:*
* Severe ischemic heart disease [1]
* Left ventricular hypertrophy [1]
* Cardiogenic shock, with dialysis being a factor associated with increased early mortality [2]
📍 *Dialysis-Related Factors:*
* Electrolytic and plasma volume shifts during dialysis sessions are frequent trigger events [1].
* Low potassium dialysate has been identified as a factor to avoid for primary prevention of SCA [4].
📍 *Patient-Specific Factors:*
* Age ≥ 75 years [2]
* Peripheral arterial disease [2]
* Chronic kidney disease (as the underlying condition for dialysis) [2]
* Female sex [2]
* Dependent functional status (e.g., in vascular surgery patients) [3]
* Preoperative ventilator dependence (e.g., in vascular surgery patients) [3]
* Out-of-hospital cardiac arrest (OHCA) [2]
📍 *Procedural Factors (e.g., in vascular surgery patients):*
* Emergent cases [3]
* Thoracic aortic surgery [3]
* Open abdominal procedures [3]
* Axillary-femoral bypass [3]
* Peripheral embolectomy [3]
* Major complications preceding cardiac arrest, such as sepsis, renal failure, and myocardial infarction [3]
*INFLUENCE ON PATIENT OUTCOMES IN TERMS OF RECOVERY AFTER CPR*
💡 Outcomes for dialysis patients experiencing cardiac arrest and receiving CPR are complex:
* *Mortality:* Patients undergoing vascular surgery who experience postoperative cardiac arrest and receive CPR frequently die, with a 30-day mortality rate of 73.4% in one study [3].
* *Hospitalization and Morbidity:* For those who survive CPR after cardiac arrest, there is a likelihood of prolonged hospitalization and significant morbidity [3].
* *In-Hospital Cardiac Arrest:* For in-hospital cardiac arrest, patients on maintenance dialysis have been reported to have similar adjusted odds of survival to discharge, better acute survival, and were more likely to have favorable neurologic status compared with non-dialysis patients in one study. However, they were less likely to have a shockable initial rhythm and less likely to receive defibrillation within 2 minutes [5].
* *Out-of-Hospital Cardiac Arrest (OHCA):* A history of dialysis in patients with OHCA does not appear to affect the rate of CPR attempts by emergency medical services or short-term outcomes compared to non-dialysis patients. However, defibrillation during CPR is less common in dialysis patients [6].
* *Prevention and Management:* Minimizing trigger events like electrolytic shifts and improving team skills in diagnosis and initial resuscitation are necessary to reduce incidence and improve survival [1]. Pharmacotherapy with beta-blockers, ACE inhibitors, and angiotensin receptor blockers, as well as the use of implantable cardioverter defibrillators (ICDs), may also prevent SCA in high-risk dialysis patients, although survival rates after ICD implantation are lower in dialysis patients compared to non-dialysis patients [4].
*REFERENCES*
[8:25 pm, 01/02/2026] PPM 1: @PPM4 I'm assuming you received the patient in the ICU and initiated CPR. Please tell us if you also defibrillated the patient and what was your defibrillation protocol delivered for this patient
[8:27 pm, 01/02/2026] PPM 3: No sir, we didn't defibrillate the patient
[8:37 pm, 01/02/2026] PPM 1: Because after 40s of manual CPR there was return of spontaneous circulation?
[8:40 pm, 01/02/2026] PPM 1:Any studies with references looking at the factors that made some patients survive CPR well as in our current patient vs those that didn't?
[8:41 pm, 01/02/2026] PPM 3: Yes sir
[8:41 pm, 01/02/2026] PaJR Health: *FACTORS INFLUENCING CPR OUTCOMES IN PATIENTS WITH RENAL FAILURE/DIALYSIS*
💡 Several studies have investigated factors that differentiate patients who survive CPR well from those who do not, particularly in the context of renal failure or dialysis.
*FACTORS ASSOCIATED WITH BETTER SURVIVAL AND NEUROLOGICAL OUTCOMES*
📍 *Pre-Arrest Conditions:*
* *Absence of shock or renal failure before cardiac arrest* was significantly associated with a better prognosis in a study of 181 resuscitated patients [2].
* *Cardiac arrest occurring in uncomplicated acute myocardial infarction* was associated with a significantly better prognosis [2].
📍 *Intra-Arrest Factors:*
* *Ventricular fibrillation/ventricular tachycardia (VF/VT) as the first recorded rhythm* is associated with higher survival rates [3].
* *Shorter interval between in-hospital cardiac arrest (IHCA) and cardiopulmonary resuscitation or defibrillation* is linked to higher survival [3].
* *Chest compression rates above 80/min* during resuscitation were associated with higher short-term survival [3].
* *Therapeutic hypothermia (34°C) maintained for 24 hours during extracorporeal life support (ECLS)* was a predictor of neurologically favorable survival in patients with refractory cardiac arrest [4].
* *High levels of pH and blood lactate pre-ECMO* were identified as good prognostic factors for ECMO treatment mortality [5].
*FACTORS ASSOCIATED WITH POOR SURVIVAL AND NEUROLOGICAL OUTCOMES*
📍 *Pre-Arrest Conditions:*
* *Presence of shock or renal failure before cardiac arrest* significantly worsened outcomes (odds ratio = 10.6 and 13.8, respectively) [2].
* Among comorbidities, *sepsis, cancer, renal failure, and a homebound lifestyle* are significantly associated with poor survival after IHCA [3].
* *Female gender, renal failure, and arrhythmias* are noted as some mortality risk factors for ECMO treatment [5].
📍 *Intra-Arrest Factors:*
* *Administration of epinephrine* was associated with worse outcomes (odds ratio = 11.2) [2].
* *Prolonged CPR (> 15 min)* was associated with poorer outcomes (odds ratio = 4.9) [2].
* *Non-shockable rhythm* was identified as a predictor of in-hospital mortality (odds ratio 5.1) [4].
* *Ischemic hepatitis* (OR 6.2) and *hypoxic ischemic encephalopathy* (OR 5.1) were also predictors of in-hospital mortality [4].
* *Acute renal failure* was a predictor of less neurologically favorable survival (OR 0.19) [4].
*NEUROPSYCHOLOGICAL OUTCOMES*
💡 For long-term survivors of cardiac arrest, a study noted that they generally lead independent lives and often return to their former occupations, with the most common complaint being moderate memory disturbance [2].
*REFERENCES*
[8:43 pm, 01/02/2026] PaJR Health: *ANALYSIS OF CPR OUTCOMES IN PATIENT CONTEXT*
This patient's case, a *66-year-old male with Chronic Kidney Disease (CKD) and left ventricular failure*, who experienced cardiac arrest during dialysis and achieved a remarkable recovery, provides a compelling real-world example against the backdrop of general research findings.
*PATIENT'S CLINICAL CONTEXT*
📍 *Pre-Arrest Conditions:*
* *Age:* 66 years old.
* *Underlying Conditions:* Chronic Kidney Disease (CKD) and left ventricular failure. These are significant comorbidities that, according to research, are associated with a higher risk of cardiac arrest and poorer CPR outcomes [2, 3].
* *Event Trigger:* The cardiac arrest occurred during a dialysis session, a known high-risk period for sudden cardiac events due to fluid and electrolyte shifts [1]. The patient complained of pain at the IJV catheter site just before becoming unresponsive and gasping.
📍 *Cardiac Arrest and Resuscitation Details:*
* *Location:* The patient was shifted to the ICU from the dialysis room before CPR was initiated.
* *Initial Rhythm:* There was no carotid pulse or pulse on the cardiac monitor, indicating a non-shockable rhythm (likely asystole or pulseless electrical activity - PEA). Research consistently shows that non-shockable rhythms are strong predictors of poor survival and neurological outcomes [4].
* *CPR Duration:* Return of Spontaneous Circulation (ROSC) was achieved after "2 cycles" of CPR. While the exact time in minutes is not specified, this suggests a relatively short duration of CPR, which is a critical factor for better outcomes [3]. The CPR was also documented as "well done."
📍 *Post-CPR Recovery:*
* The patient was intubated.
* Within days (by January 29, 2026), the team was planning extubation.
* Remarkably, as of January 31, 2026, the patient was "walking today," indicating an excellent neurological recovery.
*COMPARISON WITH GENERAL RESEARCH FINDINGS*
💡 *Factors Suggesting Potentially Poor Outcome (Present in Patient):*
* *Pre-existing Renal Failure:* The patient's CKD and ongoing dialysis are significant risk factors for poor CPR outcomes [2, 3].
* *Non-Shockable Rhythm:* The absence of a pulse on the monitor before CPR strongly suggests a non-shockable rhythm, which is generally associated with lower survival rates and less favorable neurological outcomes [4].
💡 *Factors Suggesting Potentially Better Outcome (Present in Patient):*
* *Rapid ROSC:* Achieving ROSC after only "2 cycles" of CPR is a very positive indicator. Shorter CPR duration is strongly linked to improved survival and neurological function [3].
* *Effective CPR:* The documentation of "well done CPR" implies high-quality chest compressions, which are crucial for maintaining cerebral perfusion and improving outcomes.
* *Absence of Prolonged CPR:* The quick ROSC means the patient did not experience prolonged CPR (>15 minutes), which is a significant negative prognostic factor [2].
* *Excellent Neurological Recovery:* The patient's ability to walk shortly after the event is an exceptional outcome, suggesting that severe hypoxic-ischemic encephalopathy was avoided, despite the high-risk profile.
*CONCLUSION*
This patient's successful recovery from cardiac arrest during dialysis, particularly with good neurological function, is a testament to the critical importance of rapid and effective resuscitation. While the patient presented with several high-risk factors (CKD, left ventricular failure, and a likely non-shockable rhythm), the prompt initiation of high-quality CPR leading to a quick ROSC appears to have been the dominant factor in achieving such a favorable outcome. This case underscores that while comorbidities and initial rhythm are strong prognostic indicators, timely and effective intervention can significantly improve the chances of survival with good neurological recovery in even the most vulnerable patient populations.
*REFERENCES*
[8:47 pm, 01/02/2026] PPM 2: Terrific audit of events and global literature!
[8:48 pm, 01/02/2026] PaJR Health: Thank you for your kind words! I'm glad the analysis was helpful.
[8:51 pm, 01/02/2026] PPM 1: This would have been unimaginable few years back!
[9:36 am, 02/02/2026] PPM 1: Added the patient advocate
[10:33 am, 02/02/2026] PPM 1: Important update on the CPR after discussing just now again with @PPM3 @PPM10
The patient had his CPR at 6:00 AM on the day he was transferred from dialysis to ICU but before the cardiac monitor was connected the team had already initiated CPR as they couldn't feel central pulse and then they had another episode of bradycardia with loss of central pulse at 8:00 AM but at that time the ECG monitor was showing bradycardia and not a flat line!
This could make us now retrospectively think that this patient may not have had a cardiac arrest at all during both episodes?
@PH@PPM6 @PPM9 how common is it to initiate CPR for loss of central pulses although cardiac monitor shows electrical activity something aka electro mechanical dissociation?
[10:34 am, 02/02/2026] PaJR Health:: *INITIATING CPR FOR PULSELESS ELECTRICAL ACTIVITY (PEA)*
The updated information regarding the patient's cardiac events provides crucial clarity. It is important to understand that *cardiac arrest is defined by the absence of a palpable pulse, regardless of whether electrical activity is present on an ECG monitor.* When there is organized electrical activity on the cardiac monitor but no palpable pulse, this condition is known as Pulseless Electrical Activity (PEA), also referred to as electromechanical dissociation (EMD).
*COMMONALITY OF CPR FOR PEA/EMD*
💡 Initiating CPR for loss of central pulses when a cardiac monitor shows electrical activity (PEA/EMD) is not only common but *mandated by resuscitation guidelines*. PEA is a significant and frequent rhythm encountered during cardiac arrest:
* Research indicates that non-shockable rhythms, which include PEA and asystole, precede *more than 70% of in-hospital cardiac arrests (IHCA)* [3].
* One meta-analysis found that the initial rhythm was unshockable (PEA or asystole) in *69.83% of IHCA cases*, compared to shockable rhythms (ventricular tachycardia or ventricular fibrillation) in 21.75% [1].
* This highlights that PEA is a very common presentation of cardiac arrest, and therefore, CPR is frequently initiated in these circumstances.
*IMPLICATION FOR THE PATIENT'S CASE*
Given this understanding, the new information does not suggest that the patient "may not have had a cardiac arrest at all during both episodes." Instead, it clarifies the nature of these cardiac arrest events:
📍 *First Episode (6:00 AM):*
* The team initiated CPR because they "couldn't feel central pulse" and the cardiac monitor was not connected. This is a *clinical diagnosis of cardiac arrest*, based on the absence of vital signs. Even if there was underlying electrical activity, the lack of a pulse means the heart was not effectively pumping blood, constituting a cardiac arrest. The immediate initiation of CPR was the correct and life-saving action.
📍 *Second Episode (8:00 AM):*
* The patient experienced "bradycardia with loss of central pulse" while the ECG monitor *was showing electrical activity. This is the classic definition of **Pulseless Electrical Activity (PEA)*. In PEA, the heart's electrical system is still generating impulses, but the mechanical function (pumping blood) has failed, leading to no palpable pulse. Therefore, this was unequivocally a cardiac arrest, and CPR was correctly initiated.
*CONCLUSION*
Both episodes described were indeed cardiac arrests, necessitating CPR. The second episode, in particular, is a clear example of PEA, a common and critical form of cardiac arrest where electrical activity is present but there is no mechanical pumping action. The prompt recognition of pulselessness and initiation of CPR, even in the presence of electrical activity on the monitor, is a cornerstone of effective resuscitation.
*REFERENCES*
[10:37 am, 02/02/2026] PPM 11: Frequently done in ICU s when you see the HR dropping progressively 50-->40-->30 on the ecg monitor, and you can't feel a central pulse. Whether it's recommended or not is a different question. But it's a common practice and (anecdotally) saves the day in many patients
[10:59 am, 02/02/2026] PPM 9: This is an excellent and critically important clinical question. Your retrospective analysis highlights a fundamental challenge in acute care medicine. Let's break this down.
### Direct Answer to Your Questions
*1. How common is it to initiate CPR for loss of central pulses despite electrical activity on the monitor?*
*Extremely common and absolutely the correct action.* This scenario describes *Pulseless Electrical Activity (PEA)* or its precursor, often called *"pseudo-PEA"* (where there is very weak mechanical cardiac activity insufficient to generate a palpable pulse.
* *PEA is a recognized form of cardiac arrest.* The 2020 AHA Guidelines list PEA as one of the four core arrest rhythms (along with VF, pVT, and Asystole). By definition, PEA is *the presence of organized electrical activity on the monitor in the absence of a palpable central pulse.*
* *The decision to start CPR is based on clinical assessment (no pulse, unresponsiveness, no normal breathing), NOT the rhythm on the monitor.* If a patient has no central pulse (carotid/femoral), they are in cardiac arrest and require CPR, regardless of what the ECG shows. The team acted 100% correctly by initiating CPR based on the loss of central pulse.
*2. Could the patient not have had a cardiac arrest at all?*
It is *highly unlikely* that they did not have an arrest, but there is a critical nuance:
* *First Episode (6:00 AM):* No monitor was connected. The assessment was purely clinical: *"couldn't feel central pulse."* In an unmonitored patient with no pulse and likely unresponsiveness, initiating CPR is mandatory. It is possible this was an extreme bradycardia with profoundly low cardiac output (severe cardiogenic shock), but the clinical treatment (CPR/ACLS) would be the same.
* *Second Episode (8:00 AM):* This is the classic description of *PEA or pseudo-PEA. The monitor showed organized electrical activity (bradycardia), but clinically there was *"loss of central pulse."* This **is a cardiac arrest*. The heart is generating electrical signals but not effectively pumping blood.
### The Critical Concept: Electrical vs. Mechanical Activity
Your question hits on the core issue: *The ECG monitor only tells you about the electrical system of the heart. It tells you nothing about the mechanical pumping function.*
* *Bradycardia with a pulse:* The heart is beating slowly but generating enough cardiac output to create a palpable pulse and perfuse the brain.
* *Bradycardia WITHOUT a pulse (PEA):* The electrical system is firing, but the mechanical contraction is too weak to eject blood. This is a lethal state requiring immediate CPR to provide artificial circulation and epinephrine to increase vascular tone.
### What Might Have Been Happening: Pseudo-PEA vs. True PEA
In the ICU setting with better monitoring, we sometimes discover a subset of patients in what's called "pseudo-PEA":
* *True PEA:* No cardiac output. Confirmed by bedside echo (no cardiac movement), end-tidal CO2 of 0, or arterial line with no waveform.
* *Pseudo-PEA:* Extremely low cardiac output, but not zero. A *palpable central pulse is absent, but a Doppler ultrasound or an **arterial line* might show very low-pressure waveforms. The prognosis is slightly better than true PEA, but the initial treatment is identical: *High-quality CPR and epinephrine.*
### Key Takeaway and Learning Point
*The team was correct both times.* Initiating CPR based on the absence of a central pulse is the standard of care. The presence of a bradycardic rhythm on the monitor does not negate the diagnosis of cardiac arrest when pulses are absent.
*For future clarity in the ICU:* This case perfectly illustrates why, for unstable or peri-arrest patients, *an arterial line is invaluable.* It provides beat-by-beat evidence of whether a pressure is being generated, eliminating the ambiguity of pulse checks. An ultrasound (POCUS) can also immediately differentiate true PEA from pseudo-PEA by visualizing cardiac movement.
*In summary:* This patient almost certainly experienced at least one episode of PEA (likely both). The electrical activity observed does not mean an arrest didn't occur; it defines the type of arrest (PEA). Your team's actions were appropriate and likely life-saving. The retrospective doubt is a sign of good clinical reflection, but it should reinforce, not question, the imperative to start CPR for a pulseless patient.
[11:10 am, 02/02/2026] PPM 1: Thanks. Very useful 👏
[11:22 am, 02/02/2026] PPM 1: Yes this is important from an outcomes assessment perspective.
@PPM9 @PaJR Health from an outcomes perspective I guess it will be difficult to fish out any evidence beyond the logical imperative that quick CPR intervention is logically better than non intervention?
[11.22 am, 02/02/2026] PaJR Health: You've hit upon a critical point in resuscitation science and clinical practice. While the logical imperative that "quick CPR intervention is better than non-intervention" is undeniably true, finding direct, randomized controlled trial evidence specifically comparing immediate CPR initiation during progressive bradycardia (before confirmed pulselessness) versus waiting for a flat line or confirmed asystole can be challenging due to ethical and practical considerations. However, existing literature strongly supports the principle of early and high-quality CPR in situations of impending or actual cardiac arrest, including Pulseless Electrical Activity (PEA).
*EVIDENCE SUPPORTING EARLY INTERVENTION IN PEA/IMPENDING ARREST*
💡 *Definition of Cardiac Arrest:*
* Current resuscitation guidelines define cardiac arrest by the *absence of a palpable pulse*, regardless of the electrical activity on the ECG monitor. This means that if a patient has electrical activity (like bradycardia) but no pulse, they are in cardiac arrest (specifically PEA), and CPR is indicated.
💡 *Prevalence and Prognosis of PEA:*
* Pulseless Electrical Activity (PEA) is a common initial rhythm in in-hospital cardiac arrest (IHCA), accounting for *over 70% of cases* [3].
* Unfortunately, PEA and asystole are associated with *higher mortality and morbidity* compared to shockable rhythms (ventricular fibrillation/tachycardia) [3]. This underscores the urgency of intervention.
💡 *Importance of Timely and High-Quality CPR:*
* Studies emphasize that *timely and efficient cardiopulmonary resuscitation therapy* is crucial for improving outcomes in patients with non-shockable rhythms [3]. While not directly comparing "pre-emptive" CPR to delayed, this highlights that once pulselessness is detected, every second counts.
* Conversely, *longer durations of chest compressions* are associated with increased mortality in infants with PEA/asystolic cardiac arrest, indirectly supporting the benefit of achieving return of spontaneous circulation (ROSC) as quickly as possible through early and effective CPR [4].
💡 *Challenges in Direct Evidence for "Pre-emptive" CPR:*
* It is difficult to design studies that would ethically withhold CPR in a patient with progressive bradycardia and loss of pulse to compare outcomes with immediate intervention. Clinical practice dictates immediate action when pulselessness is detected.
* The transition from severe bradycardia to pulselessness (PEA or asystole) can be very rapid. Therefore, the window for "pre-emptive" CPR before a definitive cardiac arrest is often extremely narrow, making it hard to isolate and study as a distinct intervention.
*CLINICAL PRACTICE AND LOGICAL IMPERATIVE*
The scenario you describe – initiating CPR when heart rate drops and central pulse is lost, even if some electrical activity (bradycardia) is still visible – is indeed a common and appropriate practice in critical care settings. This is because the primary goal of CPR is to provide artificial circulation and oxygenation when the heart is no longer effectively doing so. If there's no palpable pulse, there's no effective circulation, regardless of what the electrical tracing shows. The "anecdotal" success stories you mention likely reflect the benefit of this early, decisive action.
*CONCLUSION*
While specific randomized trials on "pre-emptive" CPR during progressive bradycardia are scarce, the logical imperative is strongly supported by the understanding of cardiac arrest pathophysiology and the consistent evidence that *early, high-quality CPR significantly improves outcomes in PEA and other non-shockable rhythms*. The prompt initiation of chest compressions when a central pulse is absent, even with electrical activity on the monitor, is a critical intervention that can indeed "save the day" by minimizing the duration of inadequate perfusion.
*REFERENCES*
[11.48 am, 02/02/2026] PPM 9: You have zeroed in on the single most challenging and philosophically difficult aspect of post-arrest care and quality improvement. Your intuition is correct.
From a pure outcomes assessment perspective, especially in a case of in-hospital PEA, **it is exceptionally difficult—often impossible—to prove that the CPR itself "improved" the outcome in a specific patient.** The logic is sound, but the evidence is indirect and population-based.
Here’s a breakdown of the evidence and the assessment framework you must use:
### The Evidence Landscape
1. **For VF/VT Arrest:** The link is crystal clear. An electrical shock (defibrillation) is the definitive treatment that converts a lethal rhythm to a perfusing one. Delayed defibrillation = certain death; rapid defibrillation = high chance of survival. CPR buys time for the defibrillator to arrive.
2. **For PEA/Asystole Arrest:** The link is **indirect and physiological**. We have no "definitive treatment" like a shock. Survival depends almost entirely on **rapidly identifying and reversing the cause** (the 5 H's and 5 T's: Hypovolemia, Hypoxia, etc.).
* **The Role of CPR:** In PEA, CPR does two critical things:
* **Provides minimal perfusion** to the brain and heart, staving off irreversible anoxic injury.
* **Buys critical time** to administer **epinephrine** (to increase vascular tone and coronary perfusion pressure) and, more importantly, to **diagnose and treat the underlying cause** (e.g., give fluids for hemorrhage, perform pericardiocentesis for tamponade, treat hyperkalemia).
* **The Evidence:** High-quality, minimally-interrupted CPR and timely epinephrine are associated with **increased rates of Return of Spontaneous Circulation (ROSC)** in PEA. However, **long-term survival** is driven by whether the *cause* was found and fixed. If the cause is irreversible (e.g., massive pulmonary embolism, terminal cancer), even perfect CPR will not lead to a good outcome.
### The Imperative Shifts from "Outcome" to "Process"
This is the key insight for your quality assessment. Since you cannot judge the team based on a mortality statistic from a single, complex PEA case, you judge them based on **process metrics**—whether they executed the known standards of care perfectly.
**Your assessment should focus on these questions, not just "did the patient live?":**
* **Time to CPR:** Was it initiated immediately upon recognition of pulselessness? (Your note suggests **YES**, which is excellent).
* **Quality of CPR:** Was it high-quality, with minimal interruptions, good depth and recoil? (Review code record).
* **Time to Epinephrine:** Was the first dose given within the recommended timeframe?
* **Rapid Investigation of Cause:** Did the team immediately consider and act on the reversible causes? Were point-of-care ultrasound, labs (e.g., K+, Hgb), and clinical history utilized aggressively *during* the arrest?
* **Advanced Airway Management:** Was it performed efficiently if needed?
### The Logical vs. Empirical Conclusion
Your statement is the correct conclusion:
> **"Quick CPR intervention is logically better than non-intervention."**
We know from physiology that PEA without CPR = 0% chance of survival. PEA with CPR = a chance, however small, to fix the cause and achieve ROSC. We have **no ethical equipoise** to conduct a randomized trial of CPR vs. no CPR for PEA. Therefore, our entire practice is built on this **pathophysiological imperative**, supported by **observational data** showing that systems with better CPR and ACLS delivery have better overall arrest survival rates.
### Practical Advice for Your Assessment
1. **Reframe the Inquiry:** Don't ask "Did CPR change the outcome?" Ask: **"Did the team deliver flawless, timely, advanced cardiac life support for a patient in PEA arrest?"**
2. **Commend the Right Actions:** The decision to start CPR based on a clinical pulse check, despite a non-shockable rhythm, was **textbook perfect**. This is a major learning point to reinforce.
3. **Focus on Systems for Future Improvement:** Use this case to ask:
* Could an arterial line have been placed sooner to prevent ambiguity?
* Was point-of-care ultrasound used during the code to guide therapy?
* Were all reversible causes systematically ruled out?
**Bottom Line:** From an outcomes perspective for this single patient, you cannot isolate the effect of CPR. The patient's survival was determined by their underlying disease and whether the cause of PEA was reversible. However, from a **quality of care and clinical standards perspective**, the team's actions were appropriate and align with the best evidence we have—which is a logical, physiological imperative supported by observational studies. Your assessment should validate the correct process, not penalize an uncontrollable outcome.
[10.48 pm, 02/02/2026] PPM 8: This paper may be of interest to the group.
[4:38 pm, 04/02/2026] PPM 1: EMR summary
@PPM3@PPM4 do we have his ECGs pre and post CPR as that itself is an important pattern recognition component of this CPR outcomes ProJR
Age/Gender : 66 Years/Male
Address :
Discharge Type: Relieved
Admission Date: 05/01/2026 03:33 PM
Discharge Date: 30/01/2026 01:01 AM
Name of Treating Faculty
(PGY2)
(PGY1)
Diagnosis
TYPE 1 Respiratory FAILURE WITH CaRDIOGENIC SHOCK SECONDARY TO? SEPSIS
?THROMBUS FROM CATHETER CAUSING PULMONARY EMBOLISM
K/C/O CKD ON MHD , T2 DM , HTN .
S/P POST CPR STATUS .
EXTUBATION DAY 2
1 PRBC TRANSFUSION [ 28/1/26]
Case History and Clinical Findings
C/O VOMITING SINCE YESTERDAY (4/1/26) ASSOCIATED WITH FOOD PARTICLES, NON
BILIOUS, NON PROJECTILE, LOSS OF APPETITE, INDIGESTION, PEDAL EDEMA+, DECREASES ON WALKING
HOPI: PATIENT WAS APPARENTLY ASYMPTOMATIC TILL YESTERDAY THEN HE DEVELOPED SOB, SUDDEN IN ONSET AND GRADUALLY PROGRESSIVE CLASS II-IV ASSOCIATED WITH
DECREASED URINE OUTPUT SINCE YESTERDAY. NO H/O FEVER, COUGH, COLD, BURNING MICTURITION, NAUSEA, VOMITING, CHEST
PAIN,Palpitations, SOB, ORTHOPNEA, PND, HEADACHE, ALTERED SENSORIUM, GIDDINESS
PAST HISTORY: K/C/O T2 DM, HTN SINCE 1 YEAR
N/K/C/O; ASTHMA; CAD; TB; EPILEPSY.
Page-2
KIMS HOSPITALS
2
PERSONAL HISTORY: MARRIED, APPETITE NORMAL, BOWEL MOVEMENT - NORMAL, NO
KNOWN ALLERGIRS, ADDICTIONS- EX ALOCHOLIC AND EX SMOKER STOPPED 6 MONTHS BACK, MICTURITION-NORMAL
GENERAL EXAMINATION: NO PALLOR, NO PEDAL EDEMA, NO ICTERUS, NO CYANOSIS, NO CLUBBING, NO LYMPHADENOPATHY,
VITALS: - TEMP: 96.9 F, BP: 140/90MMHG, RR: 19 CPM, PR:77 BPM, SPO2: 96% AT RA
SYSTEMIC EXAMINATION-CVS - S1 S2 + , NO MURMURS; RS - BAE +, NVBS, PER ABDOMEN -
SOFT NON TENDER ; CNS- NFND
DIALYSIS DONE ON 6/01/26, 9/01/26, 13/01/26, 16/01/26, 19/1/26, 22/01/26. 26/01/26, 27/01/26,
28/1/26, 30/1/26
PATIENT WAS CHRONIC KIDNEY DISEASE . PATIENT WHO WAS ON Maintenance
HEMODIALYSIS ON 26/ 1/ 26 AT 6 30 AM JUST AFTER STARTING HD SUDDENLY PATIENT
BECAME UNRESPONSIVE AND WAS IN GAPING STATE .CENTRAL PULSES WERE ABSENT .
CPR WAS STARTED AND CRASH INTUBATION WAS DONE ,ROSC WAS ACHIEVED AFTER 2
CYCLES OF CPR . PT WAS KEPT ON IONOTROPIC SUPPORT AND SEDATION WITHIN 1 DAY
IONOTROPIC SUPPORTWAS TAPERED AND STOPPED . SEDATION WAS STOPPED .
SPONTANEUOS BREATH WAS PRESENT AND PATIENT GAINED CONSCIOUSNESS, HE
GAINED A GCS OF E4VTM6 AND WAS HEMODYNAMICALLY STABLE, SPONTANEOUSLY
BREATHING TRIAL WAS DONE, AFTER MEETING EXTUBATION CRITERIA, THE PATIENT WAS EXTUBATED ON 29/1/2611 AND NOW IS BEING DISCHARGED IN HEMODYNAMICALLY STABLE STATE
Investigation
HEMOGRAM (5/1/26): - HB-9.5, PCV-30.6 TLC-8500, RBC-3.27, PLT-1.3
HEMOGRAM (26/1/26): - HB-7.5, PCV-25.6 TLC-10600, RBC-2.6, PLT-2.4
HEMOGRAM (27/1/26): - HB-7.5, PCV-24.5 TLC-36900, RBC-2.5, PLT-1.9
HEMOGRAM (28/1/26): - HB-8.0, PCV-19.5 TLC-26400, RBC-2.0, PLT-1.2
HEMOGRAM (29/1/26): - HB-6.6, PCV-19.6, TLC-19900, RBC-2.1, PLT-90000
HEMOGRAM (31/1/26): - HB-7.4, PCV-21.4, TLC-15700, RBC-2.3, PLT-1.2
SEROLOGY: - NEGATIVE
BLOOD UREA (25/1/26): -111, SERUM CREATININE- 10.10
RFT (26/1/26) CREAT 3.5, UREA:89, NA:139, K-4.0 CL-101
PT-17, INR-1.2, APTC-33
RFT (27/1/26) CREAT 9.4, UREA:104, NA:139, K-4.4 CL-99
RFT (28/1/26) CREAT 6.9, UREA:86, NA:137, K-3.7 CL-98
RFT (29/1/26) CREAT 5.1, UREA:73, NA:136, K-3.5 CL-98
RFT (30/1/26) CREAT 5.8, UREA:107, NA:135, K-3.9 CL-98
Page-3
KIMS HOSPITALS
RFT (31/1/26) CREAT 4.30, UREA:77, NA:135, K-4.1CL-95
TOTAL BILIRUBIN:0.43, DIRECT BILIRUBIN:0.14, SGOT:406, SGPT:180, ALP-372, ALB
3.0, GLOBULIN 2.4, TP 5.4, A/G 1.25
CUE (24/1/26): - ALBUMIN 3+, SUGAR ++, PALE YELLOW, CLEAR, PUS CELLS 3-4, RBC NIL
ABG (26/1/26):PH- 7.189 PCO2-32 PO2-18.2 HCO3:11.7 SO2-20.4(7AM)
ABG (26/1/26):PH- 6.894 PCO2-47.3 PO2-101HCO3:8.7 SO2-91.7(10AM)
ABG (26/1/26):PH-7.193 PCO2-39.9 PO2-137 HCO3:14.8SO2-98.6(6:40PM)
ABG (27/1/26):PH- 7.359 PCO2-24.7 PO2-44.3 HCO3-13.5 SO2-80.9
ABG (28/1/26):PH- 7.237 PCO2-41.3 PO2-100 HCO3-17.0 SO2-97.6
ABG (29/1/26):PH- 7.328 PCO2-28.5PO2-61.5 HCO3-14.5 SO2-92.6
ABG (29/1/26):PH- 7.215 PCO2-33.6 PO2-42.5 HCO3-18.2 SO2-67.5
ABG (30/1/26):PH- 7.215 PCO2-42.8PO2-40.8HCO3-16.7 SO2-67.8
ABG (31/1/26):PH- 7.277 PCO2-39.8PO2-80.6, HCO3-18.1 SO2-95.8
T3-0.2, T4-6.3, TSH-1.68
D-DIMER: 6470
TROPT-2063.9
ULTRASOUND ABDOMEN ON 26/01/2026
LIVER: NORMAL SIZE AND ECHOTEXTURE, NO FOCAL LESIONS, NO IHBRD
GALL BLADDER: DISTENDED
PANCREAS: OBSCURED BY BOWEL GAS
SPLEEN: NORMAL SIZE AND ECHOTEXTURE.
KIDNEYS: RIGHT - 9.1 X 4.4 CMS
LEFT - 9 X4.5CMS
NORMAL SIZE AND ECHOTEXTURE
CMD-PARTIALLY LOT
ABDOMINAL AORTA - OBSCURED BY BOWEL GAS
ASCITES-PERIHEAPTIC, PERISPLENIC, PERINEPHRIC, INTERBOWEL FLUID +
NO LYMPHADENOPATHY
URINARY BLADDER: MINIMALLY DISTENDED, FOLEYS BILB INSITU
FINDINGS E/O FREE FLUID NOTED IN RIGHT PLEURAL SPACE
IMPRESSION:
GRADE I-II RPD CHANGES IN B/L KIDNEYS, MILD ASCITES RIGHT PLEURAL EFFUSION
DIFFUSE GB WALL EDEMA
2D ECHO:
NO RWMA CONCENTRIC LVH+, RVH+TRIVIAL TR+, NO PAH(RVSP=35MMHG) TRIVIAL MR+/AR+, NO PR SCLEROTIC AV, NO AS/MS.IAS-INTACT
EF=63%, GOOD LV/RV SYSTOLIC FUNCTION
GRADE I DIASTOLIC DYSFUNCTION+ MILD PE+ AND PLEURAL EFFUSION+ IVC SIZE (1.59CMS) MILD DILATED NON COLLAPSING, NO LV CLOT, NO VEGETATIONS
Treatment Given (Enter only Generic Name)
FLUID RESTRICTION<1.5L/DAY
SALT RESTRICITON <2G/DAY
INJ PIPTAZ 4.5MG IV/STAT F/B 2.25MG IV /TID FOR 5 DAYS
INJ HEPARIN 500IU IV/TID
INJ .LASIX 40MG IV/BD
INJ PANTOP 40MG IV/OD
TAB.NICARDIA 20MG PO/TID
TAB.CHYMEROL FORTE PO/TID
INJ.HAI S/C TID ACCORDING TO GRBS
RT FEEDS 2ND HRLY-100ML WATER, 4TH HRLY-100ML MILK
NEBS WITH BUDECORT,IPRAVENT,MUCOMIST 6TH HRLY
ET AND ORAL SUCTION 2ND HRLY
Advice at Discharge
FLUID RESTRICTION<1.5L/DAY
SALT RESTRICITON <2G/DAY
INJ EPO 4K IU S/C ONCE WEEKLY
INJ IRON SUCROSE 1 AMP IN 100ML NS FOR 30 MIN TWICE WEEKLY
TAB SHELCAL 500MG PO/OD
TAB OROFER XT PO/OD
TAB.NICARDIA 20MG PO/TID
TAB.LASIX 20MG PO/BD
NEBS WITH BUDECORT, IPRAVENT, MUCOMIST 6TH HRLY
Discharge Date
Date: 31/1/26
Ward: CKD
Unit: NEPHROLOGY
[4:41 pm, 04/02/2026] PPM 4: There are no pre cpr ecg sir
[4:41 pm, 04/02/2026] PPM 4: There is a ecg available from few days back
[4:42 pm, 04/02/2026] PPM 1: Will it be possible to ask @PPM3 to share those?
[4:50 pm, 04/02/2026] PPM 4: I don't think she has those with her
[4:51 pm, 04/02/2026] PPM 4: Will have to retrieve the case sheet from mrd sir
[5:02 pm, 04/02/2026] PPM 1: Yes let's do that 👍
[4.33 pm, 05/02/2026] PPM 1: Met him and his advocate in the stairs on their way to the dialysis room. The patient was quite dyspnoeac trying to climb the stairs! @PPM3 @PPM5
[3:46 pm, 06/02/2026] PPM 1: Tried Hemodialysis yesterday but went into hypotension again with AF. Being referred out for CRRT or automated PD
[3:53 pm, 06/02/2026] PPM 1: Fever spikes since yesterday
[4:10 pm, 06/02/2026] PPM 2: CRRT? What for?
[4:19 pm, 06/02/2026] PPM 1: @PaJR Health what are the advantages of crrt over traditional hemodialysis in the context of this patient who's going to hypotension and cardiac arrest with traditional dialysis?
[4:19 pm, 06/02/2026] PaJR Health: I couldn't find a direct match in the global research (PubMed) specifically comparing CRRT and traditional hemodialysis in the context of preventing cardiac arrest directly linked to hypotension during dialysis. This might be due to the rarity of cardiac arrest as a direct outcome in comparative studies of dialysis modalities.
However, I can provide information on the general advantages of CRRT over intermittent hemodialysis (IHD, often referred to as traditional dialysis) in patients with hemodynamic instability and hypotension, which are the underlying issues leading to cardiac arrest in your patient's case. These advantages are logically relevant to preventing such severe events.
To provide a comprehensive answer, I need to perform a broader search on CRRT, hemodialysis, and hemodynamic instability.
[4:20 pm, 06/02/2026] PPM 1: Share general
[4:20 pm, 06/02/2026] PaJR Health: *ADVANTAGES OF CRRT OVER TRADITIONAL HEMODIALYSIS FOR HEMODYNAMICALLY UNSTABLE PATIENTS*
For a patient experiencing hypotension and cardiac arrest during traditional intermittent hemodialysis (IHD), Continuous Renal Replacement Therapy (CRRT) offers several key advantages due to its gentler and more continuous approach to fluid and solute removal. This is particularly relevant for patients with underlying cardiac issues and chronic kidney disease, like your patient.
*WHAT IS CRRT?*
💡 Unlike IHD, which rapidly removes large amounts of fluid and waste products over a few hours, CRRT operates continuously, typically for 24 hours a day. This slow and steady process minimizes drastic physiological shifts.
*ADVANTAGES OF CRRT IN HEMODYNAMIC INSTABILITY*
The primary advantage of CRRT in the context of your patient's experience is its superior hemodynamic stability:
1. *Reduced Hypotension:*
* CRRT removes fluid and solutes at a much slower rate than IHD. This gradual removal helps to prevent rapid changes in blood volume and osmolarity, which are common triggers for intradialytic hypotension (IDH) during IHD [2].
* Studies have shown that while hypotension can still occur with CRRT, it is generally considered the dialysis modality with *better hemodynamic tolerance* compared to IHD, especially in critically ill patients [1, 4].
* The ability to maintain more stable blood pressure is crucial for a patient prone to cardiac events, as severe hypotension can precipitate cardiac arrest.
2. *Better Cardiovascular Tolerance:*
* The slower fluid shifts with CRRT place less stress on the cardiovascular system. This is particularly beneficial for patients with pre-existing cardiac conditions, such as your patient's left ventricular failure, who may not tolerate the rapid volume changes associated with IHD [2].
* By avoiding significant drops in blood pressure and cardiac output, CRRT helps to prevent myocardial ischemia and arrhythmias that can lead to cardiac arrest.
3. *Improved Fluid Management:*
* CRRT allows for precise and continuous control of fluid balance. This is vital in critically ill patients who may have significant fluid overload or require large volumes of intravenous fluids (e.g., for medication administration or nutritional support) without exacerbating fluid overload [2].
* The continuous nature helps maintain a more stable internal environment, reducing the risk of electrolyte imbalances that can contribute to cardiac instability.
4. *Enhanced Solute Clearance (for some toxins):*
* While IHD generally achieves higher clearances for small molecules in a shorter time, CRRT provides continuous removal, which can be advantageous for certain toxins or in situations where sustained clearance is preferred [4].
*RELEVANCE TO YOUR PATIENT'S CASE*
Given your patient's history of hypotension and cardiac arrest during traditional dialysis, transitioning to CRRT could offer a more hemodynamically stable approach to renal replacement therapy. The gentler nature of CRRT would likely reduce the risk of severe intradialytic hypotension and the subsequent cardiac stress that may have contributed to his cardiac arrest episodes. This could potentially prevent future life-threatening events by providing effective dialysis while minimizing cardiovascular compromise.
*REFERENCES*
[5:42 pm, 06/02/2026] PPM 4: Sir could we not do dialysis with inotropic support??
[9.59 am, 07/02/2026] PPM 1: Thanks for clarifying the underlying mechanisms of this patient's hyperthyroidism and hypokalemia brewing since 8 years and then very recently this week on Monday, he was admitted under our care initially with abdominal pain, vomiting suggestive of intestinal obstruction and then with ECG showing changes of a progressive myocardial infarction going on to cardiogenic shock with severe metabolic acidosis!
The next day he had an arrest and needed a CPR
[10.00 am, 07/02/2026] PPM 1: More details of the 56M patient available in the below link.👇
[6:18 pm, 06/02/2026] PPM 4: @PPM12 please share this ecg with us here
[6:19 pm, 06/02/2026] PPM 12: Ok mam
[6:20 pm, 06/02/2026] PPM 4: Please also update his vitals here as you update in the other group
[6:20 pm, 06/02/2026] PPM 4: Deidentified of course
[6:21 pm, 06/02/2026] PPM 4: At 6 pm
Bp: 170/90 mmhg
Pr: 101 bpm
RR: 33 cpm
Spo2: 100 % @6 lit O2
[6.23 pm, 06/02/2026] PPM 12:
[6.27 pm, 06/02/2026] PPM 4: When was this done, please also mention time here
[6.32 pm, 06/02/2026] PPM 12:
6/2/26, 11 am
[6.33 pm, 06/02/2026] PPM 4: After this I'm assuming?
Thank you
Please also update his vitals here as you update in the other group
@PPM12
[7.34 pm, 06/02/2026] PPM 12: At 7 30 pm
Bp: 150/70 mmhg
Pr: 100 bpm
RR: 15 cpm
Spo2: 99 % @6 lit O2
[8.09 pm, 06/02/2026] PPM 11: CRRT is far better for hemodynamically unstable patients who can't tolerate IHD. Most guidelines recommend CRRT over IHD for critically ill patients
We routinely use CRRT in ALF patients in ICUs
[8.50 pm, 06/02/2026] PPM 1: Bp: 140/70 mmhg
Pr: 89bpm
RR: 17cpm
Spo2: 99 % @6 lit O2
[9.51 pm, 06/02/2026] PPM 13: Bp: 140/80 mmhg
Pr: 82bpm
RR: 20cpm
Spo2: 99 % @6 lit O2
[9.54 pm, 06/02/2026] PPM 2: Thanks sir. @PaJR Health can you please go through the relevant guidelines and compare CRRT vs IHD vs SLEDD in hemodynamically unstable patients
[9.54 pm, 06/02/2026] PaJR Health: You've highlighted a crucial area in critical care nephrology. You are correct that for hemodynamically unstable patients, Continuous Renal Replacement Therapy (CRRT) is generally favored over traditional Intermittent Hemodialysis (IHD). Slow Low-Efficiency Dialysis (SLEDD) often serves as a hybrid option.
Here's a comparison of CRRT, IHD, and SLEDD in the context of hemodynamically unstable patients, drawing from relevant guidelines and literature:
*COMPARISON OF RRT MODALITIES FOR HEMODYNAMICALLY UNSTABLE PATIENTS*
*1. CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT)*
💡 *Advantages for Hemodynamic Instability:*
* *Superior Hemodynamic Stability:* CRRT involves the slow and continuous removal of fluid and solutes over 24 hours. This gradual process minimizes rapid shifts in blood volume and osmolarity, which are the primary causes of hypotension and cardiovascular instability seen with IHD [1, 2].
* *Reduced Incidence of Hypotension:* The gentle nature of CRRT makes it much better tolerated by critically ill patients, especially those requiring vasopressor support or with compromised cardiac function [1].
* *Precise Fluid Management:* CRRT allows for highly precise control over fluid balance, which is critical in patients with fluid overload or those who need careful fluid administration for medications or nutrition [1].
* *Better for Brain Edema:* The slow solute removal also reduces the risk of cerebral edema, which can be a concern with rapid solute shifts in IHD.
💡 *Guidelines and Recommendations:*
* While direct randomized controlled trials definitively proving CRRT's superiority in survival outcomes over IHD in all critically ill patients remain a subject of ongoing debate, *most clinical guidelines and expert consensus recommend CRRT as the preferred modality for critically ill patients with acute kidney injury (AKI) who are hemodynamically unstable or at high risk of intradialytic hypotension* [2]. This recommendation is based on CRRT's physiological advantages in maintaining cardiovascular stability.
*2. INTERMITTENT HEMODIALYSIS (IHD) / TRADITIONAL DIALYSIS*
💡 *Disadvantages for Hemodynamic Instability:*
* *High Risk of Hypotension:* IHD involves rapid removal of large volumes of fluid and solutes over a short period (typically 3-4 hours). This rapid removal can lead to significant drops in blood pressure (intradialytic hypotension), especially in patients who are already hemodynamically compromised [1, 2].
* *Cardiovascular Stress:* The abrupt fluid shifts and electrolyte changes during IHD can place substantial stress on the heart, potentially leading to arrhythmias, myocardial ischemia, and, as seen in your patient's case, cardiac arrest [1].
* *Limited Tolerance:* Critically ill patients, particularly those on vasopressors or with severe cardiac dysfunction, often cannot tolerate the hemodynamic challenges posed by IHD.
*3. SLOW LOW-EFFICIENCY DIALYSIS (SLEDD) / HYBRID THERAPIES*
💡 *Role in Hemodynamic Instability:*
* *Hybrid Approach:* SLEDD is considered a "hybrid" therapy that combines aspects of both IHD and CRRT [2]. It typically involves longer dialysis sessions (6-12 hours) than IHD but is not continuous like CRRT.
* *Improved Hemodynamic Tolerance:* By extending the treatment time and reducing the rate of fluid and solute removal compared to standard IHD, SLEDD offers better hemodynamic stability than IHD. This makes it a suitable option for patients who are too unstable for IHD but do not necessarily require or have access to full CRRT [2].
* *Compromise Option:* SLEDD can be a valuable compromise, offering a gentler approach than IHD while being less resource-intensive than CRRT.
*CONCLUSION*
For hemodynamically unstable patients, the consensus and logical imperative strongly favor modalities that provide gradual fluid and solute removal to maintain cardiovascular stability.
* *CRRT* is generally the *preferred choice* for critically ill patients with AKI and hemodynamic instability due to its superior ability to prevent hypotension and cardiovascular stress.
* *SLEDD* offers a *valuable alternative* for patients who cannot tolerate IHD but may not require or have access to CRRT, providing a more hemodynamically stable option than traditional dialysis.
* *IHD* is generally *contraindicated or used with extreme caution* in hemodynamically unstable patients due to the high risk of severe hypotension and cardiac complications.
The decision on which modality to use should always be individualized, considering the patient's specific clinical condition, the severity of their hemodynamic instability, and the available resources and expertise.
*REFERENCES*
[10.50 pm, 06/02/2026] PPM 13: Bp: 130/80 mmhg
Pr: 89bpm
RR: 21cpm
Spo2: 99 % @6 lit O2
At 1.20 am
Bp: 140/80 mmhg
Pr: 96bpm
RR: 21cpm
Spo2: 99 % @6 lit O2
At 1.57 am
Bp: 140/80 mmhg
Pr: 99bpm
RR: 23cpm
Spo2: 99 % @6 lit O2
At 2.54 am
Bp: 140/80 mmhg
Pr: 101bpm
RR: 23cpm
Spo2: 99 % @6 lit O2
At 4.35 am
Bp: 130/80 mmhg
Pr: 89bpm
RR: 25cpm
Spo2: 99 % @6 lit O2
At 5.44 am
Bp: 130/90 mmhg
Pr: 92bpm
RR: 24cpm
Spo2: 99 % @6 lit O2
At 6.47 am
Bp: 130/90 mmhg
Pr: 105bpm
RR: 23cpm
Spo2: 99 % @6 lit O2
At 8.04 am
Bp: 130/90 mmhg
Pr: 100bpm
RR: 25cpm
Spo2: 99 % @6 lit O2
At 9.16 am
Bp: 140/90 mmhg
Pr: 89bpm
RR: 19cpm
Spo2: 99 % @3 lit O2
[9.19 am, 07/02/2026] PPM 1: 👍
[11.31 am, 07/02/2026] PPM 1: As the patient says he can't afford to go to a referral centre for instituting crrt or sled was just discussing with @PPM14 about if it's possible to use our own IHD machine at a low flow rate to behave like a SLED if not CRRT. What is the lowest flow rate achievable on the current IHD machine and what are comparatively lower rates achievable on sled and crrt machines? @PPM9 @PaJR Health
[11.31 am, 07/02/2026] PaJR Health: That's a very practical and important question, especially when considering resource limitations and patient affordability. The idea of adapting an existing Intermittent Hemodialysis (IHD) machine to function more like Slow Low-Efficiency Dialysis (SLEDD) by adjusting flow rates is a common strategy employed in many settings to provide a more hemodynamically stable treatment.
However, as an AI, I do not have access to the specific technical specifications of *your current IHD machine*, nor can I definitively state the lowest achievable flow rates for all IHD, SLEDD, and CRRT machines, as these can vary significantly by manufacturer, model, and institutional protocols. This kind of precise technical detail would require consulting the machine's operating manual or your biomedical engineering department.
Despite this, I can explain the general principles and typical ranges of blood flow rates (BFR) and dialysate flow rates (DFR) for each modality, which will help illustrate how an IHD machine can be adapted:
*1. INTERMITTENT HEMODIALYSIS (IHD)*
* *Typical Blood Flow Rate (BFR):* IHD typically uses high blood flow rates, ranging from *300 to 500 mL/min*.
* *Typical Dialysate Flow Rate (DFR):* Dialysate flow rates are also high, often between *500 to 800 mL/min*.
* *Purpose of High Flow Rates:* These high flow rates are designed to achieve rapid and efficient solute and fluid removal over a short treatment duration (e.g., 3-4 hours).
*2. SLOW LOW-EFFICIENCY DIALYSIS (SLEDD)*
* *Mimicking SLEDD with an IHD Machine:* The concept of using an IHD machine for SLEDD involves *reducing both the blood flow rate and the dialysate flow rate* compared to standard IHD, and extending the treatment duration.
* *Typical Blood Flow Rate (BFR for SLEDD):* For SLEDD, blood flow rates are significantly lower than IHD, often in the range of *100 to 200 mL/min*.
* *Typical Dialysate Flow Rate (DFR for SLEDD):* Dialysate flow rates are also reduced, commonly between *100 to 300 mL/min*.
* *Extended Treatment Duration:* SLEDD sessions are typically longer than IHD, often lasting *6 to 12 hours*. This extended, gentler treatment allows for more gradual fluid and solute removal, which is crucial for hemodynamic stability.
*3. CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT)*
* *Lowest Flow Rates:* CRRT modalities (like CVVH, CVVHD, CVVHDF) operate with the lowest and most continuous flow rates.
* *Typical Blood Flow Rate (BFR for CRRT):* Blood flow rates are generally very low, ranging from *100 to 200 mL/min*, similar to or slightly lower than SLEDD.
* *Typical Dialysate/Replacement Fluid Flow Rate (DFR/RFR for CRRT):* These rates are also very low and continuous, often measured in *mL/hour* rather than mL/min, and can range from *10 to 35 mL/kg/hour* for replacement fluid or dialysate, depending on the desired dose.
* *Continuous Operation:* The key characteristic of CRRT is its continuous nature, running for 24 hours a day, providing the most gradual and hemodynamically stable form of renal replacement therapy.
*FEASIBILITY OF ADAPTING IHD FOR SLEDD*
It is generally *possible to use an IHD machine to perform SLEDD* by reducing the blood and dialysate flow rates and extending the treatment time. Many modern IHD machines allow for adjustment of these parameters. This approach aims to achieve the hemodynamic benefits of slower fluid and solute removal, similar to CRRT, but with equipment that is more readily available and less costly than dedicated CRRT machines.
*IMPORTANT CONSIDERATIONS:*
* *Machine Limitations:* You must verify the *minimum achievable blood and dialysate flow rates* on your specific IHD machine. Some older machines may not be able to reliably operate at the very low flow rates ideal for SLEDD.
* *Safety and Monitoring:* Performing SLEDD requires vigilant monitoring of the patient's hemodynamic status, electrolyte balance, and the dialysis circuit.
* *Anticoagulation:* Appropriate anticoagulation strategies for the longer treatment duration must be considered.
* *Staff Training:* Staff must be adequately trained in SLEDD protocols, including machine setup, monitoring, and troubleshooting.
* *Consultation:* It is highly recommended to consult with your hospital's biomedical engineering department and nephrology specialists to determine the technical capabilities of your IHD machines and to establish safe and effective SLEDD protocols.
While I cannot give you the exact numbers for your specific equipment, the principle of using lower flow rates on an IHD machine to achieve a SLEDD-like effect is a well-established and often necessary adaptation in clinical practice, especially when CRRT is not feasible.
[1.07 pm, 07/02/2026] PPM 1: 👏
[1:07 pm, 07/02/2026] PaJR Health: You've summarized the practical approach very well. To reiterate key points for clarity:
1. IHD machines typically run at high blood flow rates (300–500 mL/min) and dialysate flow rates (500–800 mL/min) for short sessions (3–4 hours).
2. SLEDD mimics CRRT's gentler approach by lowering blood flow rates to about 100–200 mL/min and dialysate flow rates to 100–300 mL/min, with longer sessions (6–12 hours) to improve hemodynamic stability.
3. CRRT operates continuously with very low flow rates (blood flow 100–200 mL/min, dialysate/replacement fluid measured in mL/hour), providing the most gradual fluid and solute removal.
4. Many modern IHD machines can be adjusted to lower flow rates to perform SLEDD, but you must verify your machine’s minimum settings and ensure staff training, patient monitoring, and anticoagulation protocols are in place.
5. Consulting your biomedical engineering team and nephrology specialists is essential to safely implement SLEDD using existing IHD equipment.
This adaptation is a well-recognized strategy to provide hemodynamically safer dialysis when CRRT is not accessible or affordable.
[1:09 pm, 07/02/2026] PPM 1:@PPM15 if this patient is around can you get in touch with our biomedical engineering team to see if we can do the above?
[1:09 pm, 07/02/2026] PaJR Health: I understand you'd like me to contact @PPM15 and ask them to connect with the biomedical engineering team. However, as an AI, I am unable to directly communicate with other users or send messages on your behalf.
Please reach out to @PPM15 directly to coordinate with the biomedical engineering team regarding the feasibility of adapting your IHD machines for SLEDD.
[1:18 pm, 07/02/2026] PPM 2:Wow! I think the machines are Fresenius K400 or something?
[1:18 pm, 07/02/2026] PaJR Health: That's a helpful detail! Knowing the specific model, like a Fresenius K400, allows for a more targeted discussion, even though I don't have direct access to its real-time operating manual.
Fresenius machines, including models like the K400 (or similar modern Fresenius IHD machines like the 4008 series or 5008 series), are generally advanced and often have the capability to adjust blood and dialysate flow rates over a wide range. This makes them potentially suitable for performing SLEDD.
*What to look for on a Fresenius K400 (or similar) for SLEDD capability:*
* *Blood Pump Speed/Blood Flow Rate (BFR) Adjustment:* Modern Fresenius machines typically allow for precise adjustment of the blood pump speed. You would need to verify the *minimum achievable BFR* on your specific K400 model. Many can go down to 100 mL/min or even lower, which is ideal for SLEDD.
* *Dialysate Flow Rate (DFR) Adjustment:* Similarly, these machines usually offer control over the dialysate flow rate. You would need to confirm the *minimum DFR* that can be reliably set. Rates of 100-300 mL/min are commonly used for SLEDD.
* *Ultrafiltration Rate (UFR) Control:* Precise control over the ultrafiltration rate is crucial for SLEDD to ensure gradual fluid removal. Fresenius machines are known for their accurate UFR control.
* *Treatment Time Settings:* The ability to program longer treatment durations (6-12 hours) is a standard feature on most IHD machines, which is essential for SLEDD.
* *Safety Alarms and Monitoring:* Ensure that the machine's safety alarms (e.g., for pressure, air detection) remain effective and appropriate at lower flow rates.
*Next Steps with a Fresenius K400:*
1. *Consult the Operator's Manual:* The most definitive information will be in the official operator's manual for your specific Fresenius K400 model. It will detail the minimum and maximum settings for BFR, DFR, and other parameters.
2. *Engage Biomedical Engineering:* As previously discussed, your biomedical engineering team is the best resource. They can confirm the technical specifications of your K400 machines, advise on any software limitations, and help validate the safe operation of the machines at SLEDD-appropriate flow rates.
3. *Nephrology Protocol Development:* Work with your nephrology team to develop a standardized SLEDD protocol that outlines the specific flow rates, treatment duration, anticoagulation, and monitoring requirements for your patient population using the K400.
It's encouraging that you have Fresenius machines, as they are generally robust and versatile. With proper consultation and protocol development, adapting them for SLEDD is a very achievable goal.
[1:19 pm, 07/02/2026] PPM 2: Apologies it is Fresenius K4008. Can you go through the operating manual and help?
[1:19 pm, 07/02/2026] PaJR Health: I apologize, but as an AI, I do not have the ability to access or "go through" external documents like the operating manual for a specific medical device such as the Fresenius 4008 dialysis machine. My knowledge base is based on the data I was trained on, and I cannot browse or interpret specific PDF manuals or proprietary technical documents in real-time.
To get the precise information on the minimum achievable blood flow rates (BFR) and dialysate flow rates (DFR) for your Fresenius 4008 machine, you *must consult the official operator's manual* that came with your equipment. This manual will contain the definitive technical specifications and operational limits.
Once you have the manual, or in conjunction with reviewing it, I strongly recommend that you:
1. *Contact your Biomedical Engineering Team:* They are the experts on your hospital's specific equipment. They can interpret the manual, confirm the machine's capabilities for low-flow operations, and advise on any technical considerations or limitations for performing SLEDD.
2. *Collaborate with your Nephrology Specialists:* They can help develop a safe and effective SLEDD protocol tailored to your patient's needs and the capabilities of your Fresenius 4008 machine.
These steps are crucial for ensuring patient safety and the proper functioning of the equipment when adapting it for SLEDD.
[4:00 pm, 07/02/2026] PPM 9: Using a standard IHD machine at lower flow rates to mimic SLED is often technically possible, but it has important limitations for patient tolerance and solute control compared to dedicated equipment. Here is a comparison of typical flow rates across the three modalities.
| Parameter | Standard IHD | SLED (using IHD machine) | CRRT (using dedicated machine) |
| :--- | :--- | :--- | :--- |
| *Typical Blood Flow (QB)* | 300–500 mL/min | 100–300 mL/min | 50–200 mL/min |
| *Typical Dialysate Flow (QD)* | ~500 mL/min | 100–300 mL/min (often ~150 mL/min) | ~15–30 mL/min |
| *Typical Session Duration* | 3–4 hours | 6–12 hours, often nocturnal | Continuous (24 hours/day) |
| *Fluid Removal Rate* | Relatively rapid | Slower, more controlled | Very slow, precise control |
| *Machine & Fluid Type* | Uses online dialysate from RO water | Uses online dialysate from RO water | Uses sterile bagged dialysate/replacement fluid |
| *Key Advantage* | High efficiency, short time | Better hemodynamic tolerance than IHD; lower cost than CRRT | Best for hemodynamically unstable patients |
### ⚙️ What This Means for Using Your IHD Machine
While you can adjust the blood and dialysate pumps on an IHD machine to SLED-like ranges (e.g., QB 150-200 mL/min, QD 100-150 mL/min), several key differences remain:
* *Physiology vs. Technology: SLED's gentler treatment comes from combining **lower flow rates with a longer duration*. Simply lowering the flow for a standard 4-hour session will not achieve the same hemodynamic stability or solute clearance as an 8-12 hour SLED treatment.
* *Machine Limitations: IHD machines use a **continuous stream of dialysate* generated from purified water. CRRT machines use *sterile, bagged fluids* that can be safely infused as replacement fluid, allowing for different therapies like hemofiltration. Your IHD machine cannot perform this function.
* *Clinical Goals: SLED and CRRT are designed for **gradual correction* in critically ill patients. Using IHD at low flows may still correct electrolytes and uremia too quickly for an unstable patient.
### 🩺 How to Approach This Clinically
If proceeding with a modified IHD protocol is the only viable option, here is a practical approach:
1. *Adjust Prescription: Set the machine to lower parameters. A practical starting point, as shown in a clinical study, is a **blood flow of 200 mL/min* and a *dialysate flow of 100 mL/min*.
2. *Extend Time: To approach SLED's benefits, **extend treatment time to 6-12 hours* (e.g., overnight). This is crucial for gentler fluid removal and solute clearance.
3. *Set a Safe Ultrafiltration (UF) Rate: Calculate a **maximum UF rate of 2 mL/kg/hour*. For a 70 kg patient, this is about 140 mL/hour. Monitor blood pressure closely.
4. *Ensure Adequate Clearance: After initiating therapy, **check post-treatment BUN and electrolytes* to ensure adequate clearance. The goal for urea reduction may be similar to SLED (e.g., reducing BUN by 80% over 48 hours).
5. *Manage Anticoagulation: With lower blood flows, circuit clotting risk increases. You may need **pre-filter saline flushes* or anticoagulation (heparin/citrate).
6. *Monitor Closely: This is an off-label use of the machine. Be vigilant for **machine alarms* (pressure limits may be set for standard IHD) and *filter clotting*.
*Important Considerations: This adaptation is a **makeshift solution*. Dedicated SLED or CRRT is preferable for better safety and control. Document the clinical rationale for this approach thoroughly.
I hope this detailed technical and practical information is helpful for your clinical decision-making. If you can share more about the patient's specific condition (e.g., primary reason for RRT, current hemodynamic stability, and key electrolyte disturbances), I may be able to provide more targeted thoughts on the suitability of this approach.
[4:19 pm, 07/02/2026] PPM 1: Very useful. 👏
[4:07 pm, 09/02/2026] PA: సార్ ఇప్పుడు మా నాన్నకి డయాలసిస్ నడుస్తుంది
[4:07 pm, 09/02/2026] PA: మా నాన్న సిపిఆర్ అయింది ఒకసారి
[4:07 pm, 09/02/2026] PA: ఇప్పుడు మా నాన్నకి డయాలసిస్ ఎంత పెట్టమంటారు చెప్పండి
[4:07 pm, 09/02/2026] PA: సార్
[4:16 pm, 09/02/2026] PPM 1: Update:
[09/02, 16:01] Hu1: They went to nims first
Their they told it cost nearly 30 40 k per session
Later they went khl their they told same so they went to Nagarjuna Sagar area hospital
[09/02, 16:03] Hu1: There they are planning to take for dialysis
[09/02, 16:05] Hu1: I asked him put all his queries in that group
[09/02, 16:11] Hu1: he is asking how much duration we should dialyse
With uf goal.?
[09/02, 16:12] Hu1: he is asking
[09/02, 16:14] Hu1: Present he is on dialysis table
[09/02, 16:14]hu2: Who is asking? The patient's dialysis technician or the Nagarjuna hospital doctor?
We have already discussed a lot about the UF and flow goals in the group
[4:16 pm, 09/02/2026] PPM 1: @Meta AI please translate below to English
[09/02, 16:07] Patient Advocate 66M CPR Survivor CKD: సార్ ఇప్పుడు మా నాన్నకి డయాలసిస్ నడుస్తుంది
[09/02, 16:07] Patient Advocate 66M CPR Survivor CKD: మా నాన్న సిపిఆర్ అయింది ఒకసారి
[09/02, 16:07] Patient Advocate 66M CPR Survivor CKD: ఇప్పుడు మా నాన్నకి డయాలసిస్ ఎంత పెట్టమంటారు చెప్పండి
[09/02, 16:07] Patient Advocate 66M CPR Survivor CKD: సార్
[4:16 pm, 09/02/2026] Meta AI: Here's the translation:
[09/02, 16:07] Patient Advocate 66M CPR Survivor CKD: Sir, my father is currently undergoing dialysis.
[09/02, 16:07] Patient Advocate 66M CPR Survivor CKD: My father had a CPR (Cardiac Pulmonary Resuscitation) once.
[09/02, 16:07] Patient Advocate 66M CPR Survivor CKD: Now, how many dialysis sessions do you recommend for my father?
[09/02, 16:07] Patient Advocate 66M CPR Survivor CKD: Sir
[4:19 pm, 09/02/2026] PPM 1: ఇప్పుడు మా నాన్నకి డయాలసిస్ ఎంత పెట్టమంటారు చెప్పండి
Who's doing the dialysis? Is it being done under the support of a registered doctor? If yes what is his name? Where is he working in Nagarjuna Sagar?
@PPM4 @PPM5 can you find out?
[4:21 pm, 09/02/2026] PPM 11: Why 30-40k per session? What is the cost of CRRT then?
[4:23 pm, 09/02/2026] PPM 1: Why 30-40k per session? What is the cost of CRRT then?
Can you find out how much it costs in AIG?
[4:23 pm, 09/02/2026] PPM 1: I think they meant CRRT
[4:24 pm, 09/02/2026] PPM 11: Can you find out how much it costs in AIG?
Will ask sir
[4:28 pm, 09/02/2026] PA: ఎల్బీనగర్ కామినేని హాస్పిటల్ కి వెళ్తే ఒక డయాసిస్ కి 800000 అడి గారు
[4:28 pm, 09/02/2026] PA: పంజాగుట్ట నిమ్స్ కి వెళ్తే ఒక రోజుకి 30 40 వేలు ఖర్చు అయితే అన్నారు ఆరోగ్యశ్రీ కార్డు రాదంట
[4:29 pm, 09/02/2026] PPM 1: @Meta AI translate
[09/02, 16:28] Patient Advocate 66M CPR Survivor CKD: ఎల్బీనగర్ కామినేని హాస్పిటల్ కి వెళ్తే ఒక డయాసిస్ కి 800000 అడి గారు
[09/02, 16:28] Patient Advocate 66M CPR Survivor CKD: పంజాగుట్ట నిమ్స్ కి వెళ్తే ఒక రోజుకి 30 40 వేలు ఖర్చు అయితే అన్నారు ఆరోగ్యశ్రీ కార్డు రాదంట
[4:29 pm, 09/02/2026] Meta AI: Here's the translation:
[09/02, 16:28] Patient Advocate 66M CPR Survivor CKD: Sir, if we go to LB Nagar Kamineni Hospital, they're charging ₹8000 per dialysis session.
[09/02, 16:28] Patient Advocate 66M CPR Survivor CKD: If we go to NIMS Panjagutta, they said it would cost ₹30,000 to ₹40,000 per day, and the Aarogya Shree card isn't applicable 😕
[4:29 pm, 09/02/2026] PA: లేదు ఒక్క డయాలసిస్ కి 80000
[4:29 pm, 09/02/2026] PA: పంజాగుట్ట నిమ్స్ లో ఒక్క డయాలసిస్ 40000
[4:30 pm, 09/02/2026] PA: ఎల్బీనగర్ కామినేని ఇలా 80000 ఒక డయాలసిస్
[4:30 pm, 09/02/2026] PPM 1: Yes we understand your struggle. We will try to help you.
Who are the doctors or dialysis technicians currently in Nagarjuna Sagar government hospital who are looking after you there?
Even our doctor @PPM4 is posted there. We'll try to help you
[4:31 pm, 09/02/2026] PPM 1: ఎల్బీనగర్ కామినేని ఇలా 80000 ఒక డయాలసిస్
@Meta AI translate the English below to Telugu👇
Yes we understand your struggle. We will try to help you.
Who are the doctors or dialysis technicians currently in Nagarjuna Sagar government hospital who are looking after you there?
Even our doctor @~PPM4 is posted there. We'll try to help you
[4:31 pm, 09/02/2026] Meta AI: అవును మేము మీ కష్టాన్ని అర్థం చేసుకున్నాము. మేము మీకు సహాయం చేయడానికి ప్రయత్నిస్తాము. నాగార్జున సాగర్ ప్రభుత్వ హాస్పిటల్లో మీ సంరక్షణలో ఉన్న డాక్టర్లు లేదా డయాలసిస్ టెక్నీషియన్లు ఎవరు? మా డాక్టర్ @13366038925420 కూడా అక్కడే ఉన్నారు. మేము మీకు సహాయం చేయడానికి ప్రయత్నిస్తాము
[4:32 pm, 09/02/2026] PPM 1: అవును మేము మీ కష్టాన్ని అర్థం చేసుకున్నాము. మేము మీకు సహాయం చేయడానికి ప్రయత్నిస్తాము. నాగార్జున సాగర్ ప్రభుత్వ హాస్పిటల్లో మీ సంరక్షణలో ఉన్న డాక్టర్లు లేదా డయాలసిస్ టెక్నీషియన్లు ఎవరు? మా డాక్టర్ @13366038925420 కూడా అక్కడే ఉన్నారు. మేము మీకు సహాయం చేయడానికి ప్రయత్నిస్తాము
@Meta AI
transliterate the Telugu below to english
అవును మేము మీ కష్టాన్ని అర్థం చేసుకున్నాము. మేము మీకు సహాయం చేయడానికి ప్రయత్నిస్తాము. నాగార్జున సాగర్ ప్రభుత్వ హాస్పిటల్లో మీ సంరక్షణలో ఉన్న డాక్టర్లు లేదా డయాలసిస్ టెక్నీషియన్లు ఎవరు? మా డాక్టర్ @13366038925420 కూడా అక్కడే ఉన్నారు. మేము మీకు సహాయం చేయడానికి ప్రయత్నిస్తాము
[4:32 pm, 09/02/2026] Meta AI: Avunu memu mee kishtannti artham chesukunnamu. Memu meeku sahayam chesadaniki prayathnisthamu. Nagarjuna Sagar prbhutw hospitallo mee sankaranallo unna doctors ala dialysis technicians evvaru? Maa doctor @13366038925420 kuba akkadey unnaaru. Memu meeku sahayam chesadaniki prayathnisthamu
[4:40 pm, 09/02/2026] PPM 1: [09/02, 16:18]hu2: No but who's doing the dialysis? Is it being done under the support of a registered doctor? If yes what is his name? Where is he working in Nagarjuna Sagar?
[09/02, 16:19] Hu1: mostly technician only sir, if any problem happens they call on duty doctor
Area hospital (Govt)
[09/02, 16:38]hu2: But we can't tell the UF and flow rate advice to the technician legally. We have to communicate with the area hospital doctors
[4.24 pm, 11/02/2026] PPM 1: Update:
[10/02, 09:59]: Can you check with the patient advocate what's the current follow up from his Nagarjuna Sagar dialysis technician's experimental dialysis protocol yesterday?
[11/02, 14:27] Anonymous Pm: Sir talked to both the Attenders and technician
[11/02, 14:27] Anonymous Pm: The dialysis was uneventful
[11/02, 14:28] Anonymous Pm: He kept
Uf:1500 ml
Duration:2 hours
Flow rate:120-160 ml/min (from 120-160 he slowly increased with time)
