Questions related to Cardiac Arrest
Ventilation during adult cardiopulmonary resuscitation (CPR) is poorly understood. Therefore, guideline recommendations are limited. The use of waveform capnography is in part recommended to monitor frequency. Other ventilation measurements such as tidal volume or inspiratory pressure are not regularly obtained, especially when a bag-valve system is used. The use of new monitoring devices can improve guideline adherence and could lead to better understanding of ventilation during CPR. Different EMS systems have varying levels of training, equipment and resources during CPR of out-of-hospital cardiac arrest (OHCA) patients. To better understand the current state of ventilation monitoring during OHCA CPR researcher/practitioner feedback and international perspectives on this question are needed and very much appreciated.
The study of ventilation during adult cardiac arrest remains challenging due to the unexpected nature of sudden cardiac arrest and the limited resources/personnel on site. This is especially true for interventions that influence outcomes when applied early in the cardiac arrest phase. Therefore, animal models (i.e. pigs, dogs), manikins, human cadavers and computer models have been used to study intra-arrest ventilation. Also, some data has been made available from registries and clinical studies in humans.
While the possible answers to my question heavily depend on the respective research question, personal perspectives on the well known experimental models, as well as lesser known models for this niche of cardiac arrest research, would be very much appreciated.
Please note, that I do not to intend to discuss airway management during cardiac arrest. Although, I'm aware that both intra-arrest ventilation and airway management are closely connected.
Dear all Professors & fellows,
Respected to you all.
Thank u for looking this question and adding your valuable comments or understandings to this question.
I saw few published manuscripts & found that, authors have evaluated TAWSS & OSI for rigid case of CFD simulations.
My question is that, actual meaning of TAWSS is - Avgd WSS over one cardiac cycle, which is used to determine the shear stress magnitude applied on vascular wall surfaces during one cardiac cycle.
So, how & for what reasons TAWSS & OSI parameters were calculated when they have done CFD simulations where they don't have vascular wall surfaces or absence of wall.
As of my understanding I believe that, these parameters can be only evaluate if you are doing FSI simulations (fluid structure interaction studies) but not for CFD (Rigid wall) cases because that give incorrect results as CFD cases doesn't have surfaces or walls.
SO, can you please tell me how much I am correct here .
I am saying that, TAWSS, OSI should be evaluated for Fluid structure interaction cases only but not give correct results for CFD (rigid wall cases) so not necessary to calculate in rigid cases of artery.
is that I am correct??
Please clarify me by your valuable comments or reply me.
Thanking you in anticipation,
why do not we start considering the death as the brain one not the cardiac ?
Here is a question for everyone that I am currently stumped on:
Is there some standardized metrics or quality targets for in-hospital cardiac arrests rates?
Its related to the work I am doing to implement CCOT at SPH. The CCOT literature uses a variety of measures and it gets a little confusing:
· Code blue (all types) per 1000 admissions or per 1000 discharges
· Cardiac Arrest (only code blue with CPR) per 1000 admissions or per 1000 discharges
· Code blue or Cardiac arrest excluding critical care areas (i.e., ED, ICU, CCU, CSICU, OR/PACU) per 1000 admissions or discharges
I looked through CIHI and it does not look like they have any stats on in-hospital cardiac arrest rates that I could find. We keep track of code blue data, but I don’t think it is reported to any external organizations. The UK and Australia have done rapid response systems for far longer, but I haven’t come across any official standardized metrics or definitions of what is considered good, bad or ugly in the way of targets.
Thanks in advance for any assistance you can offer.
Sri Lankan Journal of Cardiology- January 2019 (Official Publication of Sri Lanka Heart Association) We are pleased to inform you that the above mentioned issue of SLJC has been published. The next issue has to be published in time for the Annual Academic sessions of the Sri Lanka Heart Association, in June 2019. Hence, we earnestly solicit a contribution from you .It would be greatly Appreciated and extremely valuable. We welcome, Reviews, Therapeutic Reviews, Research, Audits,Critiques of Guidelines, Analysis of important Trials, Milestones in achievements, Tutorials, Case Reports and Updates etc ,as contributions for the next issue of the SLJC.Could you please prepare your manuscripts and submit the same by end of April so that the editorial work could be completed in time (email@example.com). The PDF version of this issue is attached herewith. Thanking you in advance for your kind cooperation. Yours Sincerely, With Best regards,RuvanDr Ruvan EkanayakaMBBS,MD,MRCP(UK),FRCP(Lond),FRCP(Edin),FRCP(Glsg),FCCP, FACC,FESCConsultant Cardiologist / Editor in Chief SLJC
What is the effect of cardiac arrest on GI perfusion?
What are the short term (acute) consequences of cardiac arrest on GI function?
If someone were to restore spontaneous circulation, would the gut have taken a significant enough beating to not be able to well absorb an oral medication for example?
Dissertation is questioning whether CPR is the main priority in a traumatic cardiac arrest.
We recently had a patient with major thoracic trauma with lung dilaceration, major thoracic bleeding and hemorrhagic shoc leading to cardiac arrest at arrival. We performed a right thoracotomy with clamping of hilum and total pneumonectomy to control the bleeding, while CPR was performed. We stopped the bleeding but the patient unfortuneatly died anyway.
Have you ever had a survivor of a total pneumonectomy for bleeding control ?
Have you ever had the case with a patient in cardiac arrest and on-going CPR ?
patient post cardiac arrest with blood sugars >300 but on insulin drip at 30 units per hour but decreasing electrolytes. Is there research supporting permissive hyperglycemia during the maintenance phase of TTM in order to prevent severe hypokalemia
I will be presenting this topic at the International Conference in Emergency Medicine, Cape Town, next week and so far nobody that I have asked has come across it
I'm doing some work on improving outcomes in patients who suffer traumatic cardiac arrest.
Case history: a 30 year old male motorcyclist is brought to the emergency department having crashed his motorbike into a tree. He has multiple injuries, but was conscious with a palpable pulse at scene. He deteriorates en route. On arrival in your resuscitation room he is not breathing and has no palpable pulse.
Quick poll - who would initiate chest compressions in this case?
Determining the "Cause of death" is the most important thing after the death of a person. The cause of death is the underlying disease process or injury or any abnormality, which sets in motion a physiologic process (mechanism), which may be brief or prolonged but which ultimately gives rise to death.
Often in death certificates issued by Medical Officers, the "Cause of death" is mentioned as "Cardio-pulmonary Arrest".
It is obviously true that when we die our heart stops beating & we no longer breath. This however can neither be a cause of death nor the mechanism of death. Isn't this just a description of a person being dead ?
It is for my 3 year nursing dissertation. The initial proposal being: The use of vasopressin and epinephrine during a paediatric cardiac arrest versus epinephrine alone.
We have developed some novel algorithms in our group for early prediction of SCA using MIT-BIH database. We now need some other data sets to validate our algorithms.
Last I heard, this trial (https://www.thapca.org/) was completed, and results were about to be published, however have not seen anything yet. Anyone have any updates or knowledge?
Thanks in advance,
Common non invasive methods use blankets or ice, cold water immersion would be probably faster, but current guidelines for therapeutic hypothermia do not consider it.
Could cold water immersion be useful for other than heat stroke and hyperthermia treatment?
Results of the THAPCA OH trial NEJM :In comatose children who survived out-of-hospital cardiac arrest, therapeutic hypothermia, as compared with therapeutic normothermia, did not confer a significant benefit in survival with a good functional outcome at 1 year .....
Maybe we must use normothermia in pediatric cardiac arrest and traumatic brain injury in ours PICU ....
I have the data of 1000 cardiac patients, in this data many of the patients have high uric acid & high homocysteine levels.
Published or unpublished data about cardiac arrests (affecting children or adults) occurring on school grounds.
Is there any proven role of NaHCO3 in cardiac arrest before getting ABG report as most of pt of cardiac arrest will be in acidosis so give some article please. Thank you
What it is the percentage of shockable rhythms in hospital and non-hospital cardiac arrest?
Can someone share link to research paper or review?
We have recently published 2 experimental studies that show positive inotropic effect of the PDE3 inhibitor milrinone and the calcium sensitizer levosimendan during hypothermia and rewarming. This is different from studies on B-receptor agonists like epinephrine and isoprenaline, which show that such drugs have diminished or negative inotropic effects during hypothermia.
I therefore want to know whether anyone have clinical experience with use of PDE3 inhibitors or calcium sensitizers in patients that are treated with therapeutic hypothermia (eg. during surgery or after cardiac arrest) or during rewarming from accidental hypothermia?
the indication is cardiac arrest usually or tamponade which is not giving us time enough to shift the patient back to theater. but when exactly should we say lets re-open the patient and stop defibrillating etc any more.?
this is somewhat of a hot topic. 75 y.o. male, BMI 27, comes in for a STEMI with cardiac arrest, primary PCI of prox LAD (2 overlapping DES, radial approach) in 3-VD, ICU, LV EF 25%.
On day 5 he undergoes completion of revascularization with 2 DCBs in the Circ, and 1 DES in the RCA (radial approach).
Hemoglobin begins with 14.5 g/dl on admission and then drops progressively to 12, 10, and then, after the second PCI to 7.5 g/dl, without signs of overt bleeding except for an already known hemorragic gastritis.
Patient currently suffers heart failure.
Should I go for blood transfusion now, or not?
Currently there seems to be a standard rule of waiting for 20 mins of asystole prior to actually terminating resuscitative efforts in the pre-hospital environment (including a load-and-go to hospital approach). This seems reasonable for the non-trauma patient especially if an automatic chest compression device (LUCAS) is available.
For the critically injured trauma patient, these automatic devices are generally contra-indicated and furthermore, doing CPR in the back of a fast-moving ambulance is both ineffective and dangerous. A lot of these patients present with a PEA rhythym for long periods as well as with injuries that appear to be incompatible with life.
So, what does the paramedic do in these situations? Continue a futile resuscitation or terminate? Any thoughts or experience with this situation will be appreciated.
I think not!. The articles recently appeared in JAMA and PLOSONE are greatly flawed. I am wondering as to why they have been processed by right peer reviewers. Before answering me, please give a look to our reply. I'll keep you posted regarding a letter to JAMA editor asking retraction of Vigen's article
As you may possibly know, LCA ligation is a surgical approach used to induce ischemia in heart for ischemic/perfusion studies. I`m about to follow this method to start a new project, however I`m facing some interesting challenges. I'd really appreciate if someone could give me some tips on the following matters:
1. Is performing a thoracotomy in a rat possible without a ventilator machine? I mean if we don't have a ventilator, can we build up a simpler apparatus (like a hand-made balloon or something) to use as a ventilator during the procedure instead?
2. How can I regenerate the negative pressure of the thoracic cavity before the closure of the surgical site?
3. What are the key points to help the animal survive about a month after the procedure (so that the infarction is induced)?
4. Since the LCA is not so distinctively recognizable after the beating heart is exposed, how can we identify the LCA better?
Which anesthetics do you recommend to perform such a procedure? A combination of ketamine and xylazine or pentobarbital or what?
A patient around 55/m (70kg) year was admitted in ED with hypoxia condition, diabetic, hypertension and cardiac arrest. CPR was also done for around 20 minutes.
Primary atrial blood gas analysis of PCO2 was 210 mm of Hg. A mixed respiratory acidosis and metabolic acidosis condition.
patient's weight =70 kg
ventilator condition (mode=SIMV, VT=480,RR=16,PEEP=5, Fio2=95%, Bicarbonate is lower than expected so Na2CO3- was administered (IV).
After 4 hr on Ventilator atrial blood is taken for AVG analysis and AVG is done . PCO2 value was 184 mm of Hg on ventilator and PO2 was in Range.
Why did it slightly decrease as i expected ? or patient have other complicated diseases.
Therapeutic hypothermia is a common procedure in comatose survivors of cardiac arrest. I'm interested in knowing which inotropic drugs are used for cardiac support by different centres.
I'm currently studying pathophysiology in the development of J-waves in the ecg-recordings from hypothermic hearts. As my research is primarily focused on accidental hypothermia, It would be interesting to know how relevant this is in therapeutic hypothermia as well.
Lowering body temperature during the first hours after cardiac arrest reduces neurologic injury by disrupting pathological cellular events and cascades that might lead to secondary brain injury. Randomized trials demonstrated that therapeutic hypothermia early after cardiac arrest reduces mortality and improves outcome. Based on preliminary results, it was postulated that a shorter delay to target temperature would further improved outcome. However, those early results were not verified in following randomized trials. Thus, the question if time or delay to therapeutic hypothermia matter in patients resuscitated from cardiac arrest...
A Cardiac Arrest Center is a multi-disciplinary group of emergency physicians, cardiologists, neurologists and intensive care physicians with the goal of providing excellence in care to post-cardiac arrest patients. Are there good data around that a CAC performs better than others ?
How far would you transport patients with OHCA to a specialized CAC ? What should be standard of care in these centers (hypothermia, cath lab, ECMO, surgery .....) ?