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Cardiac Arrest - Science topic

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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.
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Current guidelines recommend giving the maximum feasible inspired oxygen during CPR based on the premise that restoring depleted oxygen levels and correcting tissue hypoxia improves survival.
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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.
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Yet to be developed
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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,
Regards,
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Hi.
The source of the wall shear stress (either oscillatory or averaged) is the velocity gradient in the fluid at the wall boundary. In other words, it is the force (or stress if you consider it per unit area) applied on the wall by the fluid. Therefore, you do not need to calculate/simulate the stress tensor in the wall to calculate TAWSS or OSI.
However, if the movement of the wall is significant in a way that it changes the velocity field in the fluid and its gradients at the wall boundary, you need to perform FSI. It is not to calculate to shear stresses, but to calculate the fluid velocity field accurately.
So, essentially you do NOT need FSI to calculate wall shear stress as they are basically related to the fluid velocity and the fluid viscosity only.
I hope it's clear.
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why do not we start considering the death as the brain one not the cardiac ?
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I do not know in your country, but in Spain following the indications in this regard of the WHO and the current Health CCs and, in particular of Neuroscience, the "official diagnosis", if it is indicated or required to specify it -for example, to extract organs for transplantation- it is established by means of a totally flat EEG for at least three minutes, confirmed (according to the means that are possessed) by another Health Professional, EVEN THOUGH THE HEART, FOR WHAT IT IS, KEEPS BEATING.
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The new modifications that were applied to the ACLS algorithm
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I think it should be added clearly that endotracheal tube or the supra-glottic device should be connected first to the bacterial/viral filter before its insertion inside the trachea or the pharynx. This will limit possibility of viral transmission if the patient was coughing.
Muscle relaxants usage is preferred if the incubator is experienced in intubation.
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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.
Thoughts?
Thanks in advance for any assistance you can offer.
Vini
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I agree with Nikola Bradic
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Dear Colleague,
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 (ruvan_nishali.ekanayaka@yahoo.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
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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 (ruvan_nishali.ekanayaka@yahoo.com).
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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?
Thank you
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Dissertation is questioning whether CPR is the main priority in a traumatic cardiac arrest.
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HI Tammy In attached file, you can find HOT algorithm. Hope that will help Nikola
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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 ?
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Thank you for your answer!!
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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
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Insulin for the treatment of hyperkalemia: a double-edged sword?
Tingting Li, MD and Anitha Vijayan, MD
See the article "Hypoglycemia in the treatment of hyperkalemia with insulin in patients with end-stage renal disease" in volume 7 on page 248.
 
Potassium plays a critical role in cellular metabolism and normal neuromuscular function. Tightly regulated homeostatic mechanisms have developed in the process of evolution to provide primary defense against the threats of hyper- and hypokalemia. The kidney plays a primary role in potassium balance, by increasing or decreasing the rate of potassium excretion. Distribution of potassium between the intracellular and the extracellular fluid compartments is regulated by physiologic factors such as insulin and catecholamines which stimulate the activity of the Na+-K+ ATPase. Only about 10% of the ingested potassium is excreted via the gut under normal physiologic conditions [1].
For more plz read at the following link.
Regards
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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
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Hi Richard!
Yours is an interesting case. Anyone looking at that ECG would have missed lead misplacement. As a rule, I always look at aVR and any positive wave in aVR alerts me for possible lead misplacement.
In addition, I have found that if more than one leads show all three waves (P, QRS, and T wave) inversion, then one must rule out lead misplacement. Normally, aVR is the only lead with all three waves inverted.
This can avoid most confusions while reporting ECGs.
I found another case report of similar lead misplacement for your review.
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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?
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I would not do external massage, but open chest / clamp descending thoracic aorta/ open pericardium while ET intubation is being done. Others would argue REBOA is warranted because of dismal prognosis.
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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 ?
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"Cardiorespiratory Arrest" is not the cause of death rather it is a mode of death.
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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. 
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Some papers tries to compare epinephrine vs nothing or vs vasopressin or vs both
I don't think there are very recent , a new incpmming is for neonate ressuscitation perhaps , see down :
Vasopressin improves survival compared with epinephrine in a neonatal piglet model of asphyxial cardiac arrest
Patrick J. McNamara, Doreen Engelberts, Michael Finelli, Khosrow Adeli & Brian P. Kavanagh
Neural injury after use of vasopressin and adrenaline during porcine cardiopulmonary resuscitation
A Comparison of Vasopressin and Epinephrine for Out-of-Hospital Cardiopulmonary Resuscitation
Volker Wenzel, M.D., Anette C. Krismer, M.D., H. Richard Arntz, M.D., Helmut Sitter, Ph.D., Karl H. Stadlbauer, M.D., and Karl H. Lindner, M.D. for the European Resuscitation Council Vasopressor during Cardiopulmonary Resuscitation Study Group
N Engl J Med 2004; 350:105-113January 8, 2004DOI: 10.1056/NEJMoa025431
Peter Halvorsen,1 Hari Shanker Sharma,1 Samar Basu,2 and Lars Wiklund
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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.
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Dear Brunett Parra
Thanks for your valuable information.
Regards
M Murugappan
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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,
Erik
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Quite the contrary; the THAPCA study had a profound effect size favoring the colder arm, and showed statistical significance in outcome (albeit, this was buried in the appendix, so those that don't read the whole article will miss it).  
From the point estimates, we're looking at a Number Needed to Treat (NNT) of 12.5 (20% vs. 12% to primary outcome of survival at 12 months after cardiac arrest with a VABS-II score of 70 or higher). This is amazingly large. And an overall 1-year survival of 38% in the hypothermia group vs. 29% in the normothermia group gives us an NNT of 11.
This study was underpowered to find the statistical significance, but that shouldn't affect the obvious effect size signal. The goal was 276 patients, the analyzed number was short of that, and the sensitivity analysis (reported only in the Supplementary Appendix), despite being downplayed somewhat, suggests that in fact the results were quite close to crossing into significance had the trial ran a bit longer.
Survival over time was significantly longer with therapeutic hypothermia than with therapeutic normothermia (mean survival, 149±14 days vs. 119±14 days; P = 0.04 for the comparison of survival between the two treatment groups by means of the log-rank test) (Fig. S1 in the Supplementary Appendix). Looking at Figure S1 (way down on page 22 of the Supplementary Appendix), I think it's pretty clear which arm you'd put your loved one in if faced with that decision.
The authors rightly emphasize though that this was not a study against a non-treated arm, but rather was a comparison between two very rigorously treated arms (for out to 120 hours).
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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?
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I'll preface this with the disclosure that I do have a conflict of interest with the company involved in this, but an alternative method for cooling, followed by maintenance and then rewarming, is described in these articles:  
[1] Markota A, Kit B, Fluher J, Sinkovic A. Use of an oesophageal heat transfer device in therapeutic hypothermia. Resuscitation. 2015;89:e1-2.
[2] Hegazy A, Lapierre D, Althenayan E. Targeted temperature management after cardiac arrest and fever control with an esophageal cooling device. Critical Care. 2015;19:P424.
There's also a company, Life Recovery Systems (no conflict of interest) that sells an immersion device along the lines of what you asked originally.  They've published some data showing safety in defibrillation, but I'm not sure about overall ease of use.
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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 ....
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I would be careful before interpreting the results of the THAPCA trial as negative here.  I think there will be a lot of debate over the way this was reported. The main concern I see is that to say the findings aren't "significant" is dubious. From a purely statistical standpoint (and classical/frequentist, at that, which itself brings up the unfortunate fact that we're not doing studies such as this in more advanced Bayesian Adaptive approaches...) this may be correct for some of the measures. But from the point estimates, we're looking at a Number Needed to Treat (NNT) of 12.5 (20% vs. 12% to primary outcome of survival at 12 months after cardiac arrest with a VABS-II score of 70 or higher). This is amazing. And an overall 1-year survival of 38% in the hypothermia group vs. 29% in the normothermia group gives us an NNT of 11.
This was clearly underpowered to find the statistical significance, but that shouldn't affect the obvious effect size signal. The goal was 276 patients, the analyzed number was short of that, and the sensitivity analysis (reported only in the Supplementary Appendix), despite being downplayed by the authors, suggests that in fact the statistical results were quite close to crossing into significance had the trial ran a bit longer. For some reason, the authors also buried a statistically significant finding in an appendix: "Survival over time was significantly longer with therapeutic hypothermia than with therapeutic normothermia (mean survival, 149±14 days vs. 119±14 days; P = 0.04 for the comparison of survival between the two treatment groups by means of the log-rank test) (Fig. S1 in the Supplementary Appendix)." Looking at Figure S1 (way down on page 22 of the Supplementary Appendix), I think it's pretty clear which arm you'd put your loved one in if faced with that decision.  
Finally, it's important to note (and fortunately the authors are good at emphasizing this) that this was not a study against a non-treated arm, but rather was a comparison between two very rigorously treated arms (for out to 120 hours), with one arm being colder than the other, but both arms being carefully treated to maintain a goal temperature, and avoid febrile/hyperthermic excursions which are generally agreed upon to be detrimental to outcome.  
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I have the data of 1000 cardiac patients, in this data many of the patients have high uric acid & high homocysteine levels.
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Uric acid is a risk factor for cardiovascular complications in individuals with and without diabetes. It is also a modifiable risk factor with the availability of drugs like allopurinol. I would read the following paper: 
Feig DI1, Kang DH, Johnson RJ. Uric acid and cardiovascular risk. N Engl J Med. 2008 Oct 23;359(17):1811-21. doi: 10.1056/NEJMra0800885: http://www.ncbi.nlm.nih.gov/pubmed/18946066 
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Published or unpublished data about cardiac arrests (affecting children or adults) occurring on school grounds.
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Thank you. One last question: how many were there it total for adults? 
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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 
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The key to successful resuscitation is a well thought out and high functioning system which delivers prompt CPR and ACLS. While bicarbonate is never monotherapy for any cardiac arrest, it may play a small modulatory role is patient with severe metabolic acidosis, such as those who have sustained a prolonged arrest.
The experimental evidence suggests that after a brief cardiac arrest (5 min or less), bicarbonate is neither helpful nor harmful. For arrest intervals of 10 min or more, the preponderance of experimental evidence suggests benefit. In a randomized trial of the empirical early administration of sodium bicarbonate (1 mEq/kg) in pre-hospital cardiac arrest, bicarbonate had no effect on the overal survival but there was a trend toward increased survival in prolonged (> 15 min) arrest.
Vukmir RB, Katz L, Sodium Bicarbonate Study Group: Sodium bicarbonate improves outcome in prolonged prehospital cardiac arrest. Am J Emerg Med 24: 156-161, 2006
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What it is the percentage of shockable rhythms in hospital and non-hospital cardiac arrest?
Can someone share link to research paper or review?
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Hello Marco,
Some Swedish data: in the Swedish Cardiac Arrest Registry, I found that 35% of cardiac arrest patients at hospital had VF (38% of those who were monitored by ECG), and 33% of those having out-of-hospital cardiac arrest presented with initial VF.
Concerning TIME, as mentioned by Guido Francesco Villa, I can recommend a little calculation of ours "Improvements in logistics could increase survival after out-of-hospital cardiac arrest in Sweden", presented in J Int Med 2013;273:622-7. Strömsöe A is the first author.
Best wishes
Mats Enlund
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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?
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my experience is the clinical data of  kidney stones and gall bladder stones with hypercalcemia in primary hypothyroidism  with duodenal kissing ulcer and renal acidosis in the same patient with goitrous polyseritis.
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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.? 
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Massive bleeding 300 ml or more/h,3 or 4 consecutive hours is reason for reopen patients after cardiac surgery. Second reason is clinical signs of cardiac tamponade with hemodynamic unstabile patients.To reduce te risk of infection surgeon reopen patients in operating room. Some times ,very poor LVEDP end EF requires a reopen patients.
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Hi,
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?
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Thank you, I believe your considerations are absolutely competent and I would advise the same. Besides, recently a new paper went out (JACC) saying that in case of acute MI blood transfusion is not harmful as previously thought (it could be of some benefit). This is just a retrospective study, but strong as regards statistical methods. Please take your time for a rapid scanning here: http://www.medscape.com/viewarticle/830202
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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.
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Dear Yugan,
Your question is one of those questions that is both simple and difficult in that it appears simple, but is in fact quite difficult.  As a Mobile Intensive Care Ambulance Paramedic in Victoria, Australia, I worked in a system which permitted ambulance officers of all levels to declare a patient deceased at the scene.  The written certification of death and the completion of the final 'death certificate' were restricted to medical practitioners.  However, the field declaration of death by an ambulance paramedic entailed the cessation of all treatment and, very often, the leaving of the body at the scene.
Although I cannot speak with any authority, I have suspicions that a percentage of these declarations lacked rigour and were conducted on the spur of the moment.  This does not mean that the decision taken was wrong, just that no one knows.  In the absence of a closely monitored process for making such decisions, there will be a degree of institutional blindness as to the appropriateness of the practice. This is the crux of the problem as flexibility and control collide.
In researching this question it would pay for you to look at the experience in the USA.  Until recently, many US jurisdictions restricted the declaration of death to qualified medical practitioners.  This led to many, many corpses being transported under emergency conditions to already overcrowded emergency departments.  This practice killed and injured ambulance personnel who were performing CPR when their vehicles suffered accidents.
It also ensured that hospital mortuaries were constantly overflowing with remains and it tied up valuable time in the emergency department, particularly physician time, as the legal paperwork was completed.
For all of these reasons and more, jurisdictions began to move towards legally empowering ambulance paramedics to declare death in the field.  The fears of some were that there would be a spate of declarations as paramedics wielded their new powers.  However, and I have no evidence for this assertion, I suspect the real problem will be breaking the culture of performing CPR en-route to the hospital.  I would be interested to hear what our US colleagues have to say on this matter.
Some of my thoughts on the pros of allowing paramedics to declare death are:
1. It quickly releases valuable ambulance resources for the next emergency or case
2. It lowers the administrative overhead on physicians by keeping the deceased out of the hospital and it removes the risk of the physician being called before the courts to give routine evidence on the process used.
3. It reduces the cost of handling the deceased as the funeral arrangements can be done from the home resulting in a single ambulance trip to the scene and a return funeral vehicle trip from mortuary to home and back.  This also reduces the number of times the deceased needs to be lifted and moved from nine to four.  With hospital based declarations there can be up to three other transportation legs and nine lifts involved.
4.  It leaves the deceased within the control of the family.  This lowers stress, allows grieving and leaves the family in charge of what actually happens to the remains.  This is, as far as I am concerned, the major benefit of the system.
5.  Paramedics in many jurisdictions have proven themselves highly competent in declaring death.  With good training, proper peer review of cases and transparency of medical oversight, I believe the system works well.
The Cons.
1.  There will be a level of risk that mistakes will be made.
2.  There needs to be an acceptance for field declarations by paramedics within the culture of the medical practitioners over-sighting the system.  The US experience of keeping medical control of declarations of death before then relaxing and removing the restrictions on paramedics may be due to the growth in confidence of the medical profession in the reliability of their paramedics.  In your own situation, this is the starting point.  You need to win the confidence of your peers.
3.  Public expectations.  This cannot be discounted.  There are some ethnic and religious groups who require that everything possible be done for the sick or injured patient.  This expectation needs to be met.  This again requires the creation of confidence within the community concerned and this may take some time.  This confidence will only arise from knowledge imparted by those whom the public respects.  Education and information from the medical profession concerned is essential, particularly where the highly skilled paramedic is a new addition to the health care team.
4.  There will be a reduction in the transportation of patients suffering the more extensive and untreatable injuries that are presently being seen.  When surgeons or physicians are attempting to push the boundaries of what can be done, the declaration of death by paramedics on scene will impact the availability of the very marginal case.  This requires that a system of varying the procedures be available for research purposes so that recently deceased patients fitting particular clinical criteria are transported.  Again, this will require close co-ordination with ethics committees and other stake holders.
5.  Too tight a procedure or protocol for declaring death in the field will not work.  There has to be a balance between flexibility and central control.  Usually, the best way forward is a graduated approach where field declarations can be used on the most obvious cases and, as confidence in the capacity of the paramedics increases, the range of cases can be widened.
I believe that paramedics are more than capable of declaring death in the field and that by doing so, they lower the pressure on physicians and hospitals.  However, the oversight of the medical system is vested in the physician and the first thing that must be done is to interest the physicians in how this practice will benefit them.  If this can be demonstrated, then it is essential to show them how their standards will be maintained by the paramedics, so that they can become confident that their patients are getting the best available care.
Field declarations of death by paramedics can only really occur where physicians feel confident.
Hope this helps you.
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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
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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?
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Yes, the procedure of MI in small size rat is the same as in mice. For detail please check my two papers.
erhe
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I think it's not feasible, but someone else doesn't agree.
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If they need analgesia, they don't need CPR; if they need CPR, they don't need analgesia.
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The article by Nielsen et al, November 17, 2013DOI: 10.1056/NEJMoa1310519 questioned the effectiveness of hypothermia in this situation.
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Normothermia 36ºC should be the end point after cardiac arrest based on the most precise RCT performed till nowadays (TTM trial).
N Engl J Med 2013;369:2197-206.
The question could be...should we cool all our patients after cardiac arrest or only those whom present temperature above 37ºC...?
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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.
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With rescue of spontaneous circulation the close system (central venous blood) with high pCO2 became open system and pCO2 decrease, but tissue and cellular pCO2 is much higher than venous pCO2 and CO2 wash out slowly to venous system. Your hypoventilated patient had much than one reason tohave high pCO2. Note that pO2 in physiologic range with FiO2=95% get a critically low P/F value
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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.
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The use of inotropic drugs in patients in coma after cardiac arrest and receiving target temperature management is debatable. The cardiac index may be 40-50% less in a patient who has reached a temperature of 33C. The patient may have a bradycardia as well. There is probably not much need to treat a pulse >40/min or a CI of 1.5L/min. Inotropic drugs will increase the work of the heart, and therefor the oxygen consumption. As most of these patients have experienced an ischemic cardiac event, using (high doses of) inotropic drugs may not be a good idea. In general avoid drugs, that cause tachycardia.
Blood pressure may be more important, as the auto-regulation of the brain may not function very well, and the cerebral blood flow may greatly depend on the blood pressure. So, norepinephrine may be the drug of choice for that.
Central or mixed venous oxygen saturation (ScvO2 or SvO2) could used to monitor supply and demand of oxygen; monitoring lactate may be less useful, as this is often increased during hypothermia.
We have to await RCT's looking into this problem. The TTM-trial, which will be published next week, will have data in secondary analysis looking into cardiovascular data, and may shed some light on this topic.
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Grand rounds on survived cardiac arrest in pregnancy with a live baby
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Dear Jules. Here in the UK, Myocardial Infarction is a rare but catastrophic event in pregnancy. The incidence of Ischaemic Heart Disease has risen over the last few years and in the indigenous population replaces previous cardiac deaths due to rheumatic fever (see:CMACE, 2011). Due to increased training there is evidence that more women survive cardiac arrest provided it is detected in the golden window period. See below for papers. Also, you might be aware that the United Kingdom Obstetric Surveillance System [UKOSS] (NPEU, Oxford) is currently undertaking a national audit on the incidence and outcomes for cardiac arrest in pregnancy.
RCOG (2007) Managing obstetric emergencies and trauma. MOET course manual. 2nd Edition. London: RCOG press. Dijkman A, et al., (2010) Cardiac arrest in pregnancy: increasing use of perimortem caesarean section due to emergency skills training? BJOG 2010; 117:282-287
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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.
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@33 C
We reported one case in Polish Heart Journal (Kardiologia Polska), you can download the article here: http://ojs.kardiologiapolska.pl/kp/article/viewFile/7621/7141
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We use an intravascular (femoral vein) cooling device. I agree cold saline in the ED is a good way to start the ball rolling. We cool to 33 C for 24 hours. We rewarm at 0.25-0.5C/hour to 36 C and hold there for 6 hours or so then allow passive temperature changes. We leave the intravascular catheter in place and control the temperature to not exceed 37 for a further 24 hours as post-rewarming hyperthermia is very common and likely not positive. We also apply balanced cutaneous counterwarming (forced air) which we find really cuts down on shivering and minimises metabolic changes without diminishing the cooling efficacy. We don't routinely paralyse the patients beyond a single bolus at induction of hypothermia if there is shivering, and we maintain sedation with propofol and remifentanil.
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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...
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Dear Michael, dear Ingo,
thank you both very much for sharing your experience and your preliminary data. It seems more than important to perform prospective multicenter trials in this context. Regarding the possible confounders (e.g., baseline temperature, length of CPR, ...) it would be interesting to know how your results (Michael) are influenced after adjusting the multivariable analysis.
Once again - thank you for your contributions and best regards
Raoul
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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 .....) ?
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Although I am not taking care of cardiac patients but I do believe the existence of CAC is important for countries like USA and Canada where cardiac specialsits are most of time are hundreds of miles away. Centralized special centers are needed just like ECMO or trauma centers. However, in small countries where doctors sometimes are within walking distance or level III centers are within 30 minutes for the general population a CAC may not be beneficial. Also need to consider the fiscal burden to have a specialized center which may sometimes increase the cost so as to maintain a lot of specialized facilities and doctors. Every single life deserves to be saved but a bankrupt system will definitely not helping in the long run.