Guest guest Posted October 31, 2003 Report Share Posted October 31, 2003 The answer is simple. If the patient is acidotic, then the bicarb will improve the pH in the short term which may help correct and stabilize the cardiac electrical system Don't give it unless you are properly ventilating the patient! If the patient is hyperkalemic to start off with, as in the cause of arrest.... then bicarb won't help. If working a dialysis code, after infusing large amounts of fluid and starting with epi and atropine/lidocaine, then giving calcium, then try some bicarb. It wont hurt to try albuterol as well, but it really isnt a code drug.... fact is, they all take time, more time then we are going to give most codes. If the patient has arrested for some cause other then acidocis or hypoxia, it is doubtful that by the time you get to bicarb you will saving anything. Save your bicarb for post-arrest resuscitations, TCA OD's, respiratory arrests leading to cardiac arrests, where it is more likely to be of benefit. ;-) Nick ____________________________________________ Nick Nudell, NREMT-P, CCEMT-P California nudell@... " Perception is reality " - Wise Old Paramedic bicarb Ok here is a question for the group. I had the chance to ask this of three cardiologist and got three differnt answers and caused a very intense discussion amungst them. In a cardiac arrest situation, would the use of sodium bicarbonate be an advantage? I do not know the answer to this. Nor of any study on the subject. This is simply a question and maybe even something to think about. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 31, 2003 Report Share Posted October 31, 2003 Nick: I am not sure where you get your medical facts, but may want to re-check them before posting to a list. 1. There are some codes where bicarb will help, although most simply require ventilation. 2. Dialysis patients with hyperkalemia need calcium (calcium gluconate, calcium chloride). All the other drugs are useless unless you lower the potassium. 3. How many people have cardiac arrests secondary to " acidosis " (except in patient restraint with excited delirium)? The remainder of which have acidosis secondary to other causes. Re: bicarb The answer is simple. If the patient is acidotic, then the bicarb will improve the pH in the short term which may help correct and stabilize the cardiac electrical system Don't give it unless you are properly ventilating the patient! If the patient is hyperkalemic to start off with, as in the cause of arrest.... then bicarb won't help. If working a dialysis code, after infusing large amounts of fluid and starting with epi and atropine/lidocaine, then giving calcium, then try some bicarb. It wont hurt to try albuterol as well, but it really isnt a code drug.... fact is, they all take time, more time then we are going to give most codes. If the patient has arrested for some cause other then acidocis or hypoxia, it is doubtful that by the time you get to bicarb you will saving anything. Save your bicarb for post-arrest resuscitations, TCA OD's, respiratory arrests leading to cardiac arrests, where it is more likely to be of benefit. ;-) Nick ____________________________________________ Nick Nudell, NREMT-P, CCEMT-P California nudell@... " Perception is reality " - Wise Old Paramedic bicarb Ok here is a question for the group. I had the chance to ask this of three cardiologist and got three differnt answers and caused a very intense discussion amungst them. In a cardiac arrest situation, would the use of sodium bicarbonate be an advantage? I do not know the answer to this. Nor of any study on the subject. This is simply a question and maybe even something to think about. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 31, 2003 Report Share Posted October 31, 2003 After reading what you wrote, I thought we were saying the same thing. Thanks... Nick bicarb Ok here is a question for the group. I had the chance to ask this of three cardiologist and got three differnt answers and caused a very intense discussion amungst them. In a cardiac arrest situation, would the use of sodium bicarbonate be an advantage? I do not know the answer to this. Nor of any study on the subject. This is simply a question and maybe even something to think about. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 31, 2003 Report Share Posted October 31, 2003 I did some research this afternoon while the doorbell was ringing.... I looked back on Medline for 30 years regarding hyperkalemia and about 8 years for bicarb. I did not look at the titles related to arrests from blood transfusions, surgeries or other etiologies not pertinent to this discussion. I also ignored some but not all animal studies. I found some interesting reading and am sharing some of those abstracts with you here. AHA lists both calcium and bicarb as class Indeterminate drugs. This is because no study has shown that either medication will benefit a significant number of patients. This does not mean that some people will not benefit from them (for example, hyperK patients). I have included a couple abstracts that are related to some of the recent research on delayed defibrillation that show some promising results. The studies are geared towards neurologic function post-resuscitation but are postive nonetheless. In every single case, except for one that did not provide adequate info to determine if its true or not, the published cases of hyperkalemic patients who have been resuscitated... were resuscitated after long periods of CPR (like 90-120 minutes) and standard ACLS as well as 'standard' treatments for hyperK, which where then followed by hemodialysis leading to SROSC (Spontaneous return of circulation). These cases were not in the context of my previous message but are discussed when I am teaching ACLS to nurses and doctors who 'may' be able to initiate dialysis. So finally, my comments were within the context of the current AHA guidelines. Similar comments would have applied had anyone asked about epi or lidocaine or atropine... all have minimal impact on the greater number of arrests, while some patients will benefit from them. Basically, what every survivable arrest patient benefits from and is something we can do- circulation and ventilation. Although I have provided one or two abstracts here that would seemingly disprove that theory also. If anyone disagrees with what I have posted, please feel free to comment or discuss! That is why I am here, to learn from y'all! (in my best Texas accent) Have a great weekend! Nick ______________________________________ Resuscitation. 1996 Jul;32(1):27-9. Unexpected return of cardiac action after termination of cardiopulmonary resuscitation. Voelckel W, Kroesen G. Department of Anaesthesia and Intensive Care Medicine, Leopold-Franzens-University of Innsbruck, Austria. Application of sodium bicarbonate is still an option when resuscitation efforts remain unsuccessful. Despite this, there are no recommendations on how long resuscitation should be performed after administration of this drug. Here we describe a case in which prehospital resuscitation efforts were terminated about 35 min after cardiac arrest. Seven minutes after all efforts had been discontinued, spontaneous sinus rhythm appeared from a zero-line ECG, giving normal hemodynamic values. The underlying reason might be unexpected and unrecognized hyperkalemia, which was diminished by administration of sodium bicarbonate, even under the conditions of cardiocirculatory arrest. --------------------------------------------------------------------------------\ --------------------------- Ann Emerg Med. 1994 Aug;24(2):305-11. Prolonged asystolic hyperkalemic cardiac arrest with no neurologic sequelae. Quick G, Bastani B. Division of Emergency Medicine, St Louis University Medical Center, Missouri. We report the case of a 70-year-old man who developed cardiac arrest secondary to hyperkalemia that complicated severe chronic renal failure due to obstructive uropathy. The patient experienced electromechanical dissociation and approximately 26 minutes of asystole after which the resuscitation was suspended. However, 8 to 10 minutes after declaration of death, the patient was noted to have developed spontaneous return of circulation as the emergency department personnel were preparing to transport him to the morgue. The patient survived and was discharged without apparent neurologic sequelae. This case demonstrates the challenges facing physicians to predict the outcome of hyperkalemic cardiac arrest based on usual parameters. It also highlights the relative paucity of resuscitation guidelines to assist in the management of this medical emergency. --------------------------------------------------------------------------------\ ------------- Intensive Care Med. 1994;20(4):287-90. Outcomes of severe hyperkalemia in cardiopulmonary resuscitation with concomitant hemodialysis. Lin JL, Lim PS, Leu ML, Huang CC. Division of Nephrology, Chang Gung Memorial Hospital, Taipei, Taiwan, R.O.C. OBJECTIVE: To investigate the efficacy of hemodialysis during cardiopulmonary resuscitation as an effective adjunct to the treatment of severe hyperkalemia. DESIGN: A prospective study. SETTING: In hospital dialysis units and intensive care units. PATIENTS: Renal failure patients who developed hyperkalemia induced cardiac arrest and failed to recover from conventional cardiopulmonary resuscitation (CPR) were included. Three patients entered into this study: 2 patients with chronic renal failure maintained on regular hemodialysis and one with acute renal failure who suffered from severe hyperkalemia. INTERVENTIONS: All three patients developed asystolic cardiac arrest with unrecordable blood pressure due to severe hyperkalemia. Aggressive CPR together with intravenous epinephrine, sodium bicarbonate and calcium chloride were instituted. External cardiac massage with cardiac defibrillation was unable to restore spontaneous heart action. After lack or response to intensive resuscitation, hemodialysis was performed concomitant with CPR to eliminate the potassium load. MEASUREMENTS AND RESULTS: Sinus rhythm and blood pressure were restored in all 3 patients but one of them eventually succumbed to her underlying disease. CONCLUSION: Hemodialysis during CPR is probably an effective adjunct to the treatment of severe hyperkalemia in patients with severe hemodynamic compromise and asystolic cardiac arrest. --------------------------------------------------------------------------------\ - Heart Lung. 1993 Nov-Dec;22(6):548-53. Changes in the pharmacotherapy of CPR. Grillo JA, ER. School of Pharmacy, Virginia Commonwealth University, Medical College of Virginia. The objective of this study was to review current changes in the pharmacologic management of cardiac arrest (ventricular fibrillation, pulseless ventricular tachycardia, asystole, and electromechanical dissociation) as put fourth by the American Heart Association's 1992 Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiac Care. We concluded that the 1992 Guidelines provide a reference base for all clinicians involved in emergency cardiac care. The newly revised recommendations are classified on the basis of the true clinical merit of the intervention, for example, an intervention that has been proved effective (i.e., high-dose epinephrine) versus one that is possibly effective (i.e., high-dose epinephrine). The preferred intravenous fluid to be used in resuscitation is saline solution or lactated ringers solution because of possible adverse neurologic outcomes seen with dextrose-containing fluids. The dose of all drugs administered via the endotracheal route should be 2 to 2.5 times the intravenous dose. Modifications in the dose or dosing interval have been recommended for epinephrine, atropine, lidocaine, bretylium, and procainamide during cardiopulmonary resuscitation. Options for high-dose epinephrine therapy are offered, but neither recommended or discouraged. Magnesium sulfate has been added for the management of torsades de points, severe hypomagnesemia, or refractory ventricular fibrillation. The maximum total dose of atropine in the treatment of asystole and electromechanical dissociation has been increased from 2 mg to 0.04 mg/kg. The use of sodium bicarbonate should be limited to the treatment of hyperkalemia, tricyclic antidepressant overdose, overdoses requiring urinary alkalinization, or preexisting bicarbonate sensitive acidosis. --------------------------------------------------------------------------------\ -- Wis Med J. 1990 Aug;89(8):459-61. Hyperkalemic electromechanical dissociation. Lawton JM. St 's Regional Kidney Dialysis Program, Green Bay, WI. Two patients with hyperkalemic electromechanical dissociation are described. Electrocardiograms at the time of the cardiac arrests demonstrated normal appearing QRS complexes. Both patients responded to intravenous calcium chloride administration with prompt restoration of normal blood pressure. Implications of these observations with respect to current advanced cardiac life support guidelines are discussed. --------------------------------------------------------------------------------\ --------------------------- Ann Fr Anesth Reanim. 1990;9(3):204-7. [Pharmacology of cardiopulmonary resuscitation] [Article in French] Hoffmann AC, Scheidegger D. Departement d'Anesthesie, Hopital Cantonal Universitaire, Bale. Among the adrenergic receptor agonists, epinephrine, at alpha and beta stimulating doses, remains the drug of choice for cardiopulmonary resuscitation. However, alpha adrenergic agonists such as phenylephrine, methoxamine and dopamine (at alpha stimulating doses) result in similar success rates of resuscitation as epinephrine. In the opposite, beta adrenergic agonists, without or with only low alpha stimulating effect, such as isoproterenol or dobutamine are significantly less efficient. There are few data indicating that sodium bicarbonate improves outcome. Moreover it carries the risk of adverse effects. It may be of benefit in case of preexisting metabolic acidosis or during prolonged resuscitation with documented acidosis. Calcium remains indicated in case of hypocalcaemia, hyperkalaemia or calcium channel blocker intoxication. Severe ionized hypocalcaemia can occur after out-of-hospital cardiac arrest --------------------------------------------------------------------------------\ ------------------------------ J Emerg Med. 1989 Mar-Apr;7(2):109-13. Hyperkalemia during human cardiopulmonary resuscitation: incidence and ramifications. GB, Nowak RM, Cisek JE, Carden DL, Tomlanovich MC. Department of Emergency Medicine, Henry Ford Hospital, Detroit, MI 48202. Although hypokalemia has been reported after cardiac arrest and successful resuscitation, experimental data indicate that potassium is released from cells during ischemia. The purpose of this investigation was to study serum potassium concentration ([K+]) during closed chest cardiopulmonary resuscitation (CC-CPR) in humans. Twenty-two patients presenting to the emergency department (ED) in cardiopulmonary arrest had simultaneous measurement of central venous and arterial [K+] and blood gases during CC-CPR utilizing current advanced cardiac life support protocols and a pneumatic chest compressor and ventilator. Mean arterial and central venous [K+] were 5.0 +/- 1.3 and 5.6 +/- 2.9 mEq/L, respectively, (p greater than .05) with 7 patients having [K+] of greater than 6 mEq/L. Significant hyperkalemia does occur in some patients during cardiac arrest and CC-CPR. Because poor tissue perfusion during CC-CPR impairs exchange between the interstitial and intravascular compartments, increases in interstitial [K+] would be expected to be even greater. Interstitial hyperkalemia may play a role in the genesis of wide complex electromechanical dissociation (EMD) seen after prolonged cardiac arrest. Since calcium has long been known to be beneficial in the treatment of hyperkalemia-induced dysrhythmias, the success of calcium chloride in treating wide complex EMD may be on the basis of this phenomenon. --------------------------------------------------------------------------------\ ------------------------------------ Intensive Care Med. 1989;15(5):325-6. Hyperkalemic cardiac arrest, prolonged heart massage and simultaneous hemodialysis. Torrecilla C, de la Serna JL. Intensive Care Unit, Clinica Puerta de Hierro, Madrid, Spain. A 53 year old diabetic patient underwent CABG and aortic valve replacement in another institution and developed postoperative oliguric and hyperkalemic acute renal failure. Shortly after transferring to our unit a cardiac arrest occurred. Immediate resuscitative measures were ineffective. The serum potassium level was 10.2 mmol/l. Conventional arteriovenous hemodialysis was initiated while the patient was still undergoing cardiac massage. When the serum potassium level was lowered to 6.5 mmol/l, 90 min later, the heart began to beat. After hemodialysis was discontinued the patient was reactive and fully conscious. The use of simultaneous hemodialysis with prolonged mechanical heart massage as a reliable method for recovery in hyperkalemic cardiac standstill is stressed. -------------------------------------------------------------------------------- Am J Kidney Dis. 1985 Jan;5(1):47-8. Related Articles, Links Lethal hyperkalemia associated with severe hyperglycemia in diabetic patients with renal failure. Montoliu J, Revert L. Two patients with diabetic nephropathy on maintenance hemodialysis developed extreme hyperkalemia (7.9 and 9.3 mmol/L, respectively) in association with severe episodes of hyperglycemia (1,152 and 1,185 mg/dL, respectively). The increase in serum potassium was out of proportion to the degree of metabolic acidosis that both patients had, and no exogenous source of hyperkalemia could be identified. Despite treatment efforts both patients died shortly after arrival as a consequence of cardiac arrest. It is proposed that the hyperosmolality of extracellular fluid produced by severe hyperglycemia drives potassium passively out of the cells, therefore favoring the rapid development of hyperkalemia. Insulin deficiency could also play a role. This situation is particularly dangerous in individuals with impaired renal function. Adequate blood glucose control in diabetic patients on dialysis is important to avoid life-threatening hyperkalemia. --------------------------------------------------------------------------- Anaesthesist. 1983 Sep;32(9):443-4. [Asystole in extreme hyperkalemia, and successful resuscitation] [Article in German] Kretz FJ, Meschede V. Cardiac arrest in a twenty-year-old patient was caused by hyperkalaemia of 11.8 mmol/l. Cardiorespiratory resuscitation and emergency treatment of hyperkalaemia saved the life of this patient without residual neurological or mental disorders. We discuss pathophysiological mechanisms. ------------------------------------------------------------------------------- Resuscitation. 2001 Dec;51(3):309-15. Sodium bicarbonate improves the chance of resuscitation after 10 minutes of cardiac arrest in dogs. Leong EC, Bendall JC, Boyd AC, Einstein R. Department of Pharmacology, University of Sydney, NSW 2006, Sydney, Australia. The likelihood of successful defibrillation and resuscitation decreases as the duration of cardiac arrest increases. Prolonged cardiac arrest is also associated with the development of acidosis. These experiments were designed to determine whether administration of sodium bicarbonate and/or adrenaline in combination with a brief period of cardiopulmonary resuscitation (CPR) prior to defibrillation would improve the outcome of prolonged cardiac arrest in dogs. Ventricular fibrillation (VF) was induced by a.c. shock in anaesthetised dogs. After 10 min of VF, animals received either immediate defibrillation (followed by treatment with bicarbonate or control) or immediate treatment with bicarbonate or saline (followed by defibrillation). Treatment with bicarbonate was associated with increased rates of restoration of spontaneous circulation. This was achieved with fewer shocks and in a shorter time. Coronary perfusion pressure was significantly higher in NaHCO3-treated animals than in control animals. There were smaller decreases in venous pH in NaHCO3-treated animals than in controls. The best outcome in this study was achieved when defibrillation was delayed for approximately 2 min, during which time NaHCO3 and adrenaline were administered with CPR. The results of the present study indicate that in prolonged arrests bicarbonate therapy and a period of perfusion prior to defibrillation may increase survival. ------------------------------------------------------------------------------ Resuscitation. 2002 Oct;55(1):45-55. Buffer administration during CPR promotes cerebral reperfusion after return of spontaneous circulation and mitigates post-resuscitation cerebral acidosis. Liu X, Nozari A, Rubertsson S, Wiklund L. Uppsala University Hospital, Department of Surgical Sciences/Anesthesiology and Intensive Care, SE-751 85 Uppsala, Sweden. To explore the effects of alkaline buffers on cerebral perfusion and cerebral acidosis during and after cardiopulmonary resuscitation (CPR), 45 anaesthetized piglets were studied. The animals were subjected to 5 min non-interventional circulatory arrest followed by 7 min closed chest CPR and received either 1 mmol/kg of sodium bicarbonate, 1 mmol/kg of tris buffer mixture, or the same volume of saline (n=15 in all groups), adrenaline (epinephrine) boluses and finally external defibrillatory shocks. Systemic haemodynamic variables, cerebral cortical blood flow, arterial, mixed venous, and internal jugular bulb blood acid-base status and blood gases as well as cerebral tissue pH and PCO(2) were monitored. Cerebral tissue acidosis was recorded much earlier than arterial acidaemia. After restoration of spontaneous circulation, during and after temporary arterial hypotension, pH in internal jugular bulb blood and in cerebral tissue as well as cerebral cortical blood flow was lower after saline than in animals receiving alkaline buffer. Buffer administration during CPR promoted cerebral cortical reperfusion and mitigated subsequent post-resuscitation cerebral acidosis during lower blood pressure and flow in the reperfusion phase. The arterial alkalosis often noticed during CPR after the administration of alkaline buffers was caused by low systemic blood flow, which also results in poor outcome. -------------------------------------------------- Resuscitation. 2002 Jul;54(1):47-55. Clinical use of sodium bicarbonate during cardiopulmonary resuscitation--is it used sensibly? Bar-ph G, Abramson NS, Jansen-Mc L, Kelsey SF, Mashiach T, Craig MT, Safar P; Brain Resuscitation Clinical Trial III (BRCT III) Study Group. Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, PA 15260, USA. g_barjoseph@... This study retrospectively analyzed the pattern of sodium bicarbonate (SB) use during cardiopulmonary resuscitation (CPR) in the Brain Resuscitation Clinical Trial III (BRCT III). BRCT III was a prospective clinical trial, which compared high-dose to standard-dose epinephrine during CPR. SB use was left optional in the study protocol. Records of 2915 patients were reviewed. Percentage, timing and dosage of SB administration were correlated with demographic and cardiac arrest variables and with times from collapse to Basic Life Support, to Advanced Cardiac Life Support (ACLS) and to the major interventions performed during CPR. SB was administered in 54.5% of the resuscitations. The rate of SB use decreased with increasing patient age-primarily reflecting shorter CPR attempts. Mean time intervals from arrest, from start of ACLS and from first epinephrine to administration of the first SB were 29+/-16, 19+/-13, and 10.8+/-11.1 min, respectively. No correlation was found between the rate of SB use and the pre-ACLS hypoxia times. On the other hand, a direct linear correlation was found between the rate of SB use and the duration of ACLS. We conclude that when SB was used, the time from initiation of ACLS to administration of its first dose was long and severe metabolic acidosis probably already existed at this point. Therefore, if SB is used, earlier administration may be considered. Contrary to physiological rationale, clinical decisions regarding SB use did not seem to take into consideration the duration of pre-ACLS hypoxia times. We suggest that guidelines for SB use during CPR should emphasize the importance of pre-ACLS hypoxia time in contributing to metabolic acidosis and should be more specific in defining the duration of " protracted CPR or long resuscitative efforts " , the most frequent indication for SB administration -------------------------------------------------- Acad Emerg Med. 1995 Apr;2(4):264-73. Association of drug therapy with survival in cardiac arrest: limited role of advanced cardiac life support drugs. Stiell IG, Wells GA, Hebert PC, Laupacis A, Weitzman BN. University of Ottawa Faculty of Medicine, Ontario, Canada. OBJECTIVE: To generate hypotheses regarding the association of standard Advanced Cardiac Life Support (ACLS) drugs with human cardiac arrest survival. METHODS: This observational cohort study was conducted over a two-year period in the wards, intensive care units, and EDs of two tertiary care hospitals. Included werc adult patients who suffered cardiac arrest either inside or outside the hospital and who required epinephrine according to standard ACLS guidelines. Six standard ACLS drugs (given while CPR was in progress) were assessed for association with survival from resuscitation to one hour and to hospital discharge by univariate and multivariate logistic regression analyses. RESULTS: In the 529 patients studied, initial cardiac rhythm had no impact on the association between drug administration and survival. The time of drug administration (quartile of ACLS period) was associated with resuscitation for atropine (p < 0.05) and lidocaine (p < 0.01). The odds ratios (95% CIs) for successful resuscitation, after multivariate adjustment for potential confounders, were: a respiratory initiating cause, 3.7 (2.1 -6.4); each 5-minute increase in CPR-ACLS interval, 0.5 (0.4-0.7); each 5-minute duration of ACLS. 0.9 (()1.8- 1.0; atropine, 1.2 (1.0-1.3); bretylium. (0.4 (0.1-1.1); calcium 0.8 (0.2-2.4); lidocaine, 0.9 (0.7-1.1); procainamide. 21.0 (5.2-84.0) d sodium bicarbonate 1.2 (1.0-1.6). All other potential confounding variables entered into the model were not significantly associated with resuscitation. CONCLUSION: Initiating cause of arrest, time to ACLS, and duration of ACLS were important correlates of survival. Other than procainaimide, standard ACLS drugs had relatively little association with survival, but timing of administration may be an important factor. Further research using definitive large randomized controlled trials is warranted to assess the role of drug therapy in improving cardiac arrest survival. -------------------------------------------------------------- J Indian Med Assoc. 1999 Jul;97(7):259-64, 270. Current concepts in cardiopulmonary resuscitation in adults. Datta S, Nasr NF, Khorasani A, Datta R. Department of Anaesthesiology and Pain Management, Cook County Hospital, Chicago, USA. Cardiopulmonary resuscitation (CPR) provides artificial circulation and ventilation during cardiopulmonary arrest. CPR is further categorised as basic life support (BLS), advanced cardiac life support (ACLS) and postresuscitation support. BLS consists of provision of a patent upper airway, ventilation and circulation of blood by closed chest cardiac compressions. ACLS includes use of specialised equipment to maintain the airway, early defibrillation and pharmacologic therapy. Successful outcome from an arrest depends on the total duration of an arrest and early defibrillation, as ventricular fibrillation is the most common cardiac rhythm found in adult cardiac arrest. Initial drug therapy during CPR aims at correction of arterial hypoxaemia and restoring coronary and cerebral perfusion. Oxygen and epinephrine constitute the mainstay of drug therapy during CPR. In patients with ventricular tachycardia, lidocaine is the drug of choice, followed by bretylium. Magnesium has proved to be useful in both refractory pulseless ventricular tachycardia and fibrillation. Atropine has not been demonstrated to improve outcome from arrest but can be administered in bradyasystolic cardiac arrest. The routine administration of bicarbonate and calcium is no longer recommended but situations exist where they can be used appropriately. Administration of drugs during CPR should preferably be via a central route, but epinephrine, lidocaine and atropine can be administered via the endotracheal tube if intravenous access has not been established. Postresuscitation care includes mechanical ventilation if necessary to optimise oxygenation and ventilation and steps to maintain vital organ and optimal brain protection, which includes avoidance of hypertension, hypotension and hyperglycaemia. ____________________________________________ Nick Nudell, NREMT-P, CCEMT-P California nudell@... " Perception is reality " - Wise Old Paramedic RE: bicarb Nick: I am not sure where you get your medical facts, but may want to re-check them before posting to a list. 1. There are some codes where bicarb will help, although most simply require ventilation. 2. Dialysis patients with hyperkalemia need calcium (calcium gluconate, calcium chloride). All the other drugs are useless unless you lower the potassium. 3. How many people have cardiac arrests secondary to " acidosis " (except in patient restraint with excited delirium)? The remainder of which have acidosis secondary to other causes. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 31, 2003 Report Share Posted October 31, 2003 Nick, Have you found anything more recent? Granted, the studies seem to be very relevant, but it looks as if it is against current practice to continue CPR for any prolonged period of time. Is this a case of the medical community forgetting the science, or is it that there have been more relevant studies done? Or, am I way off base here? Thoughts? Schadone, NREMT-Paramedic City of Austin Austin/ County EMS Medic 12 / Medic 24 @... Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 31, 2003 Report Share Posted October 31, 2003 Mike I provided all that I could find/access. Some of the recent literature (under a couple years old) cannot be accessed in abstract or full-text files without paying for it, like $30 each. Keep in mind that termination of efforts should be considered when the case is futile. Known cases of hypothermia, hyperkalemia, electrocution etc should not be terminated until the conditions have been reversed, the conditions will not reverse or the available equipment/training has been fully utilized. That is the heart of the current recommendations. Peoplecicles in Montana have been successfully resuscitated, even after being pronounced twice in the field. This has not been published AFAIK. I do not have firsthand knowledge of the events. HyperK patients have spontaneously resuscitated even after 10 minutes after termination of efforts. (no this is not a Halloween joke). Pediatric primary cardiac arrest and electrocution are two cases that I can think of off the top of my head where underlying CAD would not be a predominant factor in the arrest and its possible that extended resuscitation might result in neurologically and systemically intact survivors. No I have not specifically done any recent lit searches on this... and cannot place my finger on where exactly I learned these points. Take care Nick ____________________________________________ Nick Nudell, NREMT-P, CCEMT-P California nudell@... " Perception is reality " - Wise Old Paramedic RE: bicarb Nick, Have you found anything more recent? Granted, the studies seem to be very relevant, but it looks as if it is against current practice to continue CPR for any prolonged period of time. Is this a case of the medical community forgetting the science, or is it that there have been more relevant studies done? Or, am I way off base here? Thoughts? Schadone, NREMT-Paramedic City of Austin Austin/ County EMS Medic 12 / Medic 24 @... Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 1, 2003 Report Share Posted November 1, 2003 You know I really shoud have looked over my my question befor I sent it out. Thats what I get for writting an email at 2 am I should have wrote the use of bicarb early in the code vrs. later in the code in the case of renal failure patients. When I was writting the question in my mind it sounded what I ment it to say NOT what it realy did say. So after putting egg all over my face I pose the correct question to the group , That will teach me not to send emails out when I am tired/ One of the answers I did recieve was this. Renal failure patients have a ph that acidotic on a normal bases. Normal for their condition that is. If a RF pt, did suffer cadiac arrest the use of bicarb early vrs. late would depend on how resent their last dialysis treatment was. One of the Md.s I asked said that if the pt. had not hafd a treatment in two or more days that indeed early bicarb maybe of an advantage. He also stated that there has not been a study done to determine this question one way or the other. The Doctors in questions or from St. Lukes and I asked them this when I was transporting them to Hobby Airport. Now that the correct question has been asked the post will make more sence to all who answered it. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 1, 2003 Report Share Posted November 1, 2003 Ok, for your specific question... I did not find any studies that said after X number of days since last dialysis you should use bicarb early. I agree that renal failure patients are likely to be in an acidotic state, if you find them arrested. This acidosis is a result of the hyperkalemic condition caused by the renal failure. If you do not correct the hyperkalemia, then all other treatments MAY be useless. In my previous post I had provided one case example of a patient who had been treated for acidosis primarily, and was resuscitated. I do not have access to the full case, so cannot be sure if treatments for hyperkalemia were given as well. So basically it will depend on your protocols.... you should start with your 'standard' ACLS meds (an exception possibly being a known dialysis patient), because without having an I-Stat or some other electrolyte measuring device on your ambulance, you cannot be certain if it is an electrolyte based arrest or a cardiac arrest due to AMI or arrhythmia (so says AHA). If these standard treatments do not work, then you would move on to other treatments, as per the current ACLS guidelines and depending on your protocols. You can often detect the hyperkalemia prior to arrest by a 12 lead EKG (I think I read about 20-25% will have signs, which include tall symmetrical peaked T waves and an IVCD or intraventricular conduction delay). The treatments for hyperkalemia include bicarb (2 or more amps plus a drip which is D5 1L with 3 amps bicarb added), insulin IVP(10u of regular), calcium (either gluconate or chloride which is preferred in arrests but is better given through central lines), 25g glucose (unless they are already hyperglycemic <like over 450-500>, then they will possibly be unable to reabsorb the potassium as one paper I referenced indicates), 25-50g of kayexelate (PO <via NG> or PR <via enema>), 10mg of albuterol in continuous neb or IV (salbutamol)(will bring the K+ level down about 0.5 which isn't much but will help). Then hemodialysis (might take 20-30 minutes of CPR during this to get an effect). Since insulin is not in most ambulance drug packs, and is a prime med for hyperkalemia, will your protocols allow you to administer a patients own insulin if found in a refrigerator in their house or from a dialysis clinic perhaps??? Just remember that these meds will take time to work, maybe something like half an hour, I have been told. The current research, as I already mentioned, indicate that epi and bicarb might be more beneficial in cardiac arrest patients if given prior to defibrillation, and that 2 minutes is the most optimal time to defibrillate. This was not a study specifically for hyperkalemia or dialysis. The bicarb in this case is thought to reduce cerebral acidosis, which is believed to be a prime factor in poor neurologic outcomes in the post-arrest patients. I am not an expert on the subject but I have transported many renal failure patients in the past leading me to become interested in the treatments they specifically require. I am interested in whether the scope in Texas allows you folks to be more aggressive with these patients then other states...?? Any comments regarding this info? Take care Nick ____________________________________________ Nick Nudell, NREMT-P, CCEMT-P California nudell@... " Perception is reality " - Wise Old Paramedic Re: bicarb You know I really shoud have looked over my my question befor I sent it out. Thats what I get for writting an email at 2 am I should have wrote the use of bicarb early in the code vrs. later in the code in the case of renal failure patients. When I was writting the question in my mind it sounded what I ment it to say NOT what it realy did say. So after putting egg all over my face I pose the correct question to the group , That will teach me not to send emails out when I am tired/ One of the answers I did recieve was this. Renal failure patients have a ph that acidotic on a normal bases. Normal for their condition that is. If a RF pt, did suffer cadiac arrest the use of bicarb early vrs. late would depend on how resent their last dialysis treatment was. One of the Md.s I asked said that if the pt. had not hafd a treatment in two or more days that indeed early bicarb maybe of an advantage. He also stated that there has not been a study done to determine this question one way or the other. The Doctors in questions or from St. Lukes and I asked them this when I was transporting them to Hobby Airport. Now that the correct question has been asked the post will make more sence to all who answered it. Quote Link to comment Share on other sites More sharing options...
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