Cardiology ACLS (and PALS) =============== þ 2010-2011 update, BCLS/Initial Actions: - Check for responsiveness and absent or agonal breaths, call for help, call for AED, start CPR - CPR Depth: 2" for adults and kids, 1.5" for infants - Single-rescuer: 30:2 ratio (same), 15:2 with two rescuers - NOT ABC, but CAB - do 30 compressions first - Ventilation: 8-10/min, one breath Q 6-8 seconds - NO cricoid pressure - Healthcare Professional: + OK to do 10 sec pulse check (healthcare professional only, not for public) + Can do brief check for respirations - EMS with AED: 10 sec check þ 2010-11 update, Drug Changes - PEA/Asystole: no atropine (OK for bradycardia) - PEA/Asystole same for PALS and ACLS - Adenosine: + OK for monomorphic wide complex tachycardia (> 0.09 seconds) + NO for polymorphic - Epi and Vasopressin: + Epi OR Vasopressin 40 units for 1st and 2nd doses - Bradycardia: + Atropine 0.5 mg up to 3 mg total + Dopamine: 2-10 mcg/min + Epi: 2-10 mcg/min + keep sats 94%-99% (not 100% in infants: hyperoxia is bad) - Calcium: deprecated, unless + hypocalcemia + calcium channel blocker OD + hypermagnesemia + hyperkalemia þ 2010-11 update: electricity - Single Shock then long CPR rather than stacked shocks - SVT: regular: 50100 J, irregular 120-200 J - May do precordial thump but only for witnessed V Tach (useless for VF) - Kids: 2-4 (-9) J/kg - AP or Ant/Lat OK for pacer/AICD þ 2010-11 update: dead - if prehospital BLS, and + unwitnessed by BLS or first responder + no ROSC (return of spontaneously circulation) after three rounds of CPR and AED analyses + no AED shock advised - if prehospital ALS, and + unwitnessed + no CPR done prior to ALS arrival + no ROSC after ACLS þ 2010-11 recommendations, PALS specific - If congenital heart disease such as single ventricle, consider transfer for early ECMO. (extracorporeal membrane oxygenation) - Channelopathies: may be in relatives so good reason for autopsy. - Neonatal: + Still ABC, not CAB (unless known to be cardiac) + still 3:1 compression/ventilation ratio (15:2 for cardiac) + (primarily ashpyxial) + no 100% oxygen + can take 10 minutes to get sats from 60% to >90%; that's OK, it's normal + use R wrist or palm for pulse oximiter + suction only if needed, or ET suction (still) if meconium-stained + delay cord clamping for a minute, at least for healthy-born babies (unclear if needed for those requiring resuscitation) + newborn with no heart rate for 10 minutes despite resuscitation: consider calling the code. þ Ventilation - Excess ventilation, common in prehospital CPR, is bad: increased intrathoracic pressure, decreased survival. - Average 30 breaths/minute, each lasting 1 second (WAY too much) [Aufderhide T. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation 2004;109(April 27):1960-1965.] - After trauma, even normal ventilation rates are bad; lower respiratory rates are better. [Pepe P. Emergency ventilatory management in hemorrhagic states: Elemental or detrimental? J Trauma 2003;54:1048-1057.] - 100:2 chest compression-ventilation ratio had better neurological outcome. [Sanders A. Survival and neurologic outcome after cardiopulmonary resuscitation with four different chest compression-ventilation ratios. Ann Emerg Med 2002;40:553-562.] þ Aminophyline for Asystole - University of British Columbia Study SAEM 2004 - 250 or 500 mg aminophylline given to those in asystole after full treatment with epi/atropine without ROSC. - slight increase in ROSC but not statistically significant; no impact on survival but study didn't have power to show. - Didn't look at giving aminophylline first. - Adenosine produced in cardiac arrest, thought to be deleterious; aminophylline may block. [Riyad B. Aminophylline in bradyasystolic arrest: A randomized placebo-controlled trial. AEM 2004:11(5):435] þ Vasopressin - IIb per AHA: 1997 + study, but 44 physician-staffed units randomized to vasopressin vs. epinephrine: better for asystole (? worse for other groups) but only in subgroup analysis. 40% more likely to reach hospital alive, 8 more survivors to discharge, but not neurologically intact, 8 were vegetative, though none with epi were vegetative. Editorial by MD/JD internist @ Boston VA says "make into a new standard." ?!?! Similar to high-dose epi. þ Defibrillation þ Amiodarone for V.Fib arrest þ Which is best, femoral or subclavian? þ How big of an IV flush do you need during CPR? þ Cough CPR variant: - "I once saw a cardiologist in the ED talking to a patient who brady-> asystolic arrested whilst talking to him (the patient arrested that is). The cadiologist got him to cough with good effect till the defib was a bit closer, the patient stopped to question why he was suddenly asked to cough all the time on command and promptly passed out. The cardiologist then rhymically tapped the sternum with his fist as per precordial thumps and this was effective enough to enduce an ECG output and a radial pulse with each blow. Successful resus in the end after the usual stuff. Dr Garry Wilkes MBBS FACEM Department of Emergency Medicine Royal Brisbane Hospital Queensland, Australia Email G.Wilkes@mailbox.uq.edu.au" þ When to quit CPR: þ Neurological survival vs. CPR times: þ Are endotracheal intubation and positive pressure ventilation needed? þ Drugs down ET tube þ Does Valium work via ET tube? See also about IM midazolam for seizures - A number of years ago an animal study confirmed that, although ET diazepam was well absorbed, it had toxic pulmonary effects. An option, when IV access is not available, is the use of rectal diazepam particulary in children (2). Currently, I beleive that most physicians with experience in this area, find that IV lorazepam is more effective and has the advantage of a much longer half-life. There is some anectodal experience with the use of rectal lorazepam as well (3)." --H. Louzon MD (1) Rusli M, Spivey WH, Bonner H, McNamara RM, Aaron CK, Lathers CM Endotracheal diazepam: absorption and pulmonary pathologic effects. Ann Emerg Med 1987 Mar;16(3):314-8 We conducted a study to evaluate the absorption of endotracheally administered diazepam and the pulmonary pathologic changes induced by its administration. Six cats received diazepam and five cats received saline endotracheally. Serial blood gases and serum diazepam levels were drawn at intervals for 90 minutes after the administration of diazepam. The cats were sacrificed after two days and their lungs were examined by a pathologist. Mean diazepam levels reached a peak two minutes after the administration of diazepam and remained elevated above therapeutic levels for 90 minutes. There was no significant change in pH, PO2, or PCO2 for either group. Histologic examination of the lungs showed a significantly increased incidence of pneumonitis in the diazepam group as compared to the saline group. This study demonstrates that although diazepam is well absorbed when administered endotracheally, it has adverse effects on the lungs that may preclude endotracheal use in the currently available commercial form. (2) Dieckmann RA Rectal diazepam for prehospital pediatric status epilepticus. Ann Emerg Med 1994 Feb;23(2):216-24 STUDY OBJECTIVES: To compare the feasibility, effectiveness, and safety of rectal diazepam and intravenous diazepam in the treatment of pediatric prehospital status epilepticus. DESIGN AND SETTING: Retrospective analysis of a 30-month consecutive sample of ambulance-transported children in a large urban emergency medical service region. TYPE OF PARTICIPANTS: Study group included 324 patients with seizure who were less than 18 years of age; 36 had status epilepticus, of whom 16 received rectal diazepam and 15 received IV diazepam. INTERVENTIONS: For children with status epilepticus, paramedics administered the 5-mg/mL IV solution of diazepam by one of two routes: rectally either through a 5F feeding tube with an attached syringe or by lubricated tuberculin syringe inserted 4 to 5 cm into the rectum at a one-time dose of 0.2 to 0.5 mg/kg or intravenously using a one-time dose of 0.1 to 0.3 mg/kg. Cardiopulmonary status was carefully monitored in the field and emergency department. MEASUREMENTS AND MAIN RESULTS: Thirteen of 16 children (81%) who received rectal diazepam stopped seizing after a single dose ranging from 0.16 to 0.57 mg/kg. Convulsions recurred before arrival at the ED in four of the 13 (30.8%). All of three patients who did not respond to rectal diazepam initially were 3 to 5 years old and had serious underlying comorbidity; two required endotracheal intubation in the ED and multiple anticonvulsants to terminate the seizure. No child treated with rectal diazepam required prehospital endotracheal intubation. All children who received IV diazepam stopped seizing after one dose ranging from 0.04 to 0.33 mg/kg. Convulsions recurred before arrival at the ED in nine of 15 children (60%); two required prehospital endotracheal intubation for profound respiratory depression. CONCLUSION: Rectal diazepam is a simple, effective, and safe method of prehospital management of pediatric status epilepticus. Compared with IV diazepam, rectal diazepam is easier to administer, especially in infants and toddlers; is equally efficacious; and is less likely to produce respiratory depression. Although respiratory depression is rare with rectal diazepam, prehospital personnel must be prepared to provide definitive respiratory support. Short duration of action is an important limitation of both treatments. (3) Appleton R, Sweeney A, Choonara I, Robson J, Molyneux E Lorazepam versus diazepam in the acute treatment of epileptic seizures and status epilepticus. Dev Med Child Neurol 1995 Aug;37(8):682-8 Lorazepam was compared with diazepam for the treatment of acute convulsions and status epilepticus in 102 children in a prospective, open, 'odd and even dates' trial. Convulsions were controlled in 76 per cent of patients treated with a single dose of lorazepam and 51 per cent of patients treated with a single dose of diazepam. Significantly fewer patients treated with lorazepam required additional anticonvulsants to terminate the seizure. Respiratory depression occurred in 3 per cent of lorazepam-treated patients and 15 per cent of diazepam-treated patients. No patient who received lorazepam required admission to the intensive care unit for either respiratory depression or persisting status epilepticus. Rectally administered lorazepam appeared to be particularly valuable (100 per cent efficacy) when venous access was not possible. --------------------- If one has to given an anticonvulsant ET, midazolam would be a better choice than diazepam. It's in an aqueous vehicle, and should cause little or no pulmonary damage. It has been also reported to be almost miraculously (!) effective in terminating status when other benzo's fail. I'm away from my cache of articles at the moment, but if anyone is interested, I can post a reference for this. -J Schoffstall, M.D. þ VF þ Asystole AHA algorithm for "stable wide QRS tachycardia of ?? etiology" is: L = lidocaine A = adenosine P = procainamide B = bretylium S = shock Harvey Louzon's comments on wide-complex tachycardia: þ EMD = PEA global ischemia mimickers tension PTX tamponade Massive PE hypovolemia þ "Cosmic Classification" - Predictable Sick enough to die Getting worse despite the best you can do. Question "If your best therapy was ineffective while the patient was alive, why will it work better after he is dead?" "If a patient person who is nearly dead arrests and you resuscitate him, isn't he still nearly dead?" (asystole and EMD) - Unpredictable (but not unexpected) Most primary arrhythmias (Massive PE) (Myocardial rupture) (VF) þ Recurrent VF: try decreasing energy, antiarrhythmics þ Refractory VF: try increasing energy, perfusing myocardium megadose epi is 1,2,5 mg - if young, may be catecholamine storm from cocaine: try inderal 1 mg q 1' in between defibrillation. - may try magnesium 2g - try amiodarone þ Catecholamines definitely increase myocardial and brain blood flow in CPR. þ Epinephrine shows better survival than pure alpha agents. þ Lidocaine vs. Bretylium: both increase VF threshold. But, dog studies: defibrillation threshold increased by BOTH! Haynes R, et al Amer J Cardiol 1981 (no control): no difference between the two for defibrillation. In the study from from the Annals of Internal Medicine 1989 (4), that I reviewed, all of the patients who repsonded to amiodarone did indeed have recurrent, as opposed to, incessant v-fib. All of them had brief periods of perfusing rhythms related to the use of conventional treatment prior to it's administration. Two case reports, however, descibed patients with unrelenting v-fib. Both were from the Br Med J. In one (1) (massive digoxin overdose) v-fib unresponsive to epi, lidocaine and countershock. Amiodarone was administered 50 minutes into the resusitation attempt and he was sucessfully defibrillated 10 minutes later. The second case (2) was a postoperative patient who went into v-fib unresponsive to lidocaine, disopyramide (! no wonder they couldn't convert him) and 15 (!) defibrillation attempts over a period of 75 minutes. Three minutes after administration of amiodarone he was sucessfully converted with 400 j. What is one to make of case reports like this? Probably very little. Unless it is that "Acts of God" do appear to happen and physician's sometimes take the credit for it. I recall the initial enthusiasm over the use of bretyllium when it first came out. There was talk about "chemical defibrillation". After more sober reflection (read controlled studies), no advantage in comparison to the use of lidocaine could be consistantly demonstrated. If amiodarone turns out to be only useful in cases where rythyms (perfusing or otherwise) are transiently restored please consider that this would not necessarily be a bad thing. After all, lidocaine increases the DEfibrillation thresh- hold at the same time that it increases the fibrillation thresh-hold. Thus it probably makes defibrillation MORE difficult than it otherwise would be. As the ERC summary stated "...adjunctive administration of lidocaine to patients in ventricular fibrillation may indeed hinder successful defibrillation" (3). H. Louzon MD (1) Massive Digoxin Overdose: Successful Treatment with Intravenous Amiodarone. Maheswaran et. al. Br Med J 1983 287:392-393 (2) Intravenous Amiodarone in Ventricular Fibrillation. Chapman et. al. Br Med J 1981 282:951-952 (3) Drug Treatment of Arrhythmias During Cardiopulmonary Resusitation: A Statement of the Advanced Life Support Working Party of the European Resusitation Council. Resusitation 24 (1992) 227-232 (4) Intravenous Amiodarone During Prolonged Resusitation from Cardiac Arrest. Williams et. al. Ann Int Med 1989;11:839-842 POSTCOUNTERSHOCK PULSELESS RHYTHMS: HEMODYNAMIC EFFECTS OF GLUCAGON IN A CANINE MODEL Niemann, J.T., et al, Crit Care Med 15(6):554, June 1987. ---------------------- The evidence appears to show that endotracheal adrenaline is probably inneffective in cardiac arrest. Studies 1-3 shown below all suggest that ET adrenaline is unlikely to be effective in arrested patients. It must be remembered that even in cardiac arrest with good BLS, cardiac output is only likely to be 30% of normal, therefore the effects seen at the doses given in papers 1-3 (all with spontaneous circulation) are likely to be less in arrest. However, studies in anaesthetised patients are potentially compounded by the effect of the anaesthetic agents themselves. I have read other studies that show that adrenaline does not reach the systemic circulation during cardiac arrest but I am unable to find the references on healthgate. Simon Carley Clinical Fellow Department of Emergency Medicine Manchester Royal Infirmary Manchester England 1. Haemodynamic effects of tracheally administered adrenaline in anaesthetised patients. Kestin IG; McCrirrick AB Anaesthesia, 1995 Jun, 50:6, 514-7 Abstract Ten patients undergoing arterial surgery in the leg received a combined general anaesthetic, which included muscle relaxation and intubation of the trachea, and a regional anaesthetic using a lumbar extradural catheter. The radial arterial pressure was measured. Adrenaline 0.1 micrograms.kg-1 was administered intravenously and the heart rate, arterial pressure and oxygen saturation were recorded every 15 s for 10 min. Adrenaline in 5 ml of saline was given into the trachea at 10 min intervals. The first was saline only, and successive injections contained 0.5 micrograms.kg-1, 1 microgram.kg-1, 2 micrograms.kg-1, and 3 micrograms.kg-1 of adrenaline. The mean maximum rise in systolic arterial pressure after adrenaline given intravenously was 30 (SD 11) mmHg, and 15 (SD 16) mmHg after the maximum dose of adrenaline given into the trachea (p < 0.05). The mean systolic arterial pressure was significantly increased between 45 s and 4.5 min after the adrenaline given intravenously, and 2 min after adrenaline given into the trachea. Of seven patients who received adrenaline 3 micrograms.kg-1 into the trachea, six had no noticeable effect and in the other patient, the increase in arterial pressure was less than 90% of the maximum rise after the adrenaline. We conclude that adrenaline given into the trachea is unreliable in humans with very large doses necessary in some patients to produce a clinically useful haemodynamic effect. 2. Comparison of i.v. and intra-tracheal administration of adrenaline [see comments] McCrirrick A; Monk CR Br J Anaesth, 1994 May, 72:5, 529-32 Abstract Adrenaline is the single most important therapeutic agent used in advanced cardiac life support (ACLS). Ideally it should be given into a large central vein but the European Resuscitation Council, the American Heart Association and the Resuscitation Council (U.K.) advise that adrenaline may be given into the trachea if i.v. access is not available. We have studied the effects of intra-tracheal and i.v. adrenaline in 16 patients undergoing mechanical ventilation. Log dose-response curves were constructed for systolic arterial pressure and heart rate responses. Intra-tracheal doses of adrenaline up to 10 micrograms kg-1, approximately one-third of that recommended for resuscitation, had no effect on arterial pressure or heart rate, whereas adrenaline 0.1 microgram kg-1 i.v. produced a mean increase in systolic pressure of 24 mm Hg. The intra-tracheal doses recommended for resuscitation (2-3 mg) are likely to be ineffective and consideration should be given to abandoning the tracheal route for adrenaline in ACLS. 3. Haemodynamic effects of tracheal compared with intravenous adrenaline [see comments] McCrirrick A; Kestin I Lancet, 1992 Oct 10, 340:8824, 868-70 Abstract If intravenous access is not available during cardiopulmonary resuscitation, tracheal administration of adrenaline 0.02 mg/kg, twice the intravenous dose, is recommended. In a randomised crossover study we investigated the haemodynamic effects of low doses of tracheal versus intravenous adrenaline. 12 anaesthetised patients having a hip replaced received one dose of adrenaline intravenously (0.1 microgram/kg) and the other tracheally (0.5 microgram/kg). There was a mean increase in systolic arterial pressure of 40.5 mm Hg (range 16-81) after the intravenous injection, with little effect on heart rate. Tracheal adrenaline had no effect on arterial pressure or heart rate. Thus low doses of tracheal adrenaline have no haemodynamic effects. We believe that the recommended tracheal dose of twice the intravenous dose is likely to be ineffective for the treatment of cardiac arrest. Animal studies suggest that a tracheal dose at least ten times the intravenous dose is required. Unique Identifier 91144181 Authors Crespo SG. Schoffstall JM. Fuhs LR. Spivey WH. Institution Department of Emergency Medicine, Medical College of Pennsylvania, Philadelphia 19129. Title Comparison of two doses of endotracheal epinephrine in a cardiac arrest model. Source Annals of Emergency Medicine. 20(3):230-4, 1991 Mar. Local Messages Currently received at CC + MOORE Abstract STUDY OBJECTIVE: The objective of this study was to measure plasma catecholamine levels and the cardiovascular response before and after endotracheal administration of epinephrine in a swine cardiac arrest model. DESIGN: Prospective, controlled laboratory investigation. TYPE OF PARTICIPANTS: Twenty-one swine weighing 10 to 12 kg, anesthetized with ketamine and alpha-chloralose and ventilated with room air. INTERVENTIONS: Ventricular fibrillation was induced with 90 V of 60 Hz current delivered to the right ventricle by transvenous pacemaker. Blood samples for epinephrine were drawn before arrest and every two minutes thereafter. At five minutes, external mechanical cardiac compressions were initiated. Nine animals received no further therapy and served as controls. Two groups of six animals received either 0.01 mg/kg or 0.1 mg/kg of epinephrine through the endotracheal tube at ten and 20 minutes. Blood samples were assayed for epinephrine. MEASUREMENTS: Arterial blood pressure, lead II ECG, and plasma epinephrine. MAIN RESULTS: Swine receiving epinephrine 0.01 mg/kg had an increase in epinephrine levels after drug administration, but these were not significantly different from control levels. The 0.1-mg/kg dose group had a significant increase in plasma epinephrine levels compared with controls and the 0.01-mg/kg dose group after receiving epinephrine at ten and 20 minutes. These increases were from 14 +/- 3 to 215 +/- 40 ng/mL (+/- SEM) at 12 minutes after arrest and from 151 +/- 56 to 402 +/- 80 ng/mL at 22 minutes after arrest. CONCLUSION: These data suggest that standard dosing of epinephrine through the endotracheal tube during arrest does not produce significant increases in plasma catecholamines or blood pressure. Epinephrine 0.1 mg/kg produces a significant increase in plasma epinephrine levels, but it is not sufficient to produce a significant change in blood pressure. Registry Numbers 51-43-4 (Epinephrine). Authors Ralston SH. Tacker WA. Showen L. Carter A. Babbs CF. Title Endotracheal versus intravenous epinephrine during electromechanical dissociation with CPR in dogs. Source Annals of Emergency Medicine. 14(11):1044-8, 1985 Nov. Local Messages Currently received at CC + MOORE Abstract The dose-response curves of epinephrine given either IV or endotracheally (ET) were compared during resuscitation from electromechanical dissociation (EMD). Ten anesthetized dogs were subjected to a two-minute period of electrically induced ventricular fibrillation (VF) followed by defibrillation without CPR to produce EMD. Mechanical CPR was followed by injection of either ET or IV epinephrine. Successful response was defined as a return of pulsatile blood pressure within two minutes of drug administration. Using log-dose increments of epinephrine, experimental trials were repeated in each animal. The IV and ET median effective doses were 14 and 130 micrograms/kg, respectively. When the trials were successful, the time between drug administration and either arterial blood pressure increases or return of spontaneous circulation did not differ significantly for the ET and IV groups. These results show that the dosage for epinephrine delivered ET must be higher than the IV dosage to achieve the same response during CPR.