European Resuscitation Council Guidelines for Resuscitation ... - CPR

that may be hazardous. In these patients, or if injected into a centralvein, reduce the initial dose of adenosine to 3 mg. In the presenceof WPW syndrome, blockage of conduction across the AV node byadenosine may promote conduction across an accessory pathway.In the presence of supraventricular arrhythmias this may cause adangerously rapid ventricular response. In the presence of WPWsyndrome, rarely, adenosine may precipitate atrial fibrillation associatedwith a dangerously rapid ventricular response.AmiodaroneIntravenous amiodarone has effects on sodium, potassium andcalcium channels as well as alpha- and beta-adrenergic blockingproperties. Indications for intravenous amiodarone include:• control of haemodynamically stable monomorphic VT, polymorphicVT and wide-complex tachycardia of uncertain origin;• paroxysmal SVT uncontrolled by adenosine, vagal manoeuvres orAV nodal blockade;• to control rapid ventricular rate due to accessory pathway conductionin pre-excited atrial arrhythmias;• unsuccessful electrical cardioversion.Give amiodarone, 300 mg intravenously, over 10–60 mindepending on the circumstances and haemodynamic stability ofthe patient. This loading dose is followed by an infusion of 900 mgover 24 h. Additional infusions of 150 mg can be repeated asnecessary for recurrent or resistant arrhythmias to a maximummanufacturer-recommended total daily dose of 2 g (this maximumlicensed dose varies between different countries). In patientswith severely impaired heart function, intravenous amiodarone ispreferable to other anti-arrhythmic drugs for atrial and ventriculararrhythmias. Major adverse effects from amiodarone are hypotensionand bradycardia, which can be prevented by slowing the rateof drug infusion. The hypotension associated with amiodarone iscaused by vasoactive solvents (Polysorbate 80 and benzyl alcohol).A new aqueous formulation of amiodarone does not contain thesesolvents and causes no more hypotension than lidocaine. 446 Wheneverpossible, intravenous amiodarone should be given via a centralvenous catheter; it causes thrombophlebitis when infused into aperipheral vein. In an emergency it can be injected into a largeperipheral vein.Calcium channel blockers: verapamil and diltiazemVerapamil and diltiazem are calcium channel blocking drugsthat slow conduction and increase refractoriness in the AV node.Intravenous diltiazem is not available in some countries. Theseactions may terminate re-entrant arrhythmias and control ventricularresponse rate in patients with a variety of atrial tachycardias.Indications include:• stable regular narrow-complex tachycardias uncontrolled orunconverted by adenosine or vagal manoeuvres;• to control ventricular rate in patients with AF or atrial flutter andpreserved ventricular function when the duration of the arrhythmiais less than 48 h.The initial dose of verapamil is 2.5–5 mg intravenously givenover 2 min. In the absence of a therapeutic response or druginducedadverse event, give repeated doses of 5–10 mg every15–30 min to a maximum of 20 mg. Verapamil should be given onlyto patients with narrow-complex paroxysmal SVT or arrhythmiasknown with certainty to be of supraventricular origin. The administrationof calcium channel blockers to a patient with ventriculartachycardia may cause cardiovascular collapse.18 de 0ctubre de 2010 www.elsuapdetodos.comC.D. Deakin et al. / Resuscitation 81 (2010) 1305–1352 1333Diltiazem at a dose of 250 gkg −1 , followed by a second dose of350 gkg −1 , is as effective as verapamil. Verapamil and, to a lesserextent, diltiazem may decrease myocardial contractility and criticallyreduce cardiac output in patients with severe LV dysfunction.For the reasons stated under adenosine (above), calcium channelblockers are considered harmful when given to patients with AF oratrial flutter associated with pre-excitation (WPW) syndrome.Beta-adrenergic blockersBeta-blocking drugs (atenolol, metoprolol, labetalol (alpha- andbeta-blocking effects), propranolol, esmolol) reduce the effects ofcirculating catecholamines and decrease heart rate and blood pressure.They also have cardioprotective effects for patients with acutecoronary syndromes. Beta-blockers are indicated for the followingtachycardias:• narrow-complex regular tachycardias uncontrolled by vagalmanoeuvres and adenosine in the patient with preserved ventricularfunction;• to control rate in AF and atrial flutter when ventricular functionis preserved.The intravenous dose of atenolol (beta 1 ) is 5 mg given over5 min, repeated if necessary after 10 min. Metoprolol (beta 1 )isgiven in doses of 2–5 mg at 5-min intervals to a total of 15 mg.Propranolol (beta 1 and beta 2 effects), 100 gkg −1 , is given slowlyin three equal doses at 2–3-min intervals.Intravenous esmolol is a short-acting (half-life of 2–9 min)beta 1 -selective beta-blocker. It is given as an intravenous loadingdose of 500 gkg −1 over 1 min, followed by an infusion of50–200 gkg −1 min −1 .Side effects of beta-blockade include bradycardia, AV conductiondelay and hypotension. Contraindications to the use ofbeta-adrenergic blocking drugs include second- or third-degreeheart block, hypotension, severe congestive heart failure and lungdisease associated with bronchospasm.MagnesiumMagnesium is the first line treatment for polymorphic ventriculartachycardia. It may also reduce ventricular rate in atrialfibrillation. 617,625–627 Give magnesium sulphate 2 g (8 mmol) over10 min. This can be repeated once if necessary.www.elsuapdetodos.com4h Post-resuscitation careIntroductionSuccessful ROSC is the just the first step toward the goal ofcomplete recovery from cardiac arrest. The complex pathophysiologicalprocesses that occur following whole body ischaemiaduring cardiac arrest and the subsequent reperfusion responsefollowing successful resuscitation have been termed the postcardiacarrest syndrome. 628 Many of these patients will requiremultiple organ support and the treatment they receive thispost-resuscitation period influences significantly the ultimate neurologicaloutcome. 184,629–633 The post-resuscitation phase startsat the location where ROSC is achieved but, once stabilised, thepatient is transferred to the most appropriate high-care area (e.g.,intensive care unit, coronary care unit) for continued monitoringand treatment. Of those patients admitted to intensive careunits after cardiac arrest, approximately 25–56% will survive tobe discharged from hospital depending on the system and qualityof care. 498,629,632,634–638 Of the patients that survive to hospital