Msurile terapeutice avansate de resuscitare (ALS)

Sudden cardiac arrest (SCA) is a leading cause of death in Europe, affecting about 700,000 individuals a year. At the time of the first heart rhythm analysis, about 40% of SCA victims have ventricular fibrillation (VF). It is likely that many more victims have VF or rapid ventricular tachycardia (VT) at the time of collapse but, by the time the first ECG is recorded, their rhythm has deteriorated to asystole. Many victims of SCA can survive if bystanders act immediately while VF is still present, but successful resuscitation is unlikely once the rhythm has deteriorated to asystole. The optimum treatment for VF cardiac arrest is immediate bystander CPR (combined chest compression and rescue breathing) plus electrical defibrillation. The predominant mechanism of cardiac arrest in victims of trauma, drug overdose, drowning, and in many children is asphyxia; rescue breaths are critical for resuscitation of these victims.For victims of witnessed VF arrest, prompt bystander CPR and early defibrillation can significantly increase the chance for survival to hospital discharge. In comparison, typical ACLS therapies, such as insertion of advanced airways and pharmacologic support of the circulation, have not been shown to increase rate of survival to hospital dischargeBasic life support (BLS) refers to maintaining airway patency and supporting breathing and the circulation, without the use of equipment other than a protective device.

CuprinsIntroducereDefibrilareaAsigurarea unui abord venosControlul cailor aerieneAlgoritm terapeutic in cazul FV/TV fara pulsAlgoritm terapeutic in cazul asistolei/disociatiei electromecaniceEtapa post-resuscitare

Access for Medications: Correct PrioritiesDuring cardiac arrest, basic CPR and early defibrillation are of primary importance, and drug administration is of secondary importance. Few drugs used in the treatment of cardiac arrest are supported by strong evidence. After beginning CPR and attempting defibrillation, rescuers can establish intravenous (IV) access, consider drug therapy, and insert an advanced airway.Cardiopulmonary arrest is usually the result of a cardiac dysrhythmia. The majority of adults (80% to 90%) with sudden, nontraumatic cardiac arrest are found to be in ventricular tachycardia (VT) when an initial electrocardiographic rhythm strip is obtained. When ventricular fibrillation (VF) occurs outside the hospital, it most commonly results from chronic myocardial ischemia with electrical instability, rather than acute myocardial infarction.Conversely, in-hospital cardiac arrest most often follows an acute myocardial infarction or is the result of severe multisystem disease; asystole, bradydysrhythmias,and pulseless electrical activity are the usual rhythms encountered in hospitalized patients.

Introducere1/3 din pacienii la care apare IMA decedeaz in etapa pre-spital, n prima or de la debutul simptomelor, ritmul cardiac fiind FV/TV fr puls defibrilarea electric precoce20% din pacientii cu stop cardiac in spital supravietuiesc si pot fi externati prevenirea aparitiei stopuluiIdentificarea si tratamentul eficient al factorilor precipitanti (hipoxia, hipotensiunea)

Sudden cardiac arrest is responsible for more than 60% of adult deaths from coronary heart disease.In Europe, the annual incidence of resuscitation for out-of-hospital cardiopulmonary arrest of cardiac aetiology is 49.566 per 100,000 populationFewer than 20% of patients suffering an in-hospital cardiac arrest will survive to go home. Most survivors have a witnessed and monitored VF arrest, primary myocardial ischaemia as the cause, and receive immediate defibrillation, These patients often have slow and progressive physiological deterioration, involving hypoxia and hypotension, that is unnoticed by staff, or is recognised but poorly treated.3,4 The underlying cardiac arrest rhythm in this group is usually non-shockable and survival to hospital discharge is very poor.Rescuers begin CPR if the victim is unconscious or unresponsive, and not breathing normally (ignoring occasional gasps). A single compressionventilation (CV) ratio of 30:2 is used for the single rescuer of an adult or child (excluding neonates) out of hospital, and for all adult CPR. This single ratio is designed to simplify teaching, promote skill retention, increase the number of compressions given and decrease interruption to compressions. Once a defibrillator is attached, if a shockable rhythm is confirmed, a single shock is delivered. Irrespective of the resultant rhythm, chest compressions and ventilations (2 min with a CV ratio of 30:2) are resumed immediately after the shock to minimise the no-flow time. Advanced life support interventions are outlined in a box at the centre of the ALS algorithm (see Section 4). Once the airway is secured with a tracheal tube, laryngeal mask airway (LMA) or Combitube, the lungs are ventilated at a rate of 10 min1 without pausing during chest compressions.

Chain of Survival.Travers A H et al. Circulation 2010;122:S676-S684Copyright American Heart AssociationChain of survival

Chain of Survival. The links in this Chain are: Immediate recognition and activation, early CPR, rapid defibrillation, effective advanced life support and integrated post-cardiac arrest care.The actions linking the victim of sudden cardiac arrest with survival are called the Chain of Survival. They include early recognition of the emergency and activation of the emergency services, early CPR, early defibrillation and early advanced life support.The importance of recognising critical illness and/or angina and preventing cardiac arrest (in- or out-of-hospital), and post resuscitation care has been highlighted by the inclusion ofthese elements in a new four-ring Chain of Survival The central links in this new chain depict the integration of CPR and defibrillation as the fundamental components of early resuscitation in an attempt to restore life The following concept of the Chain of Survival summarises the vital steps needed for successful resuscitation (Figure 1.1). Most of these links are relevant for victims of both VF and asphyxial arrest.Early recognition of the emergency and calling for help: activate the emergency medical services (EMS) or local emergency response system, e.g. phone 112.12,13 An early, effective response may prevent cardiac arrest. Early bystander CPR: immediate CPR can double or triple survival from VF SCA Early defibrillation: CPR plus defibrillation within 35 min of collapse can produce survival rates as high as 4975%. Each minute of delay in defibrillation reduces the probability of survival to discharge by 1015%.Early advanced life support and postresuscitation care: the quality of treatment during the post-resuscitation phase affects outcome

Building Blocks of CPR.Travers A H et al. Circulation 2010;122:S676-S684Copyright American Heart Association

Building Blocks of CPR.

The actions linking the victim of sudden cardiac arrest with survival are called the Chain of Survival. They include early recognition of the emergency and activation of the emergency services, early CPR, early defibrillation and early advanced life support.The importance of recognising critical illness and/or angina and preventing cardiac arrest (in- or out-of-hospital), and post resuscitation care has been highlighted by the inclusion ofthese elements in a new four-ring Chain of Survival The central links in this new chain depict the integration of CPR and defibrillation as the fundamental components of early resuscitation in an attempt to restore life The following concept of the Chain of Survival summarises the vital steps needed for successful resuscitation (Figure 1.1). Most of these links are relevant for victims of both VF and asphyxial arrest.Early recognition of the emergency and calling for help: activate the emergency medical services (EMS) or local emergency response system, e.g. phone 112.12,13 An early, effective response may prevent cardiac arrest. Early bystander CPR: immediate CPR can double or triple survival from VF SCA Early defibrillation: CPR plus defibrillation within 35 min of collapse can produce survival rates as high as 4975%. Each minute of delay in defibrillation reduces the probability of survival to discharge by 1015%.Early advanced life support and postresuscitation care: the quality of treatment during the post-resuscitation phase affects outcome

Echipament necesar monitor/defibrilatorO2 Aspirator pt. secretiiechipament de asigurare invaziva a caii aeriene: laringoscop, sonde de intubatie, pipa, balon Reuben, ventilator, etc.Medicamente: vasopresoare, antiaritmice, etc

Algoritmul terapeutic in ALSRitm cardiac la care se poate utiliza defibrilarea electrica = FV/TV fara pulsRitm cardiac la care nu se poate utiliza defibrilarea electrica = asistola/DEMEtape comune: compresia toracica, controlul cailor aeriene, calea venoasa, adm. de droguri, identificarea si corectarea factorilor reversibili

Interventii terapeutice ce duc la cresterea supravietuirii dupa stop cardiac: Defibrilarea precoce in FV/TV fara pulsBLS eficient

Defibrillation requires the delivery of sufficient electrical energy to defibrillate a critical mass of myocardium, abolish the wavefronts of VF and enable restoration of spontaneous synchronised electrical activity in the form of an organised rhythm. The optimal energy for defibrillation is that which achieves defibrillation while causing the minimum of myocardial damage.Monophasic defibrillators deliver current that is unipolar (i.e., one direction of current flow).Biphasic defibrillators, in contrast, deliver current that flows in a positive direction for a specified duration before reversing and flowing in a negative direction for the remaining milliseconds of the electrical discharge. Biphasic defibrillators compensate for the wide variations in transthoracic impedance by electronically adjusting the waveform magnitude and duration.

The most critical interventions during the first minutes of VF or pulseless VT are immediate bystander CPR (Box 1) with minimal interruption in chest compressions and defibrillation as soon as it can be accomplished (Class I). In cases of witnessed arrest with a defibrillator on-site, after delivery of 2 rescue breaths the healthcare provider should check for a pulse. If the provider definitely does not feel a pulse within 10 seconds, the provider should turn on the defibrillator, place adhesive pads or paddles, and check the rhythm (Box 2). If the healthcare provider does not witness the arrest in the out-of-hospital setting (eg, the emergency medical services [EMS] provider arrives at the scene of an arrest), the provider may give 5 cycles of CPR before attempting defibrillation. In adults with a prolonged arrest, shock delivery may be more successful after a period of effective chest compressions.

The most critical interventions during the first minutes of VF or pulseless VT are immediate bystander CPR (Box 1) with minimal interruption in chest compressions and defibrillation as soon as it can be accomplished (Class I). In cases of witnessed arrest with a defibrillator on-site, after delivery of 2 rescue breaths the healthcare provider should check for a pulse. If the provider definitely does not feel a pulse within 10 seconds, the provider should turn on the defibrillator, place adhesive pads or paddles, and check the rhythm (Box 2). If the healthcare provider does not witness the arrest in the out-of-hospital setting (eg, the emergency medical services [EMS] provider arrives at the scene of an arrest), the provider may give 5 cycles of CPR before attempting defibrillation. In adults with a prolonged arrest, shock delivery may be more successful after a period of effective chest compressions.*

Defibrilarea electrica-FV/TV fara puls Pozitie padele: marginea dreapta a sternului, sub clavicula sp.V ic pe stg.Confirmarea VT/TV, soc electric: 360 J defibrilator monofazic150-200 defibrilator bifazicRCP 2 min (30:2), apoi verifica ritmulDaca tot FV/VT, al 2-lea soc el. de 360JRCP 2 min. (30:2), verifica ritmul-pulsulDaca tot FV/VT, Adrenalina + al 3-lea soc el. de 360J + RCP 2 min, verifica ritmul-pulsulDaca tot FV/VT, bolus de Amiodarona 300 mg + RCP

the recommended initial energy level for the first shock using a monophasic defibrillator is 360 J. Although higher energy levels risk a greater degree of myocardial injury, the benefits of earlier conversion to a perfusing rhythm are paramount.

Lovitura precordialase foloseste doar de personal medical cu experienta (la a sternului)n contextul unui stop cardiac observat de martori sau pacient monitorizat, chiar nainte de montarea defibrilatoruluipoate converti VT la RSinutil atunci cnd este aplicat la peste 30 secunde de la debutul stopului cardiac.

The rationale for giving a thump is that the mechanical energy of the thump is converted to electrical energy, which may be sufficient to achieve cardioversion. in all the reported successful cases, the precordial thump was given within the first 10 s of VFConsider giving a single precordial thump when cardiac arrest is confirmed rapidly after a witnessed, sudden collapse and a defibrillator is not immediately to hand.Using the ulnar edge of a tightly clenched fist, a sharp impact is delivered to the lower half of the sternum from a height of about 20 cm, followed by immediate retraction of the fist, which creates an impulse-like stimulus.

Asigurarea unui abord venos Vena periferica vs. vena centralaAbord periferic: rapid, usor de efectuat, sigurnecesita 10-20 ml SF suplimentar dupa adm. medicamente + ridicare membru

Abord central:efect rapid al medicatiei administrateabilitati specifice, trebuie oprita RCP, prezinta complicatii

Cai alternative: intraosos, pe sonda IOT

If IV access has not been established, the provider should insert a large peripheral venous catheter. Although in adults peak drug concentrations are lower and circulation times longer when drugs are administered via peripheral sites rather than central sites, the establishment of peripheral access does not require interruption of CPR. Drugs typically require 1 to 2 minutes to reach the central circulation when given via a peripheral vein but require less time when given via central venous access.If a resuscitation drug is administered by a peripheral venous route, administer the drug by bolus injection and follow with a 20-mL bolus of IV fluid. Elevate the extremity for 10 to 20 seconds to facilitate drug delivery to the central circulation.Establish IV access with a saline lock on all appropriate medical and traumatic emergencies External Jugular access is acceptable in critical patients when other access is not available or the time to find other access would jeopardize patient outcome.Intraosseous (IO) cannulation provides access to a noncollapsible venous plexus, enabling drug delivery similar to that achieved by central venous access. IO access is safe andeffective for fluid resuscitation, drug delivery, and blood sampling for laboratory evaluation, and is attainable in all age groups. Providers may establish IO access if IV access isunavailable (Class IIa). Commercially available kits can facilitate IO access in adults.If IV and IO access cannot be established, some resuscitation drugs may be administered by the endotracheal route: lidocaine, epinephrine, atropine, naloxone, and vasopressin are absorbed via the trachea. The optimal endotracheal dose of most drugs is unknown, but typically the dose given by the endotracheal route is 2 to 212 times the recommended IV dose. Providers should dilute the recommended dose in 5 to 10 mL of water or normal saline and inject the drug directly into the endotracheal tube

Abordul intraosos

*

Controlul cailor aerieneIntubaia orotraheal metoda optim ce asigur permeabilitatea cii aeriene i permite instituirea ventilaiei artificialetrebuie facut de catre un personal medical experimentatSe pot aspira pe sonda traheal diverse secreii/materiale strine ajunse in arborele bronic distalpe sonda traheal pot fi administrate diverse medicamente (n lipsa unui abord venos).

Controlul cailor aerieneManevra IOT nu trebuie sa dureze mai mult de 30 secdupa IOT, continua compresia toracica 100/min si ventileaza cu 10 resp./minCai alternative: masca laringiana sau Combitube Situatii particulare: epiglotit acut, leziunii patologice faringiene, trauma cranian, trauma coloanei cervicale - laringoscopie cu fibroscop substante anestezice

Tehnica intubaiei OT preoxigenare poziionare n ax a laringelui, glotei i cavitaii oraleIntroducerea corecta a laringoscopului aspiraia secreiilor orofaringiene identificarea principalelor repere anatomice si introducerea sondei de intubaie, numai dupa o bun vizualizare a laringeluiumflarea cu aer a balonaului sondeiverificarea pozitionrii corecte a sondei

fixarea sondei cu fa sau leucoplast + pipa Guedel pt. a preveni mucarea sondei

*

Cai alternative masca laringiana

The laryngeal mask airway comprises a wide-bore tube with an elliptical inflated cuff designed to seal around the laryngeal opening.*

Cai alternativeCombitube

The Combitube is a double-lumen tube introduced blindly over the tongue, and provides a route for ventilation whether the tube has passed into the oesophagus (Figure 4.10a) or the trachea. The Combitube is a dual-lumen tube with a large proximal and small distal balloon. In most cases the distal balloon will be placed in the esophagus with the proximal balloon remaining in the posterior pharynx. Inflation of both balloons effectively isolates the entry point of the lower airway (larynx) from stomach contents and/or secretions from the mouth and nose. The rescuer then ventilates the patient through a tube that terminates between the two inflated balloons. The Combitube has been widely used with great success by all levels of rescue airway providers. The ease of insertion, effectiveness and simple design make it an ideal tool for rescuers that do not have a frequent opportunity to utilize their airway management skillsmbitube in CPR and successful ventilation was achieved in 7998% of patients

Cai alternative - Tubul laringian (King LT)

Cauze potential reversibile de stop cardiacHipoxiaHipovolemiaHipo/hiperK+, hipoCa2+ acidozaHipotermia

Pneumotorax compresivTamponada cardiacaToxice/medicamenteTromboembolismul SCA, TEP

Potential causes or aggravating factors for which specific treatment exists must be sought during any cardiac arrest.Minimise the risk of hypoxia by ensuring that the patients lungs are ventilated adequately with 100% oxygen. Make sure there is adequate chest rise and bilateral breath sounds. Using the techniques described below, check carefully that the tracheal tube is not misplaced in a bronchus or the oesophagus. Pulseless electrical activity caused by hypovolaemia is usually due to severe haemorrhage. This may be precipitated by trauma, gastrointestinal bleeding, or rupture of an aortic aneurysm. Restore intravascular volume rapidly with fluid, coupled with urgent surgery to stop the haemorrhage. Hyperkalaemia, hypokalaemia, hypocalcaemia, acidaemia, and other metabolic disorders are detected by biochemical tests or suggested by the patients medical history, e.g. renal failure. A 12-lead ECG may be diagnostic. Intravenous calcium chloride is indicated in the presence of hyperkalaemia, hypocalcaemia, and calcium-channel-blocking drug overdose. Suspect hypothermia in any drowning incident; use a low-reading thermometer.A tension pneumothorax may be the primary cause of PEA and may follow attempts at central venous catheter insertion. The diagnosis is made clinically. Decompress rapidly by needle thoracocentesis, and then insert a chest drain. Cardiac tamponade is difficult to diagnose because the typical signs of distended neck veins and hypotension are usually obscured by the arrest itself. Cardiac arrest after penetrating chest trauma is highly suggestive of tamponade and is an indication for needle pericardiocentesis or resuscitative thoracotomy. In the absence of a specific history, the accidental or deliberate ingestion of therapeutic or toxic substances may be revealed only by laboratory investigations. Where available, the appropriate antidotes should be used, but most often treatment is supportive. The commonest cause of thromboembolic or mechanical circulatory obstruction is massive pulmonary embolus. If cardiac arrest is thought to be caused by pulmonary embolism, consider giving a thrombolytic drug immediately. Thrombolysis may be considered in adult cardiac arrest, on a case-by-case basis, following initial failure of standard resuscitation in patients in whom an acute thrombotic aetiology for the arrest is suspected. Ongoing CPR is not a contraindication tothrombolysis.

Algoritm terapeutic in stopul cardiac prin asistola/DEMverific semnele prezentei circulaiei, inclusiv pulsul carotidian RCP 30:2 timp de 2 min, asigura abord venosAdrenalina 1mg i.v.Atropina - retrasa din protocolControlul caii aeriene Reia RCP timp de 2min, apoi Adrenalina 1mg

*

After in-hospital cardiac arrest, the division between basic life support and advanced life support is arbitrary; in practice, the resuscitation process is a continuum and is based on commonsense.The public expect that clinical staff can undertake CPR. For all inhospital cardiac arrests, ensure that: cardiorespiratory arrest is recognised immediately; help is summoned using a standard telephone number;CPR is started immediately using airway adjuncts if indicated defibrillation attempted as rapidly as possible and certainly within 3min.

An algorithm for the initial management of in-hospital cardiac arrest is shown Ensure personal safety. Check the victim for a response. When healthcare professionals see a patient collapse or find a patient apparently unconscious in a clinical area, they should first shout for help, then assess if the patient is responsive. Gently shake the shoulders and ask loudly: Are you all right? If other members of staff are nearby, it will be possible to undertake actions simultaneously. The responsive patient Urgent medical assessment is required. Depending on the local protocols, this may take the form of a resuscitation team (e.g., MET,RRT). While awaiting this team, give the patient oxygen, attachmonitoring and insert an intravenous cannula.The unresponsive patientThe exact sequence will depend on the training of staff and experience in assessment of breathing and circulation. Trained healthcare staff cannot assess the breathing and pulse sufficiently reliably to confirm cardiac arrest.226235 Agonal breathing (occasional gasps, slow, laboured or noisy breathing) is common in the early stages of cardiac arrest and is a sign of cardiac arrest and should not be confused as a sign of life/circulation. Agonalbreathing can also occur during chest compressions as cerebral perfusion improves, but is not indicative of a return of spontaneous circulation.

Etapa post-resuscitare: Respiratie

IOT si VM controlata: normocapnie, normoxieSonda NG de decompresie; Rx pulmonar pt. control CVC, sIOT, excl. pneumotorax,

Return of spontaneous circulation is just the first step towards the goal of complete recovery from cardiac arrest. Interventions in the post-resuscitation period influence the final outcome significantly. The post-resuscitation phase starts when ROSC is achieved. Once stabilised, the patient should be transferred to the most appropriate high-care area (e.g. intensive care unit or cardiac care unit) for continued monitoring and treatment.Consider tracheal intubation, sedation, and controlled ventilation in any patient with obtunded cerebral function. Adjust ventilation to achieve normocarbia and monitor this using the end-tidal CO2 and arterial blood gas values. Adjust the inspired oxygen concentrations to achieve adequate arterial oxygen saturation. Insert a gastric tube to decompress the stomach; gastric distension caused by mouth-to-mouth or bag-mask ventilation will splint the diaphragm and impair ventilation. Obtain a chest radiograph to check the position of the tracheal tube and central venous lines and exclude a pneumothorax associated with rib fractures from CPR.

Etapa post-resuscitare CirculatieCombaterea instabilitatii hemodinamice:Linie arteriala, debit cardiacRepletie volemica, inotropi, vaspresoareVasodilatatoare, diureticeK = 4-4,5 mmol/l

Haemodynamic instability is common after cardiac arrest. An arterial line for continuous blood pressure monitoring is essential, and the use of a non-invasive cardiac output monitor may be helpful. Infusion of fluids may be required to optimise filling. Conversely, diuretics and vasodilators may be needed to treat left ventricular failure. Infusion of an inotrope may be required to maintain a mean arterial blood pressure that is no lower than the normal pressure for the patient, and achieves an adequate urine output. Maintain the serum potassium concentration between 4.0-4.5 mmol l-1. If there is evidence of coronary occlusion, consider the need for immediate revascularisation by thrombolytic therapy or percutaneous coronary intervention.

Etapa post-resuscitare Recuperare neurologicaSedareControl convulsiiControl temperatura: evitare febraHipotermie moderata (32-34oC)Controlul glicemiei

If sedation is required, short-acting drugs (e.g. propofol, alfentanil, remifentanil) will enable earlier neurological assessmentSeizures are relatively common in the post-resuscitation period and may cause cerebral injury. Control seizures with benzodiazepines, phenytoin, propofol, or a barbiturate as appropriate.A period of hyperthermia is common in the first 48 h after cardiac arrest. The risk of a poor neurological outcome increases for each degree of body temperature above 37C. Treat hyperthermia occurring in the first 72 h after cardiac arrest with antipyretics or active cooling. Mild hypothermia is thought to suppress many of the chemical reactions associated with reperfusion injury. Two randomised clinical trials showed improved outcome in adults, remaining comatose after initial resuscitation from out-of-hospital VF cardiac arrest, who were cooled within minutes to hours after ROSCUnconscious adult patients with spontaneous circulation after out-of-hospital VF cardiac arrest should be cooled to 32-34C.13 Cooling should be started as soon as possible and continued for at least 12-24 h. Induced hypothermia may also benefit unconscious adult patients with spontaneous circulation after out-ofhospital cardiac arrest from a non- hockable rhythm, or cardiac arrest in hospital. Treat shivering by ensuring adequate sedation and giving neuromuscular blocking drugs. Bolus doses of neuromuscular blockers are usually adequate but infusions are occasionally necessary. Re-warm the patient slowly (0.25-0.5oC h-1) and avoid hyperthermia. The optimum target temperature, rate of cooling, duration of hypothermia, and rate of rewarming have yet to be determined; further studies are essential. External or internal cooling techniques or both can be used to initiate treatment. An infusion of 30 ml kg-1 saline at 4oC decreases core temperature by 1.5oC. Intravascular cooling enables more precise control of core temperature than external methods, but it is unknown whether this improves outcome. Complications of mild therapeutic hypothermia include increased infection, cardiovascular instability, coagulopathy, hyperglycaemia, and electrolyte abnormalities such as hypophosphataemia and hypomagnesaemia. There is a strong association between high blood glucose levels after resuscitation from cardiac arrest and poor neurological outcome. Tight control of blood glucose (4.4 - 6.1 mmol l-1) using insulin reduces hospital mortality in critically ill adults, but this has not been demonstrated in post-cardiac-arrest patients specifically. The optimal blood glucose target level in critically ill patients has not been determined. Comatose patients are at particular risk from unrecognised hypoglycaemia, and the risk of this complication occurring increases as the target blood glucose concentration is lowered.In common with all critically ill patients, patients admitted to a critical-care environment after cardiac arrest should have their blood glucose monitored frequently and hyperglycaemia treated with an insulin infusion. The blood glucose concentration that triggers insulin therapy and the target range of blood glucose concentrations should be determined by local policy. There is a need for studies of glucose control after cardiac arrest.

ConcluziiPrioritar CPR cat mai rapid dupa aparitia stopDefibrilarea precoce pt FV/TV fara pulsSecundarControl cale aeriana invazivaAbord venos si administrarea de medicamente

Bibliografie ALSAHA guidelines 2010www.erc.eduwww.resus.org.auwww.resus.org.uk

Sudden cardiac arrest (SCA) is a leading cause of death in Europe, affecting about 700,000 individuals a year. At the time of the first heart rhythm analysis, about 40% of SCA victims have ventricular fibrillation (VF). It is likely that many more victims have VF or rapid ventricular tachycardia (VT) at the time of collapse but, by the time the first ECG is recorded, their rhythm has deteriorated to asystole. Many victims of SCA can survive if bystanders act immediately while VF is still present, but successful resuscitation is unlikely once the rhythm has deteriorated to asystole. The optimum treatment for VF cardiac arrest is immediate bystander CPR (combined chest compression and rescue breathing) plus electrical defibrillation. The predominant mechanism of cardiac arrest in victims of trauma, drug overdose, drowning, and in many children is asphyxia; rescue breaths are critical for resuscitation of these victims.For victims of witnessed VF arrest, prompt bystander CPR and early defibrillation can significantly increase the chance for survival to hospital discharge. In comparison, typical ACLS therapies, such as insertion of advanced airways and pharmacologic support of the circulation, have not been shown to increase rate of survival to hospital dischargeBasic life support (BLS) refers to maintaining airway patency and supporting breathing and the circulation, without the use of equipment other than a protective device.Access for Medications: Correct PrioritiesDuring cardiac arrest, basic CPR and early defibrillation are of primary importance, and drug administration is of secondary importance. Few drugs used in the treatment of cardiac arrest are supported by strong evidence. After beginning CPR and attempting defibrillation, rescuers can establish intravenous (IV) access, consider drug therapy, and insert an advanced airway.Cardiopulmonary arrest is usually the result of a cardiac dysrhythmia. The majority of adults (80% to 90%) with sudden, nontraumatic cardiac arrest are found to be in ventricular tachycardia (VT) when an initial electrocardiographic rhythm strip is obtained. When ventricular fibrillation (VF) occurs outside the hospital, it most commonly results from chronic myocardial ischemia with electrical instability, rather than acute myocardial infarction.Conversely, in-hospital cardiac arrest most often follows an acute myocardial infarction or is the result of severe multisystem disease; asystole, bradydysrhythmias,and pulseless electrical activity are the usual rhythms encountered in hospitalized patients.Sudden cardiac arrest is responsible for more than 60% of adult deaths from coronary heart disease.In Europe, the annual incidence of resuscitation for out-of-hospital cardiopulmonary arrest of cardiac aetiology is 49.566 per 100,000 populationFewer than 20% of patients suffering an in-hospital cardiac arrest will survive to go home. Most survivors have a witnessed and monitored VF arrest, primary myocardial ischaemia as the cause, and receive immediate defibrillation, These patients often have slow and progressive physiological deterioration, involving hypoxia and hypotension, that is unnoticed by staff, or is recognised but poorly treated.3,4 The underlying cardiac arrest rhythm in this group is usually non-shockable and survival to hospital discharge is very poor.Rescuers begin CPR if the victim is unconscious or unresponsive, and not breathing normally (ignoring occasional gasps). A single compressionventilation (CV) ratio of 30:2 is used for the single rescuer of an adult or child (excluding neonates) out of hospital, and for all adult CPR. This single ratio is designed to simplify teaching, promote skill retention, increase the number of compressions given and decrease interruption to compressions. Once a defibrillator is attached, if a shockable rhythm is confirmed, a single shock is delivered. Irrespective of the resultant rhythm, chest compressions and ventilations (2 min with a CV ratio of 30:2) are resumed immediately after the shock to minimise the no-flow time. Advanced life support interventions are outlined in a box at the centre of the ALS algorithm (see Section 4). Once the airway is secured with a tracheal tube, laryngeal mask airway (LMA) or Combitube, the lungs are ventilated at a rate of 10 min1 without pausing during chest compressions.

Chain of Survival. The links in this Chain are: Immediate recognition and activation, early CPR, rapid defibrillation, effective advanced life support and integrated post-cardiac arrest care.The actions linking the victim of sudden cardiac arrest with survival are called the Chain of Survival. They include early recognition of the emergency and activation of the emergency services, early CPR, early defibrillation and early advanced life support.The importance of recognising critical illness and/or angina and preventing cardiac arrest (in- or out-of-hospital), and post resuscitation care has been highlighted by the inclusion ofthese elements in a new four-ring Chain of Survival The central links in this new chain depict the integration of CPR and defibrillation as the fundamental components of early resuscitation in an attempt to restore life The following concept of the Chain of Survival summarises the vital steps needed for successful resuscitation (Figure 1.1). Most of these links are relevant for victims of both VF and asphyxial arrest.Early recognition of the emergency and calling for help: activate the emergency medical services (EMS) or local emergency response system, e.g. phone 112.12,13 An early, effective response may prevent cardiac arrest. Early bystander CPR: immediate CPR can double or triple survival from VF SCA Early defibrillation: CPR plus defibrillation within 35 min of collapse can produce survival rates as high as 4975%. Each minute of delay in defibrillation reduces the probability of survival to discharge by 1015%.Early advanced life support and postresuscitation care: the quality of treatment during the post-resuscitation phase affects outcome

Building Blocks of CPR.The actions linking the victim of sudden cardiac arrest with survival are called the Chain of Survival. They include early recognition of the emergency and activation of the emergency services, early CPR, early defibrillation and early advanced life support.The importance of recognising critical illness and/or angina and preventing cardiac arrest (in- or out-of-hospital), and post resuscitation care has been highlighted by the inclusion ofthese elements in a new four-ring Chain of Survival The central links in this new chain depict the integration of CPR and defibrillation as the fundamental components of early resuscitation in an attempt to restore life The following concept of the Chain of Survival summarises the vital steps needed for successful resuscitation (Figure 1.1). Most of these links are relevant for victims of both VF and asphyxial arrest.Early recognition of the emergency and calling for help: activate the emergency medical services (EMS) or local emergency response system, e.g. phone 112.12,13 An early, effective response may prevent cardiac arrest. Early bystander CPR: immediate CPR can double or triple survival from VF SCA Early defibrillation: CPR plus defibrillation within 35 min of collapse can produce survival rates as high as 4975%. Each minute of delay in defibrillation reduces the probability of survival to discharge by 1015%.Early advanced life support and postresuscitation care: the quality of treatment during the post-resuscitation phase affects outcome

Defibrillation requires the delivery of sufficient electrical energy to defibrillate a critical mass of myocardium, abolish the wavefronts of VF and enable restoration of spontaneous synchronised electrical activity in the form of an organised rhythm. The optimal energy for defibrillation is that which achieves defibrillation while causing the minimum of myocardial damage.Monophasic defibrillators deliver current that is unipolar (i.e., one direction of current flow).Biphasic defibrillators, in contrast, deliver current that flows in a positive direction for a specified duration before reversing and flowing in a negative direction for the remaining milliseconds of the electrical discharge. Biphasic defibrillators compensate for the wide variations in transthoracic impedance by electronically adjusting the waveform magnitude and duration.The most critical interventions during the first minutes of VF or pulseless VT are immediate bystander CPR (Box 1) with minimal interruption in chest compressions and defibrillation as soon as it can be accomplished (Class I). In cases of witnessed arrest with a defibrillator on-site, after delivery of 2 rescue breaths the healthcare provider should check for a pulse. If the provider definitely does not feel a pulse within 10 seconds, the provider should turn on the defibrillator, place adhesive pads or paddles, and check the rhythm (Box 2). If the healthcare provider does not witness the arrest in the out-of-hospital setting (eg, the emergency medical services [EMS] provider arrives at the scene of an arrest), the provider may give 5 cycles of CPR before attempting defibrillation. In adults with a prolonged arrest, shock delivery may be more successful after a period of effective chest compressions.The most critical interventions during the first minutes of VF or pulseless VT are immediate bystander CPR (Box 1) with minimal interruption in chest compressions and defibrillation as soon as it can be accomplished (Class I). In cases of witnessed arrest with a defibrillator on-site, after delivery of 2 rescue breaths the healthcare provider should check for a pulse. If the provider definitely does not feel a pulse within 10 seconds, the provider should turn on the defibrillator, place adhesive pads or paddles, and check the rhythm (Box 2). If the healthcare provider does not witness the arrest in the out-of-hospital setting (eg, the emergency medical services [EMS] provider arrives at the scene of an arrest), the provider may give 5 cycles of CPR before attempting defibrillation. In adults with a prolonged arrest, shock delivery may be more successful after a period of effective chest compressions.*the recommended initial energy level for the first shock using a monophasic defibrillator is 360 J. Although higher energy levels risk a greater degree of myocardial injury, the benefits of earlier conversion to a perfusing rhythm are paramount.The rationale for giving a thump is that the mechanical energy of the thump is converted to electrical energy, which may be sufficient to achieve cardioversion. in all the reported successful cases, the precordial thump was given within the first 10 s of VFConsider giving a single precordial thump when cardiac arrest is confirmed rapidly after a witnessed, sudden collapse and a defibrillator is not immediately to hand.Using the ulnar edge of a tightly clenched fist, a sharp impact is delivered to the lower half of the sternum from a height of about 20 cm, followed by immediate retraction of the fist, which creates an impulse-like stimulus.If IV access has not been established, the provider should insert a large peripheral venous catheter. Although in adults peak drug concentrations are lower and circulation times longer when drugs are administered via peripheral sites rather than central sites, the establishment of peripheral access does not require interruption of CPR. Drugs typically require 1 to 2 minutes to reach the central circulation when given via a peripheral vein but require less time when given via central venous access.If a resuscitation drug is administered by a peripheral venous route, administer the drug by bolus injection and follow with a 20-mL bolus of IV fluid. Elevate the extremity for 10 to 20 seconds to facilitate drug delivery to the central circulation.Establish IV access with a saline lock on all appropriate medical and traumatic emergencies External Jugular access is acceptable in critical patients when other access is not available or the time to find other access would jeopardize patient outcome.Intraosseous (IO) cannulation provides access to a noncollapsible venous plexus, enabling drug delivery similar to that achieved by central venous access. IO access is safe andeffective for fluid resuscitation, drug delivery, and blood sampling for laboratory evaluation, and is attainable in all age groups. Providers may establish IO access if IV access isunavailable (Class IIa). Commercially available kits can facilitate IO access in adults.If IV and IO access cannot be established, some resuscitation drugs may be administered by the endotracheal route: lidocaine, epinephrine, atropine, naloxone, and vasopressin are absorbed via the trachea. The optimal endotracheal dose of most drugs is unknown, but typically the dose given by the endotracheal route is 2 to 212 times the recommended IV dose. Providers should dilute the recommended dose in 5 to 10 mL of water or normal saline and inject the drug directly into the endotracheal tube

*

*The laryngeal mask airway comprises a wide-bore tube with an elliptical inflated cuff designed to seal around the laryngeal opening.*The Combitube is a double-lumen tube introduced blindly over the tongue, and provides a route for ventilation whether the tube has passed into the oesophagus (Figure 4.10a) or the trachea. The Combitube is a dual-lumen tube with a large proximal and small distal balloon. In most cases the distal balloon will be placed in the esophagus with the proximal balloon remaining in the posterior pharynx. Inflation of both balloons effectively isolates the entry point of the lower airway (larynx) from stomach contents and/or secretions from the mouth and nose. The rescuer then ventilates the patient through a tube that terminates between the two inflated balloons. The Combitube has been widely used with great success by all levels of rescue airway providers. The ease of insertion, effectiveness and simple design make it an ideal tool for rescuers that do not have a frequent opportunity to utilize their airway management skillsmbitube in CPR and successful ventilation was achieved in 7998% of patientsPotential causes or aggravating factors for which specific treatment exists must be sought during any cardiac arrest.Minimise the risk of hypoxia by ensuring that the patients lungs are ventilated adequately with 100% oxygen. Make sure there is adequate chest rise and bilateral breath sounds. Using the techniques described below, check carefully that the tracheal tube is not misplaced in a bronchus or the oesophagus. Pulseless electrical activity caused by hypovolaemia is usually due to severe haemorrhage. This may be precipitated by trauma, gastrointestinal bleeding, or rupture of an aortic aneurysm. Restore intravascular volume rapidly with fluid, coupled with urgent surgery to stop the haemorrhage. Hyperkalaemia, hypokalaemia, hypocalcaemia, acidaemia, and other metabolic disorders are detected by biochemical tests or suggested by the patients medical history, e.g. renal failure. A 12-lead ECG may be diagnostic. Intravenous calcium chloride is indicated in the presence of hyperkalaemia, hypocalcaemia, and calcium-channel-blocking drug overdose. Suspect hypothermia in any drowning incident; use a low-reading thermometer.A tension pneumothorax may be the primary cause of PEA and may follow attempts at central venous catheter insertion. The diagnosis is made clinically. Decompress rapidly by needle thoracocentesis, and then insert a chest drain. Cardiac tamponade is difficult to diagnose because the typical signs of distended neck veins and hypotension are usually obscured by the arrest itself. Cardiac arrest after penetrating chest trauma is highly suggestive of tamponade and is an indication for needle pericardiocentesis or resuscitative thoracotomy. In the absence of a specific history, the accidental or deliberate ingestion of therapeutic or toxic substances may be revealed only by laboratory investigations. Where available, the appropriate antidotes should be used, but most often treatment is supportive. The commonest cause of thromboembolic or mechanical circulatory obstruction is massive pulmonary embolus. If cardiac arrest is thought to be caused by pulmonary embolism, consider giving a thrombolytic drug immediately. Thrombolysis may be considered in adult cardiac arrest, on a case-by-case basis, following initial failure of standard resuscitation in patients in whom an acute thrombotic aetiology for the arrest is suspected. Ongoing CPR is not a contraindication tothrombolysis.

*After in-hospital cardiac arrest, the division between basic life support and advanced life support is arbitrary; in practice, the resuscitation process is a continuum and is based on commonsense.The public expect that clinical staff can undertake CPR. For all inhospital cardiac arrests, ensure that: cardiorespiratory arrest is recognised immediately; help is summoned using a standard telephone number;CPR is started immediately using airway adjuncts if indicated defibrillation attempted as rapidly as possible and certainly within 3min.

An algorithm for the initial management of in-hospital cardiac arrest is shown Ensure personal safety. Check the victim for a response. When healthcare professionals see a patient collapse or find a patient apparently unconscious in a clinical area, they should first shout for help, then assess if the patient is responsive. Gently shake the shoulders and ask loudly: Are you all right? If other members of staff are nearby, it will be possible to undertake actions simultaneously. The responsive patient Urgent medical assessment is required. Depending on the local protocols, this may take the form of a resuscitation team (e.g., MET,RRT). While awaiting this team, give the patient oxygen, attachmonitoring and insert an intravenous cannula.The unresponsive patientThe exact sequence will depend on the training of staff and experience in assessment of breathing and circulation. Trained healthcare staff cannot assess the breathing and pulse sufficiently reliably to confirm cardiac arrest.226235 Agonal breathing (occasional gasps, slow, laboured or noisy breathing) is common in the early stages of cardiac arrest and is a sign of cardiac arrest and should not be confused as a sign of life/circulation. Agonalbreathing can also occur during chest compressions as cerebral perfusion improves, but is not indicative of a return of spontaneous circulation.Return of spontaneous circulation is just the first step towards the goal of complete recovery from cardiac arrest. Interventions in the post-resuscitation period influence the final outcome significantly. The post-resuscitation phase starts when ROSC is achieved. Once stabilised, the patient should be transferred to the most appropriate high-care area (e.g. intensive care unit or cardiac care unit) for continued monitoring and treatment.Consider tracheal intubation, sedation, and controlled ventilation in any patient with obtunded cerebral function. Adjust ventilation to achieve normocarbia and monitor this using the end-tidal CO2 and arterial blood gas values. Adjust the inspired oxygen concentrations to achieve adequate arterial oxygen saturation. Insert a gastric tube to decompress the stomach; gastric distension caused by mouth-to-mouth or bag-mask ventilation will splint the diaphragm and impair ventilation. Obtain a chest radiograph to check the position of the tracheal tube and central venous lines and exclude a pneumothorax associated with rib fractures from CPR.Haemodynamic instability is common after cardiac arrest. An arterial line for continuous blood pressure monitoring is essential, and the use of a non-invasive cardiac output monitor may be helpful. Infusion of fluids may be required to optimise filling. Conversely, diuretics and vasodilators may be needed to treat left ventricular failure. Infusion of an inotrope may be required to maintain a mean arterial blood pressure that is no lower than the normal pressure for the patient, and achieves an adequate urine output. Maintain the serum potassium concentration between 4.0-4.5 mmol l-1. If there is evidence of coronary occlusion, consider the need for immediate revascularisation by thrombolytic therapy or percutaneous coronary intervention.If sedation is required, short-acting drugs (e.g. propofol, alfentanil, remifentanil) will enable earlier neurological assessmentSeizures are relatively common in the post-resuscitation period and may cause cerebral injury. Control seizures with benzodiazepines, phenytoin, propofol, or a barbiturate as appropriate.A period of hyperthermia is common in the first 48 h after cardiac arrest. The risk of a poor neurological outcome increases for each degree of body temperature above 37C. Treat hyperthermia occurring in the first 72 h after cardiac arrest with antipyretics or active cooling. Mild hypothermia is thought to suppress many of the chemical reactions associated with reperfusion injury. Two randomised clinical trials showed improved outcome in adults, remaining comatose after initial resuscitation from out-of-hospital VF cardiac arrest, who were cooled within minutes to hours after ROSCUnconscious adult patients with spontaneous circulation after out-of-hospital VF cardiac arrest should be cooled to 32-34C.13 Cooling should be started as soon as possible and continued for at least 12-24 h. Induced hypothermia may also benefit unconscious adult patients with spontaneous circulation after out-ofhospital cardiac arrest from a non- hockable rhythm, or cardiac arrest in hospital. Treat shivering by ensuring adequate sedation and giving neuromuscular blocking drugs. Bolus doses of neuromuscular blockers are usually adequate but infusions are occasionally necessary. Re-warm the patient slowly (0.25-0.5oC h-1) and avoid hyperthermia. The optimum target temperature, rate of cooling, duration of hypothermia, and rate of rewarming have yet to be determined; further studies are essential. External or internal cooling techniques or both can be used to initiate treatment. An infusion of 30 ml kg-1 saline at 4oC decreases core temperature by 1.5oC. Intravascular cooling enables more precise control of core temperature than external methods, but it is unknown whether this improves outcome. Complications of mild therapeutic hypothermia include increased infection, cardiovascular instability, coagulopathy, hyperglycaemia, and electrolyte abnormalities such as hypophosphataemia and hypomagnesaemia. There is a strong association between high blood glucose levels after resuscitation from cardiac arrest and poor neurological outcome. Tight control of blood glucose (4.4 - 6.1 mmol l-1) using insulin reduces hospital mortality in critically ill adults, but this has not been demonstrated in post-cardiac-arrest patients specifically. The optimal blood glucose target level in critically ill patients has not been determined. Comatose patients are at particular risk from unrecognised hypoglycaemia, and the risk of this complication occurring increases as the target blood glucose concentration is lowered.In common with all critically ill patients, patients admitted to a critical-care environment after cardiac arrest should have their blood glucose monitored frequently and hyperglycaemia treated with an insulin infusion. The blood glucose concentration that triggers insulin therapy and the target range of blood glucose concentrations should be determined by local policy. There is a need for studies of glucose control after cardiac arrest.