Università degli Studi di Perugia ALS Advanced Life

Università degli Studi di Perugia ALS Advanced Life Support Simonetta Tesoro Dipartimento di Medicina Clinica e Sperimentale Sezione di Anestesia, Analgesia e Terapia Intensiva Dir. Prof. Vito Aldo Peduto

HOSPITAL CARDIAC ARREST • Fewer than 20% of patients suffering an in-hospital cardiac arrest will survive to go home. Most survivors have monitored VF arrest (primary myocardial ischaemia) and receive immediate defibrillation • Cardiac arrest in patients in unmonitored ward areas isn’t usually caused by primary cardiac disease but by a progressive physiological deterioration, involving hypoxia and hypotension and it is usually non-shockable. The survival to hospital discharge is very poor. The records of patients who have a cardiac arrest often contain evidence of unrecognised, or untreated, breathing and circulation problems. European Resuscitation Council Guidelines 2005

IN-HOSPITAL CARDIAC ARREST • Hipoxia and incorrect use of oxygen therapy • Fluid and electrolyte balance • Poor analgesia • Lack knowledge about drug doses • Failure to monitor patients

EARLY WARNING SCORING EWS Early warning scoring systems allocate points to routine vital signs measurements on basis of their derangement from an arbitrarily agreed normal range. May be used to call ward doctors or critical care out-reach teams to the patient. THE IMPORTANCE OF EARLY RECOGNITION AND TREATMENT OF CRITICALLY ILL PATIENTS TO PREVENT CARDIAC ARREST

MEDICAL EMERGENCY TEAM MET It is a team that responds, not only to patient in cardiac arrest, but also to those with acute physiological deterioration The MET usually comprises medical and nursing staff from intensive care and general medicine

GUIDELINES FOR PREVENTION OF HOSPITAL CARDIAC ARREST • Provide care for patients who are critically ill in appropriate areas. • Critically ill patients need regular observation of vital signs. • Use EWS to identify patients at risk of clinical deterioration. • The hospital should have a MET capable of responding to acute clinical crises avaible 24 h per day IN- • Identify patients for whom cardiopulmonary arrest is an anticipated terminal event and in whom CPR is inappropriate • Ensure accurate audit of cardiac arrest, “false arrest”, unexpected deaths and unanticipated ICU admissions

STEPS FOR SUCCESSFUL RESUSCITATION 1. Early recognition of the emergency and calling for help. 2. Early bystander CPR: immediate CPR can CPR double or triple survival. 3. Early defibrillation: CPR + defibrillation within 3 -5 min can produce survival rates as high as 49 -75%. Each minute of delay in defibrillation reduces the probability of survival to discharge by 10 -15%. 4. Early Advanced Life Support and post resuscitation care: the quality of treatment affects outcome.

GUIDELINES Based on the document 2005 International Consensus on Cardiopulmonary Resuscitations and Emergency Cardiovascular Care Science with Treatment Recommendations. November 2005 • • American Heart Association (AHA) European Resuscitation Council (ERC) Italian Resuscitation Council (IRC) International Liaison Commitee on Resuscitation (ILCOR)

CHAIN OF SURVIVAL Cummins 1991…. . BLS-D ALS GOLD STANDARD • GOOD NEUROGICAL OUTCOME

CHAIN OF SURVIVAL Cummins 1991…. . • ALS: Advanced Life Support • ACLS: Adult Cardiac Life Support ALS FOR NO LAY RESCUER

HOSPITAL RESUSCITATION

CHECK THE VICTIM FOR A RESPONSE: gently shake his shoulders and ask loudly: ”are you all right? ” SHOUT FOR HELP

A = Airway OPEN THE AIRWAY

HEAD TILT AND CHIN LIFT • Place your hand on his forehead and gently tilt his head back keeping your thumb. • With your fingertips under the point of the victim’s chin, lift the chin to open the airway. JAW THRUST The rescuer’s index and other fingers are placed behind the angle of the mandible. Using the thumbs, the mouth is open slightly by downward displacement of the chin

INSERTION OF OROPHARYNGEAL AIRWAY

AIRWAY OBSTRUCTION 1. LOOK-LISTEN-FEEL 2. In partial obstruction air entry is diminished and usually noisy. 3. Inspiratory stridor is caused by obstruction at the laryngeal level or above • GURGLING is caused by liquid or semisolid foreign material • SNORING arises when the pharynx is partially occluded by the soft palate or epiglottis • CROWING is sound of laryngeal spasm

B = Breathing

• L = LOOK chest movement • L = LISTEN at the victim’s mouth for breath sounds • F = FEEL for air on your cheek NO MORE THAN 10 S … 1, 2, 3, 4, 5, 6, 7, 8, 9, 10 HE IS BREATHING

IF HE IS BREATHING NORMALLY • Turn him into the recovery position • Chek for continued breathing DO NOT CONFUSE BARELY BREATH NOISY GASPS WITH NORMAL BREATHING

• L = LOOK chest movement • L = LISTEN at the victim’s mouth for breath sounds • F = FEEL for air on your cheek NO MORE THAN 10 S … 1, 2, 3, 4, 5, 6, 7, 8, 9, 10 HE ISN’T BREATHING

CHEST COMPRESSION • Place the heel of one hand in the centre of the victim’s chest; place the heel of your hand on top of the first hand. Interlook the fingers of your hands. Ensure that pressure is not applied over the victim’s ribs. Do not apply any pressure over the upper abdomen or the bottom end of bony sternum • Position yourself vertically above the victim’s chest and, with your arm straight • • Press down on the sternum 4 -5 cm. After each compression, release all the pressure on the chest without losing contact between your hands and the sternum • Take approxmately the same amuont of time for compression and relaxation. Minimise interruptions in chest compression.

GUIDELINES CHANGES 1. Increase the number of chest compressions 30: 2 2. No cheking carotid pulse 3. One-shock versus three-shock sequence 4. Time of adrenaline

Coronary Artery Perfusion Pressure Improves With Longer Series of Chest Compressions in Adult Victims Coronary Artery Pressure at 5: 1 ratio Pressure at 15: 2 ratio

GUIDELINES CHANGES 1. Increase the number of chest compressions 30: 2 2. No cheking carotid pulse 3. One-shock versus three-shock sequence 4. Time of adrenaline

CHECK CIRCULATION • If the patient has NO signs of life –lack of movement, normal breathing, coughing- start CPR • Those experienced in clinical assessment should assess the CAROTID PULSE whilst simultaneously looking for signs of lif for not more than 10 s If there is doubt start CPR immediately MUST BE AVOID DELAY IN DIAGNOSIS !

VENTILATION BAG-MASK VENTILATION • One person holds the facemask in place using a jaw thrust with both hands • An assistant squeezes the bag 10 BREATHS min-1 DO NOT HYPERVENTILATE MOUTH TO MASK VENTILATION

D = Defibrillation

DEFIBRILLATORS • Automated External Defibrillators AED The defibrillators assess the rhythm with waveform analysis and give automatically a shock. • Manual defibrillators It is used healthcare rescuers because they have to do diagnosis and give a shock. It’s used for synchronised cardioversion • Semi-autometed external defibrillator The defibrillators assess the rhythm with waveform analysis and the rescuer has to give a shock.

ELECTRODE POSITION Apply paddles or self-adhesive pads to the chest

SEQUENCE FOR USE OF AN AED 1. 2. 3. 4. 5. 6. 7. MAKE sure you, the victim and any bystanders are safe. If the victim is unresponsive and not breathing normally, send someone for the AED and to call for an ambulance. Start CPR according to the guidelines for BLS As soon as the defibrillator arrives: -switch on the defibrillator and attach the electrode pads -ensure that no body touches the victim while the AED is unlysing the rhythm If a shock is indicated: push shock button as directed If no shock indicated: immediately resume CPR Continue until: -qualifield help arrives and takes over -the victim starts to breathe normally -you become exhaustead

AED ALGORITHM

GUIDELINES CHANGES 1. Increase the number of chest compressions 30: 2 2. No cheking carotid pulse 3. One-shock versus three-shock sequence 4. Time of adrenaline

PRECORDIAL THUMP Consider giving a single precordial thump when cardiac arrest is confirmed rapidly after a witnessed, sudden collapse and a defibrillator is not immediatele to hand. Using the ulnar edge of a tightly cleneched fist, deliver a sharp impact to the lower half of the sternum from a height of about 20 cm. A precordial thump is most likely to be successful in converting VT to sinus rhythm. Successful treatment of VF is much less likely: if it was given within the first 10 s of VF

SOMMINISTRATION ROUTE • INTRAVENOUS: drugs injected perperipherally must be followed by a flush of at least 20 ml. insertion of central venous catheter requires interrumpion of CPR • TRACHEAL ROUTE: if intravenous can’t be established. Unpredictable plasma concentration are achieved and equipotent dose is unknown. DOSE: three to ten times higher diluited in 10 ml

HOSPITAL RESUSCITATION

ADRENALINE • Adrenaline is the first drug used in cardiac arrest of any aetiology: it is included in the ALS ALGORITHM for use 1 mg every 3 -5 min of CPR • • Its primary efficacy is due to its alpha-adrenergic vasoconstrictive effects causing systemic vasoconstriction, which increases coronary and cerebral perfusion pressures. The beta adrenergic actions of adrenaline increases miocardial oxygen consumption, ectopic ventricular arrhythmias and transient hypoxaemia due to pulmonary arteriovenous shunting. CPR 2 min - SHOCK CPR 2 min – ADRENALINE - SHOCK

GUIDELINES CHANGES 1. Increase the number of chest compressions 30: 2 2. No cheking carotid pulse 3. One-shock versus three-shock sequence 4. Time of adrenaline

AMIODARONE It is a membrane-stabilising anti-arrhythmic drug that increase the duration of the action potential • INDICATION ü Refractory VF/VT ü Heamodynamically stable ventricular tachycardia (VT) and other resistant tachyarrhythmia • DOSE 300 mg in 20 ml dextrose 5% • ADVERSE EFFECTS ü May be arrhythmogenic ü Hypothension ü Bradycardia

LIDOCAINE Until 2000 it was the antiarrhytmic drug of choice Now it is recommended only when amiodarone is unavailable • DOSE 1 -1. 5 mg/kg Additional bolus 50 mg Max 3 mg/kg during first h Its half-life is prolonged during cardiac arrest It is less effective in the presence of hypokalaemia and hypomagnesaemia

MAGNESIUM SULPHATE It is an important constituent of many enzyme and improves the contractile response of the stunned myocardium • INDICATION Ø Shock-refractory VF in the presence of possible hypomagnesaemia Ø Ventricular tachyarrhythiamias in the presence of possible hypomagnesaemia Ø Torsades de pointes Ø Digoxin toxicity • DOSE 2 g in 1 -2 min It may be repeated after 10 -15 min

ATROPINE • INDICATION Ø Asystole Ø Pulseless electrical activity (PEA) with a rate <60 min-1 Ø Sinus, atrial or nodal bradycardia when the haemodynamic condition of the patient is unstable • DOSE 3 mg ev

SODIUM BICARBONATE The best treatment of acidemia in cardiac arrest is chest compression – – – NOT INDICATED DURING CPR: It exacerbates intracellular acidosis It causes generation of carbon dioxide It produces a negative inotropic effect on ischaemic myocardium It presents a large, osmotically active, sodium load It produces a shift to the left in the oxygen dissociation curve, further inhibiting release of oxygen to the tissues. Following resuscitation from cardiac arrest, consider giving small doses of sodium bicarbonate 50 ml of an 8. 4% solution CONSIDER SODIUM BICARBONATE: – Life-threatening hyperkalaemia/ cardiac arrest associated hyperkaelemia – Severe metabolic acidosis – Tricyclic overdose

VF and VT pulseless LIDOCAINA now recommended only when amiodarone is unavailable / in refractory FV-VT 1 -1. 5 mg/kg ev 1 additional bolus dose max 3 mg/kg AMIODARONE CLASSE IIb 300 mg ev additional bolus ev 150 mg dose max 2. 2 gr in 24 h Mg. SO 4 CLASSE IIb 1 -2 gr ev • shock-refractory VF + Hypo. Mg. SO 4 • Ventricular tachyarrhythmias + Hypo. Mg. SO 4 • Torsades de pointes + Hypo. Mg. SO 4 PROCAINAMIDE CLASSE IIb nella FV/TV recidivante/intermittente 30 mg/min dose max 17 mg/kg ACCETTATA MA NON RACCOMANDATA PER LUNGHI TEMPI DI SOMMINISTRAZIONE

BRADYCARDIA