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Acute coronary disorders Drugs in cardiopulmonary resuscitation Advanced Life Support (ALS) algorithm Acute coronary syndromes Definitions The acute coronary syndromes comprise: • Unstable angina • Non-Q wave myocardial infarction • Q wave myocardial infarction These process is triggering: • Hemorrhage into the plaque causing it to swell and restrict the lumen of the artery • Contraction of smooth muscle within the artery wall causing further constriction of the lumen • Thrombus formation on the surface of the plaque, which may lead ultimately to complete obstruction of the lumen of the coronary artery Unstable angina Angina – a pain resulting from myocardial ischaemia and is felt usually in or across the centre of the chest as tightness or an indigestion-like ache, radiates into the throat, arms, back or epigastrium, sometimes is perceived as discomfort Unstable angina Defined by one or more of: • Angina of effort occuring over few days with increasing frequency, • Episodes of angina occuring recurrently and unpredictably, may be relatively short-lived or be relieved temporarily by sublingual glyceryl trinitrate, • An unprovoked and prolonged episode of the chest pain raising suspicion of myocardial infarction but without ECG evidence Unstable angina The ECG may: • Be normal • Show evidence of acute myocardial ischaemia (ST segment depression) • Show non-specific abnormalities (e.g. T wave inversion) Non-Q wave myocardial infarction • The clinical syndrome presenting with symptoms suggestive of acute MI and nonspecific ECG abnormalities: – Often ST segment depression – T wave inversion • Lab tests are positive – indicating that myocardial damage has occured • Treatment – essentially the same like in the unstable angina Q wave myocardial infarction • The clinical syndrome presenting with prolonged chest pain, accompanied by acute ST segment elevation • Laboratory evidence of myocardial damage in the form of raised cardiac enzymes or other biochemical markers – creatine kinase (CK), aspartate transaminase (AST), lactate dehydrogenase (LDH), cardiac troponins (TrI, TrT) • Clinical examination – limited benefit, severe chest pain may provoke – sweating, pallor, tachycardia, nausea Q wave myocardial infarction Immediate treatment General measures in all acute coronary syndromes: • • • • Rapid initial assessment Provide prompt relief of symptoms Limit myocardial damage and risk of the cardiac arrest Coronary reperfusion therapy – thrombolytic therapy, percutaneous transluminal coronary angioplasty (PTCA), coronary artery bypass graft (CABG) surgery „MONA” – initial general treatment • M – morphine, titrated intravenously to avoid sedation and respiratory depression • O – oxygen, in high concentration • N – nitroglycerine, as sublingual glyceryl trinitrate (tablet or spray) • A – aspirin, 300mg orally as soon as practicable Patients with cardiac pain will be more comfortable sitting up !!! Peri-arrest arrhythmias • Cardiac arrhythmias - well rocognised complications of myocardial infarction • The treatment of all arrhythmias poses two basic questions – How is the patient? – What is the arrhythmia? • The presence or absence of certaine adverse signs or symptoms will dictate the appropriate treatment Adverse signs of peri-arrest arrhythmias • Clinical evidence of low cardiac output – pallor, sweating, cold, clammy extremities, impaired consciousness, hypotension • Excessive tachycardia – very high rates (>150 beats/min) reduce coronary flow resulting in myocardial ischeamia • Excessive bradycardia – may not be tolerated by patients with poor cardiac reserve (<60 beats/min) • Heart failure – arrhythmias reduce the efficiency of the heart as a pump (pulmonary oedema) Treatment options • Have determined the rhythm and find the presence or absence of adverse signs • Options available in the immediate treatment of arrhythmias: – Antiarrhythmic drugs – absence of adverse signs – DC shock to attempt cardioversion – converting a tachycardia to sinus rhythm – Cardiac pacing – treating symptomatic bradycardias Bradycardia – heart rate < 60/min Möbitz Type II Block Adverse signs: • Systolic blood pressure < 90 mmHg • Heart rate < 40/min • Ventricular arrhytmias requiring suppresion • Heart failure Treatment: • Atropine • Cardiac pacing – presence the risk os asystole Narrow Complex Tachycardia Adverse sins: • Systolic blood pressure < 90 mmHg • Chest pain • Heart failure • Impaired consciousness • Heart rate > 200 beats/min Treatment: • Antiarrhythmic drugs – esmolol, amidarone • DC shock Broad Complex Tachycardia Adverse signs: • Rate > 150/min • Chest pain • Heart failure • Systolic blood pressure < 90 mmHg Treatment: • Amidarone, lidocaine • DC shock Atrial fibrillation Adeverse signs: • Rate > 150/min • Ongoing chest pain • Critical perfusion • Breathlessness Treatment: • Anticoagulation, beta-blockers, digoxin, amiodarone • Synchronised DC shock DRUGS for cardiac arrest There are 3 groups of drugs relevant to the management of cardiac arrest: ―Vasopressors ―Anti-arrhytmics ―Other drugs Drugs should be considered only after initial shocks have been delivered and chest compressions and ventilation have been started. Adrenaline (epinephrine) primery agent for the management of cardiac arrest Its primary efficacy is due to effects: -adrenergic – arterial vasoconstriction systemic vascular resistance coronary and cerebral perfusion pressures -adrenergic – coronary blood flow force of contraction myocardial O2 consumption (may increase ischaemia) Adrenaline Indications: • The first drug used in cardiac arrest of any ethiology • Second-line treatment for cardiogenic shock • Preferred in the special circumstances: – anaphylaxis Adrenaline Dose: • 1 mg intravenous (1 ml sol. 1:1,000) every 35 min of CPR • 2-3 mg diluted to 10ml with sterile water via tracheal tube • 2–10 mcg/min continous infusion for atropine resistant bradycardia, hypotensive patients • 0.5ml 1:1,000 i.m., 3-5 ml (sol.1:10,000) i.v. in anaphylaxis, depending on severity Vasopressin • Naturally occuring antidiuretic hormone • High doses – powerful vasoconstricor that acts by stimulation of smooth muscle V1 receptors • AHA – recommended vasopressin as an alternative to adrenaline for the treatment of adult shock-refractory VF • Dose – 40 U (comp. 1mg adrenaline) • Currently – insufficient evidence of improvement in survival to discharge Anti-arrhythmics Amiodarone - membrane-stabilising drug that increases: – duration of the action potential – refractory period in atrial and vetricular myocardium – mild negative inotropic action - may cause hypotension – appers to improve the response to defibryllation Amiodarone Indications: • Refractory VF / Pulseless VT • Haemodynamically stable VT • Other resistant tachyarrhythmias Amiodarone Dose: • Refractory VF / Pulseless VT – 300 mg diluted in 5% dextrose to a volume of 20ml, • Stable tachyarrhythmias – 150 mg in 5% dextrose over 10 min – Repeat 150 mg if necessary – 300 mg in 100 ml 5% dextrose over 1 hour Lidocaine Membrane-stabilising drug that acts by: • increasing the myocyte refractory period • decreases vetricular automaticity • Suppresses ventricular ectopic activity – mainly in arrhythmogenic tissues, minimally with electrical activity of normal tissues Lidocaine toxicity: • paraesthesia • drowsiness • confusion • convulsions Lidocaine Indications: • Refractory VF / Pulseless VT – when amiodarone is unavailable • Haemodynamically stable VT – as an alternative to amiodarone Lidocaine Dose: • Refractory VF / Pulseless VT – initial 100 mg i.v. (1 – 1.5mg/kg) – further boluses 50mg, • Haemodynamically stable VT – 50 mg i.v. – further boluses of 50 mg, • Total dose should not exceed 3mg/kg during the firt hour • Reduce dose in elderly or hepatic failure Adenosine Naturally occuring purine nucleotide: • • • • Slows conduction across the AV node, Has little effect other myocardial cells Has short duration of action May reveal the underlying atrial rhythms by slowing the ventricular response Should be used in a monitored environment only Adenosine Indications: • Undiagnosed narrow complex tachycardia • Paroxysmal supraventricular tachycardia Adenosine Dose: • 6 mg intravenously, by rapid injection to achieve adequate and effective blood levels If necessary, three further doses each of 12 mg can be given every 1–2 min Magnesium sulphate Constituent involved in ATP generation in muscle, neurochemical transmission: • • • • • decreases acetylcholine release reduces the sensivity of the motor endplate improves the contractile response limits infarct size acts as a physiological calcium blocker Hypomagnesaemia contribute to arrhythmias and cardiac arrest !!! Magnesium sulphate Indications: • Shock refractory VF (in the presence of possible hypomagnesaemia) • Ventricular tachyarrhythmias (in the presence of possible hypomagnesaemia) • Digoxin toxicity (hypomagnesaemia increases myocardial digoxin uptake) Magnesium sulphate Dose: Shock Refractory VF • Initial dose – 2g (4 ml (8 mmol)) of 50% magnesium sulphate i.v. over 1 – 2 min • It may be repeated after 10-15 min Other drugs OXYGEN – high concentration should be given to all patients in cardiac arrest Atropine Antagonises the action of the parasympthatetic neurotransmitter acetylcholine at muscarinic receptors: • blocks effects of the vagus nerve on SA and AV nodes • increases sinus node automaticity • increases atrioventricular conduction Atropine Indications: • Asystole • PEA (rate < 60 beats/min) • Sinus, atrial or node bradycardia – unstable haemodynamic condition Atropine Dose: • Asystole / PEA (rate < 60 beats/min) – 3 mg i.v., single bolus – 6 mg via tracheal tube • Bradycardia – 0.5 mg i.v., repeated as necessary, maximum 3 mg Theophylline Phosphodiesterase inhibitor that: • Increases tissue concentrations of cAMP and releases adrenaline from adrenal medulla • Has chronotropic and inotropic action Theophylline Indications: • Asatolic cardiac arrest • Peri-arrest bradycardia refractory to atropine Doses: Recommended for adults: 250 – 500mg (5mg/kg) (narrow therapeutic window, optimal plasma concentration 10 – 20mg/l) • Side effects: arrhythmias, convulsions Sodium Bicarbonate (Buffer) Indications: • Severe metabolic acidosis (pH < 7.1) • Hyperkalaemia • Special circumstance – Tricyclic antidepressant poisoning Sodium Bicarbonate (Buffer) Agent used in treatment of acidaemia in cardiac arrest but generate carbon dioxide, which diffuses rapidly into cells: – exacerbates intracellular acidosis – produces a negative inotropic effect on ischaemic myocardium – causes hypernatraemia – Compromises circulation and brain – interact with adrenaline Sodium Bicarbonate Dose: • 50 mmol (50 ml of 8.4% solution) i.v. Calcium Constituent essential for normal cardiac contraction, but: •high plasma concentrations are harmful to the ischaemic myocardium and impair cerebral recovery • excess may lead to arrhythmias Calcium Indications: • Pulseless electrical activity caused by: – severe hyperkalaemia – severe hypocalcaemia – overdose of calcium channel blocking drugs Dose • 10 ml 10% calcium chloride (6.8 mmol) • May be repeated (Do not give immediately before or after sodium bicarbonate) Naloxone Indications: • Opioid overdose • Respiratory depression secondary to opioid administration Naloxone Actions: • Opioid receptor antagonist • Reverses all opioid effects, particularly respiratory and cerebral • May cause severe agitation in opioid dependence Naloxone Dose: • 0.2 - 2.0 mg i.v. • May need to be repeated up to a maximum of 10 mg • May need an infusion Route alternative routes for drug delivery • If a peripheral cannula is in place and working, use it initially • Central veins are the route of choice if expertise is available • The tracheal route can be used with appropriate adjustment of dose • Intraosseous route – drugs will achieve adequate plasma concentrations, safe and effective, may be used for children and adults Tracheal administration of drugs • • • • Drugs that can be given via the trachea: Adrenaline Lidocaine Atropine Naloxone Drugs that cannot be given via the trachea • Amiodarone • Sodium bicarbonate • Calcium European Resuscitation Council Guidelines for Resuscitation Adult advanced life support ALS Algorithm Unresponsive ? Open Airway Look for signs of life Call Resuscitation Team CPR 30:2 Until defibrillator / monitor attached Assess Rhythm Shockable Non-shockable (VF/ Pulsless VT) (PEA / Asystole) 1 Shock 150-360 J biphasic lub 360 J monophasic During CPR: •Correct reversible causses •Check electrode position and contact •Attempt / verify: •IV access •Airway and oxygen •Give uninterrupted compressions when airway secure •Give adreanline every 3-5 mins •Consider: amiodarone, atropine, magnesium Immediately resume: CPR 30:2 For 2 min CPR 30:2 For 2 min * Reversible Hipoxia Hipovolaemia Hipo/Hiperkalaemia / Metabolic Hipothermia Immediately resume: causes Tension pneumothorax Tamponade cardiac Toxins Thrombosis (coronary or pulmonary) Confirm Cardiac Arrest Precordial thump CPR 30:2 Until defibrillator / monitor attached Call Resuscitation Team Assess rhythm The interventions that contribute to improved survival after CA: •Early defibryllation (VT/VF) •Prompt and effective bystander basic life support (BLS) •Advanced airway intervention and the delivery of drugs – have not been shown to increase survival after cardiac arrest (CA) •During ALS – attention must be focused on early defibrillation and high-quality, uninterrupted BLS Precordial thump • Indication: – witnessed or monitored cardiac arrest (defibrillator is not immediately to hand) A precordial thump is most likely to be sucessful in converting VT Converting VF to sinus rhythm is much less likely Shochable rhythms (ventricular fibryllation / pulsless ventricular tachycardia) Assess rhythm Shockable (VF/pulsless VT) 1 Shock 150-360 J (biphasic) or 360 J (monophasic) Immediately resume: CPR 30:2 for 2 min If shockable rhythm is confirmed: •Charge the defibrillator •Give one shock (biphasic or monophasic energy) •Resume CPR immediately after shock without reassessing the rhythm for 2 min(CV ratio 30:2) •Check the monitor •If there is still VF/VT give next shock •Resume CPR immediately - 2min •Check the monitor •If there is still VF/VT give adrenaline followed immediately by a third shock •Resumption of CPR SEQUENCE •DRUG – shock – CPR – rhythm check •Minimise the delay between stopping chest Compressions and delivery of shock ERC Guidelines 2005 Cardiac arrest VF/VT •Adrenaline – give immediately before the shock 1 mg every 3-5min (start followed the third shock) •Amiodarone – if VT/VF persists after third shock 300 mg iv bolus during rhythm analysis before delivery of the fourth shock •Drug – shock – CPR – rhythm check SEQUENCE STOP of the algorithm •If signs of life return during CPR – movement, normal breathing or coughing •Check the monitor: •Organised rhythm present •Check for a pulse •Pulse palpable •ROSC •Continue post-resuscitation care (PRC) •Pulse not present •Continue CPR During CPR: •Correct reversible causses •Check electrode position and contact •Attempt / verify: •IV access •Airway and oxygen •Give uninterrupted compressions when airway secure •Give adreanline every 3-5 mins •Consider: amiodarone, atropine, magnesium Airway and ventilation • Personnel skilled in advanced airway management: – Attempt laryngoscopy and tracheal intubation • Personnel not skilled: – Laryngeal mask (LMA) – Laryngeal tube (LT) – Combitube • After airways insertion: – Attempt to deliver continous chest compressions, uninterrupted durin ventilation – Ventilate the lungs at 10 breaths per min Intravenous access and drugs • Central venous drug delivery • Peripheral venous drug delivery – flush cannula of 20ml fluid and elevate of the extremity • Intraosseous route – alternative route for vascular access in children (drug dose like in iv access) • Tracheal route – dose of adrenaline is 3mg diluted to 10ml with sterile water Non-shockable rhythms (PEA and asystole) Assess rhythm Nonshockable (PEA / asystole) Immediately resume: CPR 30:2 for 2 min Asystole • Start CPR (CV ratio 30:2) – Check that the leads are attached correctly • Give adrenaline – as soon iv access is achieved 1 mg every 3 - 5 mins • Atropina 3 mg i.v. – will provide max. vagal blokade • Secure the airway • After 2 min CPR – No change in ECG appearance – resume CPR – Organised rhythm is present – check the pulse • Pulse is present – begin PRC • Pulse is not present – resume CPR Pulseless electrical activity (PEA) • Start CPR (CV ratio 30:2) – Check that the leads are attached correctly • • • • • Give adrenaline Atropine 3 mg i.v. – rhythm rate < 60/min Secure the airway Check potentially reversible causes (4 Hs, 4Ts) After 2 min CPR – No change in ECG appearance – resume CPR – Organised rhythm is present – check the pulse • Pulse is present – begin PRC • Pulse is not present – resume CPR Potentially reversible causes: •Hypoxia •Hypovolaemia •Hypo / hyperkalaemia, metabolic disorders •Hypothermia •Tension pneumothorax •Cardiac tamponade •Toxins •Thrombosis (coronary or pulmonary) Post Resuscitation Care The goal: • Normal cerebral function • Stable cardiac rhythm • Adequate organ perfusion Summary • In patients in VF/pulseless VT attempt defibrillation without delay • In patients in refractory VF or with a non-VF/VT rhythm identify and treat any reversible cause