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Acute coronary disorders Drugs in cardiopulmonary resuscitation

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

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Acute coronary disorders Drugs in cardiopulmonary resuscitation

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  1. Acute coronary disordersDrugs in cardiopulmonary resuscitation Advanced Life Support (ALS) algorithm

  2. Acute coronary syndromes

  3. 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

  4. 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

  5. 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

  6. 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)

  7. Non-Q wave myocardial infarction • The clinical syndrome presenting with symptoms suggestive of acute MI and non-specific 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

  8. 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

  9. Q wave myocardial infarction

  10. 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

  11. „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 !!!

  12. 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

  13. 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)

  14. 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

  15. Möbitz Type II Block Bradycardia – heart rate < 60/min 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

  16. 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

  17. Broad Complex Tachycardia Adverse signs: • Rate > 150/min • Chest pain • Heart failure • Systolic blood pressure < 90 mmHg Treatment: • Amidarone, lidocaine • DC shock

  18. Atrial fibrillation Adeverse signs: • Rate > 150/min • Ongoing chest pain • Critical perfusion • Breathlessness Treatment: • Anticoagulation, beta-blockers, digoxin, amiodarone • Synchronised DC shock

  19. DRUGSfor cardiacarrest

  20. Thereare 3 groups of drugsrelevant to the management of cardiacarrest: Vasopressors Anti-arrhytmics Otherdrugs Drugsshould be consideredonlyafterinitialshockshavebeendelivered and chestcompressions and ventilationhavebeenstarted.

  21. Adrenaline (epinephrine)primery agent for the management of cardiacarrest Itsprimaryefficacyisdue to effects: -adrenergic – arterial vasoconstriction •  systemic vascular resistance • coronary and cerebralperfusionpressures -adrenergic – coronarybloodflow  force of contraction  myocardial O2consumption (may increase ischaemia)

  22. Adrenaline Indications: • The first drugusedincardiacarrest of anyethiology • Second-linetreatment for cardiogenicshock • Preferredinthe special circumstances: • anaphylaxis

  23. Adrenaline Dose: • 1 mg intravenous (1 ml sol. 1:1,000) every 3-5 min of CPR • 2-3 mgdiluted to 10ml withsterilewater via tracheal tube • 2–10 mcg/mincontinousinfusion for atropine resistant bradycardia, hypotensivepatients • 0.5ml 1:1,000 i.m., 3-5 ml (sol.1:10,000)i.v. - in anaphylaxis, depending on severity

  24. Vasopressin • Naturallyoccuringantidiuretichormone • High doses – powerfulvasoconstricorthatacts by stimulation of smoothmuscle V1 receptors • AHA – recommendedvasopressin as an alternative to adrenaline for thetreatment of adultshock-refractory VF • Dose – 40 U (comp. 1mg adrenaline) • Currently – insufficientevidence of improvementinsurvival to discharge

  25. Anti-arrhythmics

  26. Amiodarone - membrane-stabilisingdrugthatincreases: • duration of theaction potential • refractory period inatrial and vetricularmyocardium • mild negative inotropic action - may cause hypotension • appers to improvetheresponse to defibryllation

  27. Amiodarone Indications: • Refractory VF / Pulseless VT • Haemodynamically stable VT • Other resistant tachyarrhythmias

  28. Amiodarone Dose: • Refractory VF / Pulseless VT • 300 mg dilutedin 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

  29. Lidocaine Membrane-stabilisingdrugthatacts by: • increasingthemyocyterefractory period • decreasesvetricularautomaticity • Suppressesventricularectopicactivity – mainlyinarrhythmogenictissues, minimallywithelectricalactivity of normaltissues Lidocainetoxicity: • paraesthesia • drowsiness • confusion • convulsions

  30. Lidocaine Indications: • Refractory VF / Pulseless VT • when amiodarone is unavailable • Haemodynamically stable VT • as an alternative to amiodarone

  31. Lidocaine Dose: • Refractory VF / Pulseless VT • initial100 mg i.v. (1 – 1.5mg/kg) • further boluses 50mg, • Haemodynamically stable VT • 50 mg i.v. • further boluses of 50 mg, • Total doseshould not exceed 3mg/kg duringthefirthour • Reduce dose in elderly or hepatic failure

  32. Adenosine Naturallyoccuringpurinenucleotide: • Slows conduction across the AV node, • Has littleeffectothermyocardialcells • Has shortduration of action • May revealtheunderlyingatrialrhythms by slowingtheventricularresponse Should be used in a monitored environmentonly

  33. Adenosine Indications: • Undiagnosednarrowcomplex tachycardia • Paroxysmal supraventricular tachycardia

  34. Adenosine Dose: • 6 mg intravenously, by rapid injection to achieveadequate and effectivebloodlevels If necessary, three further doses each of 12 mg can be given every 1–2 min

  35. Magnesiumsulphate Constituentinvolvedin ATP generationinmuscle, neurochemicaltransmission: • decreasesacetylcholinerelease • reducesthesensivity of the motor endplate • improvesthecontractileresponse • limitsinfarctsize • acts as a physiological calcium blocker Hypomagnesaemiacontribute to arrhythmias and cardiacarrest !!!

  36. Magnesiumsulphate Indications: • Shock refractory VF (inthepresence of possible hypomagnesaemia) • Ventricular tachyarrhythmias (inthepresence of possible hypomagnesaemia) • Digoxintoxicity (hypomagnesaemiaincreasesmyocardialdigoxinuptake)

  37. Magnesiumsulphate Dose: Shock Refractory VF • Initialdose – 2g (4 ml (8 mmol)) of 50% magnesiumsulphatei.v. over 1 – 2 min • Itmay be repeated after 10-15 min

  38. Other drugs OXYGEN – high concentration should be given to all patients in cardiac arrest

  39. Atropine Antagonisesthe action of theparasympthateticneurotransmitteracetylcholineatmuscarinicreceptors: • blocks effects of thevagus nerve on SA and AV nodes • increases sinus node automaticity • increasesatrioventricular conduction

  40. Atropine Indications: • Asystole • PEA (rate < 60 beats/min) • Sinus, atrialornodebradycardia – unstablehaemodynamiccondition

  41. 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

  42. Theophylline Phosphodiesterase inhibitor that: • Increases tissue concentrations of cAMP and releases adrenaline from adrenal medulla • Has chronotropic and inotropic action

  43. Theophylline Indications: • Asatoliccardiacarrest • Peri-arrestbradycardiarefractory to atropine Doses: Recommended for adults: 250 – 500mg (5mg/kg) (narrowtherapeuticwindow, optimalplasmaconcentration 10 – 20mg/l) • Sideeffects: arrhythmias, convulsions

  44. Sodium Bicarbonate(Buffer) Indications: • Severe metabolic acidosis (pH < 7.1) • Hyperkalaemia • Special circumstance • Tricyclic antidepressant poisoning

  45. Sodium Bicarbonate(Buffer) Agent usedintreatment of acidaemiaincardiacarrest butgeneratecarbondioxide, whichdiffusesrapidlyintocells: • exacerbatesintracellularacidosis • produces a negativeinotropiceffect on ischaemicmyocardium • causeshypernatraemia • Compromisescirculation and brain • interact with adrenaline

  46. Sodium Bicarbonate Dose: • 50 mmol (50 ml of 8.4% solution) i.v.

  47. Calcium Constituent essential for normal cardiac contraction, but: • high plasmaconcentrationsareharmful to theischaemicmyocardium and impaircerebralrecovery • excess may lead to arrhythmias

  48. 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)

  49. Naloxone Indications: • Opioid overdose • Respiratory depression secondary to opioid administration

  50. Naloxone Actions: • Opioid receptor antagonist • Reverses all opioid effects, particularly respiratory and cerebral • May cause severe agitation in opioid • dependence

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