Acute coronary disordersDrugs in cardiopulmonary

resuscitationAdvanced 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 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

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

Adverse signs:• Systolic blood pressure < 90 mmHg• Heart rate < 40/min• Ventricular arrhytmias requiring suppresion• Heart failureTreatment:• Atropine• Cardiac pacing – presence the risk os asystole

Möbitz Type II Block

Narrow Complex Tachycardia

Adverse sins:• Systolic blood pressure < 90 mmHg• Chest pain• Heart failure• Impaired consciousness• Heart rate > 200 beats/minTreatment:• Antiarrhythmic drugs – esmolol, amidarone• DC shock

Broad Complex Tachycardia

Adverse signs:• Rate > 150/min• Chest pain• Heart failure• Systolic blood pressure < 90 mmHgTreatment:• Amidarone, lidocaine• DC shock

Atrial fibrillation

Adeverse signs:• Rate > 150/min• Ongoing chest pain• Critical perfusion• BreathlessnessTreatment:• Anticoagulation, beta-blockers, digoxin, amiodarone• Synchronised DC shock

DRUGSDRUGSfor cardiac arrestfor 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)Adrenaline (epinephrine)primery agent for the management of cardiac arrestprimery agent for the management of cardiac arrest

Its primary efficacy is due to effects:Its primary efficacy is due to effects:

-adrenergic – -adrenergic – arterial vasoconstrictionarterial vasoconstriction systemic vascular resistance systemic vascular resistance coronary and cerebral perfusion coronary and cerebral perfusion pressurespressures

-adrenergic – -adrenergic – coronary blood flowcoronary blood flow force of contractionforce of contraction myocardial Omyocardial O22 consumptionconsumption (may increase ischaemia)(may increase ischaemia)

AdrenalineAdrenaline

Indications:Indications:

• The first drug used in cardiac arrest of The first drug used in cardiac arrest of any ethiologyany ethiology

• Second-line treatment for cardiogenic Second-line treatment for cardiogenic shockshock

• Preferred in the sPreferred in the special circumstances:pecial circumstances:– anaphylaxisanaphylaxis

AdrenalineAdrenalineDose:Dose:

• 1 mg intravenous (1 ml 1 mg intravenous (1 ml sol.sol. 1:1,000) every 1:1,000) every 3-3-55 min min of CPRof CPR

• 2-3 mg2-3 mg diluted to 10ml with sterile water diluted to 10ml with sterile water via via tracheal tubetracheal tube

• 2–10 mcg2–10 mcg//minmin continous infusion continous infusion for for atropine resistant bradycardiaatropine resistant bradycardia, hypotensive , hypotensive patientspatients

• 0.5ml 1:1,000 i.m., 3-5 ml 0.5ml 1:1,000 i.m., 3-5 ml (sol.(sol.1:10,0001:10,000)) i.v. i.v. - - in anaphylaxis, depending on severityin 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

AmiodaroneAmiodarone

- membrane-stabilising drug that - membrane-stabilising drug that increases:increases:– duration of duration of the the action potentialaction potential– refractory period in atrial and vetricular refractory period in atrial and vetricular

myocardiummyocardium– mmild negative inotropild negative inotropic actionic action - may cause - may cause

hypotensionhypotension– appers to improve the response to appers to improve the response to

defibryllationdefibryllation

AmiodaroneAmiodarone

Indications:Indications:

• Refractory VF / Pulseless VTRefractory VF / Pulseless VT• Haemodynamically stable VTHaemodynamically stable VT• Other resistant tachyarrhythmiasOther resistant tachyarrhythmias

AmiodaroneAmiodaroneDose:Dose:

• Refractory VF / Pulseless VTRefractory VF / Pulseless VT– 300 mg 300 mg diluted diluted in 5% dextrosein 5% dextrose to a volume of 20ml to a volume of 20ml, ,

• Stable tachyarrhythmiasStable tachyarrhythmias– 150 mg in 5% dextrose over 10 min150 mg in 5% dextrose over 10 min– Repeat 150 mg if necessaryRepeat 150 mg if necessary– 300 mg in 100 ml 5% dextrose over 1 hour300 mg in 100 ml 5% dextrose over 1 hour

LidocaineLidocaineMembrane-stabilising drug that acts by:Membrane-stabilising drug that acts by:• increasing the myocyte refractory periodincreasing the myocyte refractory period• decreases vetricular automaticitydecreases vetricular automaticity• Suppresses ventricular ectopic activity – mainly in Suppresses ventricular ectopic activity – mainly in

arrhythmogenic tissues, minimally with electrical arrhythmogenic tissues, minimally with electrical activity of normal tissuesactivity of normal tissues

Lidocaine toxicity:Lidocaine toxicity:• paraesthesiaparaesthesia• drowsinessdrowsiness• confusionconfusion• convulsionsconvulsions

LidocaineLidocaine

Indications:Indications:

• Refractory VF / Pulseless VTRefractory VF / Pulseless VT– when amiodarone is unavailablewhen amiodarone is unavailable

• Haemodynamically stable VTHaemodynamically stable VT– as an alternative to amiodaroneas an alternative to amiodarone

LidocaineLidocaine

Dose:Dose:• Refractory VF / Pulseless VTRefractory VF / Pulseless VT

– initial initial 100 mg i.v.100 mg i.v. (1 – 1.5mg/kg) (1 – 1.5mg/kg) – further bolusesfurther boluses 50mg, 50mg,

• Haemodynamically stable VTHaemodynamically stable VT– 50 mg i.v.50 mg i.v.– further boluses of 50 mg,further boluses of 50 mg,

• Total dose should not exceed 3mg/kg Total dose should not exceed 3mg/kg during the firt hourduring the firt hour

• Reduce dose in elderly or hepatic failureReduce dose in elderly or hepatic failure

AdenosineAdenosine

Naturally occuring purine nucleotide:Naturally occuring purine nucleotide:• Slows conduction across the AV nodeSlows conduction across the AV node,,• Has little effect other myocardial cellsHas little effect other myocardial cells• Has short duration of actionHas short duration of action• May reveal the underlying atrial rhythms by slowing May reveal the underlying atrial rhythms by slowing

the ventricular responsethe ventricular response

ShouldShould be used in a monitored environment be used in a monitored environment onlyonly

AdenosineAdenosine

Indications:Indications:

• Undiagnosed narrow Undiagnosed narrow complex tachycardiacomplex tachycardia

• Paroxysmal supraventricular tachycardiaParoxysmal supraventricular tachycardia

AdenosineAdenosine

Dose:Dose:

• 6 mg intravenously, by rapid injection6 mg intravenously, by rapid injection to achieve adequate and effective to achieve adequate and effective blood levelsblood levels

If necessary, three further doses each of If necessary, three further doses each of 12 mg can be given every 1–2 min12 mg can be given every 1–2 min

MagnesiumMagnesium sulphate sulphate

Constituent involved in ATP generation in Constituent involved in ATP generation in muscle, neurochemical transmission:muscle, neurochemical transmission:

• decreases acetylcholine releasedecreases acetylcholine release• reduces the sensivity of the motor endplatereduces the sensivity of the motor endplate• improves the contractile responseimproves the contractile response• limits infarct sizelimits infarct size• aacts as a physiological calcium blockercts as a physiological calcium blocker

Hypomagnesaemia contribute to arrhythmias Hypomagnesaemia contribute to arrhythmias and cardiac arrest !!!and cardiac arrest !!!

MagnesiumMagnesium sulphate sulphate

Indications:Indications:

• Shock refractory VF Shock refractory VF ((in the presence ofin the presence of possible hypomagnesaemia) possible hypomagnesaemia)

• Ventricular tachyarrhythmias Ventricular tachyarrhythmias ((in the presence ofin the presence of possible hypomagnesaemia) possible hypomagnesaemia)

• Digoxin toxicityDigoxin toxicity(hypomagnesaemia increases myocardial digoxin (hypomagnesaemia increases myocardial digoxin

uptake)uptake)

MagnesiumMagnesium sulphate sulphateDose:Dose:

Shock Refractory VFShock Refractory VF• Initial dose – Initial dose – 22g (g (4 ml (8 mmol)4 ml (8 mmol)) of 50% magnesium ) of 50% magnesium

sulphatesulphate i.v. over i.v. over 1 – 21 – 2 min min• It mayIt may be repeated after 10-15 min be repeated after 10-15 min

Other drugs

OXYGEN – high concentration should be given to all patients in cardiac

arrest

AtropineAtropine

AAntagonises the action of the parasympthatetic ntagonises the action of the parasympthatetic

neurotransmitter acetylcholine at muscarinic neurotransmitter acetylcholine at muscarinic

receptors:receptors:• bblocks effects of locks effects of the the vagus nervevagus nerve on SA and on SA and

AV nodes AV nodes • iincreases sinus node automaticityncreases sinus node automaticity• iincreases atrioventricular conductionncreases atrioventricular conduction

AtropineAtropine

Indications:Indications:

• AsystoleAsystole• PEA (rate < 60 beatsPEA (rate < 60 beats//min)min)• Sinus, atrial or node bradycardia – Sinus, atrial or node bradycardia –

unstable haemodynamic conditionunstable haemodynamic condition

AtropineAtropineDose:Dose:• Asystole / PEA (rate < 60 beatsAsystole / PEA (rate < 60 beats//min)min)

– 3 mg i.v., 3 mg i.v., single bolussingle bolus– 6 mg via tracheal tube6 mg via tracheal tube

• BradycardiaBradycardia– 0.5 mg i.v., repeated as necessary, 0.5 mg i.v., repeated as necessary,

maximum 3 mg 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 atropineDoses:Recommended for adults: 250 – 500mg (5mg/kg)(narrow therapeutic window, optimal plasma

concentration 10 – 20mg/l)

• Side effects: arrhythmias, convulsions

Sodium BicarbonateSodium Bicarbonate (Buffer)(Buffer)

Indications:Indications:

• Severe metabolic acidosis (pH < 7.1)Severe metabolic acidosis (pH < 7.1)

• HyperkalaemiaHyperkalaemia

• Special circumstanceSpecial circumstance– Tricyclic antidepressant poisoning Tricyclic antidepressant poisoning

Sodium BicarbonateSodium Bicarbonate (Buffer)(Buffer)

Agent used in treatment of acidaemia in Agent used in treatment of acidaemia in cardiac arrest bcardiac arrest butut generate carbon generate carbon dioxide, which diffuses rapidly into cellsdioxide, which diffuses rapidly into cells::

– exacerbates intracellular acidosisexacerbates intracellular acidosis– produces a negative inotropic effect on produces a negative inotropic effect on

ischaemic myocardiumischaemic myocardium– causecausess hypernatraemia hypernatraemia– Compromises circulation and brainCompromises circulation and brain– interact with adrenalineinteract with adrenaline

Sodium BicarbonateSodium Bicarbonate

Dose:Dose:

• 50 mmol (50 ml of 8.4% solution) i.v.50 mmol (50 ml of 8.4% solution) i.v.

CalciumCalcium

Constituent eConstituent essential for normal cardiac ssential for normal cardiac contractioncontraction, but:, but:

•high plasma concentrations are harmful to high plasma concentrations are harmful to the ischaemic myocardium and impair the ischaemic myocardium and impair cerebral recoverycerebral recovery

• eexcess may lead to arrhythmiasxcess may lead to arrhythmias

CalciumCalcium

Indications:Indications:• Pulseless electrical activity caused by:Pulseless electrical activity caused by:

– severe hyperkalaemiasevere hyperkalaemia– severe hypocalcaemiasevere hypocalcaemia– overdose of calcium channel blocking drugsoverdose of calcium channel blocking drugs

DoseDose• 10 ml 10% calcium chloride (6.8 mmol)10 ml 10% calcium chloride (6.8 mmol)• May be repeatedMay be repeated

(D(Do not give immediately before or after sodium bicarbonateo not give immediately before or after sodium bicarbonate))

NaloxoneNaloxone

Indications:Indications:

• Opioid overdoseOpioid overdose

• Respiratory depression secondary to Respiratory depression secondary to opioid administrationopioid administration

NaloxoneNaloxone

Actions:Actions:

• Opioid receptor antagonistOpioid receptor antagonist• Reverses all opioid effects, particularly Reverses all opioid effects, particularly

respiratory and cerebralrespiratory and cerebral• May cause severe agitation in opioid May cause severe agitation in opioid dependencedependence

NaloxoneNaloxone

Dose:Dose:

• 0.2 - 2.0 mg i.v.0.2 - 2.0 mg i.v.• May need to be repeated up to a May need to be repeated up to a

maximum of 10 mgmaximum of 10 mg• May need an infusionMay need an infusion

RouteRoutealternative routes for drug deliveryalternative routes for drug delivery

• If a peripheral cannula is in place and working, If a peripheral cannula is in place and working, use it initiallyuse it initially

• Central veins are the route of choice if expertise is Central veins are the route of choice if expertise is availableavailable

• The tracheal route can be used with appropriate The tracheal route can be used with appropriate adjustment of dose adjustment of dose

• Intraosseous route – drugs will achieve adequate Intraosseous route – drugs will achieve adequate plasma concentrations, safe and effective, may be plasma concentrations, safe and effective, may be used for children and adultsused for children and adults

Tracheal administration of drugsTracheal administration of drugs

Drugs that Drugs that cancan be be given via the given via the trachea:trachea:

• AdrenalineAdrenaline• LidocaineLidocaine• AtropineAtropine• NaloxoneNaloxone

Drugs that Drugs that cannotcannot be be given via the tracheagiven via the trachea

• AmiodaroneAmiodarone• Sodium bicarbonateSodium bicarbonate• CalciumCalcium

European Resuscitation Council Guidelines for Resuscitation

Adult advanced life supportALS Algorithm

CPR 30:2Until defibrillator / monitor attached

AssessRhythm

Shockable(VF/ Pulsless VT)

Non-shockable(PEA / Asystole)

1 Shock150-360 J biphasic

lub 360 J monophasic

Immediately resume:

CPR 30:2 For 2 min

CallResuscitationTeam

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

* Reversible causesHipoxia Tension pneumothorax Hipovolaemia Tamponade cardiacHipo/Hiperkalaemia / Metabolic Toxins Hipothermia Thrombosis (coronary or pulmonary)

Immediately resume:

CPR 30:2For 2 min

Open AirwayLook for signs of lifeUnresponsive ?

CPR 30:2Until defibrillator / monitor attached

Assessrhythm

CallResuscitationTeam

Precordial thump

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

Confirm Cardiac Arrest

Precordial thumpPrecordial thump

• Indication:Indication:– witnessed or witnessed or

monitored cardiac monitored cardiac arrestarrest

(defibrillator is not immediately to (defibrillator is not immediately to

hand)hand) A precordial thump is most A precordial thump is most

likely to be sucessful in likely to be sucessful in converting VTconverting VT

Converting VF to sinus Converting VF to sinus rhythm is much less rhythm is much less likelylikely

Shochable rhythms(ventricular fibryllation / pulsless ventricular tachycardia)

Shockable(VF/pulsless VT)

1 Shock150-360 J (biphasic)

or 360 J (monophasic)

Immediately resume:

CPR 30:2 for 2 min

Assess rhythm

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 CPRSEQUENCE•DRUG – shock – CPR – rhythm check•Minimise the delay between stopping chest Compressions and delivery of shock

ERC Guidelines 2005Cardiac 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

Assessrhythm

Non-shockable(PEA / asystole)

Immediately resume:

CPR 30:2 for 2 min

Non-shockable rhythms (PEA and asystole)

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 CarePost Resuscitation Care

The goal:The goal:

• Normal cerebral functionNormal cerebral function

• Stable cardiac rhythmStable cardiac rhythm

• Adequate organ perfusionAdequate organ perfusion

SummarySummary

• In patients in VF/pulseless VT attempt In patients in VF/pulseless VT attempt defibrillation without delaydefibrillation without delay

• In patients in refractory VF or with a In patients in refractory VF or with a non-VF/VT rhythm identify and treat non-VF/VT rhythm identify and treat any reversible causeany reversible cause