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 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 ( 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 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 3-
5 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 Drugs that cannot be
given via the given via the trachea
trachea: • Amiodarone
• Adrenaline • Sodium bicarbonate
• Lidocaine • Calcium
• Atropine
• Naloxone
European Resuscitation Council
Guidelines for Resuscitation
Adult advanced life support
ALS Algorithm
Call
Open Airway Resuscitation
Unresponsive ? Look for signs of life Team
CPR 30:2
Until defibrillator / monitor attached
Assess
Rhythm
Shockable Non-shockable
(VF/ Pulsless VT) (PEA / Asystole)
During CPR:
1 Shock •Correct reversible causses
•Check electrode position and contact
150-360 J biphasic •Attempt / verify:
lub 360 J monophasic •IV access
•Airway and oxygen
•Give uninterrupted compressions when airway secure
•Give adreanline every 3-5 mins
•Consider: amiodarone, atropine, magnesium
Immediately resume: Immediately resume:
CPR 30:2 CPR 30:2
For 2 min For 2 min
* Reversible causes
Hipoxia Tension pneumothorax
Hipovolaemia Tamponade cardiac
Hipo/Hiperkalaemia / Metabolic Toxins
Hipothermia Thrombosis (coronary or pulmonary)
Confirm
Cardiac Arrest
Call
Precordial thump CPR 30:2 Resuscitation
Until defibrillator / monitor attached 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
If shockable rhythm is confirmed:
•Charge the defibrillator
Shockable •Give one shock (biphasic or monophasic energy)
(VF/pulsless VT)
•Resume CPR immediately after shock without
reassessing the rhythm for 2 min(CV ratio 30:2)
•Check the monitor
1 Shock •If there is still VF/VT give next shock
150-360 J (biphasic) •Resume CPR immediately - 2min
or 360 J •Check the monitor
(monophasic)
•If there is still VF/VT give adrenaline followed
immediately by a third shock
•Resumption of CPR
Immediately resume:
CPR 30:2 SEQUENCE
for 2 min •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
Non-
shockable
(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