Adult ACLS 2010
อ.นพ.อนทนนท อมสุวรรณ
โครงการจัดตัวรรณ
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คณะแพทยงภาควชาเวชศาสุวรรณ
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eกเฉุกเฉิน
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eน
คณะแพทยศาสุวรรณ
โครงการจัดตัตั้งภาควิชาเวชศาสตร์ฉุกเฉิน
คณะแพทยร มหาวทยา"ยธรรมศาสุวรรณ
โครงการจัดตัตั้งภาควิชาเวชศาสตร์ฉุกเฉิน
คณะแพทยร

Key changes from the 2005 ACLS
Guidelines
 Continuous

quantitative waveform capnography is recommended for confirmation and monitoring of endotracheal t ube placement

 Cardiac

arrest algorithms are simplified and redesigned to emphasize the importance of hig h-quality CPR

Key changes from the 2005 ACLS Guidelines


Atropine is no longer recommended for routine use in the management of PEA/asystole

 There

is an increased emphasis on physiologic monitoring to optimize CPR quality and detec t ROSC

Key changes from the 2005 ACLS Guidelines
 Chronotropic

drug infusions are recommended as an alternative to pacing in symptomatic and unstable bradycardia

 Adenosine

is recommended as a safe and potentially effective therapy in the initial mana gement of stable undifferentiated regular mono morphic wide-complex tachycardia

Topic in ACLS 2010
 Management
 Management

of Cardiac Arrest

of Symptomatic Bradycardia and Tachycardia

Management of Cardiac Arrest

Management of Cardiac Arrest
 Early

CPR and rapid defibrillation can significantly increase the chance for survival to hospital discharge

Management of Cardiac Arrest
 Medications

and advanced airways associated with an increased rate of ROSC
• But have not been shown to increase the rate of

survival to hospital discharge

 Higher

quality CPR and post– cardiac arrest interventions improved long-term outcomes

 Vascular

access, drug delivery, advanced airway placement should not cause significant

interruptions in chest compression or delay defibrillation Drug Therapy in VF/
Pulseless VT
Amiodarone
• First-line antiarrhythmic agent given during

cardiac arrest
• Clinically demonstrated to improve the rate of

ROSC and hospital admission in adults with refract ory VF/pulseless VT

 Amiodarone

• Considered for VF or pulseless VT unresponsive

to CPR, defibrillation, vasopressor therapy(Clas s IIb, LOE B)

• Initial dose 300 mg IV/IO followed by 1

dose of 150 mg IV/IO

Lidocaine
• A retrospective review
 association between improved hospital admission rates and use of lidocaine in patients with out-of-hospital VF ca rdiac arrest

• Lidocaine has not been demonstrated to improve

rates of ROSC and hospital admission compared wit h amiodarone

Lidocaine
• Alternative antiarrhythmic
 long-standing and widespread familiarity with fewer immediate side effects

• No proven short- or long-term efficacy in cardiac

arrest
• Lidocaine may be considered if amiodarone is not

available (Class IIb, LOE B)

Lidocaine
• Initial dose is 1 to 1.5 mg/kg IV
• If VF/pulseless VT persists
 additional doses of 0.5 to 0.75 mg/kg IV push
 administered at 5- to 10-minute intervals to a maximum dose of 3 mg/kg

Interventions Not Recommended for
Routine Use During Cardiac Arrest
 Routine

use atropine

• No prospective controlled clinical trials have

examined the use of atropine in asystole or bradycar dic PEA cardiac arrest
 Pro

• There is no evidence that atropine has detrimental

effects during bradycardic or asystolic cardiac arres t  Cons

• Lower-level clinical studies provide conflicting

 Routine

use of atropine during PEA or asystole is unlikely to have a therapeutic benefit Interventions Not Recommended for
Routine Use During Cardiac Arrest
 Sodium

Bicarbonate

 Pro

• Two studies demonstrated increased ROSC, hospital

admission, and survival to hospital discharge associated with use of bicarbonate
 Cons

• Majority of studies showed no benefit or found a

relationship with poor outcome

 Disadvantages

of sodium Bicarbonate

• Compromise CPP by reducing systemic vascular

resistance
• Exacerbate central venous acidosis
• Create extracellular alkalosis
 Shift the oxyhemoglobin saturation curve ,inhibit oxygen release • Produces excess CO2
 Freely diffuses into myocardial and cerebral cells and may paradoxically contribute to intracellular acidosis

 Advantages

• Preexisting metabolic acidosis
• Hyperkalemia
• Tricyclic antidepressant overdose

 Routine

use of sodium bicarbonate is not recommended for patients in cardiac arrest (Class
III, LOE B)

 Dose

• Initial dose of 1 mEq/kg
• Bicarbonate therapy should be guided by
 bicarbonate concentration or calculated base deficit obtained from blood gas analysis or laboratory measurement

• To minimize the risk of iatrogenically induced alkalosis
 providers should not attempt complete correction of the calculated base deficit

Interventions Not Recommended for
Routine Use During Cardiac Arrest
 Calcium

• No trial has found a beneficial effect on survival either

in or out of hospital
• Routine administration is not recommended (Class

III, LOE B)

Monitoring During CPR
 Mechanical

Parameters

 Physiologic

Parameters

 Pulse
 End-Tidal
 Coronary

CO2
Perfusion Pressure and Arterial

 Relaxation
 Central
 Pulse

Pressure

Venous Oxygen Saturation

Oximetry

Physiologic Parameters
 ECG

leads and pulse checks

 PETCO2

Physiologic Parameters
 PETCO2

• Correlate with cardiac output and myocardial blood

flow during CPR
• Threshold values below which ROSC is rarely

achieved have been reported

End-Tidal CO2
 CO2

detected by capnography in exhaled air is produced in the body and delivered to the lungs by circulating blood

End-Tidal CO2
Under normal conditions
•
PETCO2 is in the range of 35 to 40 mm Hg
•
During untreated cardiac arrest
•
CO2 continues to be produced in the body
•
but there is no CO2 delivery to the lungs
•
Under these conditions PETCO2 will approach zero with continued ventilation •

 With

initiation of CPR

• Cardiac output is the major determinant of CO2

delivery to the lungs
 If

ventilation is relatively constant

• PETCO2 correlates well with cardiac output during

CPR

 Abrupt

increase in any of these parameters

• sensitive indicator of ROSC that can be monitored

without interrupting chest compressions

Capnography waveform to comfirm endotracheal tube placement and monitor resuscitative effort

 Persistently

low PETCO2 values (10 mm Hg) during CPR in intubated patients
• Suggest that ROSC is unlikely
• Consider trying to improve CPR quality by optimizing

chest compression parameters

 Specific

target PETCO2 value that optimizes the chance of ROSC has not been established

 Monitoring

PETCO2 trends during CPR

 To guide individual optimization of compression depth and rate
 To detect fatigue in the provider performing compressions  Abrupt

sustained increase in PETCO2 during
CPR (35-40 mm Hg)is an indicator of ROSC

 It

is reasonable to consider using quantitative waveform capnography in intubated patients
• To monitor CPR quality, optimize chest compressions
• Detect ROSC during chest compressions or when

rhythm check reveals an organized rhythm

 Value

of using quantitative waveform capnography in nonintubated patients to monitor and optimize CPR quality and detect ROSC is unc ertain Management of
Symptomatic
Bradycardia and Tachycardia

Management of
Symptomatic
Bradycardia

 ECG

and rhythm information

• should be interpreted within the context of total patient

assessment
 Providers

must evaluate

• Patient’s symptoms
• Clinical signs
• Ventilation, oxygenation, heart rate, blood pressure,

level of consciousness, signs of inadequate organ per fusion Unstable and symptomatic
 Unstable

• Refers to a condition in which vital organ function is

acutely impaired or cardiac arrest is imminent
• Immediate intervention is indicated

Unstable and symptomatic
 Symptomatic

• Palpitations, lightheadedness, dyspnea
• Patient is stable and not in imminent danger
• More time is available to decide on the most

appropriate intervention

 In

both unstable and symptomatic cases

• Provider must make an assessment whether it is the

arrhythmia that is causing the patient to be unstable
• Patient in septic shock with sinus tachycardia 140 /

min is unstable
 Electric cardioversion will not improve this patient’s condition  If

patient with respiratory failure and severe hypoxemia becomes hypotensive and develops bradycardia

 Bradycardia

is not the primary cause of

instability
• Treating the bradycardia without treating the

hypoxemia is unlikely to improve the patient’s condition

Atropine
 First-line

drug for acute symptomatic bradycardia (Class IIa, LOE B)
• improved heart rate, symptoms, signs of bradycardia
• Should be considered a temporizing measure while

awaiting a transcutaneous or transvenous pacemaker

 Caution

• Doses < 0.5 mg may paradoxically bradycardia
• Cautiously in the presence of acute coronary ischemia
 Increased heart rate may worsen ischemia

• Atropine will likely be ineffective in patients who have

undergone cardiac transplantation
 transplanted heart lacks vagal innervation

 Caution

• Type II second-degree or third degree AV block
 These are not likely to be responsive to reversal of cholinergic effects by atropine

• Preferably treated with TCP or -adrenergic support as

temporizing measures while the patient is prepared for transvenous pacing

Pacing
 RCT

show atropine and glycopyrrolate were compared with TCP showed few differences in outcome and survival
• In a study evaluating the feasibility of treatment with

dopamine as compared with TCP
• No differences were observed between treatment

groups in survival to hospital discharge

 TCP

is painful in conscious patients

• HCP should initiate TCP in unstable patients who do

not respond to atropine (Class IIa, LOE B)
• Immediate pacing might be considered in unstable

patients with high-degree AV block when IV access i s not available(Class IIb, LOE C)

 If

the patient does not respond to drugs or TCP

• Transvenous pacing is probably indicated (Class IIa,

LOE C)
• Patient should be prepared for transvenous pacing and

expert consultation

Alternative Drugs to Consider
 Although

not first-line agents for treatment of symptomatic bradycardia

 Dopamine,

epinephrine, and isoproterenol

• β-blocker or calcium channel blocker overdose

Dopamine
 Dopamine

hydrochloride

• Catecholamine with α- and β-adrenergic actions
• At lower doses dopamine : inotropy
• At higher doses (10 mcg/kg /min) :vasoconstrictive

effects
 Dopamine

infusion

• Used for patients with symptomatic bradycardia
• Particularly if associated with hypotension, in atropine

fails (Class IIb, LOE B)

Epinephrine
 Epinephrine

• Used for patients with symptomatic bradycardia,

particularly if associated with hypotension for whom at ropine may be inappropriate or after atropine fails (Clas s IIb, LOE B)
• Infusion at 2 -10 mcg/min and titrate to patient

response

Isoproterenol
 Isoproterenol

• β-adrenergic agent with β1, β2 effects
• Increase in heart rate and vasodilation
• Infusion at 2 -10 mcg/min and titrate to patient

response

Management of
Symptomatic
Tachycardia

Classification of Tachyarrhythmias
 Narrow–QRS-complex

tachycardias

• QRS < 0.12 second
• Sinus tachycardia
• Atrial fibrillation
• Atrial flutter
• AV nodal reentry
• Accessory pathway–mediated tachycardia
• Atrial tachycardia (including automatic and reentry

forms)

Classification of Tachyarrhythmias
 Wide–QRS-complex

tachycardias

• QRS > 0.12 second
• Ventricular tachycardia (VT)
• ventricular fibrillation(VF)
• SVT with aberrancy
• Pre-excited tachycardias
 (Wolff-Parkinson-White[WPW] syndrome)

• Ventricular paced rhythms

Tachycardia with pulses

Synchronized Cardioversion
 Synchronized

cardioversion

• If cardioversion is needed and it is impossible to

synchronize a shock
 use high-energy unsynchronized shocks (defibrillation doses)

 Synchronized

cardioversion is recommended

to treat
• unstable SVT
• unstable atrial fibrillation
• unstable atrial flutter
• unstable monomorphic (regular) VT

 Cardioversion

of atrial flutter

• Initial energy of 50 J to 100 J is often sufficient
• If the initial 50-J shock fails
 Should increase the dose in a stepwise fashion

• Cardioversion with monophasic waveforms should

begin at 200 J
 increase in stepwise fashion if not successful (Class IIa, LOE
B)

 Cardioversion

of atrial fibrillation is 120 to 200 J

(Class IIa, LOE A)
 Monomorphic

VT with a pulse responds well to monophasic or biphasic waveform cardioversion s hocks at initial energies of 100 J

Vagal Maneuvers
 Valsalva

maneuver or carotid sinus massage

• Terminate up to 25% of PSVTs
 For

other SVTs

• May transiently slow the ventricular rate
• Potentially assist rhythm diagnosis but will not usually

terminate such arrhythmias

Adenosine


If PSVT does not respond to vagal maneuvers • Give 6 mg of IV adenosine as a rapid IV push through

antecubital vein followed by a 20 mL saline flush (Cla ss I, LOE B)
 If

the rhythm does not convert within 1 to 2 minutes • Give a 12 mg rapid IV push using the method above

 Because

of the possibility of initiating AF with rapid ventricular rates in a patient wit h WPW
• Defibrillator should be available when adenosine is

administered to any patient in whom WPW is a conside ration Narrow-complex irregular tachycardia  Atrial

fibrillation with uncontrolled ventricular response  MAT
 sinus

rhythm/tachycardia with frequent atrial premature beats

Therapy
 General

management of AF should focus on

• Rate control
• Rhythm control
 Conversion of hemodynamically unstable atrial fibrillation to sinus rhythm

 Patients

with an atrial fibrillation duration of 48 hours
• increased risk for cardioembolic events
• although shorter durations of atrial fibrillation do not

exclude the possibility of such events
• Electric or pharmacologic cardioversion should not

be attempted in these patients unless the patient is uns table  Alternative

strategy

• Perform cardioversion following anticoagulation

with heparin and TEE to ensure the absence of a left atrial thrombus

Rate Control
 Unstable

patients

• Prompt electric cardioversion
 Stable

patients

• Ventricular rate control as directed by patient symptoms
• IV nondihydropyridine calcium channel blockers
 Diltiazem are drugs of choice for acute rate control in most individuals with atrial fibrillation and rapid ventricular respo nse (Class IIa, LOE A)

 Digoxin

and amiodarone

• may be used for rate control in patients with CHF
 Amiodarone

• Potential risk of conversion to sinus rhythm should be

considered

Therapy for Regular
Wide-Complex Tachycardias
 If

the etiology of the rhythm cannot be determined

 QRS

monomorphic, regular

• IV adenosine is relatively safe for both treatment and

diagnosis (Class IIb, LOE B)
 However,

adenosine should not be given for unstable or irregular or polymorphic wide complex tachycardia s • It may cause degeneration of the arrhythmia to VF (Class

III, LOE C)

Adenosine
 If

the wide-complex tachycardia proves to be
SVT with aberrancy
• transiently slowed or converted by adenosine to sinus

rhythm
 If

due to VT there will be no effect on rhythm
(except in rare cases of idiopathic VT)
• The brevity of the transient adenosine effect should be

reasonably tolerated hemodynamically

 Continuous

ECG recording is strongly encouraged to provide such written documentation

 When

adenosine is given for undifferentiated widecomplex tachycardia
• Defibrillator should be available

Verapamil
 Verapamil

• Contraindicated for wide-complex tachycardias

unless known to be of supraventricular origin (Class III,
LOE B)
 Adverse

effects when the rhythm was due to VT were shown in 5 small case series
• Profound hypotension was reported in 11 of 25 patients

known to have VT treated with verapamil

IV antiarrhythmic drugs
 For

patients who are stable with likely VT

 IV

antiarrhythmic drugs or elective cardioversion is the preferred treatment strategy • Amiodarone (Class IIb, LOE B)
• Procainamide (Class IIa, LOE B)
• Sotalol (Class IIb, LOE B)
• Procainamide and sotalol should be avoided in

patients with prolonged QT, CHF

 If

one of these antiarrhythmic agents is given

• second agent should not be given without expert

consultation (Class III, LOE B)
 If

antiarrhythmic therapy is unsuccessful

• cardioversion or expert consultation should be

considered (Class IIa, LOE C)

Amiodarone
 Amiodarone

• Effective in preventing recurrent monomorphic VT
• Treating refractory ventricular arrhythmias in patients

with coronary artery disease and poor ventricular functi on • 150 mg IV over 10 minutes
• Dosing should be repeated as needed to a maximum

dose of 2.2 g IV per 24 hours

Lidocaine
 Lidocaine

• less effective in terminating VT than procainamide,

sotalol, amiodarone
• When given to patients with or without a history of MI

with spontaneous sustained stable VT in the hospital set ting • Lidocaine has been reported to variably terminate VT

when administered intramuscularly to patients with AM
I and VT in the out-of-hospital setting

 Considered

second-line antiarrhythmic therapy for monomorphic VT
• 1 to 1.5 mg/kg IV bolus
• Maintenance infusion is 1 -4mg/min (30 -50 mcg/kg /

min)

Wide-complex irregular rhythm  Should

be considered preexcited atrial fibrillation

 Expert

consultation is advised

 Avoid AV

nodal blocking agents

• adenosine, calcium channel blockers, digoxin, and

possibly β-blockers
• paradoxical increase in the ventricular response

Polymorphic (Irregular) VT
 First

step

• Stop medications known to prolong the QT interval
• Correct electrolyte imbalance
• Acute precipitants: drug overdose or poisoning

 Prolong

QT interval(Torsade de pointes)

• IV magnesium 1 to 2 g IV over 15 minutes
 Normal

QT interval

• Most common cause is myocardial ischemia
• IV amiodarone and β-blockers may reduce the

frequency of arrhythmia recurrence (Class IIb, LOE C)

 If

a patient has polymorphic VT, treat the rhythm as
VF and deliver high-energy unsynchronized shocks

สุวรรณ
โครงการจัดตัรปเปร%ยบเท%ยบการเป"%ยนแป"งของ
ACLS 2005 & 2010

CPR 2005

CPR 2010

ขนตอนการทำ BLSླ8า
BLS

A-B-C

C-A-B

การประเมินระดับนระดับความรู้สึกบ
ความินระดับรสึกตัวẨ㿰P獴Ƌ腘὿ꄬกตว

เรยกและเขยาทำ BLSླ8ไหลทำ BLSླ8ง เนนใหสึกตัวẨ㿰P獴Ƌ腘὿ꄬงเกตการหายใจ
สึกตัวẨ㿰P獴Ƌ腘὿ꄬองขาง
บ%คคลทำ BLSླ8วไป ถ้าไม่หายใจหราไมินระดับหายใจหร'อ
หายใจไมินระดับปกต ใหกดับความรู้สึกหนาอก
ทำ BLSླ8นทำ BLSླ8
บ%คลากรการแพทำ BLSླ8ย) ใหคลาชีพจรก่อนได้ แต่ไม่เกินพจร
กอนไดับความรู้สึก แตไมินระดับเกน 10 วนาทำ BLSླ8 ถ้าไม่หายใจหรา
คลาไมินระดับไดับความรู้สึก ใหกดับความรู้สึกหนาอก

การกดับความรู้สึกหนาอกสึกตัวẨ㿰P獴Ƌ腘὿ꄬลบ
การเป+าปาก

30: 2 หลงกดับความรู้สึกหนาอก 30: 2 หลงกดับความรู้สึกหนาอก ใหเป1ดับความรู้สึก
ใหเรมินระดับ A, B โดับความรู้สึกย วธีตาดู หูฟัง แก้มสัมผัส䂸萀䂻 軨಻
: 軌 ทำ BLSླ8างเดับความรู้สึกนหายใจและเป+าปากเลย

ความินระดับเร2วในการกดับความรู้สึก
หนาอก

CPR 2005
CPR 2010
ประมินระดับาณ 100 ครงตอ อยางนอย100 ครงตอนาทำ BLSླ8
นาทำ BLSླ8

ความินระดับลกในการกดับความรู้สึก
หนาอก

ผัส䂸萀䂻 軨಻
: 軌಻┼᪤￨Ὂ┼᪤ห躴಻躜಻嬘ἺㅜƓễ⑰᪤$ꋠ᪲ꌠ᪲ꌠ᪲ꄠἇ㊈᪤富⊧횬ဂธีใหญ่ 1½ 1½ -2 นว
(4-5 ซมินระดับ)

Cricoid pressure ใชีพจรก่อนได้ แต่ไม่เกินป6องกน aspiration Airway

ผัส䂸萀䂻 軨಻
: 軌಻┼᪤￨Ὂ┼᪤ห躴಻躜಻嬘ἺㅜƓễ⑰᪤$ꋠ᪲ꌠ᪲ꌠ᪲ꄠἇ㊈᪤富⊧횬ဂธีใหญ่ 1½ 2 นว (5 ซมินระดับ) และเนน
ปลอยใหหนาอกคลายตวใหสึกตัวẨ㿰P獴Ƌ腘὿ꄬ%ดับความรู้สึก
ไมินระดับแนะนา เพราะอาจทำ BLSླ8าใหใสึกตัวẨ㿰P獴Ƌ腘὿ꄬ
ทำ BLSླ8อชีพจรก่อนได้ แต่ไม่เกินวยหายใจยากและไมินระดับ
สึกตัวẨ㿰P獴Ƌ腘὿ꄬามินระดับารถ้าไม่หายใจหรปองกน aspiration
6
ไดับความรู้สึก

Head tilt, Chin เหมินระดับ'อนเดับความรู้สึกมินระดับ lift ถ้าไม่หายใจหราใสึกตัวẨ㿰P獴Ƌ腘὿ꄬทำ BLSླ8อชีพจรก่อนได้ แต่ไม่เกินวยหายใจ พจารณาใชีพจรก่อนได้ แต่ไม่เกิน
ETCO2 เพ'อย'นยนตาแหนง

CPR 2005
อตราเร2วในการชีพจรก่อนได้ แต่ไม่เกินวย 1 ครง ทำ BLSླ8%ก 5-6
หายใจ
วนาทำ BLSླ8( 10-12 ครงตอ
นาทำ BLSླ8)

CPR 2010
1 ครง ทำ BLSླ8%ก 6-8 วนาทำ BLSླ8( 8-10
ครงตอนาทำ BLSླ8)

การกดับความรู้สึกหนาอก

เนน high quality CPR
พจารณาใชีพจรก่อนได้ แต่ไม่เกิน ETCO2 เพ'อ
เพมินระดับประสึกตัวẨ㿰P獴Ƌ腘὿ꄬทำ BLSླ8ธีตาดู หูฟัง แก้มสัมผัส䂸萀䂻 軨಻
: 軌ภาพในการ CPR

Defibrillation Unwitnessed
ถ้าไม่หายใจหรา AED มินระดับาใหใชีพจรก่อนได้ แต่ไม่เกินทำ BLSླ8นทำ BLSླ8 ไมินระดับตอง cardiac arrest ใหกดับความรู้สึก รอใหกดับความรู้สึกหนาอกครบ แตใหกดับความรู้สึก
หนาอกไปจนครบ 5 รอบ หนาอกตอจนกวาเคร'องพรอมินระดับ
หร'อ 2 นาทำ BLSླ8
Shock เสึกตัวẨ㿰P獴Ƌ腘὿ꄬร2จ กดับความรู้สึกหนาอก Shock เสึกตัวẨ㿰P獴Ƌ腘὿ꄬร2จ กดับความรู้สึกหนาอกตอ
ตอทำ BLSླ8นทำ BLSླ8 ไมินระดับตองคลาชีพจรก่อนได้ แต่ไม่เกินพจร ทำ BLSླ8นทำ BLSླ8 ไมินระดับตองคลาชีพจรก่อนได้ แต่ไม่เกินพจร

Defibrillation energy Algorithm

Post CPR care

CPR 2005
ไมินระดับมินระดับตวเลขชีพจรก่อนได้ แต่ไม่เกินดับความรู้สึกเจนสึกตัวẨ㿰P獴Ƌ腘὿ꄬาหรบ cardioversion ใน monomorphic VT
Asystole/PEA ใชีพจรก่อนได้ แต่ไม่เกิน epinephrine, atropine

CPR 2010
มินระดับตวเลขพลงงานเรมินระดับตน
ชีพจรก่อนได้ แต่ไม่เกินดับความรู้สึกเจน สึกตัวẨ㿰P獴Ƌ腘὿ꄬาหรบ biphasic
ใน AFใหเรมินระดับทำ BLSླ8 120-200
J
ไมินระดับแนะนาใหใชีพจรก่อนได้ แต่ไม่เกิน atropine
(IIb) ใน
Asystole/PEA
แนะนาใหใชีพจรก่อนได้ แต่ไม่เกิน adenosine
ไดับความรู้สึกใน stable regular
WCT
Therapeutic hypothermia ใชีพจรก่อนได้ แต่ไม่เกินออกซเจนขนาดับความรู้สึกนอยทำ BLSླ8สึกตัวẨ㿰P獴Ƌ腘὿ꄬดับความรู้สึก
%

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