BRADYCARDIAS

Slow (absolute bradycardia=rate < 60 bpm

or
Relatively slow (rate less than expected relative to
underlying condition or cause)
PRIMARY ABCD SURVEY
Assess ABCs
Secure airway noninvasively
Ensure monitor / defibrillator is available

SECONDARY ABCD SURVEY

Assess secondary ABCs (invasive airway
management needed?)
Oxygen - IV access - monitor - fluids
Vital signs, pulse oximeter, monitor BP
Obtain and review 12-lead ECG
Obtain and review portable chest x-ray
Problem-focused history
Problem-focused physical examination
Consider causes (differential diagnoses)

Next slide

SERIOUS SIGNS OR SYMPTOMS ?

Due to the bradycardia?

No
Type II second-degree AV block
or
Third-degree AV block?

Yes

Intervention Sequence
Atropine 0.5 1.0 mg
Transcutaneous pacing if available
Dopamine 5-20 g/kg per minute
Epinephrine 2-10 g/min
Isoproterenol 2-10 g/min

Yes

No
Observe

Prepare for transvenous pacer

If symptoms develop, use
transcutaneous pacemaker until
transvenous pacer placed

The Tachycardias: Overview Algorithm

Evaluate patient
Is patient stable or unstable?
Are there serious signs or symptoms?
Are signs and symptoms due to tachycardia?

Unstable

Stable
Stable patient: no serious signs or symptoms
Initial assessment identifies 1 of 4 types of
tachycardias

1. Atrial fibrillation
Atrial flutter

2. Narrow-complex
tachycardia

Unstable patient: serious signs or symptoms

Establish rapid heart rate as cause of signs and
symptoms
Rate-related signs and symptoms occur at many rates,
seldom < 150 bpm
Prepare for immediate cardioversion (see Fig. 10)

3. Stable wide-complex
tachycardia: unknown type

4. Stable monomorphic VT
and/or polymorphic VT

Next slide

Evaluation focus: 4 clinical

features
1. Patient clinically unstable?
2. Cardiac function impaired?
3. WPW present?
4. Duration <48 or >48 hours?
Treatment focus: clinical
evaluation
1. Treat unstable patients urgently
2. Control the rate
3. Convert the rhythm
4. Provide anticoagulation

Treatment of
atrial
fibrillation/
atrial flutter
(see following
table)

Attempt to establish a
specific diagnosis
12-lead ECG
Clinical information
Vagal maneuvers
adenosine

Attempt to establish a
specific diagnosis
12-lead ECG
Esophageal lead
Clinical information

Diagnostic efforts yield

Ectopic atrial tachycardia
Multifocal atrial tachycardia
Paroxysmal supraventricular
tachycardia (PSVT)

Treatment of SVT
(see narrow-complex
tachycardia algorithm)

Confirmed
SVT

Wide-complex
tachycardia of
unknown type

Preserved
cardiac function
DC cardioversion
or
Procainamide
or
Amiodarone

Confirmed
stable SVT

Ejection fraction <40%

Clinical CHF
DC cardioversion
or
Amiodarone

Treatment of stable
monomorphic and
polymorphic VT
(see stable VT:
monomorphic and
polymorphic algorithm)

Tachycardia: Atrial Fibrillation and Flutter

Control of Rate and Rhythm (Continued from Tachycardia Overview)

Atrial fibrillation/
atrial flutter with
Normal heart

1.

Control Rate

Impaired heart
WPW

Heart Function
Preserved

Impaired
Heart EF
<40% or CHF

Note: If AF>48 hours

duration, use agents
with potential to
convert rhythm with
extreme caution in
patients not receiving
adequate
anticoagulation
because of possible
embolic
complications.

(Does not
apply)

Use only 1 of the

following agents (see
note below):
Calcium channel
blockers (Class I)
-Blockers (Class I)

Next slide

2. Convert Rhythm

Duration <48 Hours

Consider
DC carioversion
Use only 1 of the
following agents
(see note below ):
Amiodarone
(Class lla)
Ibutilide (Class lla)
Flecainide
(Class lla)
Propafenone
(Class lla)
Procainamide
(Class lla)

Duration >48 Hours or

Unknown
Avoid nonemergent
cardioversion unless
anticoagulation or clot
precautions are taken (see
below).
Note: Conversion of AF to
NSR with drugs or shock may
cause embolization of atrial
thrombi unless patient has
adequate anticoagulation.
Use antiarrhythmic agents
with extreme caution if AF >48
hours duration (see note
above).
or
Delayed cardioversion
Anticoagulation x 3 weeks at
proper levels
Cardioversion, then
Anticoagulation x 4 weeks
more
or

 For additional
drugs that are
Class IIb
recommendation
s,
see Guidelines
or ACLS text

Impaired
heart (EF
<40% or
CHF)

(Does not apply)

Note: If AF>48 hours

duration, use agents
with potential to convert
rhythm with extreme
caution in patients not
receiving adequate
anticoagulation because
of possible embolic
complications.
Use only 1 of the
following agents (see
note below):
Digoxin (Class IIb)
Ditiazem (Class IIb)
Amiodarone (Class IIb)

For additional
drugs that are
Class IIb
recommendation
s , see
Guidelines or
ACSL text

Early cardiovesrsion
Begin IV heparin at once
TEE to exclude atrial clot
Then
Cardioversion within 24 hours
Then
Anticoagulation x 4 more weeks

Consider
DC
Cardioversion
Or
Amiodarone
(Class IIb)

Aviod nonemergent
cardioversion unless
anticoagulation or clot
precautions are taken (see
above).
Anticoagulation as described
above, follow by
DC cardioversion

Tachycardia: Atrial Fibrillation and flutter

Atrial fibrillation/
atrial flutter with
Normal heart
Impaired heart
WPW

WPW

1. Control Rate

2. Convert Rhythm

Heart Function
Preserved

Impaired Heart EF
<40% or CHF

Duration <48 Hours

Duration >48
Hours or Unknown

Note: If AF >48
hours duration, use
agents with potential
to convert rhythm
with extreme caution
in patients not
receiving adequate
anticoagulation
because of possible
embolic
complications
DC cardioversion
Or
Primary
antiarrhytmic
agents

Note: If AF >48 hours

duration, use agents
with potential to
convert rhythm with
extreme caution in
patients not receiving
adequate
anticoagulation
because of possible
embolic
complications.
DC cardioversion
Or
Amiodarone
(Class IIb)

DC cardioversion
Or
Primary
antiarrhythmic agents
Use only 1 of the
following agents (see
note below):
Amiodarone
(Class IIb)
Flecainide
(Class IIb)
Procainamide
(Class IIb)
Propafenone
(Class IIb)
Sotalol
(Class IIb )

Avoid
nonemergent
Cardioversion
unless
anticoagulation or
clot precautions are
taken (see above).
Anticolagulation
as described above,
followed by
DC cardioversion

Next slide

Use only 1 of the

following agents
(see note below):
Amiodarone (Class
IIb)
Flecainide
(Class IIb)
Procainamide
(Class IIb)
Profenone
(Class IIb)
Sotalol (Class IIb)

Class III
(can be harmful)
Adenosine
-Blockers
Calcium blockers
Digoxin
Impaired heart
(EF <40% or CHF)
DC cardioversion
Amiodarone (Class
IIb)

Class III syndrome: AF, atrial fibrillation; NSR, normal sinus rhythm; TEE, transesophageal
WPW indicates Wolff-Parkinson-White
echocardiogram; and EF, ejection
(can befraction.
harmful)
Adenosine

Note: Occasionally 2 of the named antiarrithmic agents may be used, but use of these agents in combination may have
-Blockers
proarrhythmic potential. The classes listed represent the Class of Recommendation rather than the Vaughn-Williams
Calcium blockers
classification of antiarrhythmics.

Digoxin

Narrow-Complex Tachycardia
Narrow-Complex SupraventricularTachycardia, Stable

Attempt therapeutic diagnostic maneuver

Vagal stimulation
Adenosine
Preserved
Heart function

Junctionalnct
tachycardia

EF <40%, CHF

- Blocker
Ca+ channel blocker
Amiodarone
NO DC cardioversion!

Amiodarone
NO DC cardiversion!
Next slide

Preserved
heart function

Priority order:
AV nodal blockade
-Blocker
Ca2+ channel blocker
Digoxin
DC cardioversion
Antiarrhythmics:
consider procainamide,
amiodarone, sotalol

EF <40%, CHF

Priority order:
DC cardioversion
Digoxin
Amiodarone
Diltiazem

Paroxyamal supraventricular
tachycardia

Preserved
Heart function

Ectopic or multifocal
atrial tachycardia
EF <40%, CHF

-Blocker
Ca2+ channel blocker
Amiodarone
NO DC cardioversion!
Amiodarone
Diltiazem
NO DC cardioversion!

Stable Ventricular Tachycardia: Monomorphic and Polymorphic

Stable Ventricular Tachycardia
Monomorphic or Polymorphic?

Monomorphic VT
Is cardiac function impaired
Preserved
heart function

Poor ejection fraction

Medications: any one

Procainamide
Sotalol
Others acceptable
Amiodarone
Lidocaine

Note!
May go direcly to
cardioversion
Normal baseline
QT interval

Polymorphic VT
Is Baseline QT interval prolonged?
Prolonged baseline
QT interval(suggests torsades)

Normal baseline QT Interval

Long baseline QT interval

Treat ischemia
Correct electrolytes

Correct abnormal electrolytes

Medications: any one

-Blockers or
Lidocaine or
Procainamide or
Sotalol

Therapies: any one

Magnesium
Overdrive
Isoproterenol
Phenytoin
Lidocaine

Next slide

Cardiac function
impaired
Amiodarone
150 mg IV over 10 minutes
or
Lidocaine
0.5 to 0.75 mg/kg IV push
Then use
Synchronized cardioversion

Acute Pulmonary Edema, Hypotension, Shock

Clinical signs: Shock, hypoperfusion,
congestive heart failure, acute pulmonary edema
Most likely problem?

Acute pulmonary edema

Volume Problem

Pump problem

Brandycardia
(see algorithm)
1st Acute pulmonary adema
Furosemide IV 0.5 to 1.0 mg/kg
Morphine IV 2 to 4 mg
Nitroglycerin SL
Oxygen/intubation as needed

Administer
Fluids
Blood transfusion
Cause-specific interventions
Consider vasopressors

Rate problem

Tachycardia
(see algorithm)

Blood
pressure?

Next slide

Systolic BP BP
defines 2nd line
of action (See
below)

Systolic BP
<70 mm Hg
Signs/symptoms
of shock

Norepinephrine
0.5 to 30 g/min IV

Systolic BP
70 to 100 mm Hg
Signs/symptoms
of shock

Dopanime
5 to 15 g/kg per
minute IV

Systolic BP
70 to 100 mm Hg
No signs/symptoms
of shock

Dobutamine
2 to 20 g/kg per
minute IV

2nd Acute pulmonary edema

Nitroglycerin/nitroprusside if BP >100 mm Hg
Dopamine if BP = 70to 100 mm Hg, signs/symptoms of shock
Dobutamine if BP> 100 mm Hg, no signs/symptoms of shock
Futher diagnostic/therapeutic
considerations
Pulmonary artery catheter
Intra-aortic ballon pump
Angiography for AMI/ischemia
Additional diagnostic studies

Systolic BP
>100 mm Hg

Nitroglycerin
10 to 20 g/min IV
Consider
Nitroprusside 0.1 to
5.0 g/kg per minute IV

Ischemic Chest Pain Algorithm

Chest pain
suggestive of ischemia
Immediate assessment (<10 minutes)
Measure vital signs (automatic/standard BP cuff)
Measure oxygen saturation
Obtain IV access
Obtain 12-lead ECG (physician reviews)
Perform brief, targeted history and physical exam;
focus on eligibility for fibrinolytic therapy
Obtain initial serum cardiac marker levels
Evaluate initial electrolyte and coagulation studies
Request, review portable chest x-ray (<30 minutes)

Immediate general treatment

Oxygen at 4 L/min
Aspirin 160 to 325 mg
Nitroglycerin SL or spray
Morphine IV (if pain not relived with
nitroglycerin)
Memory aid: MONA greets all patients
(Morphine, Oxygen, Nitroglycerin,
Aspirin)

EMS personnel can

perform immediate
assessment and
treatment (MONA),
including initial 12-lead
ECG and review for
fibrinolytic therapy
indications and
contraindications.

Assess initial 12-lead ECG

ST elevation or new or
presumably new LBBB:
strongly suspicion for injury

ST depression or dynamic T-wave

inversion: strongly suspicious for
lachemia

Nondiagnostic ECG: absence of

change in ST segment or T
waves

ST-elevation AMI

High-risk unstable angina/ non-ST

elevation AMI

Intermediate/low-risk unstable
angina

Next slide

Start adjunctive treatments

Start adjunctive treatments

(as indicated: no reperfusion delay)

(as indicated: no contraindications)

-Adrenoceptor blockers IV

Heparin (UFH/LMWH)

Nitroglycerin IV

Aspirin 160 to 325 mg qd

Heparin IV

Glycoprotein IIb/IIIa receptor

inhibitors

ACE inhibitors (after 6 hours or

when stable)

Meets criteria for unstable

Yes

or new-onset angina?
Or
Troponin positive?

Nitroglycerin IV

No

-Adrenergic receptor blockers

Time from onset of symptoms

>12 hours

Admit to ED chest pain

unit

Assess clinical status

<12 hours
Select a reperfusion
strategy based on local
resources:
Angiography
PCI (angioplasty stent)
Cardiothoracic surgery
backup

Or to monitored bed
if signs of cardiogenic shock
or contraindications to
fibrinolytics, PCI is treatment
of choice (Class I) if available

High-risk patient: defined

by

If PCI is not available, use

fibrinolystics (if no
contraindications)

Recurrent ischemia

Persistent symptoms
Depressed LV function
Widespread ECG changes
Prior AMI, PCI, CABG

Clinically
stable

In ED follow
serial cardiac markers
(including troponin)
Repeat ECG/continuos
ST monitoring
Consider imaging
study (2D
echocardiogharphy or
radionuclide)

Next slide

No
Fibrinolytic therapy selected

Primary PCI selected

Front-loaded alteplase or

Door-to-ballon
inflation 90 30
minutes

Streptokinase or
APSAC or
Reteplase or

Experienced
operators

Tenecteplase

High-volume center

Goal: door-to-drug <30

minutes

Cardiac surgical
capabillity

Perform cardiac
catheterization:
anatomy suitable for
revascularization?
Yes
Revascluraization
PCI
CABG

Yes

Admit to CCU/ monitored bed

Continue or start adjunctive
treatments as indicated
Serial cardiac markers

Evidence
of ishemia
or
infraction
No

Serial ECG

Discharge
acceptable

Consider imaging study (2D

echocardiography or raionuclide)

Arrange
follow-up

This algorithm provides general guidelines that may not apply to all patients. Carefully consider proper indications and contraindications.

The Acute Coronary Syndromes

Initial Management in the Field and Emergency Department
Immediate Treatment

Prehospital Fibrinolytic Therapy

(memory aid: MONA greets all patients

Morphine
Oxygen
Nitroglycerin
Aspirin

Key to benefits of fibrinolysis: start EARLY.

Prehospital fibrinolytics have the greatest effect
when they are routinely administered at least 1
hour before they would be administered inhospital.
EMS assessment (12-lead ECG and chest
pain checklist in field), triage, and prearrival
notification reduce time to in-hospital
fibrinolytics. EMS hospital systems with a
hospital door-to drug (fibrinolytic) interval of
<30 minutes cancel most benefits of
prehospital fibrinolytics.
Prehospital fibrinolytic therapy is
recommended only in special settings with
a physician present in the ambulance/practice
site/home or when prehospital transport time is
60 minutes.

Immediate Assessment
Vital signs, including blood pressure
Oxygen saturation
IV access
12-lead ECG
Brief, targeted history and physical exam (to
identify reperfusion candidates)
Initial cardiac markers
Initial electrolyte and coagulation studies
Portable chest x-ray <30 minutes
Assess for the following:
- heart rate 100 bpm and SBP 100 mmHg
or
- pulmonary edema (rates > way up) or
- signs of shock
If any of these conditions is present, consider
triage to a facility capable of cardiac
catheterization and revascularization.

Oxygen
Immediate General Treatment for
Suspected Ischemic Chest Pain
Oxygen at 4 L/min per nasal cannula
If no contraindications, add
Aspirin 160 to 325 mg
Nitroglycerin SL or spray
Morphine IV (pain unrelieved by
nitroglycerin)
Rationale
Supplementary oxygen may limit ischemic
myocardial injury.
Oxygen reduces the amount of STsegment elevation (effect on morbidity or
mortality in acute infarction unknown)

Oxygen
Recommendation
Uncomplicated
Oxygen at 4 L/min per nasal cannula for
first 2 to 3 hours (Class IIa)
Probably not helpful beyond 3 to 6 hours
Complicated MI (Overt Pulmonary
Congestion, SaO2 <90%)
Oxygen at 4 L/min per nasal cannula,
titrate as needed (Class I)
Continue therapy until patient is stable or
hypoxemia corrected

The Acute Coronary Syndromes

Nitrates and Nitroglycerin
Recommendations
Effects
Vasodilatation through nitric oxideinduced relaxation of vascular smooth
muscle in veins, arteries, and arterioles
Indications
- Initial antianginal for suspected
ischemic pain
- For the first 24 to 48 hours in patients
with acute MI and CHF, large anterior
wall infarction, persistent or recurrent
ischemia, or hypertension
- Continued use (beyond 48 hours) for
patients with recurrent angina or
persistent pulmonary congestion

Initial dose, route

- IV: 12.5 to 25.0 g bolus, 10 to 20
g/min infusion, titrated or
- SL: 0.4 mg, repeat x 2 at 5 minute
intervals or
- Spray: 2 metered doses under or
onto tongue
Contraindications
- Systolic blood pressure <90 mmHg
- Severe bradycardia or severe
tachycardia
- RV infarction
- Use of Viagra within 24 hours

The Acute Coronary Syndromes

Morphine

Morphine
Effects: Analgesia; venodilation reduces
ventricular preload and oxygen
requirements.
Indications: Treatment of ischemic pain
not relieved by nitroglycerin; also useful to
redistribute blood volume in patients with
pulmonary edema.
Cautions and complications: Do not use
in patients with suspected hypovolemia. If
hypotension develops in absence of
pulmonary congestion, elevate patients legs
and administer normal saline (200 to 500 mL
bolus).

Recommendations
Action
- Predominantly a venodilator that decreases LV
preload
- Decreases systemic vascular resistance, reducing
LV afterload
- CNS analgesia decreases anxiety by
sympatholytic effects
Indications
- Ischemic chest pain
- AMI without hypotension
- Acute pulmonary edema
Dose
- 2 to 4 mg IV, titrated to effect; based on the
ACC/AHA Practice Guidelines
- Repeat every 5 minutes to effect
Precautions
- Do not administer if hypotensive
- Low volume states; respiratory depression
If hypotension develops, give 200 to 500 mL normal
saline if no pulmonary congestion

Aspirin
Rationale
Effects: A dose of 160 to 325 mg causes immediate
and near-total inhibition of thromboxane A2 production.
This rapid inhibition reduces coronary reocclusion and
recurrent eents after fibrinolitic therapy. Also effective
for patients with unstable angina.
Indications: Administer to all with suspected
ACS, particulary reperfusion candidates, unless
hypersensitive to aspirin (ticlopidine/clopidogrel may
be helpful).
Dose, route: In the early hours after infraction, aspirin
is absorbed more quickly when chewed than when
swallowed, particularly if morphine has been given.
Aspirin suppositories (325 mg) are recommended for
patients with severe nausea, vomiting, or upper GI
disorders.
Cautions, contraindications: Relatively
contraindicated in patients with active peptic ulcer
disease, a history consistent with aspirin
hypersensitivity, or bleeding disorders.

Aspirin
Recommendations
Action
Irreversibly inhibits platelet cyclo-oxygenase
Inhibits thromboxane A2 pletelet aggregation
Indications
Acute ST-elevation infraction
Coronary angioplasty
Suspected ischemic-type pain
Dose
160 to 325 mg orally, crushed or chewed
325 mg suppository if nausea, vomiting
Precautions
Active peptic ulcer disease (use rectal
suppositories)
History of hypersensitivity or allergy
Bleeding disorders, serve hepatic disease

The Acute Coronary Syndromes

Assess the initial ECG
The 12-lead ECG is central to triage of ACS in the Emergency
Department
Classify patients as being in 1 of 3 syndromes within 10 minutes of
arrival

ST-segment elevation or
new LBBB

ST elevation 1 mm in 2 or
more contiguous leads
New or presumably new
LBBB (BBB obscuring STsegment analysis)

ST-segment depression/
dynamic T-wave Inversion:
strongly suspicious for
ischemia

Nondiagnostic or normal
ECG

ST depression >1 mm

ST depression 0.5 to 1.0 mm

Marked symmetrical T-wave

inversion in multiple precordial leads

T-wave inversion or flattening

in leads with dominant R waves

Dynamic ST-T changes with pain

Normal ECG

Next slide

 >90% of patients with ischemictype chest pain and ST-segment

elevation will develop new Q waves
or positive serum markers for AMI.
Patients with hyperacute T waves
benefit when AMI diagnosis is
certain. Repeat ECG may be
helpful.

High-risk subgroup with increased

mortality:

Heterogeneous group: rapid

assessment needed by

Persistent symptoms, recurrent

ischemia

Serial ECGs

Diffuse or widespread EG
abnormalities

ST-segment monitoring
Serum cardiac markers

Depressed LV function

Further risk assessment helpful

Patients with ST depression in

early precordial leads who have
posterior MI benefit when AMI
diagnosis is certain

Congestive heart failure

Perfusion radionuclide imaging

Serum marker release: positive

troponin or CK-MB+

Stress echocardiography

Reperfusion therapy

Antithrombin therapy with

heparin

Aspirin
Heparin (if using fibrinspecific lytics)
-Blockers
Nitrates as indicated

Antiplatelet therapy with

aspirin
Glycoprotein Iib/Iia Inhibitors
-Blockers
Nitrates

Aspirin
Other therapy as
appropite
Patients with positive
serum markers, ECG
changes, or functional
study: manage as high
risk

The Acute Coronary Syndromes

ST-segment Depression, Dynamic T-Wave Changes:
Non-Q-Wave Infarction Unstable Angina
Non-Q-Wave Infarction
Epidemiology
Unstable angina and non-Q-wave infarction are pathological processes on a continuum:
chronic stable minimal myocardial damage unstable angina + no non-Q-wave typical Q-wave
angina
(troponin positive/CK-MB
serum marker release infarction
MI
negative)

Incidence of non-Q-wave MI is increasing for several reasons:

- increasing pool of patients who are older and have more advanced disease
- wider use of acute reperfusion strategies for ST-elevation infarction (limited infarction):
fibrinolytic therapy and angioplasty
- prophylactic effects of greater use of aspirin, -blocker
On presentation these patients are in a high-risk subgroup with a relatively high mortality
rate.
Next slide

MANAGEMENT
Major limitation: fibrinolytic therapy does not benefit patients with ST-segment depression.
-blockade: start as key adjunctive therapy and optimize.
Add calcium channel blockers for persistent symptoms if any of the following are present:
- -blockade intolerance
- contraindications to -blockers
- adequate blockade fails to reduce symptoms
Potential benefit: new antithrombin and antiplatelet agents have shown significant benefit in
selected patients with non-ST-elevation MI and unstable angina.
- antiplatelet therapy with GP IIb/IIIa inhibitors.
- antithrombin therapy with low molecular weight heparin.
Refer to emergency coronary angiography and possible revascularization (with PCI or
CABG) if treating high-risk patients with
- Recurrent ischemia
- Depressed LV function
- Widespread ECG changes
- Prior MI
When appropriate, continue medical therapy and further risk stratification if clinically stable.

The Acute Coronary Syndromes

ST-segment Depression, Dynamic T-Wave Changes:
Non-Q-Wave Infarction Unstable Angina
Recommendations for Initial Management and Therapy
In general, treat these patients
with both
- Antithrombin (heparin) and an

Antithrombin (heparin)
plus
Antiplatelet (aspirin)

- Antiplatelet agent (aspirin)

Modify this treatment if patient

meets criteria for high risk

Next slide

High-Risk Criteria
ST depression 1 mm
Persistent symptoms; recurrent
ischemia
Diffuse or widespread ECG
abnormalities
Depressed LV function
Congestive heart failure
Cardiac marker release: positive
troponin or CK-MB+

Patients who meet high-risk criteria

benefit from treatment with
Aspirin and
GP IIb/IIIa inhibitors and
unfractionated heparin or
Low molecular weight heparin
(efficacy and safety combined with
GP IIb/IIIa inhibitors under review)

Antithrombin (heparin)
plus
Antiplatelet (aspirin)
Plus
Glycoprotein IIb/IIIa inhibitors

All patients without contraindications

should receive

-Blockers

Patients who suffer recurrent angina

should also receive

Nitrates

As a third agent to use for refractory

angina or in patients with a
contraindications to -blockers

Calcium channel blockers

FARMAKOLOGI ACLS
Ingat tujuan utama dalam ACLS:
Koreksi hiposekmia
Membuat sirkulasi spontan dengan tekanan darah yang adekuat
Mengoptimalkan fungsi jantung
Menekan dan mencegah aritmia yang bermakna
Menghilangkan sakit
Mengoreksi asidosis
Mengobati gagal jantung kongestif

Next slide

Klasifikasi rekomendasi penggunaan obat-obatan atau tindakan:

Class I: Indicated, acceptable, useful & effective
Class II: Acceptable, uncertain efficacy, maybe controversial
Class IIa: Favour of its usefulness & eficacy
Class IIb: Maybe helpful, probably not harmful
Class III: Inappropriate, no scientific supporting data, maybe harmful
Pendekatan untuk mempelajari farmakologi dalam ACLS dengan
why, when, how, watch out:
Why an agent is used (action) / kenapa suatu obat digunakan
When to use an agent (indication) / kapan obat tersebut digunakan
How to use an agent (dosage) / bagaimana menggunakannya
What to watch out for (precaution) / awasi

OXYGEN
Why
Meningkatkan tekanan oksigen arterial
Meningkatkan kandungan oksigen arterial
Memperbaiki oksigen jaringan
When
Nyeri dada akut yang mungkin disebabkan oleh iskemia jantung
Hiposekmia oleh berbagai sebab
Henti jantung dan nafas
How
Tanpa henti jantung : 2 L / m
Dengan gangguan nafas ringan : 5 6 L / m
Watch Out
Keracunan oksigen
Mengurangi rangsangan pernafasan pada pasien dengan retensi CO2

EPINEPHRINE
Why
Meningkatkan :
Resistensi vaskuler sistemik
Tekanan darah sistolik dan diastolik
Aktivitas darah ke seberal dan koroner
Aliran darah ke serebral dan koroner
Kekuatan kontraksi miokard
Kebutuhan oksigen miokard
Otomatisitas
When
Ventricular ectopy, wide complex tachycardias, ventricular tachycardia dan VF
Pulseless VT dan VF yang refrakter terhadap terapi listrik dan epinefrin
Pasien dengan risiko terjadinya aritmia ventrikel yang maligna
Tak direkomendasikan lagi untuk pemberian pencegahan rutin pada pasien dengan
IMA
Next slide

EPINEPHRINE
How
Dosis awal : 1,0-1,5 mg/ kg I.V. bolus
Via EET : 2-2,5 x IV dose
Bolus kedua : 0,5-0,75 mg/ kg setelah 10
Bolus tambahan : 0,5-0,75 mg/ kg every 5-10 (bila masih tetap ada aritmia), sampai
total:3 mg/kg
Continuous iv infusion : 2-4 mg/min (pada sirkulasi spontan)
Watch out
Perubahan neurologis
Depresi miokard & sirkulasi

ADENOSINE
Why
Memperlambat konduksi melalui AV node
Menghentikan jalur re-entri di AV node
Mengembalikan ke irama sinus pada pasien dengan PSVT
Respon farmakologinya singkat
Watch out
Atrial flutter / fibrillation dengan sindrom WPW
VT, dapat menyebabkan hipotensi atau VF
Hypotension, A-V block

AMIODARONE
Why
Efektif untuk supraventricular arrhythmia, ventricular arrhythmia
Ventricular rate control
Kardioversi farmakologik
Menguah konduksi yang melalui accesory pathway.
When
Terapi tambahan setelah electrical cardioversion pada PSVT yang refrakter (II a)
Kardioversi farmakologis untuk AF (IIa)
Atrial tachycardia (II b)
Ventricular rate control pada rapid atril arrhythmia pada pasien dengan fungsi
ventrikel yang buruk, atau pada pasien dengan konduksi accesory pathway

Next slide

AMIODARONE
When
Menghentikan SVT yang melibatkan jalur rentri AV node
How
Dosis awal : 6 mg bolus cepat dalam 1-3 diikuti flush cepat normal
saline
Dosis ulangan : 12mg, jika tak berespon dalam 1-2 menit
Teofilin menyebabkan kurang sensitif
Watch out
Flushing, dyspnea, chest pain (biasanya hilang dalam 1-2 menit)
Transient bradycardia dan ventricular ectopy
Tak terlalu berpengaruh pada hemodinamik

Ventricular Fibrillation / Pulseless Ventricular Tachycardia

Primary ABCD Survey
Focus: basic CPR and defibrillation
Check responsiveness
Activate emergency response system
Call for defibrillator
A
Airway: open the airway
B
Breathing: provide positive-pressure ventilations
C
Circulation: give chest compressions
D
Defibrillation: assess for and shock VF/pulseless VT, up to 3
times
(200 J, 200 to 300 J, 360 J, or equivalent biphasic) if
necessary
Rhythm after first 3 shocks?
Persistent or recurrent VF / VT
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Secondary ABCD Survey

Focus: more advanced assessments and
treatments
A
Airway: place airway device as
soon as possible.
B
Breathing: confirm airway
device placement by exam plus
confirmation device
B
Breathing: secure airway
device; purpose-made tube holders
preferred
B
Breathing: confirm effective
oxygenation and ventilation
C
Circulation: establish IV
access
C
Circulation: identify rhythm
monitor
C
Circulation: administer drugs
appropriate for rhythm and condition
D
Differential Diagnosis: search
for and treat identified reversible causes

Epinephrine 1 mg IV push, repeat every 3 to 5 min

or
Vasopressin 40 U IV, single dose, 1 time only

Resume attempts to defibrillate

1 x 360 J (or equivalent biphasic) within 30 to 60
seconds

Consider antiarrhythmias :
Amiodarone (IIb for persistent or recurrent VF/VT)
Lidocaine (indeterminate for persistent or recurrent
VF/pulseless VT)
Magnesium (IIb if known hypomagnesemic state)
Procainamide (indeterminate for persistent VF/
pulseless VT; IIb for recurrent VF/pulseless VT)

Resume attempts to defibrillate

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