Emergency in Medicine 2012

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Emergency in medicine

4 April 2012



Scope

Cardiopulmonary resuscitation

Cardiac arrhythmia

Acute coronary syndrome

Fast track MI



Cardiopulmonary

resuscitation













VF/ Pulseless VT



Ventricular Fibrillation

Multiple ventricular foci rapidly discharge

producing a totally erratic ventricular

rhythm without identifiable waves



Ventricular tachycardia



Ventricular Tachycardia (VT)

•Regular rhythm (may be slightly irregular)•Rate ~150-250/min

•Wide QRS complex



Polymorphic VT

+ Prolong QT = Torsades de pointes



Defibrillation Provide most effective

treatment for

ventricular fibrillation

as soon as possible





Manual Defibrillator



Manual Defibrillators





1.Turn on or monitor on

Step Manual Defibrillation



2. Set lead select•Paddle lead

•Lead I, II, III



3. Analyze rhythm

4. If VF or pulseless VT Defibrillation



Select energy level•Monophasic :360J

•Biphasic:120-200 J

(If unknown use 200J)



5. Apply gel to paddle

or use adhesive pad6. Apply paddle or pad

at correct position





7.Charge defibrillator by

•Press button on control panel

•Or at right hand apex paddle





8. When fully charged : voice &

number

9. Say One , I am clear Two , you are clear

Three , everybody is clear



10. Press 2 discharge button simultaneously

11. Check monitor. If VF/VT remains , startCPR for 5 cycles

VF/P l l VT



VF/Pulseless VT Give 1 shock •Manual biphasic:120-200J•Monophasic:360J• AED: device specificResume CPR immediately

Shockable rhythm?

•Give 1 shock •Resume CPR immediately after the shock

• Vasopressor when IV/IO available•Epinephrine 1mg IV/IO every 3-5 min or• Vasopressin 40 U IV/IO

Give 5 cycles of CPR

Shockable rhythm?

Give 5 cycles of CPR

Shockable

•Give 1 shock •Resume CPR immediately after the shock

•Consider antiarrhythmics• Amiodarone 300 mg IV/IO then consider additional 150 mg IV/IO•Lidocaine (1-1.5 mg/kg then 0.5-0.75 mg/kg IV/IO)

•Magnesium 1-2 g IV/IO for torsades de pointes

Shockable



Asystole/ PEA



Asystole



Confirm true asystole

Check lead & cable connections

Monitor power on?

Monitor gain up?

Verify asystole in another lead?



Pulseless Electrical activity

(PEA)Electrical mechanical dissociation

Treatment goal is to bring back perfusion

(pulse and blood pressure)Correct the reversible cause is the key

factor for success resuscitation

The process is to perform cardiopulmonarysupport and try to identify and correct the

causes





Search for & treat possible

contributing factors

5HHypovolemia

Hypoxia

Hydrogen ion

(acidosis)

Hypo/hyperkalemia

Hypoglycemia

Hypothermia

5TToxins

Tamponade (cardiac)

Tension

pneumothorax

Thrombosis (coronary

or pulmonary)

Trauma

(hypovolemia,increased ICP)





Key changes from the 2005 ACLS

Guidelines

Continuous quantitative waveform capnography for confirmation andmonitoring of endotracheal tube placement

Emphasize the importance of high-quality CPR (including chest

compressions of adequate rate and depth, allowing complete chestrecoil after each compression, minimizing interruptions in chestcompressions and avoiding excessive ventilation)

Atropine is no longer recommended for routine use in themanagement of pulseless electrical activity (PEA)/asystole

There is an increased emphasis on physiologic monitoring tooptimize CPR quality and detect ROSC



Cardiac arrhythmia

Tachyarrhythmia

Bradyarrhythmia



Approach to cardiac arrhythmia

Rhythm –

qu ick look

Flat l ine

Use electrod e and loo k for 2 leads

Look for connect ion

Sti l l f lat l ine

= Asysto le

VF QRS com plex

Rate > 100

Tachycardia

Rate < 60

Bradycard ia

Narrow QRS Wide QRS

Regular Irregular

SVT

Regular Irregular

AF

Atr ial f lut ter

MAT

VT

SVT with

aberrant

SVT with BBB

AF

with

WPW



Tachyarrhythmia





Tachyarrhythmia-Management in CPR

Identify the hemodynamic effects of tachyarrhythmia

Electrical therapy should be

performed at any time if the patientbecomes unstable.

Antiarrhythmic medication could be

used initially in stable tachyarrhythmia



Unstable Tachycardia



Cardioversion

St C di i



Step Cardioversion

! Consider sedation

1. Turn on or Monitor on

2. Attach monitor leads

3. Press “ sync ” button at control panel 4. Look for marker on R wave

5. Adjust monitor gain until sync marker occur

6. Select energy level and charge

7. Apply gel and place paddle at correct position

8. Clear : One , Two , Three



9. Press discharge botton10. Analyze rhythm again

Narrow regular 50-100 jNarrow irregular 120-200 j (Bi), 200 j (Mo)

Wide regular 100 j

Wide irregular Defib



Synchronized



Narrow QRS complex

Wide QRS complex

Stable Tachycardia



Narrow QRS-ComplexTachycardia



Narrow Complex Tachycardia

Regular Irregular

No P waveP wave

-AF-PAC

-MAT

-AT with block

-A.Flutter + block

A.Flutter 2:1

PSVT-AVNRT

-AVRT

-AT

Sinus tachycardia



Irregular Narrow QRS-

Complex Tachycardia



Atrial Fibrillation (AF)

Irregular rhythm

Not seen P wave

(fibrillate baseline)

Atrial rate ~350-500/min

Ventricular ratevariable



Atrial Fibrillation (AF)

•Irregular rhythm

•Not seen P wave (fibrillate baseline)

• Atrial rate ~350-500/min

•Ventricular rate variable



Atrial Flutter

Regular or irregular

rhythm

Atrial rate 250-

350/minVentricular rate 1/2,

1/3, … of atrial rate

“Saw tooth”

appearance

AV block 2:1, 3:1,…



Atrial Flutter

•Regular or irregular rhythm

• Atrial rate 250-350/min

•Ventricular rate 1/2, 1/3, … of atrial rate

•“Saw tooth” appearance

•AV block 2:1, 3:1,…



Recommendations for Pharmacological or

Electrical Cardioversion of AF

Class I

1. Immediate electrical cardioversion in patients with

paroxysmal AF and a rapid ventricular response who have

ECG evidence of acute MI or symptomatic hypotension,angina, or HF that does not respond promptly to

pharmacological measures. (Level of Evidence: C )

2. Cardioversion in patients without hemodynamicinstability when symptoms of AF are acceptable.

(Level of Evidence: C )



Electrical cardioversion

Synchronized mode, Initial energy 200 J

Increments of 100 J until a maximum of

400 J

Lower energies are required with biphasicwaveforms

Interval between 2 consecutive shocks

should not be < 1 min.



Risk & Complication of electrical

cardioversion

Embolism

– 1-7% : if no prophylactic anticoagulant before

cardioversion

Arrhythmia

– Hypokalemia

– Digitalis intoxication

Myocardial Injury

– Transient ST elevation and small increased bloodlevel of CK-MB.

– Probably not clinically significant



Prophylaxis of Thromboembolism

before Cardioversion

Anticoagulate patients with AF lasting more than 48 h or of unknown duration, for at least 3 to 4 weeks before

and after cardioversion (INR 2 to 3).

Screening for the presence of thrombus in the LA or LAA by TEE is an alternative for routinepreanticoagulation in candidates for cardioversion of AF.

M di l i At i l fib ill ti



Medical conversion Atrial fibrillation



Typical Doses of Drugs Used to Maintain Sinus Rhythm

in Patients With Atrial Fibrillation







Anticoagulant

CHADS2 ( CHF , HT , age > 75 yrs , DM ,stroke ) ≥ 2

no contraindication

keep INR 2-3



Vascular disease (prior MI, PAD, Aortic plaque ) ESC 2010



Regular Narrow QRS-

Complex Tachycardia

Paroxysmal Supraventricular



Paroxysmal Supraventricular Tachycardia (PSVT)

Rate ~150-250/min,Regular rhythm

Abrupt onset &termination

Not seen sinus Pwave (usually notseen P wave or retrograde P wave)

Usually narrow QRScomplex

Paroxysmal Supraventricular



Paroxysmal Supraventricular Tachycardia (PSVT)

•Rate ~150-250/min, Regular rhythm

•Usually narrow QRS complex

•Abrupt onset & termination

•Not seen sinus P wave (usually not seenP wave or retrograde P wave)



Management

Unstable VS : sedation+Cardioversion synchronized

biphasic 50-100 j , adenosine

Stable VS : Adenosine 6 mg rapidly iv if ineffective within 1-2 min give 12 mg

Nausea,light-headedness,flushing

Contraindication in asthma, second or third degree AV

block , sick sinus syndrome



Management

Diltiazem 0.25 mg/kg over 2 min, further 0.35 mg/kg after 15 min if

required

Initial infusion 5-10 mg/hr , increased 5-15 mg/hr up to

24 hr, maintainance 120-360 mg oral daily

Verapamil 5-10 mg slowly iv (over 2-3 min) repeated 10 mg in 10-

15 min , oral maintainance 120-480 mg daily divided in

3-4 doses

Contraindication in hypotension , bradycardia , wide

complex tachycardia , VT

Narrow QRS



Narrow QRS

• Attempt vagal maneuvers•Give adenosine 6 mg IV push.If no conversion give 12 mg IV push

Irregular Narrow-ComplexTachycardia AF/atrial flutter/MAT•Consider expert consultation•Control rate

Convert?

If rhythm convertsProbable reentry SVT

If rhythm does not convertPossible atrial flutter, atrial tachycardia,

junctional tachycardia

Regular Irregular

Converts Does not convert



Wide QRS-ComplexTachycardia



Approach to wide complex tachycardia

History of MI favor VT

Age,rate and hemodynamic cannot differentiate

Differential diagnosis of wide complex tachycardia

1) Ventricular tachycardia

2) SVT with aberrant conduction

3) SVT with preexisting bundle branch block

4) circus movement tachycardia in WPW



Clues for VT

AV dissociation

Fusion beat

Capture beat

Axis : No man’s land , LBBB with RAD

QRS morphology

Precordial concordance : negative specific more

than positive



AV dissociation in VT

VA conduction are also seen

Positive concordance



VT N ’ l d



VT – No man’s land



Management

Amiodarone Oral loading dose 1200-1600 mg daily , maintainance

200-400 mg daily

Intravenous loading 150 mg over 10 min then 360 mg

over 6 hr then 560 mg over remaining 18 hr then 0.5

mg/min

Contraindication in severe bradycardia , prolong QT

V t i l T h di (VT)



Ventricular Tachycardia (VT)

•Regular rhythm (may be slightly irregular)

•Rate ~150-250/min

•Wide QRS complex

P l hi VT



Polymorphic VT

Like VT but QRS complexes different inmorphology

Typical: QRS complexes spiral around the

baseline, changing their axis andamplitude.

Polymorphic VT + prolong QT interval =

Torsades de pointes



Bradyarrhythmia



Bradyarrhythmia



Bradyarrhythmia

Sinus node dysfunction AV block

1st degree AV block

2nd degree AV block

3nd degree AV block

2nd degree AV block type I

2nd

degree AV block 2:1

2nd degree AV block typeII

Advanced 2nddegree AV block

Sinus arrest /pause

Sinus exit block

Sinus bradycardia

Tachy-brady syndrome



E Rh th



Escape Rhythms

Escape beats= rescuing beats originatingoutside the sinus node

AV Node (junctional rhythm): 40 to 60

beats/minute , narrow QRS

Ventricles: 30 to 40 beats/minute , wide

QRS



Sinus bradycardia

Sinus rhythm

Rate<60/min



Sinus Arrestand SA Exit

Block

T h b d d



Tachy-brady syndrome

J ti l h th



Junctional rhythm

J ti l h th



Junctional rhythm

Rate 40-60/min

Most often not seen P wave (Occasional

retrograde P wave)

Narrow QRS complex

Idio entric lar rh thm



Idioventricular rhythm

Rate 30-40 /min

Wide QRS complex

AV Block



First degree AV block

Second degree AV block

– Type I (Wenchkebach)

– Type II

– 2:1 second degree AV block

– Advanced second degree AV block

Third degree AV block

AV Block

1st DEGREE AV BLOCK



1st DEGREE AV BLOCK

PR interval >0.2 sec

All beats are conducted through to the ventricle

2nd DEGREE AV BLOCK: Mobitz



type I (Wenckebach)

Progressive prolongation of the PR interval until

a QRS is dropped

2nd DEGREE AV BLOCK: Mobitz



type II

QRS complexes are dropped at regular intervals

without prolongation of the PR interval

2nd DEGREE AV BLOCK 2:1



2nd DEGREE AV BLOCK 2:1

2 sinus P wave: 1 QRS complex

Constant PR interval(Impossible to tell whether it is Mobitz I or II)

High grade AV block



g g

(Advanced AV block)

≥ 3:1 AV block

Constant PR interval





No beats are conducted through to the

ventricles.

AV dissociation: atrium and ventricles are driven

by independent pacemakers

Bradycardias

• slow (rate < 60 bpm)

BradycardiaAlgorithm



( p )

• relatively slow

Primary CAB survey

Serious signs or symptoms ?

Due to Bradycardia ?

Type II second-degree AV block

Third-degree AV block

Intervention sequences

• Atrop ine 0.5-1 mg

• Transcu taneous pacing

• Dopamine 5-20 ug/kg/min

• Epinephr ine 2-10 ug/min

•Isoproterenol 2-10ug/kg

Observe • Prepare for transvenous pacer

• If symptoms develop, transcutaneous pacing

----> transvenous pacing placed

NO YES

NO YES

g

Search for & treat possible



contributing factors

5HHypovolemia

Hypoxia

Hydrogen ion

(acidosis)

Hypo/hyperkalemia

HypoglycemiaHypothermia

5TToxins

Tamponade (cardiac)

Tension

pneumothorax

Thrombosis (coronary

or pulmonary)Trauma

(hypovolemia,increased ICP)



Transcutaneous Pacing



Pacing Control



Pacing Control

Method



Method

1. Attach electrode.

2. Turn on pacemaker at desire rate.

3. In bradyasystolic arrest, set initial output tomaximum; once capture has been confirmed,↓output until threshold determined.

4. In conscious patient, start with minimumoutput and↑ until threshold is achieved.

5. Set output at 10-20% above capture

threshold.6. Give sedative & analgesia as needed.

Capture



Capture Definition:Cardiac depolarization and

resultant contraction caused by

pacemaker stimulus



Acute coronary syndrome



References

Guideline UA/NSTEMI ACC/AHA

2007

Guideline STEMI ACC/AHA 2007 ,

2009

Pathophysiology of ACSL



Fuster V et al NEJM 1992;326:310 – 318

Davies MJ et al Circulat ion 1990;82(Suppl II):II –

38, II –

46

Lipid pool

Macrophages

Stress, tensile,internal

Shear forces,external Fissure

Largefissure

Smallfissure

Mural thrombus(unstable angina/NSTEMI)

Occlusive thrombus(STEMI)

Atheroscleroticplaque

Plaquedisruption

Thrombus

Example of atherosclerosis

disease progression

Spectrum of Acute Coronary



Spectrum of Acute Coronary

Syndrome

Q-wave MIUnstable Angina

Ischemic Discomfort at Rest

No ST Elevation ST Elevation

Non ST Elevation MI

Braunwald E et al . J Am Coll Cardiol 2000;36:970 – 1062.

≥0.2 mV in V1-3

≥0.1 mV in other lea

>2 contiguous leads

Di i



Diagnosis

Clinical presentation

ECG finding

Cardiac Biomarker

Clinical presentation



AnginaRetrosternal chest pain, burning, heaviness

Radiating to neck,jaw,epigastrium,shoulder ,Lt arm

Precipitated by exercise,cold weather,emotional stress

Duration < 2-10 min

Rest or unstable anginaSame as angina , more severe

Typical <20 min

Acute myocardial infarctionSame as angina , more severe

Sudden onset, often with shortness of breathing,weakness, nausea , vomitting

Usually lasting 30 min or longer

PericarditisSharp, pleuritic pain

Aggravated by changes in positions, variable in duration, pericardial friction rub

Braunwald’ s Heart disease ,textbook of cardiovascular medicine eight edition

ED Evaluation of

Patients With STEMI



Patients With STEMI

Aortic dissection

Pulmonary embolus

Perforating ulcer

Tension pneumothorax

Boerhaave syndrome

(esophageal rupture with

mediastinitis)

Differential Diagnosis of STEMI: Life-Threatening

ED Evaluation of

Patients With STEMI



Gastroesophageal reflux

(GERD) and spasm

Chest-wall pain

PleurisyPeptic ulcer disease

Panic attack

Cervical disc or neuropathic

pain

Biliary or pancreatic pain

Somatization andpsychogenic pain disorder

Patients With STEMI

Differential Diagnosis of STEMI: Other Noncardiac

ECG fi di



ECG finding

ST Elevation

> 0.2 mV in leads V1-3

> 0.1 mV in other leads

Elevation in at least 2 contiguous leads







Comparison of EKG Changes Associated with Acute Pericarditis,



Myocardial Infarction and Early Repolarization

ECG Finding

Acute

Pericarditis

Myocardial

Infarction

Early

Repolarization

ST-segment shape Concave upward Convex upward Concave upward

Q waves Absent Present Absent

Reciprocal ST-

segment changes

Absent Present Absent

Location of ST-

segment elevation

Limb and precordial

leads

Area of involved

artery

Precordial leads

ST/T ratio in lead V6 >0.25 N/ A <0.25

Loss of R-wave

voltage

Absent Present Absent

PR-segment

depression

Present Absent Absent

Marriott Practical Electrcaediography 10th

edition

Early repolarization



y p





LVH LBBB pericarditisHyper K

ASMI Brugada







Acute Inferior wall MI



Acute Anterior wall MI



Wall ST elevation



Wall

Septal

Anterior

Anteroseptal

Extensive anterior

LateralHigh lateral

Anterolateral

Inferior

RV infarctposterior

ST elevation

V1-V2

V3-V4

V1-V4

V1-V6

V6, I, AVLI, AVL

V3-V6, AVL

II, III, AVF

V3R-V4RTall R in V1

Corelation of Wall and coronary vessel



Progression of Nonreperfused Q-

AMI



wave AMI

Biochemical Cardiac Markers





ESC/ACCF/AHA/WHF Expert Consensus Document,

JACC Vol. 50, No. 22, 2007 :2173 –95

Management



g

Generalmanagement

Oxygenation

AnalgesiaNTG

Blood sugar control

Specificmanagement

Reperfusion

Antiplatelets Anticoagulant

Betablocker

ACEI/ARB Aldosterone blockade

Statin

Analgesia



Morphine remains Class I for STEMIalthough may increase adverse events in

UA/NSTEMI

NSAID medications increase mortality,reinfarction, and heart failure in proportion

to degree of COX-2 selectivity

– Discontinue on admission for STEMI– Do not initiate during acute phase of

management

ACC/AHA guideline for STEMI 2007

Oxygen



Supplemental oxygen should be administered topatients with arterial oxygen desaturation (SaO2

< 90%).

It is reasonable to administer supplemental

oxygen to all patients with uncomplicated STEMI

during the first 6 hours.

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III


Nitroglycerin



Patients with ongoing ischemic discomfort should

receive sublingual NTG (0.4 mg) every 5 minutes for atotal of 3 doses, after which an assessment should be

made about the need for intravenous NTG.

Intravenous NTG is indicated for relief of ongoing

ischemic discomfort that responds to nitrate therapy,

control of hypertension, or management of pulmonary

congestion.




Nitroglycerin Contraindications



Nitrates should not be administered when:

Nitrates should not be administered to

patients who have received aphosphodiesterase inhibitor for erectile

dysfunction within the last 24 hours (48

hours for tadalafil).

• systolic pressure < 90 mm Hg or ≥ to 30 mm Hg

below baseline

• severe bradycardia (< 50 bpm)

• tachycardia (> 100 bpm) or • suspected RV infarction.



Specific management

Reperfusion Options for STEMIPatients



Reperfusion Options for STEMI PatientsSelect Reperfusion Treatment.



Fibrinolysis generally preferred

Early presentation ( ≤ 3 hours from symptom

onset and delay to invasive strategy)

Invasive strategy not an option

Cath lab occupied or not available Vascular access difficulties

No access to skilled PCI lab

Delay to invasive strategy

Prolonged transport Door-to-balloon more than 90 minutes

> 1 hour vs fibrinolysis (fibrin-specific agent) now

If presentation is < 3 hours and there is no delay to an invasive

strategy, there is no preference for either strategy.


Reperfusion Options for STEMI PatientsSelect Reperfusion Treatment.



Invasive strategy generally preferred

Skilled PCI lab available with surgical backup

Door-to-balloon < 90 minutes

• High Risk from STEMI

Cardiogenic shock, Killip class ≥ 3

Contraindications to fibrinolysis, including

increased risk of bleeding and ICH

Late presentation > 3 hours from symptom onset

Diagnosis of STEMI is in doubt

If presentation is < 3 hours and there is no delay to an invasive strategy,

there is no preference for either strategy.


Primary PCI



STEMI patients presenting to a hospital with PCIcapability should be treated with primary PCI within

90 min of first medical contact as a systems goal.

STEMI patients presenting to a hospital without PCI

capability, and who cannot be transferred to a PCI

center and undergo PCI within 90 min of first

medical contact, should be treated with fibrinolytic

therapy within 30 min of hospital presentation as asystems goal, unless fibrinolytic therapy is

contraindicated.




Application of PCI for STEMI



STEMI

Thrombolysis Primary PCI

Success Failure

Rescue PCI Routine

immediateor urgent PCI

RoutineDeferred CAG+ PCI

Selective CAG

+ PCI only for High-risk pts

Curr Prob l Cardiol, January 2003

Facilitated PCI



Rescue and Late PCI

Assessment of Reperfusion

It is reasonable to monitor the pattern of ST elevationIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII



It is reasonable to monitor the pattern of ST elevation,

cardiac rhythm and clinical symptoms over the 60 to 180

minutes after initiation of fibrinolytic therapy.

Noninvasive findings suggestive of reperfusion include:

Relief of symptoms

Maintenance and restoration of hemodynamic and/or

electrical instability

Reduction of ≥ 50% of the initial ST-segment elevation

pattern on follow-up ECG 60 to 90 minutes after

initiation of therapy.

ACC/AHA guideline 2007

Rescue PCI



PCI in no reperfusion after fibrinolytic therapy

Failed reperfusion

ongoing chest pain

resolution of ST elevation < 50 %

Early peak of cardiac enzyme

Benefit ( Meta-analysis in 2007)

Mortality rate 10.4% to 7.3 % ( RR 0.69, 95% CI 0.46-1.05 ; p=0.09)

Reinfarction 10.7% to 6.1 % ( RR 0.58, 95% CI 0.35-0.97 ; p=0.04)

Heart failure 17.8% to 12.7 % ( RR0.73,95% CI 0.54-1.00 ; p=0.05)

Thrombolytic Therapy



y y

Indications ?

Contraindications ?Which drug ?

How fast to be given ?

Conjunctive antithrombotics ?

ST segment elevation

> 0 2 mV in leads V1-3



Indicationfor

fribinolysis

TherapyIn STEMI

> 0.2 mV in leads V1 3

> 0.1 mV in other leads

Elevation in at least 2 continuous leadsor new LBBB

Duration < 12 hr (class I)

12-24 hr with ongoing pain ( class IIa)

No contraindications

TIMI Risk Score for STEMI Risk Score Odds of death by 30D*

Mortality prediction of STEMI



Age65-74 75

DM/HTN or angina

Weight < 67 kg

Time to rx > 4 hrs

Anterior STE or LBBB

HR >100

SBP < 100

Historical

Exam

Presentation

Killip II-IV

2 points3 points

1 point

3 points

2 points

1 point

1 point

1 point

2 points

Risk Score = Total (0 -14)

0

12

3

4

56

7

8

>8

0.1 (0.1-0.2)

0.3 (0.2-0.3)

0.4 (0.3-0.5)

0.7 (0.6-0.9)

1.2 (1.0-1.5)

2.2 (1.9-2.6)

3.0 (2.5-3.6)

4.8 (3.8-6.1)

5.8 (4.2-7.8)

8.8 (6.3-12)

*referenced to average mortality

(95% confidence intervals)






Indications ?




Absolute Contraindications for

Thrombolytic Rx



y

Any prior ICHKnown structural cerebral vascular lesion

Malignant intracranial neoplasm

Ischemic stroke within 3 monthsSuspected aortic dissection

Active bleeding diathesis (excluding menses)

Significant closed-head or facial traumawithin 3 months

Relative Contraindications for

Thrombolytic Rx



Chronic severe poorly controlled HTN

Severe uncontrolled HTN on presentation SBP>180,DBP>110

Prior ischemic stroke > 3 months, intracranialpathology

Traumatic or prolonged >10 min CPR or major surgerywithin 3 weeks

Recent within 2-4 weeks internal bleeding

Noncompressible vascular puncture

SK, anistreplase: prior exposure > 5 days ago or prior

allergic reactionPregnancy

Active peptic ulcer

Current use of anticoagulation

Risks for ICH After Thrombolysis



Age > 65

Weight < 70 kg

FemaleHypertension

Use of tPA




Indications ?




Thrombolytic Agents



First generation Second generation Third generation

Streptokinase* APSAC Reteplase* (r-PA)

Urokinase Alteplase* Lanoteplase* (n-PA)

Staphylokinase Saruplase TNK-PA

Staphylokinase

Thrombolytic Agents in

Clinical Practice



• SK 1.5 mu IV > 1 hr

• Accelerated tPA 15 mg IV bolus

50 mg (0.75 mg/kg) IV in 30 min

35 mg (0.5 mg/kg) IV in 60 min

Clinical Practice

Comparison



Streptokinase Alteplase Reteplase Tenecteplase

•Dose 1.5 MU over Up to 100mg in 10U x 2 30-50mg

30-60 min 90 min (wt-based) each over 2 min based on weight

•Bolus Admin. No No Yes Yes

•Antigenic Yes No No No

•Allergic React Yes No No No

•Systemic Marked Mild Moderate Minimal

Fibrinogen Depletion

• ~90-min patency 50 75 75? 75

rates (%)•TIMI grade 3 flow, % 32 54 60 63

Antiplatelets



Aspirin

Thienopyridines

Glycoprotein IIb/IIIa receptor antagonist

Aspirin



Reduce mortality

Reduce coronary reocclusion

Reduce recurrent ischemic events

Aspirin



Aspirin should be chewed by patients who

have not taken aspirin before presentation

with STEMI. The initial dose should be

162 mg to 325 mg

Although some trials have used enteric-coated aspirin for initial dosing, more rapid buccal absorption occurs with

non –enteric-coated formulations.


Complementary Mode of Action between

Clopidogrel and ASA



p g

COX, cyclooxygenase; ADP, adenosine diphosphate; TxA2,

thromboxane A2

Schafer AI Am J Med 1996;101:199 209

Clopidogrel is an advanced ADP receptor antagonist and

inhibits platelet aggregation by antagonizing the effects of ADP

ST-Elevation MI: ClopidogrelTrials



COMMIT / CCS-2

46,000 patients

Mortality, D / MI / CVA

AMI < 24 hrs

Age up to 100

~ 50% lytic

No loading dose China

Non-invasive strategy

3,500 Patients

Infarct artery patency

AMI < 12 hrs

Age < 75

100% fibrinolytic

Loading dose Europe / N. America

Invasive strategy

Thie

nopyridines



Clopidogrel 75 mg per day orally should be added toaspirin in patients with STEMI regardless of whether

they undergo reperfusion with fibrinolytic therapy or

do not receive reperfusion therapy.

Treatment with clopidogrel should continue

for at least 14 days.




Thie

nopyridines



In patients < 75 years who receive fibrinolytic

therapy or who do not receive reperfusion therapy, it

is reasonable to administer an oral clopidogrel

loading dose of 300 mg. (No data are available to

guide decision making regarding an oral loading

dose in patients ≥ 75 years of age.)

Long-term maintenance therapy (e.g., 1 year) with

clopidogrel (75 mg per day orally) can be useful in

STEMI patients regardless of whether they undergo

reperfusion with fibrinolytic therapy or do not

receive reperfusion therapy.


I IIa Ia Ia IIb Ib Ib III II II IIa Ia Ia IIb Ib Ib III II II IIa Ia Ia IIb Ib Ib III II II Ia Ia Ia IIb Ib Ib III II II









Anticoagulant



Anticoagulant

Reduce reocclusion

Reduce reinfarction

Reduce recurrent ischemia



Heparin

LMWH

Fondaparinux

Bivalirudin

Anticoagulants



Patients undergoing reperfusion with fibrinolytics

should receive anticoagulant therapy for a minimum of

48 hours (Level of Evidence: C) and preferably for the

duration of the index hospitalization, up to 8 days

(regimens other than unfractionated heparin [UFH] are

recommended if anticoagulant therapy is given for morethan 48 hours because of the risk of heparin-induced

thrombocytopenia with prolonged UFH treatment).

(Level of Evidence: A)

Anticoagulant regimens with established efficacyinclude:

♥ UFH (LOE: C)

♥ Enoxaparin (LOE:A)

♥ Fondaparinux (LOE:B)



ACC/AHA guideline STEMI 2007






Beta-Blockers

Beta-Blockers



Reduce reinfarct size

Reduce reinfarction

Reduce life threatening ventricular tachyarrhythmias

Beta-Blockers



Oral beta-blocker therapy should be initiated in the first 24

hours for patients who do not have any of the following: 1)signs of heart failure, 2) evidence of a low output state, 3)

increased risk* for cardiogenic shock, or 4) other relative

contraindications to beta blockade (PR interval > 0.24 sec,

2nd- or 3rd-degree heart block, active asthma, or reactive

airway disease).

It is reasonable to administer an IV beta blocker at the time of

presentation to STEMI patients who are hypertensive and who

do not have any of the following: 1) signs of heart failure, 2)

evidence of a low output state, 3) increased risk* for

cardiogenic shock, or 4) other relative contraindications to

beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart

block, active asthma, or reactive airway disease).






Inhibition of the Renin-Angiotensin Aldosterone

System

Inhibition of the Renin-Angiotensin-Aldosterone System



Aldosterone System

ACEI/ARB

Reduce mortality

Aldosterone

blockadeReduce mortality

Reducehospitalization

ACE/ARB: Within 24 Hours

An ACE inhibitor should be administered orally

ithi th fi t 24 h f STEMI t th f ll i




within the first 24 hours of STEMI to the following

patients without hypotension or known class of contraindications:

• Anterior infarction

Pulmonary congestion

LVEF < 0.40

An ARB should be given to ACE-intolerant patients

with either clinical or radiological signs of HF or LVEF< 0.40.







Roles of statins in ACS



Improve endothelial function

Repair ruptured atherosclerotic plaques

Improve plaque stabilization

Reduce thrombus formation on ruptureplaques

Cardiol Rev1999;16(Suppl.):1-6.

Prefer high dose atrovastation 80 mg/day

(MIRACL, PROVE-IT)

ST elevation

ASA clopidogrel Beta blocker statin



ASA, clopidogrel,Beta-blocker,statin

< 12 hours

Thrombolytic Rx

contraindicated

SK Cardiac cath with

primary PTCA

Not candidate for

reperfusion Rx

Medical Rx: ACEI, Nitrates

> 12 hours

No Yes

Consider

reperfusion Rx

Persistent

symptoms

If failed SK,

rescue (salvage)

PTCA

Eligible for

thrombolytic Rx

D to N time <30 minD to balloon time 90+30 min



1st

24 h

During Hosp Hosp DC +

Long Term

Summary of Pharmacologic Rx: LVD, Sec. Pre



24 h Long Term

ACEI Anterior MI,Pulm Cong., EF < 40 Oral

Daily

OralDaily

IndefinitelyARB ACEI intol.,

HF, EF < 40

Aldo

Blocker

No renal dysf,

K+ < 5.0 mEq/L

On ACEI,

HF or DM

Same as

during

Hosp.

Statin Oral daily Oral daily Indefinitely,LDL <70-100

JACC 2004;44:671 , Circ 2004;110:588





Fast Track MI



การด แลผ ป วยโรคกลามเนอหัวใจตายเฉยบพลัน โรงพยาบาลสม ทรปราการ

checklist ตามแบบคัดกรองอาการเจบหนาอก

ผปวยเจบหนาอก



แนวทางการด แลผ ป วย

แพทยซักประวัตตรวจรางกาย ตรวจคล นไฟฟ าหัวใจ และ Non invasive procedure เพ อทาการวนจฉัยและวนจฉัยแยกโรค



ภาวะหัวใจขาดเลอดเฉยบพลัน โรคหัวใจขาดเลอดเร อรัง

เหมาะสมก ับการให SK หรอไม

ST Elevation Non ST elevation

ใหยาละลายล มเลอด (SK)

เปดหลอดเลอดดวย SK ไดหรอไม

ICU / CCU

มภาวะแทรกซอนหรอไม

ตดตามและรักษาอย างต อเน อง

สงตอเพ อทา Invasive procedure

เหมาะสม

ได

ไมม

ไมเหมาะสม

ไมได

ม

แบบคั ดกรองผ ปวยกลามเน อหัวใจตายเฉยบพ ลัน ช อ – สกล ............................................................................................................

HN. ………………………………….

วันท …………………………………. เวลา ………………………………….

เพ ………………………………….

รคประจาตัว



รคประจ าตว ……………………………………………………………………………………

การแพยา ……………………………………………………………………………………

อาการ ขะซักประวัต 1. มอาการเจบหนาอกอย

2. ไมมอาการเจบหนาอกแลว

ลักษะการเจ บหนาอก 3. เจบแนนเหมอนถกทับกลางหนาอก

4. เจบราวไปทองแขนขางซาย, ราวข นกราม

5. เจบนานกวา 20 นาท 6. อาการเจบมากข นเม อออกแรง

7. เจบขะพัก

อาการรวม 8. เปนลมหมดสต 9. เหน อยหอบนอนราบไมได 10. อดอัดหายใจไมออก

11. เหง อแตก

12. ใจส ัน

13. คล นไสอาเจยน

ตรวจรางกายเบ องตน 14. Vital Sign BP_________mmHg, P_________ คร ัง/นาท, R_________ คร ัง

15. ซด

16. กระสับกระสาย

สงตอผ ปวยไปยัง ER [ถาเขาเก 1, 3 – 5, 8 – 10, 15 – 16 และตรวจรางการเบ องตน

SBP≥ 180, SBP < 100, P ≥ 100, P≤ 40, R ≥ 24, R ≤ 6]

หองทา ECG

พบแพทยอายรกรรม พบแพทย GP

แบบคัดกรองอาการเจบหนาอก





ER

Activate fast track MI

แนวทางการดแลผ ปวย Acute STEMI (Fast Track )

ผ ปวยมาดวยอาการเจบหนาอก

*Onset เวลา .............../....................(พยาบาลER )

เวลาท มาถงหองฉกเฉน .............../....................(พยาบาล ER )

ECG 12 Lead เวลา.............../....................(พยาบาล ER )

ช อ............................สกล...................

HN………………………………….

วันท ...................................................



ประวัต / ตรวจรางกาย / แปลผล ECG โดยแพทยประจาหองฉกเฉน

เวลา.............../....................(แพทยประจาหองฉกเฉน)

ASA gr V 1 เมดเค ยวทันท เวลา .............../....................(พยาบาลER )

Clopidogrel 4 เมด ทันท (งด ถาอาย > 75 ป) เวลา.............../....................(พยาบาลER )

Troponin T เวลา.............../....................(พยาบาลER )

ปรกษาแพทยอายรกรรมมาด เวลา.............../....................(แพทยอายรกรรม) วนจฉัย...............................................

Admit เวลา.............../....................(แพทยอายรกรรม)

ออกจากหองฉกเฉน เวลา.............../....................(พยาบาลER )

เขาหอผ ปวย.......................................... เวลา.............../....................(พยาบาลWard)

รายงานแพทยประจา Ward เวลา.............../....................(พยาบาลWard)

แพทยประจา Ward ประเมนผ ปวยเวลา.........../..........(แพทย Ward) วนจฉัย...........................Killip……………..

*เร ม Streptokinase เวลา.............../....................(พยาบาลWard)

ประเมนผ ปวย (Symptom , ECG) หลังได Streptokinase 90 นาท เวลา.............../....................(พยาบาลWard)

ภาวะแทรกซอน (Major bleeding) ( ) ไมม ( ) ม ........................................................................

จาหนายจากหอผ ปวย ................................................................................

ถานการจาหนาย ( ) ทเลา ( ) เสยชวต

( ) ปเสธการรักษา ( ) สงตอไปท .............................................

Door to Needle time ……………hr ……………..min

าเหตท ไดรับการรักษาลาชา..................................................................................................................................................

................................................................................................................................................................................................

Fast track MI





ER หองทาECG

Activate fast track MI

Admit

ผล ECGเขาไดก ับ STEMI

ดแลรักษาตาม Caremap

standing order

เก บขอมลตามตัวช วดั

yes no

ส ง ER เขา fast track MI

Admit ward เขา fast track MI

พบอายรแพทยถามECGผดปกต

พบแพทยท ัวไปถาECG ปกต

D/C

แผนการรักษา Acute ST Elevation MI

Fast Track



หนังสอยนยอม / ไมยนยอม การใหยาละลายล มเลอด

(Streptokinase)

http://f/MI26-05-53/%E0%B9%81%E0%B8%9C%E0%B8%99%E0%B8%81%E0%B8%B2%E0%B8%A3%E0%B8%A3%E0%B8%B1%E0%B8%81%E0%B8%A9%E0%B8%B2%20Acute%20ST%20Elevation%20MI%20Fast%20Track.doc



( p )

แนวทางการด แลผ ป วย

แพทยซักประวัตตรวจรางกาย ตรวจคล นไฟฟ าหัวใจ และ Non invasive procedure เพ อทาการวนจฉัยและวนจฉัยแยกโรค

http://f/MI26-05-53/%E0%B8%82%E0%B9%89%E0%B8%AD%E0%B8%AB%E0%B9%89%E0%B8%B2%E0%B8%A1%E0%B8%81%E0%B8%B2%E0%B8%A3%E0%B9%83%E0%B8%AB%E0%B9%89%E0%B8%A2%E0%B8%B2%E0%B8%A5%E0%B8%B0%E0%B8%A5%E0%B8%B2%E0%B8%A2%E0%B8%A5%E0%B8%B4%E0%B9%88%E0%B8%A1%E0%B9%80%E0%B8%A5%E0%B8%B7%E0%B8%AD%E0%B8%94.doc



ภาวะหัวใจขาดเลอดเฉยบพลัน โรคหัวใจขาดเลอดเร อรัง

เหมาะสมก ับการให SK หรอไม

ST Elevation Non ST elevation

ใหยาละลายล มเลอด (SK)

เปดหลอดเลอดดวย SK ไดหรอไม

ICU / CCU

มภาวะแทรกซอนหรอไม

ตดตามและรักษาอย างต อเน อง

สงตอเพ อทา Invasive procedure

เหมาะสม

ได

ไมม

ไมเหมาะสม

ไมได

ม

แนวทางในการรับสงตอผ ป วย



ส งต อกรเก นศกัยภาพในการดแล Contraindication of thrombolytic

Acute anterior wall MI killip >III

Cardiogenic shock Rescue PCI

รับดแลต อจากโรงพยาบาลชมชน

แนวทางการสงตอผ ป วย



แบบฟอรมการสงตอผ ป วยโรคกลามเนอหัวใจตายเฉยบพลันชนด

STEMI ไปโรงพยาบาลชลบ ร

http://f/MI26-05-53/%E0%B9%81%E0%B8%9C%E0%B8%99%E0%B8%A0%E0%B8%B9%E0%B8%A1%E0%B8%B4%E0%B8%97%E0%B8%B5%E0%B9%88%20%202%E0%B9%81%E0%B8%99%E0%B8%A7%E0%B8%97%E0%B8%B2%E0%B8%87%E0%B8%81%E0%B8%B2%E0%B8%A3%E0%B8%AA%E0%B9%88%E0%B8%87%E0%B8%95%E0%B9%88%E0%B8%AD%E0%B8%9C%E0%B8%B9%E0%B9%89%E0%B8%9B%E0%B9%88%E0%B8%A7%E0%B8%A2%E0%B8%AA%E0%B8%B3%E0%B8%AB%E0%B8%A3%E0%B8%B1%E0%B8%9A%E0%B8%AA%E0%B8%96%E0%B8%B2%E0%B8%99%E0%B8%9E%E0%B8%A2%E0%B8%B2%E0%B8%9A%E0%B8%B2%E0%B8%A5%E0%B8%A3%E0%B8%B0%E0%B8%94%E0%B8%B1%E0%B8%9A%201.doc



แบบฟอรมการสงตอผ ป วยโรคกลามเนอหัวใจตายเฉยบพลันชนด

STEMI ในจังหวัดสม ทรปราการ

http://f/MI26-05-53/%E0%B9%81%E0%B8%9A%E0%B8%9A%E0%B8%9F%E0%B8%AD%E0%B8%A3%E0%B9%8C%E0%B8%A1%E0%B8%81%E0%B8%B2%E0%B8%A3%E0%B8%AA%E0%B9%88%E0%B8%87%E0%B8%95%E0%B9%88%E0%B8%AD.doc



ตัวชวัด

http://f/MI26-05-53/%E0%B9%81%E0%B8%9A%E0%B8%9A%E0%B8%9F%E0%B8%AD%E0%B8%A3%E0%B9%8C%E0%B8%A1%E0%B8%81%E0%B8%B2%E0%B8%A3%E0%B8%AA%E0%B9%88%E0%B8%87%E0%B8%95%E0%B9%88%E0%B8%AD%E0%B8%9C%E0%B8%B9%E0%B9%89%E0%B8%9B%E0%B9%88%E0%B8%A7%E0%B8%A2%E0%B9%82%E0%B8%A3%E0%B8%84%E0%B8%81%E0%B8%A5%E0%B9%89%E0%B8%B2%E0%B8%A1%E0%B9%80%E0%B8%99%E0%B8%B7%E0%B9%89%E0%B8%AD%E0%B8%AB%E0%B8%B1%E0%B8%A7%E0%B9%83%E0%B8%88%E0%B8%95%E0%B8%B2%E0%B8%A2%E0%B9%80%E0%B8%89%E0%B8%B5%E0%B8%A2%E0%B8%9A%E0%B8%9E%E0%B8%A5%E0%B8%B1%E0%B8%99%E0%B8%8A%E0%B8%99%E0%B8%B4%E0%B8%94%20%20%20STEMI%20%20%E0%B9%83%E0%B8%99%E0%B8%88%E0%B8%B1%E0%B8%87%E0%B8%AB%E0%B8%A7%E0%B8%B1%E0%B8%94%E0%B8%AA%E0%B8%A1%E0%B8%B8%E0%B8%97%E0%B8%A3%E0%B8%9B%E0%B8%A3%E0%B8%B2%E0%B8%81%E0%B8%B2%E0%B8%A3.doc



1. รอยละของผ ป วย Acute STEMI ไดรับยาละลายล มเลอดภายใน 30นาท

2. รอยละการเสยชวตของผ ป วย Acute STEMI

3. รอยละการรอดชวตของผ ป วย Acute STEMI แบงตาม killip

classification

4. รอยละการเกด Major bleeding จากการไดรับยาละลายล มเลอด

ตัวชวัดเสรม



1. ระยะเวลาเฉล ยผ ป วย Acute STEMI ท ไดรับยาละลายล มเลอดตั งแตมาถงโรงพยาบาลจนถงไดรับยา

2. รอยละของผ ป วย Acute STEMI ไดรับยาละลายล มเลอดภายใน 30

นาทเฉพาะในเวลาราชการ

3. Door to EKG time ภายใน 10 นาท

4. Door to Diagnosis time ภายใน 20 นาท



Documents

Emergency in Medicine 2012