CARDIOVASCULAR EMERGENCY

From the past to the future

…time is myocardium!
santosokaro@gmail.com

No Conflict of Interest
 2

Statistics
• Cardiovascular disease (CVD) 17.3m
deaths/year ----WHO 2008.
• IHD contributes to app 7m deaths/ yr

• Sudden cardiac death accounts for

over 40% of these deaths.
 3

•The first Cardiac Emergency Room (CER) founded in 1978

by Professor Dirk Durrer in Amsterdam.

• with the initial goal of reducing time delays in patients

with acute myocardial infarction.
• have contributed to the reductions in mortality from coronary
disease in the past decades

• In later years, the focus of CERs has gradually shifted towards

ruling out acute coronary syndromes (ACS), to reduce
unnecessary hospital admissions .

•In more recent years, other clinical conditions have

been added to the case loads of CERs,
including worsening heart failure, atrial fibrillation
and syncope
 HISTORICAL REVIEW
 5000 - first artificial mouth to mouth
3000 BC ventilation
 1780 – first attempt of newborn
resuscitation by blowing
 1874 – first experimental direct cardiac
massage
 1901 – first successful direct cardiac massage
in man
 1946 – first experimental indirect cardiac
massage and defibrillation
 1960 – indirect cardiac massage
 1980 – development of cardiopulmonary
resuscitation due to the works of Peter
Safar 4
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6
 7

Cardiovascular emergencies are

life-threatening disorders that
must be recognized immediately
to avoid delay in treatment and
to minimize morbidity and
mortality.
Patients may present with chest pain,
dysrhythmia, cardiopulmonary arrest or
severe hypertension,
 8

Acute Cardiology:Symptoms
Diagnosis of cardiac emergencies:
Synthesis of symptoms and physical
examination and combination with
laboratory findings, and appealing an
expert opinion.

Main symptoms:
1- Chest pain and chest discomfort
2- Dyspnea
3- Shock
4- Fatigue
5- Palpitation
6- Syncope, Presyncope
7- Sudden death
 9

Acute Cardiology :Physical examination

CLİNİCAL KEY POİNTS OF PHYSİCAL EXAMS:
- History.
1. Blood pressure: Low, high
2. Peripheral pulses: Rapid, slow, rythmic,
arryrthmic.
3. Signs of systemic hypoperfusion:
Consciousness, skin color, warmness of the
skin, urinary output.
4. General posture of the patient: Inspection,
ortopnea, supine position, pale, sweating.
5. Killip class. (I-IV).
 10

Sudden cardiac death (SCD)

• is a syndrome defined by its clinical presentation rather

than by a discrete pathophysiology
The World Health Organization definition has been
widely accepted: sudden collapse occurring within one
hour of symptom
As the name implies, SCD is instantaneous and most
individuals become unconscious within seconds to
minutes as a result of insufficient cerebral blood
Underlying heart disease is present the vast majority of
patients with SCD
 Heart Attack vs Cardiac Arrest
Heart Attack: Cardiac Arrest:
• Blockage in coronary artery • Heart stops

• Person usually conscious • Person is unconscious

• Upper body discomfort • Often no previous symptoms

or pain
• Person may be gasping or not
be breathing at all
Underlying Arrhythmia of Sudden Death

Primary
VF
8% Torsades
de Pointes
13%

VT Bradycardia
62% 17%
 Underlying Causes of Fatal
Arrhythmias
80%
Coronary Artery
Disease
5% Other*

15%
Cardiomyopathy

Adapted from Heikki et al. N Engl J Med, Vol. 345, No. 20, 2001.
* ion-channel abnormalities, valvular or congenital heart disease, other causes
 Time references in Sudden Cardiac Deaths

Prodromes Onset of Terminal Cardiac arrest Biological

events death

New or Abrupt Sudden collapse Failure of

Worsening Changes in •Loss of effective resuscitation
CV symptoms clinical Status: circulation or
•Chest pain •Arrhythmia •Loss of failure of
•Palpitation •Hypotension Consciousness electrical,
•Dyspnea •Chest pain mechanical.
•Fatiguabilty •Dyspnea or
•Lightheadedness CNS function
after initial
resuscitation

Days to months Up to 1 hour Minutes to weeks

 ECG ABNORMALITIES
Diagnosis
• Arrhythmogenic RV dysplasia
•Hypertrophic cardiomyopathy
•Long QT syndrome
•Brugada Syndrome
•WPW Syndrome
•Short QT-syndromes
ECG Findings
T wave inversion anteriorly
Epsilon waves
RBBB complete or incomplete
LVH
Pseudoinfarct with anterior Q waves
Prolonged QTc (>450 msec in men and >460msec in
children and women )
Abnormal appearing ST segments
RBBB complete or incomplete
Anterior St elevations
Short PR
Prolonged QRS
Delta waves
QTc < 300 msec
Brugada Syndrome
 17

Importance of Early Defibrillation

% Success
100
90
Chances of success
80 decrease 7–10%
70 each minute
60
50
40
30
20
10
0
0 1 2 3 4 5 6 7 8 9
Time to Defibrillation (minutes)
 Acute Management of Specific Arrhythmias
Management of Cardiac Arrest
I IIa IIb III
For victims with ventricular tachyarrhythmic mechanisms of
cardiac arrest, when recurrences occur after a maximally
defibrillating shock (generally 360 J for monophasic
defibrillators), intravenous amiodarone should be the preferred
antiarrhythmic drug for attempting a stable rhythm after further
defibrillations.
I IIa IIb III
For recurrent ventricular tachyarrhythmias or nontachyarrhythmic
mechanisms of cardiac arrest, it is recommended to follow the
algorithms contained in the documents on CPR developed by the
AHA in association with ILCOR and/or the ERC.
I IIa IIb III
Reversible causes and factors contributing to cardiac
arrest should be managed during advanced life
support, including management of hypoxia,
electrolyte disturbances, mechanical factors, and
 Acute Management of Specific Arrhythmias

Management of Cardiac Arrest

I IIa IIb III For response times greater than or equal to 5 min, a
brief (less than 90 to 180 s) period of CPR is
reasonable prior to attempting defibrillation.
I IIa IIb III
A single precordial thump may be considered by
health care professional providers when responding
to a witnessed cardiac arrest.
 Therapies for VA

Antiarrhythmic Drugs

♥ Beta Blockers: Effectively suppress ventricular ectopic beats &

arrhythmias; reduce incidence of SCD
♥ Amiodarone: No definite survival benefit; some studies have shown
reduction in SCD in patients with LV dysfunction especially when given
in conjunction with BB. Has complex drug interactions and many
adverse side effects (pulmonary, hepatic, thyroid, cutaneous)
♥ Sotalol: Suppresses ventricular arrhythmias; is more pro-arrhythmic than
amiodarone, no survival benefit clearly shown
♥ Conclusions: Antiarrhythmic drugs (except for BB) should not be used as
primary therapy of VA and the prevention of SCD
 Something to think about
• Public access defibrillation has the potential to the
single greatest advancement in the treatment of
prehospital SCA Death since the development of
CPR

AHA Guidelines 2000 for Cardiopulmonary

Resuscitation and Emergency Cardiovascular Care Textbook.
PREVENTION OF SCD
Detection and treatment of high
risk for SCD
Early recognition
Early access to AED
Resucitation skills of the family
of patients and community
 2006 ACC/AHA/ESC recommendations on the use of the implantable cardioverter defibrillator in
the secondary prevention of sudden cardiac death.
VF, ventricular fibrillation; VT, ventricular tachycardia (*haemodynamically unstable sustained VT; **recurrent VT); MI, myocardial
infarction; NIDC, non-ischaemic dilated cardiomyopathy; EF, ejection fraction.

Rossenbacker T et al. Eur Heart J Suppl 2007;9:I50-I58

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For
permissions please e-mail: journals.permissions@oxfordjournals.org
ACUTE CORONARY SYNDROME
 Milestones in ACS Management
Anti-Thrombin Rx
Heparin LMWH Bivalirudin [ Fondaparinux ]

Anti-Platelet Rx
GP IIb/IIIa
Aspirin Clopidogrel
blockers
Treatment Strategy
Conservative Early invasive

PRISM-PLUS REPLACE 2 ICTUS

PURSUIT CURE OASIS-5 ISAR-REACT 2

ESSENCE TACTICS TIMI-18 SYNERGY ACUITY

1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006

PCI ~ 5% stents ~85% stents Drug-eluting stents

Ischemic risk

Bleeding risk
Adapted from and with the courtesy of Steven Manoukian, MD
 31
PEMAHAMAN PATOFISIOLOGI
STEMI Non-STEMI

Patology: Total oclusive/Nonocclusive thrombus

Markers of necrosis: () Markers of necrosis: N or ()

 32

Cold “Heart” Facts of STEMI

Time is myocardium

 coronary occlusion < 30min may not lead to

permanent myocardial damage
 Myocardial cell loss rapidly decreases
after 30 -120 mins of coronary occlusion

 Delaying treatment means greater

morbidity and greater risk of dying
 33

The Time Factor

 34

(Adapted from CW Hamm et al: Lancet 358:1533, 2001, an MJ Davies: Heart

83:361, 2000)
 35

ECG diagnosis:
Importance of TELEMEDICINE
and MI networks
 36

BIOMARKERS
Diagnosis of acute myocardial infarction

• Creatine-Kinase-MB isoform , Cardiac Troponin.

In 2000, Cardiac Troponin replaced CK-MB the biomarker of
choice for diagnosing a myocardial infarction .
• Troponin is a protein released from myocytes when irreversible myocardial
• damage occurs.
• highly specific to cardiac tissue and accurately diagnoses myocardial infarction
• with a history of ischaemic pain or ECG changes reflecting ischaemia

Copeptin can rule out MI earlier in addition to a negative

Troponin T test
At the time of presentation a copeptin level of < 14 pg/ml and a Trop T level of <
0.01 could rule out a myocardial infarction thus obviating the need for monitoring
and serial blood tests in a majority of patients. C
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 40

Upstream Management of Suspected ACS

► ECG and ASA within 10 min

STEMI patients directed to their pathway

► Risk stratification
Focused history and physical, biomarkers, serial ECGs, risk score,
and bleeding risk

► Patients with high ischemic risk should go for EIS

(Class I) or, in a minority of cases, for ICS (Class IIa), but
only after medical stabilization
 41

Risk stratification
Patient presents with chest pain or potential chest pain equivalent (e.g. jaw, shoulder,
arm, back, or epigastric pain, unexplained dyspnea, syncope, palpitations)

Chest pain triage and ECG (< 10 min)

Physician's history Physician's physical Prompt 12- or
examination 15-lead ECG

Prompt differentiation

ST-segment elevation
meeting fibrinolytic criteria
or new/presumably new
LBBB or evidence of acute
posterior MI
ST-segment depression > 0.5 mm ECG is nondiagnostic Very low
or transient ST-segment elevation or normal suspicion
not meeting fibrinolytic criteria Clinical suspicion of ACS
(ECG or clinical evidence of ACS
of unstable angina)

(modified from Pollack et al,2003)

43
 44

Reperfusion strategy STEMI

Pharmacology/Lysis PCI
Widely available Limited availability
Quickly administered Treatment delays
Less effective More effective
Bleeding Risk Hemorrhagic stroke
lower
Lytics
tPA,rPA,TNK > SK
 45

►There is still a role for fibrinolytic

therapy in STEMI

►Adjuvant clopidogrel and/or

enoxaparin improve outcomes in
combination with fibrinolytics

►Fondaparinux improves outcomes

relative to placebo
 Treatment Goals After MI
• Reducing the risk of another heart attack
– Antithrombotic therapy
– CABG, PTCA/stent
– ACE inhibitors
– Beta-blockers
– Statins
• Prevent the occurrence/progression of heart failure
– Aldosterone antagonists
– ACE inhibitors
– Beta-blockers
• Reducing the risk of sudden cardiac death
– Above agents especially beta-blockers, statins and
revascularization
– ICD therapy
• MADIT II provided 31% reduction in mortality in patients who were
optimized on drug therapy
 47

Improving Pre Hospital Management :

STEMI

Improved public awareness and education

- Gov,health service and Clinical network
commitment to public education

- NGO and other health promotion

agencies commitment to relevant,impactful
social marketing through modern,popular
and accessible media
 49

iSTEMI
The STEMI chain of survival must include an
integrated strategy started from patient education
and early contact with health care personnel in the
network, coordinated protocol for referral to a
reperfusion-capable facility for fibrinolysis or
primary Percutaneous Coronary Intervention (PCI),
efficient emergency medical services to shorten the
door-to-reperfusion time and implementation of
reperfusion strategy by a well-trained team.
 50

iSTEMI

Vision
Reperfusion for all STEMI patients
Mission
•To develop a healthcare facility network for acute coronary
syndrome especially STEMI from downstream to upstream
•To create strategic breakthrough to increase STEMI
reperfusion
•To shorten First Medical Contact (FMC) to reperfusion of
STEMI patients
•To increase community awareness of cardiovascular heart
disease especially acute coronary syndrome
Cardiogenic shock post STEMI
6 – 10% (decreasing in PPCI era)
Presents early : Shock registry
- 50% of CS presented within 6hrs of
symtom onset
-75% within 24 hrs
Prognosis poor – appr 50% 12mo mortality
LV dysfunction is the single strongest
predictor of mortality following STEMI
 Heart failure & Cardiogenic
Shock
SBP to determine choice of inotrope
If HF and SBP < 90mmHg : Dopamine
If HF and SBP > 90mmHg : dobutamine or
levosimedan
Noradrenaline may be preferable if signs
of cardiogenic shock
Levosimedan if patient on chronic BB
 Heart Failure
Severity and Modes of Death
NYHA II NYHA III
CHF
12% CHF
Other 26% Other
24% Sudden 59%
64% Death 15% Sudden
(N = 103) Death
(N = 103)

NYHA IV SCA Pump

CHF
Failure
33% Other
56% NYHA Class II 64% 12%
Sudden
11% Death
(N = 27) NYHA Class III 59% 26%
NYHA Class IV 33% 56%

MERIT-HF Study Group. Lancet. 1999;353:2001-2007.

Treatment of Acute Heart failure
Assessing congestion
Managing Congestion with diuretics
Use of inotropes
Chest pain in the emergency room
 3%

50 47
% Suggested initial triage in patients with suspected AHF%
syndromes
 Clinical signs:Shock, hypoperfusion, congestive heart failure
Acute pulmonary oedema
Most likely problem ?

Acute pulmonary oedema Volume problem Pump problem Rate problem

First–line actions Administer Bradycardia Tachycardia

•Oxygen and intubation p.r.n •Fluids
•Nitroglycerin S.L. •Blood transfusions Blood
•Furosemide IV 0.5- 1mg/Kg •Cause specfic interventions Pressure?
•Morphine IV 2-4 mg •Consider vasopressors

Systolic BP Systolic BP Systolic BP Systolic BP Systolic BP

BO define 2nd <70 mmHg 70-100 mmHg 70-100 mmHg 100 mmHg
Line of action Signs/symptoms Signs/symptoms No signs/symptoms
of shock of shock of shock

Nor-epinephrine Dopamine Dobutamine Nitroglycerin

0.5-30ug/min IV 2-20ug/kg/min IV 2-20 ug/Kg/min IV 10-20ug/min IV

2nd line actions-Acute pulmonary oedema: *Nitroglycerine if SBP>100 mmHg

* Dopamine if SBP 70-100 mmHg, signs/symptoms of shock *Dobutanmine if SBP >100 mmHg no sgins/sytmptoms of shock
 57

Hypertensive emergency
Definition

A hypertensive emergency is an acute, severe

elevation in blood pressure accompanied by
end-organ compromise. It is usually associated
with a systolic blood pressure (SBP) equal to
or higher than 180 mm Hg and/or a diastolic
blood pressure (DBP) equal to or higher than
120 mm Hg.
End-organ compromise includes acute renal failure
due to nephrosclerosis, ocular involvement with retinal exudates,
hemorrhages, or papilledema, hypertensive encephalopathy,
acute stroke or intracranial hemorrhage, acute myocardial
infarction, aortic dissection, and eclampsia.
 TREATMENT PRINCIPLES OF HE

► Where possible ,admit patient

► Rapid reduction BP is unnecessary,must be
be avoided and can be dangerous
> can cause cerebral n cardiac hypoperfusion
► Initial BP  25% to be achieved over 1-4 hours n
less rapid reduction over 24 hours
► In Aortic Dissection and MI must be lowered
rapidly*
PRESENT TO THE FUTURE
•CARDIOVASCULAR EMERGENCIES REMAIN HIGH
•ROLE OF FAMILY
•ROLE OF COMMUNITY
•DEVELOPMENT OF BETTER MARKERS
•MORE USE OF GADGETS Smartphones Video call and
Consultations
•PORTABLE LIFE SAVINGS APPARATUS
•REMOTE CONTROL DELIVERY
•BETTER PROTOCOLS
•HIGHLY TRANIED PERSONNEL
 66

TERIMA KASIH, THANK YOU

MEJUAH JUAH
 Treatment

► With life-threatening organ damage

 Close monitoring
 Sodium nitroprusside (Nipride)
• Arteriovenous dilator
 Gylceryl trinitrate
• Arteriovenous dilator
• Especially effective when MI/pulm edema
co-exist
 Labetalol
• An alpha and beta blocker
• Can exacerbate asthma, heart failure, heart
block
 Hydralazine and diazoxide
 Many methods to further risk stratify patients at
risk for SCA have been studied...
Test Objective Sensitivity Specificity Limitations
(%) (%) But a reduced EF
remains the single most
Echo Measurement of 55–65 75–80 important risk factor for
LVEF overall mortality and
sudden cardiac death.
HR Assessment of low 38–62 75–88 Multiple non-
variability heart rate standardized
variability methods
EP Study Induction of VA’s 48–73 65–93 Invasive, expensive

Signal Induction of late 56-68 74–81 Not useful in non-

Averaged potentials ischemic
ECG cardiomyopathy
(SAECG)

Microvolt Identification of 77–93 37–83 Cannot be used in

T-Wave repolarization AF
Alternans abnormalities
(MTWA)

Siddiqui A, Kowey PR. Curr Opin Cardiol. 2006;21:517-25.

Prior SG, et al. Eur Heart J, Vol 22:16:August 2001
 75

CV disease: US prevalence

Myocardial
ischemia
37 million*

Heart
failure
Chest Pain
5 million
4.2 million emergency visits/year
6.4 million outpatient visits/year
Acute MI
865,000/year

Peripheral
vascular Stroke
disease 5.7 million
8 million

*Symptomatic coronary artery disease (CAD) American Heart Association.

or angina pectoris. Heart Disease and Stroke Statistics—2007 Update.
 76
American Heart Association (AHA)
“Chain of Survival”
• Communities with the following things in place
tend to have the best rates of survival:
 Understanding that emergency services are needed and
calling 9-1-1 immediately.
 Early CPR, especially with quality chest compressions
 Rapid defibrillation (an electrical shock to the heart)
 Effective paramedics (advanced life support )
 Follow up care (post-cardiac arrest care)
The “Chain of Survival”
Number Needed to Treat To Save A Life
NNTx years = 100 / (% Mortality in Control Group – % Mortality in Treatment Group)

50
45
Drug Therapy
37
40
35
28
30 26
amiodarone
25 20
ICD Therapy
20 simvastatin

15 11
9 Metoprolol
succinate
10 3 4
captopril
5
0
MUSTT MADIT MADIT II AVID SAVE Merit-HF 4S Amiodarone
Meta-
analysis
(5 Yr) (2.4 Yr) (3 Yr) (3 Yr) (3.5 Yr) (1 Yr) (6 Yr) (2 Yr)
 78

What is sudden cardiac arrest?

• Electrical system in the heart
malfunctions.
• Heart unexpectedly and abruptly
stops beating.
• Sometimes caused by an abnormal
heart rhythm called ventricular
fibrillation or VF.
 About one-third caused by VF.
 Remainder caused by other lethal heart
rhythms (PEA, Asystole, Bradycardia,
Tachycardia).
• Often associated with a heart attack.
• Majority occur outside of a hospital.
 Acute Management of Specific Arrhythmias

Management of Cardiac Arrest

I IIa IIb III

After establishing the presence of definite, suspected, or

impending cardiac arrest, the first priority should be
activation of a response team capable of identifying the
I IIa IIb III
specific mechanism and carrying out prompt intervention.

CPR should be implemented immediately after contacting

I IIa IIb III a
response team.

In an out-of-hospital setting, if an AED is available, it

should
be applied immediately and shock therapy administered
according to the algorithms contained in the documents on
CPR developed by the AHA in association with the