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HEART ATTACK

dr. Dea Prista Agatha

What is it?
Heart Attack or Myocardial Infarction
is a sudden blockage of blood flow to
a portion of the heart which reduce
the oxygen levels.
As a result, some of the heart muscle
begins to die.
Without early medical treatment this
damage can be permanent.

What causes a heart


attack?

The heart is a muscular pump that needs a continuous


supply of oxygen. It gets oxygen from the blood, which
flows to the heart muscle through arteries on the hearts
surface. These arteries are called the coronary arteries.
The most common cause of heart attack is coronay heart
disease (CHD) the slow build-up of fatty deposits on the
inner wall of the arteries that supply the heart muscle with
blood. These fatty deposits, called plague, gradually clog
the inside channel of the arteries causing them to narrow. It
is a process that begins early in life and continues over the
years.
A heart attack usually begins when an area of plaque
cracks. Blood cells and other components of the blood stick
over the damaged area and form a clot that suddenly and
completely blocks the blood flow to the heart muscle. If the
artery remains blocked, the lack of blood flow through that
artery permanently damages the area of heart muscle that
it supplies blood to.

Signs and Symptoms


Pain in the chest
Pain spreading
Discomfort in the
upper body
Difficulty breathing,
nausea or vomiting,
a cold sweat, or a
feeling
of
being
dizzy or lightheaded.

Heart attack symptoms vary. Not all heart


attacks begin with a sudden, crushing pain
that is often shown on TV or in the movies. The
warning signs and symptoms of a heart attack
arent the same for everyone. Many heart
attacks start slowly as mild pain or discomfort.
Some people dont have symptoms at all (this
is called a silent heart attack).
The symptoms usually last for at least 10
minutes and you may experience more than
one of the heart attack symptoms below.

Pain in the chest


The most common symptom of heart attack is chest pain or discomfort. The
pain sometimes starts slowly, or may come on suddenly, or develop over a
few minutes. Most heart attacks involve discomfort in the center of the chest
that lasts for more than a few minutes or goes away and comes back. It may
feel like tightness, pressure, heaviness, fullness, or squeezing. The feeling has
been described as: 'like a steel band tightening around my chest', 'like an
elephant sitting on my chest' or 'like a red hot poker in the centre of my
chest'. The pain can range from severe, to moderate or even mild. Heart
attack pain can sometimes feel like indigestion or heartburn
Pain spreading
The chest discomfort may spread to the neck and throat, jaw, shoulders, the
back, either or both arms and even into the wrists and hands.
Discomfort in the upper body
Some people do not get any chest pain -only discomfort in parts of the upper
body. There may be a choking feeling in the throat. The arms may feel 'heavy'
or 'useless.

Other
symptoms
Often there may also be difficulty breathing, nausea or vomiting,
a cold sweat or a feeling of being dizzy or light-headed.
The symptoms of angina can be similar to the symptoms of a
heart attack. Angina is pain in the chest that occurs in people
with coronary artery disease, usually when theyre active. Angina
pain usually lasts for only a few minutes and goes away with rest.
Angina that doesnt go away or that changes from its usual
pattern (occurs more frequently or occurs at rest) can be a sign of
the beginning of a heart attack and should be checked by a
doctor right away.
Women's most common heart attack symptom is chest pain or
discomfort. But women are somewhat more likely than men to
experience some of the other common symptoms, particularly
shortness of breath, nausea/vomiting, and back or jaw pain.

Primary Management
Techniques

Heart Attack Treatment


First you must conduct a primary survey of the casualty;
A primary survey consists of following the DRABCD procedure, this involves;
D = DANGER If I find a heart attack casualty I should check for any surrounding
danger to myself first and for the casualty and others
R = Response I should asses whether the person is conscious or unconscious using
the COWS procedure; -Can you hear me, -Open your eyes, -What is your name,
-Squeeze my hand.
A = Airways - After response if the casualty is unconscious I should then check the
airways for any obstructions or blockages and if there is a blockage turn the victim onto
his/her side and clear the airway.
B = Breathing The next step if the patient is unconscious is to check for signs of life.
Check for breathing by using look, listen and feel technique. If breathing place the
casualty in recovery position, if not give 2 rescue breaths and...
C = Compressions - If the casualty is unconscious with no breathing, start compressions
immediately! Give 30 compressions. At a rate of 100 compressions per minute (approx 2
compressions per second). At 1/3 depth of the casualtys chest.
D = Defibrillation - If available use a defibrillator on the casualty as soon as possible.

If the casualty is conscious attempt to sit him/her in a


comfortable position and encourage relaxation and steady
breathing until emergencies arrive.
It is also vital that the blood flow to your heart is quickly
restored. This is usually achieved in one of the following ways:
Fibrinolysis
involves the use of special clot-dissolving medications which
are administered directly into the blood stream.
Angioplasty and stent implantation
Coronary angioplasty is a heart attack treatment that aims to
restore blood flow to the heart by using a special balloon to
open a blocked artery from the inside

Bypass surgery
Coronary Artery Bypass Graft Surgery is an operation in
which blood flow is redirected around a narrowed area,
allowing blood to flow more freely to the heart muscle.

Implantable cardiac defibrillators (ICDs)


After recovering from a heart attack, some people may
develop, or be at high risk of developing, abnormal heart
rhythms (arrhythmias) which could be life-threatening. In
some cases, a small device can be implanted in the
chest and connected to the heart in order to treat such
an arrhythmia if it occurs. This device is called an
implantable cardiac defibrillator (ICD).

Heart Attack Recovery


Modern treatments, along with healthy lifestyle choices, can assist
in recovering from a heart attack and greatly reduce the risk of
further heart problems and relieve or control symptoms such as
angina.
The most important things you can do to reduce your risk and aid
heart attack recovery are:
Take medications as prescribed by a doctor
Be smoke free
Enjoy healthy eating
Be physically active
Control blood pressure
Achieve and maintain a healthy body weight
If the person affected has diabetes, they should also aim to keep
their blood glucose levels within the normal non-diabetic range.

Cardiac rehabilitation
The Heart Foundation and the World Health
Organization recommend that all those who have had
a heart attack, heart surgery, coronary angioplasty,
angina or other heart or blood vessel disease are
routinely referred to an appropriate cardiac
rehabilitation and prevention program for cardiac care.
These programs are designed to help you make
practical, potentially life-saving changes to the way you
live. They can provide you and your family with
education, information, physical activity programs and
support, which can complement the help and cardiac
care you receive from your GP and/or cardiologist.

Acute Coronary Syndromes

A spectrum of clinical diagnoses comprising


unstable angina, Non-STEMI, and STEMI that
share similar pathological features involving
intracoronary thrombosis

ACS: Definition

From: Braunwalds Heart Disease

Pathophysiology
atherosclerosis with superimposed coronary thrombosis
Slowly growing high-grade stenoses can progress to complete
occlusion but do not usually precipitate acute STEMI d/t
collateral circulation
During development of plaques, abrupt transition can occur,
resulting in
Platelet activation
Thrombin generation
Thrombus formation
Blood flow occlusion leads to imbalance between supply and
demand and could lead to myocardial necrosis
Pts with non-transmural infarction more likely to have more
significan stenosis in IRA
Less severe stenosis with lipid-laden plaques and fragile caps
more likely to rupture and causing thrombsis and STEMI

Pathophysiology
Stable Angina
Progressive
narrowing of
coronary lumen
Stable fibrous cap

Unstable Angina
Progressive
narrowing
Acute worsening
of coronary lumen
due to thrombus
formation

NSTEMI
Acute worsening of
coronary lumen due
to thrombus
formation
Sub-occlusive/
transient coronary
thrombus with
myocardial necrosis

STEMI
Minimal prior
narrowing of
coronary lumen
Acute rupture of
thin fibrous cap
Occlusive
thrombus
formation
Acute injury
pattern
Myocardial
necrosis

ACS Evaluation

Angina
Definition: Discomfort in the chest/ choking,
that characteristically comes on with exertion,
relieved by rest and/or NTG
Character
Location

Provoking
Factors

Favors Ischemic
Origin

Against
Ischemic Origin

Constricting
Squeezing
Burning
Heaviness

Dull ache
Knife-like, sharp
Jabs
Pleuritic

Substernal
Anterior thorax
Arms, shoulders
Neck, teeth,
Interscapular

Left submammary area


Left hemithorax

Exertion
Excitement
Cold, meals, stress

Pain after completion


of exercise
Pain with movement

Likelihood that signs & symptoms represent an ACS secondary to CAD

Feature

High

Intermediate

Low

History

Chest or left arm pain or


discomfort as chief
symptom reproducing prior
documented angina
Known history of CAD,
including MI

Chest or left arm pain or


discomfort as chief
symptom
Age > 70
Male gender
Diabetes mellitus

Probable ischemic
symptoms in absence of
the intermediate likelihood
characteristics
Recent cocaine use

Exam

Transient MR, hypotension,


diaphoresis, pulmonary
edema or rales

Extracardiac vascular
disease

Chest discomfort
reproduced by palpation or
respiration

EKG

New or presumably new,


transient ST segment
deviation (0.05mV) or T
wave inversion (0.2mV)
with symptoms

Fixed Q waves
Abnormal ST segments or
T waves not documented to
be new

T wave flattening or
inversion in leads with
dominant R wave
Normal EKG

Cardiac
Marker

Elevated cardiac TnI, TnT


or CK-MB

Normal

Normal

Braundwald 1994 AHCPR Publication No. 94-0602

Chest Pain Classification


Substernal
Exertional
Relieved with rest
Interpretation
Typical Angina: 3 criteria from above
Atypical Angina: 2 criteria from above
Non-Anginal Chest Pain: 1 or less criteria from
above

Classification of Angina
STABLE vs UNSTABLE
CCS Classification for STABLE Angina
I: No symptoms, or angina with strenuous exertion
II: Slight limitation of ordinary physical activity
Walking more than two blocks, climbing more than one
flight of stairs brings on angina

III: Marked limitation of ordinary physical activity


Walking less than two blocks, climbing less than one
flight of stairs

IV: Any physical activity brings on angina; angina


at rest

UA/NSTEMI
THREE PRINCIPAL PRESENTATION
Rest Angina

Angina occuring at rest and


prolonged, usually > 20 minutes

New-onset Angina

New-onset angina of at least CCS


Clas III severity

Increasing Angina

Previously diagnosed angina that


has become distinctly more
frequent, longer in duration, or
lower in threshold (i.e., increased
by > 1 CCS) class to at least CCS
Class III severity

*Pts with NSTEMI usually present with angina at rest

US/NSTEMI Rx

Management of UA/NSTEMI

8 medication
Oxygen
ASA , clopidogrel
Anticoagulant: UFH, LMWH
Nitrates for pain
Nitropatch 0.4 mg/hr x 12 hours daily
IV NTG

Beta-blocker

Metoprolol 25-50 mg PO BID

+ Calcium channel blocker


ACEI for secondary prevention
Statin
Investigations:

Serial cardiac enzymes


Definitive in-hospital risk stratification.

Platelet Inhibitors in the ACS


A platelet GpIIb/IIIa receptor antagonist
should be administered, in addition to ASA
and UFH, to patients with continuing ischemia
or with other high risk features
Level of the evidence: A
ACC/AHA Guideline Circulation
2000;102:1193-1209

ANTIPLATELET Rx
Class I
Definite ACS with continuing
Possible ACS Likely/Definite ACS Ischemia or Other High-Risk
Features or planned PCI
Aspirin

ACC Slide

Aspirin
Aspirin
+
+
Subcutaneous LMWH
IV heparin
+
or
IV heparin
IV platelet GP IIb/IIIa antagonist

Exercise Stress Testing


Positive response: horizontal 1mm ST depression
and symptoms
High risk response:

Deep ST depression
Poor exercise tolerance: unable to exercise past stage 2 (<6 mins)
Exercise induced hypotension and dysrhythmias

Uninterpretable:
LBBB
Digoxin
LVH

Contra-indications:

Severe Aortic stenosis


Aortic dissection
MI/ACS within 24 h
PE

Angiography
Gold standard

Defines anatomy: 1VD, 2VD, 3VD, LM


Assesses LV function
Guides treatment: PCI, CABG or medical therapy

Indications

UA/post MI with ongoing pain, ST depresssion


Hemodynamic instability
CHF, ventricular arrhythmias
Previous PCI, CABG
High risk non-invasive test
Emerging as the strategy of choice for initial evaluation of most
ACS with elevated troponins or EKG changes
Based on FRISC II, TACTICS trials

Strategy needs to be individualized.

Indications for Invasive Risk Stratification


Strategy in UA/NSTEMI
Class I
Recurrent ischemia at rest despite medical Rx
Elevated troponin I or T
New ST depression
High risk findings on non-invasive testing
Depressed LV function
Hemodynamic instability
Sustained VT
PCI within 6 months
Prior CABG
In the absence of the above, either non-invasive or
invasive strategy can be followed.

ACC/AHA Guidelines for Management of UA/NSTEMI 2002

SUMMARY: ER Evaluation of Patient with

Chest Pain
Symptoms
Suggestive of
Cardiac Origin?

NO

YES

Consider
Alternative
Diagnosis
Stable

Unstable

Early Risk Stratification in ER

SUMMARY: Management of UA/NSTEMI


Prolonged CP (>20
minutes or ongoing), plus:
EKG:
Transient ST changes
Sustained ST depr.
Deep T wave inv. (>5
leads)
Biochemical markers:
Troponin/CKMB
abnormal
Recurrent ischemia
AMI in last 4 weeks
Hemodynamic
compromise

ASA + heparin/LMWH
GP IIb/IIIa
Early cardiac cath

INTERM. RISK
(4-8%)

LOW RISK
(<2%)

No high risk features but >=1


of:
Ongoing chest pain
Crescendo angina
Borderline positive
troponin I (0.4-2.0)
Previous intervention: PCI
or CABG
Increased baseline risk
(DM, elderly)

No high or
intermediated features
Chest pain, single
episode, exertional
EKG: normal or
nonspecific or
unchanged

ASA + clopidogrel
UFH or LMWH
Cardiac cath lab

May include previous


hx of CAD or risk
factors

ASA
No heparin
Observe/outpt
tests

*30 day rate of death or MI

HIGH RISK
(12-30%)*

STEMI
WHO defn: 2 of
characteristic chest pain
ECG changes ST elevation
Biochemical changes
ACC + ESC
Rise and fall of biochemical marker (Tn, CK-MB)
+ one of

ischemic symptoms
development of pathological Q waves
ECG changes suggestive of ischemia
Coronary angiography

STEMI
More than 1 million MIs per year in US
Fatal in 1/3 of pts, of death occurs within
1 hr of symptoms (arrhythmias)

Symptoms
prolonged pain > 30 min usually
constricting, crushing, or compressing; heaviness or
squeezing
can be choking, burning, knife-like
retrosternal, radiating to L>R side of chest, ulnar
sides of arms L>R, shoulder, upper extremity, jaw,
neck, interscapular region sometimes epigastric
pain usually implies ischemia
other sx

nausea/vomiting more common in inferior MI


weakness
dizziness
palpitation
cold perspiration
sense of impending doom

STEMI
Pre-hospital care
EMS

Dispatch, first response, EMS ambulance


AED to first responders
Relief of pain to reduce sympathetic tone
Rapid transfer to hospital

Prehosp fibrinolysis
Some evidence suggesting improved mortality

STEMI
ER Management
Early recognition
Ischemic type chest pain
ECG signs

ECG monitor rhythm


IV access
O2
Reperfusion strategy will depend on

Time since symptoms


Risk assoc with STEMI
Risk of lytics
Time required for PCI

Time to Rx

STEMI - Acute Rx
ASA

Block formation of thromboxane A2 in platelets by blocking cox


Chew 160-325 mg to allow for buccal absorption

Pain control

Try to decrease sympathetic activity


Analgesics
Nitrates

Coronary vasodilation, decrease preload by increasing venous


capacitance
Avoid if suspect RV infarct

Beta blockers

Reduce HR, decrease myocardial oxygen demand


Reduce pain
Reduce the need for analgesics
Reduce infarct size

Oxygen

STEMI - Reperfusion
Time is muscle
Increased mortality with delay in reperfusion
regardless of strategy
Less time:
Recovery of LV systolic fxn
Improved diastolic dysfxn
Reduced mortality
Post ischemic contractile dysfxn can occur after
reperfusion
Myocardial stunning

STEMI - Lytics
Benefits
Recanalize thrombotic occlusion
Restores coronary flow
Reduce infarct size
Improves myocardial function
Improves survival
May result in microvascualr damage and
reperfusion injury
STR strong predictor of reperfusion

STEMI - lytics
GISSI first trial to demonstrate benefit of
streptokinase
Other fibrinolytics
Alteplase (t-PA)
GUSTO I

Reteplace (rtPA)
GUSTO III (equivalence)

Tenecteplase (TNK)
ASSENT II (equiv with t-PA)

Evidence for Fibrinolysis: GISSI


n >11,000
ARR: 2%
RRR: 18%

Circ. 1998

ASSENT 2

N= 16949
Design: non-inferiority

Trend toward decrease in bleeding


Improve ease of use with Bolus infusion
Combination with heparin IV

Lancet 1999; 354: 716-22

Time to Rx

Choosing a Fibrinolytic
Patients in whom t-PA is proven superior to SK:
Age < 75
Anterior MI, presenting within 4 hours
High risk/extensive MI at other site within 4 hours
Cardiogenic shock
Previous SK exposure
TNK = rtPA > tPA
Easy administration
Lower chance of med error
Less non-cerebral bleeds
Patients in whom SK appears to be equivalent to t-PA:
Inferior, posterior or lateral MI
MI at any site after 6 hours
Age > 75 years

Bleeding complications with Lytics


Major bleeding 0.5-2%
Minor bleeding: 10-20 %
Intracranial hemorrhage: 0.5-2%
Management:
D/C thrombolytic
Cryoprecipitate (fibrinogen enriched)
If heparin, give protamine sulfate

Indications for Primary PCI


Class I
Alternative to thrombolytic if performed in a timely fashion by skilled
individuals
Patients within 36 hours of AMI, with cardiogenic shock, <75 years
Class IIa
Contraindication to thrombolysis
Class IIb
NSTEMI within 12 hours, with less than TIMI II flow in infarct
related artery
Class III
Elective PCI of non-IRA at time of AMI
Beyond 12 hours of symptoms, no evidence of ischemia
Successful thrombolysis

From ACC/AHA Guidelines, 2000

STEMI -PCI
Meta analyis shows improved clinical
endpoints favoring PCI
Factors to consider

Time to treatment
Risk of STEMI
Cardiogenic shock
Kilip class >= II
Risk of bleeding
Time to transport to skilled PCI center

STEMI Other Rx
ASA

ISIS-2

Thienpyridines
Clopidogrel

CLARITY

Ticlopidine

Inhibit binding to adenosine diphosphate receptor

GPIIb/IIIa inhibitors
Abciximab
Tirofiban
Eptifibatide

GUSTO V

rtPA vs 1/2rtPA and abciximab


similar efficace endpoints but increased bleeds with IIb/IIIa

ASA: ISIS 2
n > 17, 000

Lancet, 1988

STEMI Other Rx
Heparin
reduces reinfarction, stroke, PE
reduces mortality in pts receiving lytic

LMWH
ASSENT III showed benefit over UFH in pts
receiving TNK

Others
Bivalirudin (HITT)

Post- STEMI Rx
BB
ACEi

Prevents ventricular remodeling


Improved hemodynamics
Reduces CHF
Selected population: (long-term, started day 3-16)
SAVE
AIRE
TRACE

Unselected pop (short term, started early)

GISSI 3
SMILE
ISIS-4
CCS-1

Post- STEMI Rx
ARB
OPTIMAAL (losartan)
VALIANT (valsartan)

Aldasterone antagonists
EPHESUS (acute MI, LV dysfxn, HF)
Reduction in mortality

Statins
PROVE-IT

Mechanical Complications of MI
Variable

VSD

Free Wall
Rupture

Papillary
Muscle Rupture

Age

63

69

65

Days, post MI

3-5

3-6

3-5

Anterior MI

66%

50%

25%

New Murmur

90%

25%

50%

Thrill

Yes

No

Rare

Previous MI

25%

25%

30%

Echo:

VSD

Pericardial
Effusion

Flail leaflet
MR

O2 step-up
RA-RV

Equalization of
diastolic press.

Prominent Vwave

90%
50%

90%
?

90%
40-90%

PA catheter:
Mortality:
Medical
Surgical

Other Complications
Arrhythmias
Electrical instability

VPB
VT
VF
AIVR

Pump failure/inc symp drive


Sinus tachy
AFib/Flutter
SVT

Brady/conduction
Sinus brady
Junctional escape
AVB

Other Complications
Recurrent chest pain
Distinguish reinfarction from recurrent ischemia
from non-ischemic chest pain

Pericarditis
LV aneurysm

Risk Stratification
survival after STEMI depends on
LV fxn
Stress/pharma Echo, PET

Residual potentially ischemic myocardium


Submaximal ETT

Susceptibility to vent arrhythmias

Risk Stratification

Discharge Planning
usually 5 days post STEMI
counseling
ambulation but avoid heavy lifting
graded activity (symptom limited)
Rehabilitation