Acute Coronary Syndrome

Muhammad Awais Munir
Roll # 346
Batch 2011-2016
Punjab Medical College
Faisalabad

 45 year old man comes to your clinic
for routine follow up. He gives history
of chest pain on walking 500 meters
on foot. There is no history of
dyspnea, orthopnea. He smokes 2
cigarettes per day. He has got history
of angioplasty of left anterior
descending artery 5 years back.

 He is type 2 diabetic and hypertesive
taking lisinopril and glimepiride 2 mg
daily.
 His pulse is 90/minute, B.P
145/90mmHg, R/R 14/minute, Temp.
98F°
 Rest of examination is normal.
 What is your diagnosis?

 55 years old male presents in
emergency department with
central chest pain radiating to
left arm for last 20 minutes
while sitting in his study room.

 He gives h/o chest pain on
walking 1000 steps for last 2
years for which he is talking
aspirin 75mg, clopidogrel 75gm,
simvastatin 40mg and triglyceryl
spray as needed.
 What is your diagnosis?

 63 years old man known case
of ischemic heart disease
present in emergency with c/o
chest pain for last 10 minutes
while working in his garden. It
is accompanied by cold
sweating and palpitations.

 Pulse 96/-, B.P
160/110mmHg, temp. 98F°,
R/R 18/minute ECG in shown
below.
 Cardiac enzymes are normal.

 65 years old female developed
sudden central chest pain
radiating to her left arm not
relieved by nitrates. It is
associated with cold sweating
and sinking of heart.

 Pulse 100/minute, B.P
160/100mmHg, Temp. 98F°, R/R
15/minute.
 Rest of examination is normal.
 ECG is shown below.
 Cardiac Enzymes are raised.
 Trop T is positive.

 60 years old male presented
with sudden severe cental
chest pain for last 2 hours
associated with cold sweating
and sinking of heart not
relieved by rest or sublingual
nitrates.

 Pulse 90/min, B.P 180/90 mmHg,
Temp 98F°, R/R 16/min
 JVP is raised.
 Resp examination shows bibasilar fine
cackles.
 ECG is shown below.
 Cardiac enzymes are raised.
 Trop T is positive.

 Unstable Angina
 Non-ST-Segment Elevation MI (NSTEMI)
 ST-Segment Elevation MI (STEMI)

NON- MODIFIABLE
 Age
 SEX
 FAMILY HISTORY-----Event in 1st degree
relative
 <55 Male
 <65 Female

MODIFIABLE
 Smoking
 Hypertension
 Diabetes Mellitus
 Dyslipidemia
◦ Low HDL < 40
◦ Elevated LDL >100-
130
 Lack of exercise
 Obesity
 Waist circumference
 Lack of diet rich in
fruit vegetable fiber
 Homocysteinemia

Ethnic-Specific Values for Waist Circumference
Ethnic Group Waist Circumference
Japanese
Men >85 cm (33.5 in)
Women >90 cm (35 in)
South Asians and Chinese
Men >90 cm (35 in)
Women >80 cm (31.5 in)
Europeans
Men >94 cm (37 in)
Women >80 cm (31.5 in)

Unstable
Angina STEMINSTEMI
Non occlusive
thrombus
Non specific
ECG
Normal cardiac
enzymes
Occluding thrombus
sufficient to cause
tissue damage & mild
myocardial necrosis
ST depression +/-
T wave inversion on
ECG
Elevated cardiac
enzymes
Complete thrombus
occlusion
ST elevations on
ECG or new LBBB
Elevated cardiac
enzymes
More severe
symptoms

 Stable angina:
Reproducibly by exercise or emotion,
stress and relieved within 15-20 min by
rest or sublingual nitroglycerine
 Unstable angina
(A) occurs at rest or mild exertion, usually
lasts more than 30 min
(B) new onset( within 1 month)
(C ) crescendo type

Criteria.
 H/o prolonged chest discomfort or angina
equivalent > 30 min.
 Presence of more than 1 mm ST- elevation in
2 consecutive chest leads or 2mm elevation
in limb leads.
 Presence of elevated cardiac biomarkers.
 New onset left bundle branch block

• Chest pain resembles angina.
• But lasts more than 30 minutes
• It is more intense, not relieved by rest or
sublingual nitrates.
• Accompanied by dyspnoea, nausea vomiting,
fatigue, syncope and cold sweating.
• It may present as extreme exhaustion.
• Impending fear of death
• It may occur without chest pain in
hypertensive, diabetic elderly, or post
operative patients.

PHYSICAL EXAMINATION
 Patients usually appear restless and in
distress.
 Tend to lie still.
 The skin is cold and moist due to
sympathetic discharge.
 Breathing may be labored and rapid.
 Fine crackles, coarse crackles, or
rhonchi may be heard when
auscultating the lungs due to heart
failure.

 Increased blood pressure
related to anxiety or a
decreased blood pressure
caused by heart failure.
 The heart rate may vary from
bradycardia to tachycardia.
 On auscultation, the first heart
sound may be diminished as a
result of decreased
contractility.

 A fourth heart sound is heard in
almost all patients with MI, whereas a
third heart sound is detected in only
about 10% to 20% of patients due to
failure.
 Transient systolic murmurs may be
heard due to papillary muscle
ischemia
 After about 48 to 72 hours, many
patients acquire a pericardial friction
rub

• Patients with acute ST- elevation MI
are stratified into low and high risk
groups on the basis of their initial
physical examination.
1. Without pulmonary congestion or
shock. (Klipp I). Mortality rate < 5%.
2. Mild pulmonary congestion or
presence of S3(Klipp class II)
favourable prognosis.

1. Pulmonary edema(Klipp Class III)
needs aggressive management.
2. Hypotensive patients with
evidence of shock(Klipp class IV)
80% mortality rate

4 groups of investigation are
used.
 ECG.
 Cardiac biomarkers
 Cardiac imaging.
 Non specific indices of Tissue
necrosis and inflammation.

ECG CRITERA OF ACUTE MI
 Pathological q wave
 T wave inversion
 Convex ST-elevation above 1 mm.
ECG CRITERA OF old MI
 Pathological q wave
 ST in baseline
 T wave normal or inverted
 Right ventricular MI(V 4 R)

 Tall R wave, ST segment
depression and t wave
inversions in V1 and V2

 Q wave infarction means
infarction of full thickness
myocardium
 Non Q wave infarction means
infarction of subendocardium

 Trop-T and Trop- I are raised after 3-12
hours of MI..>95% sensitivity and specificity
Peak at 2 days.
Elevated for 5-14 days.
 CK-MB has sensitivity of 95 % when
measured within 24-36 hours after the onset
of chest pain. Increases within 3-4 hours of
chest pain. Peak at 24 hours. And returns to
base line at 48-72 hours.

Protein
Molecular mass
(kD)
First
detection
Duration of
detection
Sensiti
vity
Specifi
city
Myoglobin 16 1.5–2
hours
8–12 hours +++ +
CK-MB 83 2–3 hours 1–2 days +++ +++
Troponin I 33 3–4 hours 7–10 days ++++ ++++
Troponin T 38 3–4 hours 7–14 days ++++ ++++
CK 96 4–6 hours 2–3 days ++ ++

• If MI not detected on ECG, then two dimensional
echocardiography is used which shows wall motion abnormalities
and aids in management and decision.
• It also shows RV infarction, ventricular aneurysm and pericardial
effusion.
• Myocardial perfusion imaging. Very sensitive but cann’t
distinguish acute infarct from chronic infarct thus not specific for
acute MI.

 Radioneucleotide ventriculography. Tc
labelled RBCs are used which show wall
motion abnormalities.
 MRI. Can be used. It detects MI accurately.

 Immediate management.
 The goal is to identify the patient for
reperfusion therapy.
 IN IDEAL CONDITIONS Goal is door to needle
time of < 30 min and door to ballon time of
< 90 min.
 Relieves ischemic pain, provide supplemental
oxygen, recognize and treat potential life
threatening complication.

10/00medslides.com 50
ST elevation
 12 h
Aspirin
Beta-blocker
Eligible for
fibrinolytic therapy
> 12 h
Fibrinolytic therapy
contraindicated
Not a candidate for
reperfusion therapy
Persistent
symptoms ?
Primary
PTCA or CABG
Other medical therapy:
ACE inhibitors
? Nitrates
Anticoagulants
Consider
Reperfusion
Therapy
No Yes
Modified from Antman EM. Atlas of Heart Disease, VIII; 1996
ST elevation
Aspirin
Beta-blocker
 12 h > 12 h
Eligible for
fibrinolytic therapy
contraindicated
Primary
PTCA or CABG
Not a candidate for
reperfusion therapy
Other medical therapy:
ACE inhibitors
? Nitrates
Anticoagulants
Persistent
symptoms ?
No Yes
Consider
Reperfusion
Therapy

10/00medslides.com 51
ST depression/T-wave inversion:
Suspected AMI
Heparin + Aspirin
Nitrates for recurrent angina
Assess Clinical Status
Continued observation
in hospital
Consideration of
stress testing
PCI
CABG
No
Yes
Antithrombins: LMWH - high-risk patients
Anti-Platelets: GpIIb/IIIa inhibitor
Patients without prior
beta-blocker therapy or
who are inadequately
treated on current dose
of beta-blocker
Persistnet symptoms in
patients with prior
who cannot tolerate
beta-blockers
Establish adequate
beta-blockade
Add calcium antagonist
High-risk patient:
1. Recurrent ischemia
2. Depressed LV function
3. Widespread ECG changes
4. Prior MI
Clinical stability
Catheterization: Anatomy
suitable for revascularization
Medical
Therapy
Modified from Antman EM. Atlas of Heart Disease, VIII; 1996
ST depression/T-wave inversion:
Suspected AMI
Antithrombins: LMWH - high-risk patients
Anti-Platelets: GpIIb/IIIa inhibitorPatients without prior
who are inadequately
treated on current dose
of beta-blocker
Establish adequate
beta-blockade
Add calcium antagonist
Persistnet symptoms in
patients with prior
who cannot tolerate
beta-blockers
Assess Clinical Status
High-risk patient:
1. Recurrent ischemia
2. Depressed LV function
3. Widespread ECG changes
4. Prior MI
Catheterization: Anatomy
suitable for revascularization
Yes
PCI
CABG
Medical
Therapy
Clinical stability
Continued observation
in hospital
Consideration of
stress testing
Heparin + Aspirin
Nitrates for recurrent angina
No

 IV CANULA
 OXYGEN INHALATION
 MORPHINE DERIVATIVES
 NITROGLYCERINE SUBLINGUALLY
 ORAL Asprin 300mg chew and swallow THEN
75mgd
 Clopidogril. 300 bolus then 75mg/day
 Anti-coagulation
 UFH: initial bolus 60u/kg, maximum 5000u
followed by infusion of 12u/kg /hr.
maximum 1000u/hr to keep APTT of 1.5-2
times of control.
 LWMH: (enoxaparin): 1mg/kg bid.

 should be avoided in patients of hypotension.
 Right ventricular MI, bradycardia < 50/ min.
Sublingual preparation used ,If pain still
continues then IV nitroglycerine
10microgram/ min should be initiated.
 Dose adjustment may be performed every 5
min at 10 microgram/min until chest pain
resolves or heart rate increases or BP
decreases more than 10 %.

Cellular Mechanism of Vasodilatation
Nitrates Formation of
Nitric oxide (NO)
Activation of
Guanylate cyclase
Synthesis of
cyclic GMP
Relaxation of Vascular
smooth muscles

Effect of Nitrates :
Venodilatation Arteriolar
dilatation
Preload Afterload
Myocardial
Oxygen demand
2- Redistribution of coronary flow towards
subendocardium
3- Dilatation of coronary collateral vessels
1-

Adverse Reactions :
1- Postural Hypotension &
Syncope
2- Tachycardia
5- Throbbing Headache
4- Facial Flushing
3- Drug Rash
6- Prolonged high dose
Methaemoglobinaemia

 They reduce myocardial ischemia
and infarct size and myocardial
rupture.
 IV metoprolol 5 mg can be
repeated every 5 min for 3 doses.
If tolerated then can be shifted to
oral medication 25-50 mg/ 6 -12
hrly.

Fatigue &
weakness
Hyperglycemia Nightmares , Hallucinations ,
Depression.
Plasma Triglycerides & HDL
Cholesterol Discontinuation after
long ttt exacerbates
Angina
Adverse Reactions :

CHF A-V block
Peripheral
Vascular
disease
Hypotension
Contraindications :
Bronchial
asthma

 Only indicated in highest risk UA/NSTEMI
patients (dynamic changes on EKG,
elevated biomarkers, electrical
instability) and/or in whom early PCI is
planned
 Abciximab is the choice if early
angiography and PCI is planned
 Tirofiban indicated when no PCI planned

 Handle patient carefully while providing initial
care, starting I.V. infusion, obtaining baseline
vital signs, and attaching electrodes for
continuous ECG monitoring.
 Maintain oxygen saturation greater than 92%.
 Administer oxygen by nasal cannula if
prescribed

Following agents are used as
fibrinolytic agents.
 TPA
 Streptokinase.
 Tenecteplase.
 Reteplase.

 Thrombolytic therapy should be
considered in patients with ST-
elevation MI in 2 or more leads.
 Effective if given within 12 hours but
not beyond 24 hours.
 It is not indicated if symptoms have
resolved or the patient with ST-
depression.

Absolute.
• Intracranial hemorrhage
• Ischemic strokes within past year
• Head trauma
• Suspected Aortic dissection.
• Active internal bleed
• BP> 180/110

 Allergy or previous use of streptokinase------ 5
days to 2 years
 Active peptic ulcer disease
 Internal bleed 2-4 weeks
 Prolonged CPR > 10 min.
 Major surgery < 2 weeks
 Known bleeding diathesis
 hemorrhagic ophthalmic condition (e.g.,
hemorrhagic diabetic retinopathy),
 Severe menstrual bleeding.
 Pregnancy

• Streptokinase.
• 1.5 million units IV over 60 min.
• Retiplase.
• IV bolus of 10 mg over 2 min followed by
another IV bolus of 10 mg over 30 min.
• Alteplase.
• IV bolus of 15 mg followed by a 0.75mg/kg
by IV infusion over 30 min. then 0.5 mg/kg
over 60 min. maximum dose of 100mg over
90 min.

 Grade O: indicates complete occlusion.
 Grade I: some penetration beyond the part of
obstruction but without penetration distal
part.
 Grade II: perfusion of entire infarct vessel into
distal bed but flow is delayed.
 Grade III: full perfusion of infarct vessel.
 Fibrinolytic therapy reduces mortality in 50 %.

 It is alternative to thrombolytic
therapy.
 Used in patients in whom diagnosis is
in doubt.
 Cardiogenic shock, increased bleeding
risk.
 It should be considered when door to
baloon time is < 90 min.

• Primary PCI is preferred over thrombolysis in
patients < 75 years age and present with
cardiogenci shock within 36 hrs of MI. and PCI
can be performed within 18 hours of shock.
• Contraindications to fibrinolytic therapy.
• Increased risk of death or CHF.
• Underwent resent PCI.
• NOTE: emergency CABG is a high risk precedure
that should be considered if a patient has
cardiogenic shock and coronary vasculature is
not compatible for PCI or the procedure has
failed.

 (PTCA) is an effective alternative to reestablish
blood flow to ischemic myocardium.
 Primary PTCA is an invasive procedure in which
the infarct-related coronary artery is dilated
during the acute phase of an MI without prior
administration of thrombolytic agents
 These complications can include retroperitoneal
or vascular hemorrhage, other evidence of
bleeding, early acute reocclusion, and late
restenosis.

 Bed rest for 12 hrs.
 Under supervision to upright position
sitting in a chair in 24 hours.
 In absence of shock, hypotension, 2rd
day, can go to washroom on wheel
chair, can take shower or stand on the
sink.
 End of 3rd day, activity is increased.

 For 1st 4-12 hrs:
 Clear fluids or NPO.
 30% less of total calories , complex
carbohydrates should take 50% of
total calories.
 Bowels:
 Bed side comod should be used .
 Diet rich in bulk, stool softners and
lexatives.

 After medical therapy including thrombolysis:
 Stress test: Is done to determine the
prognosis or functional capacity.
 Stress test: Can be performed 4-6 days after
the MI. Can also be performed after hospital
discharge 2-3 weeks or late after discharge
3-6 weeks if the initial post infartction stress
test was sub maximal.

• The goal of secondary prevnetion is to produce a
favourable impact on the morbidity and mortality .
• Antiplatelet agents: Asprin 75- 325 mg/ day should
be used indefinitly.
• Clopidogril : 75 mg/day for a maximum of 9
months.
• Ace Inhibitors: reduce mortality and incidence of CHF.
• Treatment should be given indefinitely.
• Benefit is seen in patients with LV dysfunction,
ejection fraction less than 40 and all patients of MI.
• Beta blocker: Reduce cardiac events after MI, and
should be use indefinitly.

• B1 selective blokeres e.g Metoprolol 100mg BID,
atenolol 100mg daily, propranolol 80mg TID.
• Cholestrol treatment:
• With ACS and ST-elevation MI, it should be less
than 100mg/dl.
• Tobacco cessation
• Diet:
• A body mass index of < 25kg/m2 is desireable.
• Diabetes:
• Target HbA1C <7.
• Exercise:
• The goal is a minimum of 3-4 days per week of
30-60 min of activity in those who are physically
capable.

 Routine office visits:
 Every 4-12 months are suggested for the 1st
year.

Pericardial Complications
 Pericarditis
 Dressler’s syndrome
 Pericardial effusion
Thromboembolic Complications
 Thromboembolism
 Deep venous thrombosis
 Pulmonary embolism

Electrical Complications
 Ventricular tachycardia
 Ventricular fibrillation
 Supraventricular tachydysrhythmias
 Bradydysrhythmias
 Atrioventricular block (first, second, or
third degree)

Vascular Complications
 Recurrent ischemia
 Recurrent infarction
Mechanical Complications
 Left ventricular free wall rupture
 Ventricular septal rupture
 Papillary muscle rupture with acute
mitral regurgitation

Myocardial Complications
 Congestive heart failure
 Hypotension/cardiogenic shock
 Right ventricular infarction
 Aneurysm formation

• Post infarction ischemia:
• Nitrates. Beta blockers. Clopidogril.
Asprin.
• Arrythmias:
• Sinus bradycardia: Atropine 0.5-1 mg
IV.

 Supraventricular tachyarrthmia:
 IV beta blockers such as metoprolol 2.5-
5mg/hr.
 IV diltiazim 5-15mg/hr if beta blockers are
contraindicated.
 Digoxin 0.5mg as initial dose then 0.25mg
every 90 to 120 min.
 amiodarone 150mg IV bolus.
 Ventricular arrythmias:
 1mg/kg bolus of lidocaine if the patient is
stable.
 If not, then DC cardioversion at 100-200
jouls. IV amiodarone can be used.

 Ventricular fibrillation
 Ventricular tachycardia

Conduction disturbances:
• Ist degree heart block is the most
common and requires no treatment.
• 2nd degree block is usually of Mobitz
type I and requires treatment only if
symptomatic.
• Complete AV block occurs in 5% of
patiets and generally resolves but it
may persist for hours to several
weeks. And TPM is indicated in such
cases.

• Hypotension and shock:
• Patients with hypotension should be treated
with successive boluses of 100ml of normal
saline until PCWP reaches 15mm of Hg.
• Dopamine is the most appropriate for
the cardiogenic hypotension initiated at the
dose of 2-4mcg/kg/min.
• At low doses, < 5mcg it improves renal
blood flow.
• At intermediate dosages 2.5-10mcg, it
stimulates myocardial contractility and
above 10mcg it is a potent alpha 1
adrenergic agonist.

• It is associated with inferior wall
MI.
• Diagnosis is suggested by ST-
elevation in right sided anterior
chest leads particulary R wave in
V4 .
• Confirmed by echocardiography.

 Rupture of papillary muscles or
interventricular septa usually occurs
3-7 days.
 Detected by new systolic murmurs.
 Confirmed by doppler
echocardiography
 surgical intervention is mandatory.

• Complete rupture occurs in 1 % of
patients and results in immediate
death.
• It occurs 2-7 days post infarction.
• Involves anterior wall.
• Incomplete rupture recognized by
echocardiography, radioneucleotide
angiography.
• Early surgical repair is indicated.

• 10-20% of patients.
• Usually follows anterior wall infarction.
Recognized by persistent ST-
elevation beyond 4-8 weeks.
• They rarely rupture but associated
with arterial emboli, ventricular
arrythmias and CHF.
• Surgical resection may be performed.

 Pericardium is involved in 50 % of infarction.
 But pericarditis is often not clinically
significant.
 Pericardial pain occurs 2-7 days, recognized by
its variation with position and respiration.
 Improved by sitting.
 Often no treatment is required but Asprin
650mg 4-6hrly will usually relieve the pain.

 1-12 weeks after infarction.
 Autoimmune phenomenom.
 Presents as pericarditis associated with
◦ Fever
◦ Leucocytosis
◦ pericardial or pleural effusion.

Acute Coronary Syndrome

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