ACUTE CORONARY SYNDROME

SHAMS REHAN FINAL YR MBBS

CASE SCENARIO

A 75 years old, known diabetic(10 yrs) male patient uzadin of karak was brought to emergency dptt today at 1 pm and was admitted in/to cardiology ward bed # 5 with the c/c of:

Single episode of Sudden, rapid onset ,severe chest pain, lasting more then 30 min , radiating towards the medial aspect of his left arm associated with breathlessness , nausea , heavy perspiration, Lightheadedness, fever, cold clammy skin.

CASE SCENARIO CONTINUE

There is no PND , orthopnea nd cough.

EXAMINATION REVEALS:

Pulse : 48 bpm , regular, normal rhythm

BP= 115/70

Temperature= 99f

RR= 12/MIN

JVP = N

Apex beat non palpable

Heart sounds muffled

CONTINUE

What is your most probable diagnosis ?

What relevant investigation would u do?

What complications can arise if not managed

properly?

MYOCARDIAL INFARCTION

MI is defined by the demonstration of

myocardial cell necrosis due to significant and

sustained ischaemia.(WHO)

Myocardial ischemia cardiac

myocyte dies (pathologically)

Rupture / erosion ATH plaque

thrombosis , platelets aggregation ,

vasoconstriction coronary artery

occlusion myocardial necrosis with in 15-

30 min

CELLULAR CHANGES IN MI

The cellular changes associated with an MI

can be followed by:

1. the development of infarct extension (new

myocardial necrosis),

2. infarct expansion (a disproportionate

thinning and dilation of the infarct zone), or

3. Ventricular remodeling (a disproportionate

thinning and dilation of the ventricle

CLINICAL CLASSIFICATION OF MYOCARDIAL

INFARCTION

STEMI

non-ST elevation MI’ (NSTEMI).

Many patients with MI develop Q waves (Q

wave MI),

but others do not (non-Q MI).

Patients without elevated biomarker values

can be diagnosed as having unstable angina

ANOTHER CLASSIFICATION

Spontaneous myocardial infarction (MI

type 1 with / with out CAD)

Myocardial infarction secondary to an

ischemic imbalance (MI type 2)

CONTINUE

Cardiac death due to myocardial infarction

(MI type 3)

Myocardial infarction associated with

revascularization procedures (MI types 4 ND

5)

Initially subendocardial myocardium affected

Continued ischemia extension to

subepicardial myocardium(Q WAVE MI)

CONTINUE..

Clinical features : SYMPTOMS:

severe chest pain

Lasting more then 20 min

Radiation lower jaw, left arm , neck

Breathlessness

Collapse

Nausea , vomiting

CONTINUE

Physical signs :

restless and in distress.

SANS signs

Vagal stimulation signs

Impaired MI signs

Narrow pulse pressure

S3 and S4 heart sounds

Lung crepitaions

CONTINUE

Lung crepitations

Transient systolic murmurs may be heard

right ventricular infarcts may present with

jugular vein distension,

peripheral edema,

and an elevated central venous pressure

SILENT MI

In elderly nd diabetic ptts

Atypical symptoms like dyspnea , fatigue

syncope

DIAGNOSIS

CLINIAL HISTORY

ECG

BIOCHEMCAL MARKERS

FBC

GLUCOSE

LIPID PROFILE

TTE

CONTI..

ECG :

Ischemia, injury, infarction

Ischemia.

T-wave inversion

The inverted T wave representative of ischemia is symmetrical, relatively narrow, and somewhat pointed

ST segment depression in the leads facing the ischemic area.

ISCHEMIA ON ECG

ST segment elevations.

INFARCTION

hyperacute or peaked T waves.(MIN AFTERWARDS)

hyperacute T waves invert.(Within a few hours)

Next, the ST segments elevate, a pattern that usually lasts from several hours to several days.

reciprocal ST segment changes.

Reciprocal changes are most likely to be seen at the onset of infarction, but their presence on the ECG does not last long.

CONTINUE

Within a few days after the MI, the elevated ST segments return to baseline.

Persistent elevation of the ST segment (ventricular aneurysm.)

The T waves may remain inverted for several weeks, indicating areas of ischemia near the infarct region.

Eventually, the T waves should return to their upright configuration.

The Q waves do not disappear and therefore always provide ECG evidence of a previous MI

ECG CHANGES IN MI

BIOCHEMICAL MARKERS

Creatine Kinase :

CK-MB appears in the serum in 6 to 12 hours,

peaks between 12 and 28 hours,

and returns to normal levels in about 72 to 96 hours.

Serial samplings are performed every 4 to 6 hours for the first 24 to 48 hours after the onset of symptoms

Creatine Kinase Isoforms: CK-MB1 found in the plasma,

and CK-MB2 is found in the tissues. In MI CK-MB2 to CK-MB1 ratio greater than one

CONTINUE

Myoglobin:. release earlier than the release

of CK.

elevate within 1 to 2 hours of acute MI

peaks within 3 to 15 hours.

is not specific for the diagnosis of MI.

BIOCHEMICAL MARKERS

Troponin. (troponin T and troponin I):

Troponin -I levels rise in about 3 hours,

peak at 14 to 18 hours,

and remain elevated for 5 to 7 days.

Troponin T levels rise in 3 to 5 hours and

remain elevated for 10 to 14 days

DIFFERENTIAL DIAGNOSIS

Acute Coronary Syndrome

Angina pectoris

Anxiety

Aortic Dissection

Aortic Regurgitation

Aortic Stenosis

Asthma

Cholecystitis

COPD

Dyspepsia

DIFFERENTIAL DIAGNOSIS

Endocarditis

Esophageal reflux

Esophageal Spasm

Heart arrhythmias

Heart rupture

Mitral Regurgitation

Mitral Valve Prolapse

Pancreatitis

Pericarditis

DIFFERENTIAL DIAGNOSIS

Pneumonia

Pneumothorax

Pulmonary EmbolismPulmonary

Hypertension, Shock

Unstable Angina

Ventricular Septal Defec

MANAGEMENT

1. Early medical management:

Accident and emergency

Fibrinolysis

PCI

CABG

ACCIDENT AND EMERGENCY

Aspirin 150-300 mg

Clopidogrel 3oo mg oral gel

Sublingual GTN 0.3-1 mg

Oxygen nasal cannula 2-4 l/min

Brief HX / RF

I.V access + blood for markers

CONTINUE

Analgesic

Antiemetics

Beta blocker if no contraindication

Calcium channel blocker

(ACE) inhibitors are administered to patients with anterior wall MI and to patients who have an MI with heart failure in the absence of significant hypotension.

ACE inhibitors help prevent ventricular remodeling (dilation) and preserve ejection fraction

FIBRINOLYSIS

Fibrinolytic agents are given in conjunction with antithrombin and antiplatelet agents, which help to maintain vessel patency once the clot has been dissolved

Aspirin inhibits platelets; the recommended dose is 162-325 mg of chewable aspirin.

Clopidogrel For patients 75 years of age and younger, administer an oral loading dose of 300 mg.

In patients older than 75 years of age, administer 75 mg orally.

CONTINUE

Heparin UFH or LMWH inhibit thrombin.

UFH: intravenous (IV) bolus of 60 U/kg

(maximum, 4000 U) followed by an initial

infusion of 12 U/kg/h (maximum, 1000 U/h)

adjusted to maintain the activated partial

thromboplastin time (aPTT) at 1.5-2 times

the control value.

CONTINUE

LMWH (enoxaparin) alternative to UFH.

younger than 75 years of age;

the recommendation is a 30 mg IV bolus followed by 1 mg/kg subcutaneously every 12 hours.

For patients at least 75 years and older, subcutaneous dose is reduced to 0.75 mg/kg every 12 hours.

Regardless of age, if the creatinine clearance is less than 30 mL/min, the subcutaneous dose is 1 mg/kg every 24 hours

CONTRAINDICATIONS

Absolute Contraindications to Thrombolysis

Any previous history of hemorrhagic stroke

History of stroke, dementia, or central nervous system damage within 1 year

Head trauma or brain surgery within 6 months

Known intracranial neoplasm

Suspected aortic dissection

Internal bleeding within 6 weeks

Active bleeding or known bleeding disorder

Major surgery, trauma, or bleeding within 3 weeks

RELATIVE CI

Oral anticoagulant therapy

Acute pancreatitis

Pregnancy or within 1 week postpartum

Active peptic ulceration

Transient ischemic attack within 6 months

Dementia

Infective endocarditis

Active cavitating pulmonary tuberculosis

CONTINUE

Active cavitating pulmonary tuberculosis

Advanced liver disease

Intracardiac thrombi

Uncontrolled hypertension (systolic blood pressure >180 mm Hg, diastolic blood pressure >110 mm Hg)

Puncture of noncompressible blood vessel within 2 weeks

Previous streptokinase therapy

COMPLICATIONS

Heart failure : mild ( lasix i/v 40- 80 mg +

GTN + Oxygen + ace inhibitors)

Severe: dobutamine / dopamine

Cardiogenic shock : revascularization

ASSESS HF USING KILLIP CLASSIFICATION

Killip class I includes individuals with no clinical signs of heart failure.( no crackles nd S3)

Killip class II includes individuals with crackles in the lungs, and S3, and elevated jugular venous pressure.( less then 50%)

Killip class III describes individuals with frank acute pulmonary edema.(more then 50%)

Killip class IV describes individuals in cardiogenic shock or hypotension

COMPLICATIONS CONTINUE

Myocardial rupture

Aneurysmal dilatation

VSD

Mitral regurge

Arrythmias

Av block

Post MI pericarditis

POST MI LIFE STYLE MODIFICATION

Omega 3 FA / WEEK more then 7g

Physically active 20-30 min/day

Smoking cessation

Treat the HTN if any

Treat the diabetes if any ( HbA1c less then

7%)

POST MI DRUG THERAPY ND ASSESSMENT

Aspirin daily

Clopidogrel daily

Beta blocker daily

Ace – inhibitor rimipril 2.5 mg b.d

Valsartan 20 mg b.d

Simvastatin 20-80 mg /day

Eplerenone 25 mg/day

PRIOR TO DISCHARGE?

Uncomplicated patient with no angina

Exercise test

ETT 6 week later

IF + test coronary angiography/

stenting

JUST READ IT

I saw many people who had advanced heart

disease and I was so frustrated because I

knew if they just knew how to do the right

thing, simple lifestyle and diet steps, that the

entire trajectory of their life and health would

have been different.