myocardial infarction
TRANSCRIPT
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ACUTE CORONARY SYNDROME
SHAMS REHAN FINAL YR MBBS
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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.
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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
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CONTINUE
What is your most probable diagnosis ?
What relevant investigation would u do?
What complications can arise if not managed
properly?
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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
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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
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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
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ANOTHER CLASSIFICATION
Spontaneous myocardial infarction (MI
type 1 with / with out CAD)
Myocardial infarction secondary to an
ischemic imbalance (MI type 2)
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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)
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CONTINUE..
Clinical features : SYMPTOMS:
severe chest pain
Lasting more then 20 min
Radiation lower jaw, left arm , neck
Breathlessness
Collapse
Nausea , vomiting
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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
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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
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SILENT MI
In elderly nd diabetic ptts
Atypical symptoms like dyspnea , fatigue
syncope
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DIAGNOSIS
CLINIAL HISTORY
ECG
BIOCHEMCAL MARKERS
FBC
GLUCOSE
LIPID PROFILE
TTE
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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.
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ISCHEMIA ON ECG
ST segment elevations.
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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.
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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
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ECG CHANGES IN MI
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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
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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.
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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
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DIFFERENTIAL DIAGNOSIS
Acute Coronary Syndrome
Angina pectoris
Anxiety
Aortic Dissection
Aortic Regurgitation
Aortic Stenosis
Asthma
Cholecystitis
COPD
Dyspepsia
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DIFFERENTIAL DIAGNOSIS
Endocarditis
Esophageal reflux
Esophageal Spasm
Heart arrhythmias
Heart rupture
Mitral Regurgitation
Mitral Valve Prolapse
Pancreatitis
Pericarditis
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DIFFERENTIAL DIAGNOSIS
Pneumonia
Pneumothorax
Pulmonary EmbolismPulmonary
Hypertension, Shock
Unstable Angina
Ventricular Septal Defec
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MANAGEMENT
1. Early medical management:
Accident and emergency
Fibrinolysis
PCI
CABG
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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
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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
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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.
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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.
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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
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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
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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
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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
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COMPLICATIONS
Heart failure : mild ( lasix i/v 40- 80 mg +
GTN + Oxygen + ace inhibitors)
Severe: dobutamine / dopamine
Cardiogenic shock : revascularization
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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
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COMPLICATIONS CONTINUE
Myocardial rupture
Aneurysmal dilatation
VSD
Mitral regurge
Arrythmias
Av block
Post MI pericarditis
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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%)
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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
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PRIOR TO DISCHARGE?
Uncomplicated patient with no angina
Exercise test
ETT 6 week later
IF + test coronary angiography/
stenting
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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.