myocardial infarction - case presentation and an overview

Clinico-pathological conference

1st

Myocardial

infarctionPresentation by

1605- Abubakkar

Raheel

1622- Haider Ali

1606- Ahmed Arsalan

1611- Amaila Anam

Final Year MBBS

27th February, 2015

Long Case

• Muhammad Shareef, a 65 year old male patient from Abbottabad, known case of Diabetes since last 12 years and Coronary Artery Disease for the last 2 years presented in King Abdullah Teaching Hospital with the complaints of Chest pain and breathlessness for the last 6 hours. Patient had an episode of vomiting. He was conscious and well oriented. Overall health state was weak and meagre.

Dept of MedicineFrontier Medical and Dental College

History of Patient

• Name: Muhammad Shareef

• Sex: Male

• Age: 65 years

• Marital Status: Married

• Occupation: Retired Govt. servant

• Address: Abbottabad

• D.O.A: 20th February, 2015

• T.O.A: 9:30 am

• M.O.A: OPD


Chief Complaints

• Chest pain – 6 hrs

• Shortness of Breath – 6 hrs

• Vomiting - 5 hrs


History of Present illness

• Known case of Diabetes - 12 yrs & Ischemic Heart Disease – 2 yrs

• Chest pain started 6 hrs back

• Sudden in onset

• Retrosternal

• Crushing in nature

• Radiating to left arm, back and neck

• Aggravated on exertion



• Shortness of breath – 6hrs

• Sudden onset

• present at rest

• Vomiting – 5hrs

• 2 episodes of vomiting

• Vomitus was yellowish



Associated symptoms:

• Moderate fever

• Sweating

• Dizziness

• Patient was completely conscious

• Palpitations



• Systemic Inquiry

1. General

a. Reduced apetite

b. Sleep disturbed

c. Weakness

2. Respiration

Cough, wheezing and hemoptysis not present



• Alimentary system: Nausea & Vomiting present

• Urinary system: No significant history


History of Past illness

• Past Medical History

– Diabetes : 12 yrs

– IHD : 2 yrs

– HTN : Positive

– TB : Negative

– Asthma : Negative

• Past Surgical History

No significant past surgical history


Family History

• Positive for IHD, HTN and DM

• 2 brothers died of MI


Drug & treatment History

• Patient was taking anti diabetics and anti hypertensive drugs

• Drug compliance was poor

• No other significant drug history


Personal History

• Chronic Smoker

• No history of drinking

• Sedentary lifestyle


Socio-economic History

• Satisfactory


History based Differential Diagnosis

• Acute Myocardial Infarction

• Unstable Angina

• Pleurisy

• Pericarditis

• Pneumothorax

• Pulmonary embolism

• Reflex Esophagitis


General Physical Examination

Patients general appearance

• Pale and anxious



• Vitals

– B.P: 160/90mmHg in lying position

– Pulse: 115 b/m, regular, tachycardia

– Temp: 101 F

– Resp: 30/m



• No Clubbing, pallor, splinter hemorrhages koilonychias or leconichia

• Mild tobacco staining observed

• Xanthomas present on extensor surface of hands

• Carotid pulse: thin

• JVP: Not raised

• Eyes: Anemia not present



• Jaundice not present

• Dental hygiene good

• Carotid briut not audible

• No abnormality on fundoscopy

• No abnormality seen on thyroid examination

• Lymph nodes not palpable

• Pedal and Sacral edema absent

• No other significant findings


Systemic Examination

1. CVS Systemic Examination

a. Inspection:

• No Chest deformity

• No sternotomy or any other surgical scar

b. Palpation:

• Apex beat: Lateralized from mid clavicular line at 6th intercoastal spacecedue to LVH



• Heave: well sustained (at apex)

• No left parasternal lift

c. Auscultation:

Mitral, Tricuspid, Aortic, Pulmonary



• S1- Normal (Apex)

• S2- Audible (Left sternal edge)

• No added sounds

• No murmurs



c. GIT:

• Liver not palpable

• Spleen not palpable

• Ascites not present

d. Respiration:

• Chest clear

• No tracheal shift

• No remarkable findings



e. CNS:

No remarkable findings


Examination based Differential Diagnosis

• Myocardial Infarction

• Unstable Angina


Investigations - ECG


Investigations

ECG:

Done within 25 mins of patient arrival

Findings:

• Rate: 78.9

• Rhythm: Sinus Rhythm


Investigations

Leads showing ECG Changes:

• V1 to V6, AvL

• Changes include:

• ST Segment Elevation

• Q wave development

• Loss of R Wave

• T wave inversion


Investigations

• Left Axis deviation seen by thumb rule on Lead 1 and AvF

(For inferior wall MI, changes are seen in: Leads 2, 3 and AvF)


Investigations

Cardiac biomarkers

• Trop T raised

• CK-MB raised

Chest Xray

• Cardiothoracic ratio increased showing LV Dilatation

• Pulmonary edema not evident


Investigations – Xray


Investigations

Other Blood Tests

• ESR and CRP raised

Echocardiography could not be done due to the non availablity of facility.


Investigations based Diagnosis

Anterolateral ST Segment Elevation Myocardial Infarction with Left Axis Deviation


Management

• Patient was immediately admitted in ICU. Within 10 mins, ECG was performed and based upon diagnosis, following treatment was given.

• Oxygen + Cardiac rhythm monitoring


Management

• Aspirin 300mg PO

• (Therapy should be continued indefinitely if there are no side affects)

• Clopidogrel 600mg PO followed by 150mg daily for 1 week and 75mg daily thereafter.

• Streptokinase 1.5ml I.V in 100ml sol at 6ml/hr

• Inj Morphine

• Inj Metoclopromide I.V Stat


Late Management

• Patient advised on the following:

• Lifestyle Modification:

• Lipid Lowering diet

• Cessation of Smoking

• Regular exercise


Late Management

• Secondary Drug therapy:

• Aspirin

• B blocker

• Ace Inhibitor/ARB

• Statin

• Additional therapy for DM and HTN


The patient was given Streptokinase (Thrombolysis) within 8 hours of his arrival. He is still in the ICU undergoing 24/7 observation and treatment. He was advised angiography due to the unavailability of the facility at the Hospital. We wish him a speedy recovery.


What is MI ?

• Detection of rise and/or fall of cardiac biomarker values (preferably cardiac troponin) with atleast one of the following:

• Symptoms of Ischemia

• Significant ST segment-T wave changes or new LBBB

• Development of pathological Q waves

• Imaging evidence of new loss of viable myocardium

• Angiographic identification of Intra coronary thrombus


Types of MI

On the basis of ECG, there are two main types of MI

• STEMI (major coronary artery complete obstruction)

• Non-STEMI (Complete occlusion of a minor vessel or partial occlusion of a major coronary vessel


Arterial Supply of the Heart



There are two major arteries which supply the heart

• Left coronary artery

• Right coronary artery

1. Left Coronary Artery:

It is further divided into two main branches:

LAD (I/V septum, Ant. Wall of LV and Apex)

LCx (Lateral, Posterior and Inferior Walls)



2. Right Coronary Artery

It supplies RA, RV and inferio-posterior part of LV

Branches include:

PDA (supplies I/V septum inferior part) In 90% individuals PDA is a branch of RCA. (Right Dominant people)

In 10% individuals PDA is a branch of LCA (Left Dominant)


Arterial Supply of SA & AV Node

• SA Node: RCA in 60% individuals

• AV Node: RCA in 90% individuals

Clinical Significance:

• Proximal RCA occlusion may result in Sinus Bradycardia and may also cause AV Nodal block

• Abrupt occlusion of RCA may lead to infarction of inferior part of LV


Conducting system of Heart


Nerve Supply of Heart

• Adrenergic Nerves from the Cervical Sympathetic chain supply atria and ventricles

• Parasympathetic: Vagus nerve


Pathophysiology of MI

Atheromatous plaque formation

Interplaque haemorrhages

Exposure of Subendothelialcollagen fibers

Formation of micro thrombi

Full blown thrombus

vasospasm



• LCA Occlusion:

LAD occlusion (40-50) leads to

Anterior wall infarction of LV

Anterior portion of ventricular septum

Apex

LCx Occlusion 15-20%

Lateral wall of LV



RCA Occlusion (30-40%)

RCA occlusion leads to infarction of

• Posterior wall of RV

• Inferior wall of LV

• Posterior 1/3rd of I/V septum


Clinical features

Symptoms:

• Pain: Crushing, retrosternal chest pain radiating to back, left arm, neck or jaw

• Anxiety and fear of impending death

• Nausea and Vomiting

• Breathlessness

• Diaphoresis


Clinical features – Pain Areas


Clinical features

• Signs

Sympathetic activation:

- pallor

- sweating

- tachycardia

Vagal activation:

-bradycardia


Clinical features

vomiting

• Signs of impaired myocardial function:

Hypotention

Narrow pulse pressure

JVP may be raised


Clinical features

3rd heart sound

Quiet 1st heart sound

Diffuse apical impulse

Lung crepitations


Clinical features

• Signs of tissue damage

fever

• Signs of complications e.g Mitral regurgitation, pericarditis etc


Clinical features

• Silent MI

diabetic patients

Older individuals


Investigations

• ECG

• Cardiac biomarkers

• Chest X-Ray

• Echocardiography

• ESR & CRP

• Angiography


Investigations

• ECG

It is central to confirming the diagnosis but may be difficult to interpret if there is bundle branch block or previous MI. so repeated ECGs are very important.


Investigations – Normal ECG



Earliest changes are seen in ST-segment

1. STEMI

• ST-segment elevation

• progressive loss of R wave .

• Development of Q wave .

• Resolution of ST-segment

• T-wave inversion



2. NSTEMI

• St-segment depression

• T-wave changes

• Loss of R-wave

• Absence of Q-wave


Investigations – ECG - STEMI



Significance of chest leads

Antero-septal infarct

v1 ,v2,v3,v4

Antero-lateral

v4,v5,v6 and AVL and 1



Inferior infarction

leads II , III and AvF

Posterior wall infarction doesn’t cause ST elevation or Q-waves in the standad leads but can be diagnosed by the reciprocal changes that is stdepression and a tall R-wave and leads V1-V4.


Cardiac Biomarkers

1. Troponins

2. Creatinine kinases

3. LDH

4. AST

5. Myoglobins

6. Most specific are troponins and CK-MB


Cardiac Biomarkers

1. CK-MB

Rises in 4-6 hours and peaks a 12 hours and falls to normal within 48-72 hours . It is very important. For diagnosis of recurrent MI’s.

2. Troponins: Trop-T and trop-I are gold standards for diagnosis of MI, Troponins rise in 4 to 6 hours and remains elevated for 2 weeks


Investigations- Chest Xray

• Chest Xray to determine cardiomegaly and pulmonary edema


Investigations - Echocardiography

• Useful for assessing ventricular function and determining complications

Eg. Mural thrombus, cardiac rupture , VSD and pericardial effusion etc


Investigations - Other blood tests

1. ESR raised

2. Leucocytosis

3. CRP raised


Management


Drugs used in treatment of MI

1. Analgesics

- Opiates: Morphine Sulphate dimorphine

2. Anti-emetics: metoclopromide

3. Anti-thrombotic drugs

a. Anti platelets: Aspirin

- Clopidogrel

- Ticagrelor

- Gycoprotien 2b and 3a receptor antagonists: Abciximab



b. Anticoagulants :

– LMW Heparin, HMW Heparin, pentasaccharide - fondaparinux

– Warfarin



4. Anti anginal drugs

- Nitrates: GTN, isosorbide dinitrate

- B blockers: metoprolol and atenolol

5. Dihydropyridine CCBs:

- Nifedipine, amlodipine

6. Thrombolytics:

- Alteplase, streptokinase, retiplase, tenecteplase


Invasive modalities used in the treatment of MI

• PCI (Percutaneous Intervention)

• CABG (Coronary Artery Bypass graft) Surgery


Late Management of MI

Lifestyle modifications

Diet

Cessation of smoking

Weight control

Reguar exercise


Late Management of MI- Sec prevention

• Anti platelet therapy

• B blockers

• Ace inhibitors

• Statins

• Additional therapy for diabetes and HTN control

• Mineralocorticoid receptor antagonist

• Devices: Implantable Cardiac Defibrillators


Complications

• Arrythmias

• Bradycardia

• Acute Circulatory failure

• Pericarditis


Complications - Mechanical

• Rupture of papillary muscle

• Rupture of I/V septum

• Rupture of ventricle which can lead to fatal cardiac temponade

• Embolism

• Impaired ventricular function, remodeling and ventricular aneurysm


Prognosis

• If medical care is not provided, death occurs in almost 1/4th of the cases. Half of the death occurs within 24nhours of the onset of symptoms and about 40% of all affected patients die within the first month.

• Patients who reach the hospital and survive have much better prognosis with a 28 day survival of more than 85%. The prognosis of anterior infarcts is worse as compared to inferior infarcts.


Prognosis

OF THOSE WHO SURVIVE AN ACUTE ATTACK, MORE THAN 80% LIVE FOR A FURTHER YEAR. ABOUT 75% FOR 5 YEARS.

50% FOR 10 YEARS & 25% FOR 20 YEARS.


Thankyou everyone

Dept of MedicineFrontier Medical and Dental Collegev

myocardial infarction - case presentation and an overview

Health & Medicine

present urinary system

yrschest pain

hrs shortness of breath

hrs backsudden

complaints of chest

anti diabetics

year old male patient

episode of vomiting