1. Myocardial Infarction: - Definition. - classification. - Signs & Symptoms. - Causes. - Risk factors. - Diagnosis. - Management.

2. Amphetamine abuse: -Common names. -Reasons for abuse -Mechanism of action -Side effects - Withdrawal Symptoms - Management of toxicity

3. Case Study: -Case scenario -Physical exam -History -Lab results -Final Diagnosis -Medications -Assessment

Definition. Mana e ent. classification.

Dia nosis.

i ns y to s.

Risk factors.

Causes. 

In a myocardial infarction the heart

muscles suffer a prolonged and severe restriction of oxygenated blood. 
This is most commonly due to occlusion of

a coronary artery following the rupture of a vulnerable atherosclerotic plaque. 
The resulting ischemia if left untreated for

a sufficient period of time, can cause damage of the myocardium

1- Transmural: I v lv s t tir t ick ss f t l ft v tric lar all fr car i t icar i .

2- Subendocardial: I v lv s ltif cal ar as f cr sis t t i r 1/3 r 1/2 f t c fi l ft v tric lar all.

ST elevation MI

Normal ECG

Non ST Elevation MI

- Persistent, severe chest pain. The pain generally begins in the chest and radiates to the left arm, back neck and jaw. - Pain persists for longer than 30 min and is unrelieved by NTG. - Some patients; particularly diabetic and hypertensive s may experience abdominal pain resembling indigestion. - Other complaints: a sense of impending doom, nausea, vomiting, sweating, difficulty breathing.

Coronary artery vasospasm Ventricular hypertrophy Hypoxia Coronary artery emboli Cocaine, amphetamines, and ephedrine.

Diabetes

Tobacco smoking

Hyperlipidemia

Family history of IHD Alcohol

Hypertension

Obesity

Stress

High homocysteine levels.

Males over 45yr

Females over 55yr

Troponin. Creatine kinase. Myoglobin. 

Myocardial muscle creatine kinase (CK-MB), which is found mainly in the heart .  A level within the reference range does not exclude myocardial necrosis.  CK-MB may not be affected by very small infarcts. 

Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal muscle.  Myoglobin levels are highly sensitive but not specific

Chest Radiography Echo cardiograph

Electrocardiography Complete blood count Chemistry profile C-reactive protein (CRP)
Erythrocyte sedimentation rate (ESR Serum lactate dehydrogenase (LDH) 

The management of STEMI and NSTEMI differ in:

STEMI:
Is due to sudden thrombotic occlusion. The mainstay of treatment is thrombolytic therapy

NSTEMI
Is due to an unstable plaque with aggregation of platelets. The mainstay of treatment is anti platelet drugs and anticoagulants.

1- Thrombolytic agents 2- Antithrombotic agents 3- Platelet aggregation inhibitors 4- Nitroglycerin 5- eta blockers 6- ACE inhibitors 7- Analgesics

Alteplase & Tenecteplase.

Streptokinase.

Alteplase Very short half life, so adjunctive Heparin therapy is needed. Dose: Dose: 15 mg IV bolus then 0.75 mg/kg IV over 30 min. Contraindications: stroke within last 2 months & severe uncontrolled hypertension.

Tenecteplase Dose: Give IV bolus over 5 s using body weight dosing. not to exceed 50 mg. <60 kg: 30 mg (6 mL) 60-70 kg: 35 mg (7 mL) 70-80 kg: 40 mg (8 mL) 80-90 kg: 45 mg (9 mL) >90 kg: 50 mg (10 mL) 

Streptokinase forms a complex with plasminogen which

then converts plasminogen to plasmin. Plasmin breaks down clots as well as fibrinogen and other plasma proteins. 
Dose: 1.5 million U in 50 mL D5W IV over 60 min.  Caution in severe hypertension.

Aspiri :

Inhibits cyclooxygenase, which produces thromboxane A2, a potent platelet activator. Dose: 160-324 mg PO .
Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Dose: 60 U/kg (max 4000 U) IV bolus; followed by a 12 U/kg/h (max 1000 U/h) maintenance infusion. Inactivates activated factor X & factor II. Advantages include intermittent dosing and decreased requirement for monitoring. Dose: NSTEMI = 1 mg/kg SC bid STEMI= 30 mg IV single bolus plus 1 mg/kg SC

Hep ri :

Enox p rin:

Clopidogrel
Inhibits ADP binding to platelet receptor GP2b/3a complex, thereby inhibiting platelet aggregation.

irofib n

Abcixi

b

Chimeric humanmurine monoclonal

Antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor

antibody Binds to receptor with high affinity and reduces platelet aggregation by 80%

Dose: 75 mg PO

Dose: 0.4 µg/kg/min IV for 30 min

Dose: 0.25 mcg/kg IV bolus, followed by 10 mcg/min IV for 12 h 

Causes relaxation of vascular smooth muscle by stimulating

intracellular c-GMP production. 
Dose: 400 mcg SL

if symptoms persist, infuse IV at a rate of 5-10 mcg/min

Metoprolol

Es olol
Selective beta1-adrenergic receptor blocker

Selective beta1-adrenergic receptor blocker

Dose: 5 mg IV q. 5 min TID

Loading dose: 500 µg/kg/min IV over 1 min Maintenance dose: 0.1 mg/kg/min IV 

These agents prevent conversion of angiotensin I to angiotensin

II, a potent vasoconstrictor, causing lowered aldosterone secretion. 

Has short half-life, which makes it important drug for initiation

of ACE inhibitor therapy. 
Dosing: 6.25 mg PO TID ; may titrate to total 450 mg/d 

May provide some preload reduction as well as reducing pain

and ensuring patient comfort. 

DOC for analgesia because of reliable and predictable effects,

safety profile, and ease of reversibility with naloxone. 
Dose: 1-3 mg IV; repeat and titrate to pain relief. 

Is suitable for patients with the clinical presentation of

STEMI within 12 h after symptom onset and with persistent ST-segment elevation. 
Indicated for patients in shock and those with

contraindications to thrombolytic therapy irrespective of time delay. 

Facilitated PCI is defined as a pharmacological reperfusion treatment delivered prior to a planned PCI. Full-dose thrombolytic therapy Or half-dose thrombolytic therapy with a glycoprotein (GP)IIb/IIIa inhibitor. 

Rescue PCI is defined as PCI performed on a coronary

artery which remains occluded despite thrombolytic therapy. 
Clopidogrel should be given as soon as possible to all

patients with STEMI undergoing PCI. 
Loading dose = 300 - 600 mg  Followed by a daily dose of 75 mg.

Common names. Management of an overdose Reasons for abuse

Withdrawl Effects Side effects

Mechanism of action

A study drug

A party drug

A weight-loss drug 

Increases the levels of

dopamine, serotonin, and norepinephrine in the central nervous system. 
The major neural systems

affected by amphetamine are largely implicated in the brain s reward circuitry.

Physical: 
anorexia  dilated pupils  hyperactivity  drymouth  tachycardia  tachypnea  hypertension  acne  heart attack

Psychological: 
  

euphoria, anxiety concentration self-confidence 

  

sociability aggression grandiosity paranoia

fatigue

mental depression excessive sleep

vivid or lucid dreams

suicidal ideation.

When oral toxicity is recent activated charcoal may be given.
Benzodiazepines are the preferred initial treatment for CNS excitation, seizures, tachycardia, and hypertension.

Propofol with mechanical ventilation, may be required for severe agitation.

Hypertension that does not respond to benzodiazepines is treated with nitrates. -Blockers may be used for severe ventricular arrhythmias or tachycardia.

Case scenario Assessment Physical exam

Medications

History

Final Diagnosis

Lab results 

A 32 year old Saudi man was admitted on Dec 14th 2010 through

the ER. 

Co pl ining of: chest pain for more than 2 hours numbing in

nature & radiating to both shoulders & arms. Pain was aggravated by lying down & decreased by sitting. 

He was discharged 4 days later on Dec 18th 2010.

Gener l Blood pressure Heart Rate Chest ECG

Conscious but in pain 190/120 mmHg 150 Beats/min Dyspnea ST elevation

Known case HTN > 2yrs

Drug addict ( 5 tablets of amphetami ne/ day )

Heavy cigarette smoker 2 packs/day

Test pCO2 pO2 Na Random Glucose LDH Trop CK

P tient re ding 6.97 3.43 130 7.3 229 0.19 329

Nor

l Range

H (4.7 6.1) Kpa L (21 26) mmol/l L (135-145)mmol/l H (3.9 6.7) mmol/l H (100 190) U/l H (0 0.1) µg/l H (21-232) IU/l

Dr g name (generic)

Indication in the case

Dose 162 mg OP OD 75 mg O.P OD 40 mg O.P OD 6.25mg OP TID 8000 IU S.C 50 mg I.V TID 80 mg OD I.V 5 mg OD

Main side effect

ASA Clopidogrel Simvastatin Captopril Enoxaparin Ranitidine Tenecteplase Diazepam

Anti-platelet Anti-platelet stabilize the thrombus Antihypertensive Anti coagulant Stress ulcer Thrombolytic Amphetamine OD

Bleeding Bleeding Abdominal pain Hyperkalemia Bleeding dizziness Bleeding Sedation. 

Close monitoring for development of hypotension is

recommended due to Coadministration of diazepam and captopril. 
Concomitant use of Captopril and Enoxaparine may

increase the risk of hyperkalemia. Serum potassium and renal function should be checked regularly. 

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http://emedicine.medscape.com/article/812518-overview  http://www.medicinenet.com/script/main/hp.asp