August 16, 2009

Management for angina

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1) Treat underlying problem ie. Anemia, hyperthyroidism

2) Manage coexist problem ie. DM, HPT

3) Evaluate risk factor & control it ie. Smoking, obesity

4) Medical therapy vs revascularization


Medical therapy


a) Prognostic therapy


- Tab aspirin 75 mg daily, po

- Lipid lowering drug in pt:


i) With total cholesterol above 4.8 mmol/L.

ii) LDL more than 3.3 mmol/L

iii) HDL less than 1.0 mmol/L

iv) If TG less than 3.5 mmol/L use statin. Atorvastatin 10-20 mg daily or simvastatin 20-40 mg daily, pravastatin 40 mg daily and rosuvastatin 10-20 mg daily.

v) If TG more than 3.5 mmol/L use fibrate


b) Symptomatic


- Sublingual GTN 0.3-0.5 mg at 5 minutes interval to a max 3 tab.

- Beta blocker, tab. atenolol 50-100 mg bds, po or tab. Metaprolol 25-50 mg bds, po if renal function impaired

- Calcium channel blocker like ca2t antagonist (diltiazem, verapamil) or short acting dihydropyrides (nifedipine)

- Long acting nitrates for eg; isosorbide mononitrate (c/I with sildanefil)

- Pottasium channel activator (nicorandil)

Risk factor for IHD

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Fixed

-Age (increase with age, >40. After >65, higher chances and always complicated by calcification of vessel)

-Male sex

-Possitive family history

-Deletion polymorphism in Angiotensin Converting Enzyme gene


Changeable

-HLD

-Smoking

-HPT

-DM

-Sedentary life style

-Blood coagulation factor (high fibrinogen, factor VII)

-CRP

-Homocysteinaemia

-Obesity

-Gout

- Contraceptive pills

-Heavy alcohol consumption

-Psychososial (work stress, lack of social support, depression, personality)

Ischaemic heart disease (causes and pathophysiology)

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Myocardial ischaemic occur when there is imbalance between O2 supply and myocardial and myocardial demand.


Can be due to


1) Mechanical obstruction

- Atheroma

- Thrombosis

- Spasm

- Embolus

- Coronary ostial stenosis

- Coronary arteritis


2) Decrease blood flow of oxygenated blood to myocardium

- Anaemia

- Carboxyhaemoglobulinaemia

- Hypotension leads to decrease coronary perfusion pressure.


3) Increase demand of O2

- Increase cardiac input in thyrotoxicosis

- Myocardial hypertrophy (aortic stenosis@ hypertension)


The most common causes for IHD is Coronary artery disease (CAD) due to coronary atherosclerosis.


Mechanism responsible for thrombosis on plaque


1) Superficial endothelial injury

- Break of endothelial lining

- Platelet adhesion

- Migration of smooth muscle from tunica media to intima

- Formation of form cell

- Thrombus formation.


2) Deep endothelial fissuring

- Advanced plaque with lipid core

- Tearing of plaque cap allows entering of blood from lumen into plaque itself

- Core with lamellar lipid surface, tissue fator produced by amcrophage + exposed collegen highly thrombogenic

- Formation of thrombus and expendation of thrombus

- Thrombus extends into lumen.

5H’s and 5T’s in pulseless carotid artery

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In primary survey during emergency, we might encounter pulseless carotid artery which indicates problems with circulation. Please consider this formula when managing your patient


5H’s

-Hypovolumic

- Hypoxia

-Hypothermia

-Hyper/Hypo kalaemia

- H+ (acidosis)


5T’s

-Tension pneumothorax

-Temponade (cardiac)

-Thrombosis (massive pulmonary embolism)

-Thrombosis (MI)

-Tablet (Drug overdose)


Source: Case File™: Emergency Medicine, Eugene C. Toy MD, and et all, Mac Graw Hill company, 2005

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