IM Lec #2 by Alaa Hmadan

by **Sura** 26/10/2011, 1:42 am

http://www.mediafire.com/?449n67yxiq9gqha

by **Shadi Jarrar** 8/11/2011, 1:02 am

بسم الله الرحمن الرحيم

Internal medicine lec. 2

Dr.akram al-saleh

Alaa hamdan

Our lecture today about ischemic heart disease(IHD),,,,,

The commonest cause for death worldwide is IHD-

-Heart is a muscle that beating continuously, to maintain this contractility the heart needs blood supply.

-two big arteries that supply the heart:

Left anterior descending artery

1.Left coronary artery: divided into

circumferential artery

2.Right coronary artery

-between these two arteries there are collateral arteries , normally these collaterals not opened ,to open them there must be a stimulus & usually this stimulus is ischemia.

-IHD result from imbalance between demands & supply,,, for example: during exercise>>>increase the heart rate>>> increase the demand of blood supply>>> increase blood flow,,, blood flow of coronary increase 5 times during exercise more than resting blood flow ,,normally coronary blood flow 60-80ml/100g of muscle tissue/minute.

Normal heart weight is 250-300g,,,&this muscle contract continuously so oxygen extraction is very high ,& considered the highest one between all body muscles.

As we mentioned earlier we have demand & supply & we have factors affect both,,

Factors that affect the oxygen demand(blood flow) of myocardium:**

1.heart rate: most important one,,, increase in heart rate>>>increase oxygen demand,, in IHD we give the patient β-blockers to decrease the heart rate by that we decrease oxygen demand.

-we should not stop β-blockers immediately bcz that’s lead to reflux tachycardia.

2.contractility:the stronger contractility>>the more the oxygen demand,,, again β-blockers can do this job by decreasing the contractility ,,β-blockers has negative inotropic (contractility) effect & negative chorontropic(heart rate) effect.

3.wall tension: increase in wall tension>>>increase the oxygen demand(increase the pressure on the left ventricle).

4.muscle mass: increase in muscle mass >>>increase in oxygen demand

So sometimes we can see patient with angina due to increase in the muscle mass of the myocardium ,,,the causes that lead to increase in myocardium muscle mass:

A. hypertension :the most common cause, if hypertension not controlled the ventricle works against resistance that’s lead to hypertrophy of left or right ventricle.

B. patient with aortic valve stenosis :the same idea, the ventricle work against resistant & the left ventricle try to adapt to this condition by increasing the thickness.

C. hypertophic cardiac myopathy.

Factors that affect blood supply:**

1.patency of the artery: if the coronary is patent, this allow to more blood flow &increase in oxygen supply.

2.hemoglobin level: as we know hemoglobin is the carrier of oxygen in our tissues ,, For that we always try to keep hemoglobin level in IHD patients above 10.5mg,if the patient suffer from severe anemia he may suffer from tissue hypoxemia& heart maybe one of these tissues.

Decrease in oxygen saturation>>>>increase in tissue hypoxemia.

The main cause of IHD is coronary artery atherosclerosis which account up 95%,,atherosclerosis is diffused disease that can affect any artery in the body &coronary is one of them &that’s lead to lipid accumulation in the subintimal layer &lead to narrowing of coronary, stenosis, &maybe rupture of this plaque in a syndrome called acute coronary syndrome.

Risk factors that affect atherosclerosis divided into two big categories : modified(reversible) & non-modified(irreversible)

Modifiable(reversible) risk factors for atherosclerosis :**

1-hypertension:we have 2 types of hypertension

_systolic hypertension

-diastolic hypertension

2-smoking

3-hyperlipidemia: we have many types of hyperlipidemia,,

-high LDL

-high triglyceride

-low HDL

4-diabetes mellitus

There are many other reversible causes such as:*

1.diatery

2.lack of exercises

3.obesity

4.hypolipoprotenase

On the other side there are non-modifiable risk factors(factors we can't change theme):**

1-age & sex :male>45y female>55y considered risk factor(this difference is due to estrogen production in females)

2-family history: if the patient has first degree relative less than 55y if male or less than 65y if female

The important risk factors are the modifiable bcz we can change them.

Atherosclerosis is a diffused disease that can affect any artery in the body one of these arteries is coronary artery.

The manifestations of coronary artery disease maybe range from asymptomatic to sudden cardiac death, in between the two spectrums the patient may suffer from chest pain .

Chest pain is related to many diseases:*

-stable angina

chronic IHD or stable plaque IHD

-variant angina

-unstable angina

Acute coronary syndrome

myocardial infarction(MI)-

-heart failure

-arrhythmia

-hypotension

All these diseases maybe a presentation of IHD,the commonest for us as dentists are angina in its different types & MI

**Stable angina**:

-usually result from imbalance between demands & supply

-usually presented with chest pain that come with exercise & relief by rest or sublingual nitrate

-chest pain located commonly retrosternal & maybe present in the shoulder ,arm, throat, neck, epigastria, jaw, or teeth.

(يعني بيجي المريض بحكيلك أنا لما امشي فكي أو سني الفلاني بصير يوجعني ولما أوقف بروح الوجع)

-pain lasts for 3-5 minutes & disappear by rest or sublingual nitrate

-we diagnose it clinically just by history

Note: if the patient has chest pain lasts for few seconds (na5zat) , or has lasts for few days or weeks , we can't called that IHD maybe its musculoskeletal problem , GI problem , gallbladder,…..etc but not IHD.

-there's no specific sign for angina ,the clinical examination maybe completely normal , but the patient has signs of risk factors (hypertension, smoking, diabetes, hyperlipidemia) & you should look for other signs of atherosclerosis in other arteries, that’s mean you should look for peripheral ischemic diseases such as muscle pain during walking bcz sometimes its related to ischemia in peripheral artery.

To diagnose*

1.history (most important)

2.ECG maybe normal or abnormal

3. we can do something called angiocathornalization(??) to make appropriate diagnosis.

4.vascular ultrasound to inter inside the artery

To manage:*

The management by treat the reversible risk factors & we give antiplatelet(aspirin),

Aspirin is important drug for all patients with IHD & that makes some problems to dentist when dealing with them due to increase the incidence of bleeding .

{aspirin: antiplatelet , prevent thrombosis,,,,,,,,,,,,,,, Statin: anticoagulant }

-any patient with IHD must kept on statin to achieve the goal of LDL level which is less than 100mg/dl for any patient with IHD or diabetes ,& now the recommendation is to less than 70mg/dl.

To treat:*

1.we start by stop smoking, increase exercises, control body weight .

2.medication:aspirin, statin, β-blockers (if there's no any contraindication such as asthma, advanced heart failure, heart block, peripheral heart diseases, …etc ,all patients with IHD except variant angina should kept on β-blockers), AC inhibitors, nitrate(we start sublingually then if no response we give it orally or long acting)

3.revascularization if medication not useful.

Mortality:*

Depends on the extent of coronary artery disease, for example, if the biggest coronary is affected which is left descending artery the one year mortality will be 12%,but if small artery is affected the one year mortality will be 1%.

Variant angina**:**

-usually it due to spasm of coronary artery & decrease in the lumen & blood supply for myocardium.

-severe chest pain usually comes at rest

-ECG changes (ST segment elevation).

-relived by giving vasodilator mainly nitrate

-in this condition we must avoid β-blockers ,bcz when you give it you block β receptors which cause vasodilatation & leave α receptor which cause vasoconstriction without antagonist lead to more spasm & construction.

These two diseases called chronic IHD or stable plaque IHD))

Now we come to other category when the plaque is not intact or ruptured, we called this category acute coronary syndrome

-severe sudden myocardial ischemia that result from erosion for the plaque lead to thrombosis

-two types: MI & unstable angina

-both have the same histopathology ,,plaque erosion>>thrombosis formation

-when the plaque rupture or eroded or fissured the endothelial layer become exposed to blood stream >>this recognized by platelet ,so the platelet is the first structures to be involved in thrombus formation >>platelet will stuck(adhesion) to the rough surface area by collagen ,glycoprotein 2B3A which works as glue>>>activation of platelet which converted from spherical form to irregular one that has many projections on its surface contain thousands of receptors of glycoprotein 2B,3A >>> these receptors are so important for platelet aggregation by attached to each other by fibrinogen & that’s we called aggregation.

ADHESION>>ACTIVATION>>AGGREGATION

-its very important step in healing process for any injury & in the same time in pathogenesis of acute coronary syndrome & for that the patient must be kept on antiplatelet to decrease the activity of this process.

When glycoproteins attached to each other by fibrinogen it activate the coagulation system (we have extrinsic & intrinsic coagulation systems) that’s lead to formation of thrombus .

-there are two types of thrombus:

1.white thrombus: platelet rich thrombus

2.red thrombus: fibrin rich thrombus, this thrombus formed after platelet activation.

So if you block the first thrombus (white), you decrease the incidence of the second one(red).

Myocardial infarction (MI)**:**

-common cause of death.

-usually caused by plaque rupture which leads to blocking in one of coronary arteries.

-so MI means one of coronary arteries is totally blocked.

-presented as severe chest pain comes at rest ,it’s the worst pain that the patient suffer from during his life & he feels that he will die.

-this pain usually comes in the early morning hours (note: early morning hours are the most dangerous time to vascular accident :MI ,stroke, CVA,…, bcz this time has many things lead to increase in thrombotic process like decrease in fibrinolytic process, & increase in platelet activity)

-the pain lasts for more than 30 minutes (usually lasts for 6 hours)

-if the artery still blocked the affected segment will necrotize & dead, this necrotized segment is painless, then the pain disappear after 6 hours ,but if the segment still viable & ischemic then the severe chest pain continue.

-So the chest pain in MI disappear in one of two:

1.the the affected segment is totally necrotized & become painless.

2.the artery opened & no more ischemia is present.

-the site of pain is the same for angina ,retrostearnal (the commonest site) ,shoulder, arm, jaw, teeth, epigastria…etc.

عادة المريض بيوصف الوجع انو حاسس في صخرة على صدره وبكون حاسس بغثيان

-nausea, sweating, dyspnea, & chest pain are the main manifestations of MI.

-Again, the pain resist as long as the ischemia resist, if we remove the ischemia the pain will

-with examination the patient looks anxious, stressed, agitated, sweating, tachycardia, hypotension.

*Diagnosis:

1.history:

يعني بحكيلك المريض انو معو جلطة او عندو احتشاء او مركب شبكة

2.ECG: play a key role in MI diagnosis & gives an idea about which type of infarction , where the site of infarction,& which the most likely artery to be affected.

3.cardiac markers: like troponin or CBK or any other,, commonly we used troponin T&I which sensitive to myocardium, but we don’t use troponin C which sensitive to skeletal muscles.

What's important for us in IHD:**

1.comes with imbalance between demands & supply

2.patient must avoid anything increase the demands,& we should decrease the pain as much as we can by local anesthesia.

3.try to avoid adrenalin in local anesthesia ,bcz adrenalin cause tachycardia & that’s will increase the demands.

4.you should avoid stopping β-blockers immediately bcz it will lead to reflux tachycardia,, so always remember DON’T touch the dose of β-blockers.

5.according to antiplatelet which are most likely to be aspirin & clopidrogel ,, antiplatelet drugs will increase the chance of bleeding during dental operation ,,to manage that you must do one of two choices

A. if the patient stable you can stop the drug for 7 days before dental operation.

B. if not stable or he recently has stent you can't stop the drug.

6.some patient may takes anticoagulant drugs like warfarin ,, & you can stop it before 3 days of dental operation.

That’s itJJJ

IM Lec #2 by Alaa Hmadan

IM Lec #2 by Alaa Hmadan

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