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Pathophysiology

Challenge 2010propound

Lecture Notes

Lecture Title : CVS disorders

Prof name : Dr.Mostafa Shihebat

Done by : Pharmacy students

Corrected by : Dentistry students


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:(Ischemia)CVS disordersToday's lecture about

Anatomical and Physiological Introduction:-

Heart arteries are mainly 2 arises from the ascending

aorta (which is the largest art. In human) and supply the

oxygenated blood to the myocardium :

1- Left Coronary art. Divides into :

-anterior interventricular branch.

-circumflex branch.2- Right Coronary art. Divides into :

- posterior interventricular branch.

-marginal branch( left and right).

Drainage of veins through the Coronary sinus ( a

vascular sinus which's thin-walled that has no

smooth muscle ) which enters the blood in theright atrium.

( Note : that these art. or this system of art.

sovascularity of the heartreferred to as the

thatswhy we explained them to get the idea about

how ischemia occurs).

Normal coronary blood flow:

The resting coronary blood flow= 225

ml/min (relaxed situation e.g sleeping )

In strenuous exercise = increase three to

four folds. ( sometimes up to 7 folds)


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Now the question is when perfusion occurs

during the systole or the diastole?

Systolic pressure created from thecontraction of the left ventricle(phase of

contraction) .

Diastolic pressure created from the recoil

of the aorta (phase of relaxtion) .

During systole: arteries( thesubendocardial arteries) of the heart will

ofperfusionso most of thebe compressed

.diastoleoccurs duringheart

As you see in the following diaghram:


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Systole BF is 100 ml/minute.

Diastole BF is 300 ml/minute.

Which controls the coronary blood flow and all

arteries of the body in general ?

Need or increased demand in order to increase the

blood supply.

Otherwise ( if there's imbalance between the supply

aassumedand the demand) it's going to be

Ischemia.which is called(defect )disorder

Blood flow is controlled mainly by :-

Metabolic (activities) regulation : if it increased then

bf will increase.(Blood flow through coronary system

is regulated almost entirely by local arterialvasodilatation in response to cardiac muscle need for

nutrients which leads to increased contraction so

Increase in rate of coronary blood flow) .


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Nervous regulation : sympathetic stimulation

increase the heart rate and contractility so it will

increase the cardiac output which means increased

coronary blood flow.

Now let us start with pathophysiology:-

:Ischemia

There are two important subjects placedunder or related to ischemia generally :

-Ischemia.

-Necrosis.

Now what do we mean by Ischemia?

Lack of oxygen due to inadequate perfusion of the

myocardium, which causes imbalance between

oxygen supply and demand.

Specificly : when there's a constriction , narrowing

or subdivision(partial occlusion) in the arteries

which supply the heart(coronary arteries ).

The other part is necrosis(myocardial infarction ):

When there's complete occlusion of the blood

vessel ( not partial).


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Then the myocytes beyond the occlusion will die

and it might be fatal (this leads to a state of

necrosis) .

Ischemia equation :

e.g u need 10 liter and

blood supply only 8 ltrs ( this leads to ischemia).

-causes of myocardial ischemia :

The most common cause is Coronary atherosclerosis(

which means blockage of arteries ):

Thickening or narrowing of the wall of the arteries

due to accumulation of fatty material such as

cholesterol ( most common in old people ).

Epicardial coronary arteries are the major site.

Major risk factors that causes atherosclerosis(precipitating factors) :

Increase in LDL( low density lipoprotein) .Decrease in HDL( high density lipoprotein) .Cigarette smoking.Hypertension.


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DM (Diabetes mellitus).*Additional note : low density lipoprotein means bad cholesterol and HDL means good

cholesterol.

all of us know that smoking ,hypertension..etc are

common causes , but what the mechanism?

Because all these things leads to destruction or injury to

the endothelial (has to be smooth) layer of the arteries

which leads to aggregation of clotting factors ( platelets)

due to the fragility of its surface ( no luminar flow) .

This mechanism similar when we got injured or had an

external cut this leads to rough (fragile) surface and

aggregation of clotting factors.

*remember that blood vessels consists of 3 layers : tunica interna(endothelial) , tunica

media ,tunica externa .

*there are 2 type of blood flow : luminar flow( steady or smooth state ) and turbulentflow.

Normal function of vascular endothelium :

-Local control of vascular tone.

-Maintenance of an anticoagulant surface.-Defense against inflammatory cells.

Loss of these defensesleads to:

-Inappropriate constriction.

-Luminal clot formation.-Abnormal interactions with blood monocytes &

platelets.


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- Now the occlusion caused either by Thrombosis or

Embolism, but what the difference ?

The thrombosis is local formed clot , but in the embolismthe clot could be transferred to other sites (from artery to

another artery) & may follow deep venous thrombosis.

The Dr started to talk about angina(to know that it differs

from local spasm) it occurs in people who has neither

embolism , thrombosis nor any problem but they develop

signs and symptoms that resemble the angina ( whenthey get angry, sad or stressed.) they could feel a pain

in their chest ( thorax) this case is due to spasm of the

coronary arteries ( angina-like symptoms) that occurred

because of the deffientcy of blood perfusion (low or less)

due toover sympathetic stimulation .

And if the patient brought to ER and had an examinationit would be a normal ECG without angina.

Partial occlusion

(ischemia) may develop

to complete


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The Location of the obstruction Influence the quantity of

myocardial ischemia ,Determines the severity of the

clinical manifestations which means that if the occlusion

where in major artery then the effect will be major ( the

heart will be affected so much , massive destruction of

cells leads to massive dead myocytes) but if the artery is

small the complication will be less( why? Because there's

a less amount of dead cells).

Collateral circulation:

Before that there's a question : if where young man

had a myocardial infarction he would die but an old

or middle- aged man wouldn't?

Due to Collateral circulation that only formed in

old people and athletes .

Which means that an area(the same one) supplied

by many arteries ( network of blood vessels) it is

Complete occlusion

(necrosis) death of

the area supplied by

the artery


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not opened in young people (except athletes) but

opens when we get older.

*in athletes because they have a high demand(cardiomegaly ).

If heart rate less than 60 it's a disorder which is

called brady cardi but in athletes not ( their heart

size is larger = cardiomegady) normal to had HR


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-Fatty acid cant be oxidized.-Glucose is broken down to lactate.-Reduced intracellular PH and ATP stores.

3) Cell membrane function:

-Leakage of potassium and uptake of sodium by

myocytes.4) Electrical function:-ECG changes:Repolarization abnormalities.Transient ST segment depression.-Electrical instability:

Ventricular tachycardia and fibrillation.

Later on when we discuss arrythimia we will know

that one of its important causes is ischemia and

massive myocardial infarction ( it may lead to

ventricular fibrillation which is fatal).

-angina

there are 2 types :

-unstable angina : which is misdiagnosed between

unstable angina and acute MI(myocardial infarction


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)both of them are Acute coronary syndrome(symptoms:

retrosternal severe chest pain near to the left hand).

We can differentiate between them by ecg ,we have todo blood tests, ckmp, troponine (will be +ve for MI

patients andve for unstable angina patients) next lecture

we will discuss it in detail .

-stable angina:chronic artery disease,

Characteristics:Heaviness,Pressure, Squeezing,

Smothering and Choking pain.

Causes:

-CAD ( coronary artery disease).- Aortic valve disease.

- Hypertrophic cardiomyopathy.

History:

A man > 50 years.

A woman > 60 years.

Pain with physical & emotional

exertion.


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Last to 5-10 min (relieved by vasodilators).

But how does the pain occurs or start? Radiating pain to the

left shoulder, both arms, back, interscapular region, root of the

neck, jaw and teeth but you need to know that any other

symptoms that are not related to the heart in diagnosing angina

or MI ( e.g abdominal pain) otherwise if you didn't you might

kill the patient because you will forget or misdiagnose that he

has angina and you will give him another treatment for other

disease ( that you thought) .

Both types have the same cause(narrowing andconstriction of the coronary artery) but the stable is

relieved by Vasodilators(nitro-peceline sublingual,

nitrates,-adrenergic

blockers,Calcium,antagonist,Antiplatelet drugs.) occurs

mainly after doing exercises specially when the demand

become more than the supply which leads to a severe

chest pain but signs and symptoms will be subsided by

Vasodilators .


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But in unstable pain will not be subsided by

Vasodilators.

*tread-mill or stress test : to know if that your heart doing well ( 220- the

age) e.g ( your age is 20 then 220-20=200 this means that your HR after

doing exercise should reach 200 without feeling any chest pain otherwise

there would be a disorder .

Why are these patient given analgesics (morphine or opium) or

we call them painkillers?

Because heart pain is very severe (painful).

THE END

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