Physio 16 Cardiac Pathophysiology 1

7/27/2019 Physio 16 Cardiac Pathophysiology 1

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Circulation

Coronary Circulation & IHD


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Coronary Circulation & IHD

The normal and pathological physiology of the

Coronary circulation is one of the most

important subjects in medicine.


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Coronary Arteries


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Coronary Arteries

Only 0.1 mm of the

endocardial surface

of the heart can get

its supply of

nutrients directly

from the blood

inside the chambersof the heart.


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Coronary Arteries

The Right & the Left

Coronary arteries

arise at the root ofthe Aorta, from the

two Aortic sinuses

just above the Aorticvalve.


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Coronary Arteries

The Left Coronary

artery supplies the

anterior and leftlateral portions of

the heart


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Coronary Arteries

The Right Coronary

arterysupplies:

Most of the RightVentricle

as well as

Most of theposterior part of

the Left Ventricle.


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Cardiac Veins

Most of the Coronaryvenous blood from

the Left Ventricle

returns to the RightAtrium by way of the

Coronary sinus (about

75 % of the total

venous return)


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Cardiac Veins

The remaining

25 % 30 % of the

blood returns

through two

different pathways;


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Cardiac Veins

Most of the coronary

venous blood from

the right ventricle

returns by the small

Anterior Cardiac

veins directly to the

Right Atrium.


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Cardiac Veins

The rest returns

directly to the

various chambers of

the heart through

the various small

Thebesian veins.


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Phasic Coronary Blood Flow During

Cardiac Cycle


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Blood Supply At The Different Levels

Of The Myocardium

Due to the rhythmical contractions of the

myocardial muscles the blood vessels in the

myocardium gets powerfully squeezed during

each systole.

There exists a difference in the squeeze

experienced by different levels of the

myocardium.


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Of The Myocardium

The squeeze is the maximum in the

subendocardial layer.

The squeeze is the least in the epicardial layer

of the myocardium.


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Of The Myocardium

Intramural vessels


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Blood Supply At The Different Levels Of The

Myocardium

To compensate for the almost total lack of flow

during systole in the subendocardial layer, the

subendocardial plexus is most extensive

The epicardial plexus is the least extensive of

the 3 layers of blood vessels to the

myocardium.

This difference has important clinical

significance.


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Of The Myocardium

The subendocardial layer of the myocardium:

Always repolarizes last, even in health, causing

an upright T wave.

Most susceptible to infarction


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Control Of Coronary Blood Flow

Local Control

Release of vasodilator (Adenosine)

substances.

Lack of O2 (Nutrient) lack.

Nervous Control

Parasympathetic (very negligible supply) Sympathetic ( and receptors)


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Sympathetic supply

Epicardial vessels have mostly receptors.

Intramural arteries have mostly receptors.


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Sympathetic supply

Hence, there is a greater possibility of

sympathetic stimulation causing

vasoconstriction. However, the local metabolic factors always

have an overriding effect


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Cardiac Muscle Metabolism

Under resting conditions Cardiac tissues getabout 225 ml of blood; about 5 % of theCardiac output.

Under resting conditions, 70 - 80 % of O2 isextracted from the blood flowing in theCoronary arteries.

Hence during times of extra needs, theincrease in blood flow is the prime meansof meeting the increased demands.


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Under resting conditions, 70 % energy

requirement of the heart is derived mainly

from fatty acids.

Under ischemic conditions, the heart turns to

anerobic glycolysis for its needs, and then

large amounts oflactic acid are liberated.


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95 % of the energy derived thus is used for

the synthesis of ATP.

The energy stored in the ATP is used formuscle contraction.

The ATP is broken down to

ADP AMP Adenosine

Adenosine is reabsorbed and reutilized.


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In severe coronary ischemia, Adenosine

diffuses out from the cell and causes

vasodilatation.

Half of adenosine is lost in 30 mins. - has

serious consequences to the heart muscle.

Replacement by resynthesis occurs at the pace

of2 % per hour.


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Ischemic Heart Disease

Most common cause of deaths in the WesternCulture

35 % of the people in the USA die suddenly as

a result of Acute Coronary occlusion orFibrillation of the Heart.

Others die as a result of progressive

weakening of the pumping mechanism of theHeart


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Atherosclerosis:

This develops in certain people who have a

genetic predisposition to atherosclerosis.

Or, in those who consume excessive quantities

of Cholesterol and other fatty substances.


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Atherosclerosis:

Large quantities of Cholesterol is deposited

under the endothelium of several arteries all

over the body.

Gradually these areas of deposits are invaded

by fibrous tissue and may even have calcium

deposited in it (calcification).


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Soon the atheromatous plaques protrude into

the lumen of the artery and cause a degree of

occlusion.

This causes slowing of the blood flow.


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If the surface endothelium gets eroded,

platelets get deposited on the rough surface

laid bareThrombus formation.

Occasionally, muscular spasm at the edge of

the atheromatous plaque may result in

Secondary Thrombus formation.


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Soon the thrombus may break offand head

downstream Embolus formation.

The embolus may go and lodge at the opening

of the distal branch of the artery.


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Blockage at the mouth of the artery causes

cutting off of the blood supply to the areas of

the myocardium supplied by the same branch

of the coronary artery.

This results in ischemia of the myocardium.


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Collateral Circulation

In the normal heart,

there are

communications

between the smallerbranches of the

Coronaries.


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When suddenocclusion occurs in

one of the larger

Coronary arteries,the small

anastomoses dilate

and compensate

for the loss of

blood supply.


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If the ischemic area is small enough, these

collaterals may suffice.

In moderately larger ischemic areas, the

diameter of the collaterals open up further in

a span of 8 24 hours.


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In larger ischemic areas or where the

collaterals do not or cannot compensate the

loss, there is death of the myocardium

Myocardial infarction.


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Myocardial Infarction

The local vessels supplying the ischemic area

get disgorged despite lack of blood.

Soon the area has seepage of stagnant blood

from the collaterals.


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The ischemic myocardium sucks up the last

of the O2 present in this stagnant pool and the

hemoglobin gets totally reduced.

This imparts a bluish brown hue to the

infarcted myocardium.


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Finally the disgorged vessels become very

leaky and result in tissue edema.

The cardiac muscle cell begins to swell

because of diminished cellular metabolism

Within a few hours of almost no blood supply,

the cardiac muscle cells die.


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Normal resting cardiac muscle is supplied 8

ml of O2 / 100 gms of muscle / min.

Forsurvival, the myocardial cell needs just1.3

ml of O2 / 100 gms of muscle / min. (15

30 % of the normal resting supply)


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The subendocardial surface has extra difficulty

in getting its normal share of blood supply.

The subendocardial surface is the first to

undergo infarction.

The damage then spreads outward towards

the epicardium.


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Mortality In Acute Coronary Occlusion

Causes of death:

Decreased cardiac output

Damming of blood in the Pulmonary veins and

Pulmonary edema

Fibrillation of the heart

Rarely, rupture of the heart


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Systolic Stretch

When the normal portion

contracts, the ischemic

portion is forced outwards.

This may result in

insufficient blood supply

to the peripheral tissues

Coronary / Cardiogenic

Shock.


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Pulmonary Edema

Inadequate pumping of the heart results in:

Increase in the Right and Left Atrial pressures

Increase in capillary pressure in the lungs

Cardiac output Kidney failure

blood volume congestion in the lungs.


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Fibrillation Of The Heart

Causes of Ventricular Fibrillation:

(in the first 10 mins or during the 2ndhouronwards).

Rapid depletion of intracellular K+ions.

Ischemic part can generate abnormal impulses(Current of Injury).

Powerful Sympathetic stimulation.

Cardiac muscle weakness resulting indilatation of the heart Circus movement.


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Circus Movement


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Initiation & Propagation Of

Fibrillation


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Rupture Of The Heart

The dead muscle fibers become thin.

With each heart beat it bulges outwards.

Finally the heart ruptures.

Blood collects in the pericardial space. --

Cardiac tamponade.

Failure of the blood to flow into the rightatrium.


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Stage Of Recovery From Acute



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Pain In Coronary Disease

Pain is felt due to increased levels of:

Lactic Acid

Histamine

Kinins

Proteolytic enzymes

Which stimulate the nerve endings of thecardiac muscle.


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Angina Pectoris

Progressive constriction of the coronaries can

result in Cardiac pain (Angina Pectoris)

whenever the load on the heart becomes too

great.

There is retro-sternal pain which is described

as constricting, pressing or hot.


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Angina Pectoris

It often radiates to the tip of the left shoulder,

left arm or side of the face.

This distribution of pain is due to the

embryonic origin of the heart.


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Angina Pectoris

Treatment:

Rest

Oxygen

Vasodilator drugs (Nitroglycerine)

Beta blocker (Propranolol)

Surgical treatment (Aortic

Coronary Bypass,Coronary angioplasty)

Physio 16 Cardiac Pathophysiology 1

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