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CORONARY CIRCULATION. CORONARY CIRCULATION. The coronary circulation supplies the myocardium, a tissue that rivals the brain in terms of its nutritional demands and the critical importance of continued flow for normal function. Anatomy.

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coronary circulation
CORONARY CIRCULATION

The coronary circulation supplies themyocardium, a tissue that rivalsthe brain in terms of its nutritional demands and the critical importance ofcontinued flow for normal function.

anatomy
Anatomy

The myocardium is supplied by left and right coronary arteries thatoriginate from the root of the ascending aorta immediately above theaortic valve.

The right coronary artery generally suppliesthe right heart, whereas the left coronary artery supplies theleft.

The arteries course over the heart’s surface and then dive downthrough the muscle layers. The vasculature is notable for numerouscollaterals connecting adjacent arteries and also for the presence ofprecapillary sphincters .

coronary circulation1
Coronary Circulation

Only 1/10 mm of the endocardial surface can obtain nutrition from the blood inside the cardiac chamber

Left coronary artery supplies mainly anterior and lateral portions of the left ventricle

Right coronary artery supplies most of the right ventricle and some posterior part of the left ventricle

Most coronary venous blood returns to the right atrium by coronary sinus (75% of total coronary flow)

Anterior cardiac veins from right ventricle open directly into the right atrium

Thebesian veins empty directly into chambers of the heart

regulation
Regulation

At rest, the coronary circulation receives 5% of CO.

Cardiac muscleextracts 70% of available O2 from blood, and it has a very low capacityfor anaerobic metabolism, much like the brain.

This O2dependencemeans that any increase in work must be matched by an increase incoronary flow, achieved entirely through local control mechanisms.

slide7

Local controls:

  • Coronary resistance vessels are exceptionallysensitive to adenosine. Local control mechanisms allow for a fourfoldto fivefold increase in coronary flow when CO increases, aphenomenon called coronary reserve.
  • 2. Central controls:
  • Coronary resistance vessels are innervated byboth branches of the ANS, but their influence is overridden bylocal controls.
coronary circulation2
Coronary Circulation

Right and left coronary arteries

precapillary sphincters
Precapillary sphincters

Precapillary sphincters comprise single smooth muscle cells wrappedaround the inlets to individual capillaries . They contractand relax with changes in local metabolite concentrations and functionas on/off switches to capillary flow.

slide16

When CO is minimal, mostsphincters are contracted (“off”), and flow is inhibited. They relax intermittently

as local metabolite levels rise but again contract when theincreased flow washes the metabolites away.

At rest, only a small proportion(20%) of sphincters is relaxed, and capillaries are activelyperfused, but the pattern of capillary flow shifts continually (vasomotion).

When cardiac workload increases, levels of metabolic wasteproducts rise, and the sphincters spend a much greater percentageof time in the “on” position. At maximal levels of CO, all sphincters areopen all the time, and coronary flow rises to maximal levels also.

extravascular compression
Extravascular compression

Blood flow through most systemic vascular beds follows the aorticpressure curve, rising during systole and falling during diastole.

Flowthrough the left coronary artery drops sharply during systole and thenrises sharply with the onset of diastole. This unique flowpattern occurs because ventricular myocytes collapse the arterialsupply vessels as they contract (extravascular compression).

The effect is felt strongest during early systolebecause aortic pressure, the main force maintaining vascular patency,is at a low point. During diastole, the compressive forces areremoved, and blood surges through the musculature at peak rates.

normal coronary blood flow
Normal Coronary Blood Flow

Resting coronary blood flow (CBF) is about 225 ml/min

CBF increases in proportion to exercise or work output

Phasic changes in CBF during systole and diastole

coronary blood flow
Coronary Blood Flow

Epicardial vs subendocardial CBF (intramyocardial pressure)

Epicardial arteries in the outer surface supply most of the muscle

Subendocardial arterial plexus is beneath the endocardium

slide24

Aort kapağı

Sol koroner arter

Sağ koroner arter

control of coronary blood flow
Control of Coronary Blood Flow

Local muscle metabolism is the primary controller of CBF

Oxygen demand as a major factor in local CBF regulation

Normally about 70% of O2 is removed as the blood flows

Role of adenosine in vasodilation

And other substances

nervous control of coronary blood flow
Nervous Control of Coronary Blood Flow

Autonomicnervescan affectthe CBF bothdirectlyandindirectly

Directstimulation of coronarybloodvessels

Indirecteffectsresultfromsecondarychanges in CBF causedbyincreasedordecreasedactivity of theheart

Directeffects of nervousstimuli on coronaryvasculature

Parasympathetic fiber distribution is not great

There is moresympatheticinnervation of coronaryvessels

Constrictorreceptorsarealphaadrenoreceptors (moreepicardial)

Betareceptorsarevasodilatory (more in theintramusculararteries)

special features of cardiac muscle metabolism
Special Features of Cardiac Muscle Metabolism

At rest, cardiac muscle normally consumes fatty acids to supply most of its energy instead of carbohydrates

About 70% of total energy from fatty acids

However, under anaerobic or ischemic conditions, glycolytic mechanism is required

Glycolysis consumes tremendous amounts of blood glucose and forms large amounts of lactic acid

Hypoxia, release of adenosine and dilation of coronary artery

ischemic heart disease
Ischemic Heart Disease

The most common cause of death

Insufficient coronary blood flow

Coronary ischemia, coronary occlusion and myocardial infarction – congestive heart failure

Atherosclerosis as a cause of ischemic heart disease

Consumption of large amounts of cholesterol and lack of mobility

Development of atherosclerotic plaques in major coronary arteries

acute coronary occlusion
Acute Coronary Occlusion

Acute coronary occlusion occurs frequently in atherosclerotic heart

1) Atherosclerotic plaque can cause a local blood clot called a thrombus

Unsmooth surface, adherence of blood platelets

2) Local muscular spasm of coronary arteries may occur

Spasm may result from irritation of smooth muscle

Or from local nervous reflexes – plaque

Spasm may lead to secondary thrombosis of the vessel

value of collateral circulation in the heart
Value of Collateral Circulation in the Heart

In normal heart, there is no communication between large coronary arteries

But many anastomoses do exist among the smaller arteries (20-250 micrometre in diameter)

This collateral circulation may delay appearance of ischemic heart symptoms

collaterals
Collaterals:

Collaterals are vessels thatconnect adjacent arterioles. They are usually constricted in ahealthy heart, but, if a supply vessel becomes occluded, they dilatein response to rising metabolite levels.

Flow through collateralsmay prevent infarctionif the occluded vessel is small. In time,these channels enlarge to provide near-normal flow to the ischemicarea.

flow interruption
Flow interruption

Because the ventricular myocytes extract such high levels of O2 fromthe blood, a delicate balance exists between myocardial workloadand coronary supply. If the balance is disturbed, then myocytes become

ischemic and infarcted. Most commonly, this occurs due toatherosclerosisand coronary artery disease.

atherosclerosis
Atherosclerosis:

Atherosclerotic lesions appear at an early agein the populations of most Western countries. They evolve to becomecomplex plaques of lipids, hypertrophied myocytes, and fibrous material. Plaques enlarge at the expense of the vascularlumen and impair blood fl ow. This causes an imbalance betweencoronary supply and myocardial demand, resulting in ischemia.

Ischemic myocytes release large quantities of vasoactive compounds,such as adenosine, but vasodilators have no effect onplaque.

As the O2 deficit continues, the myocytes release lacticacid, which stimulates pain fibers within the myocardium andcauses angina pectoris.

myocardial infarction
Myocardial Infarction

After coronary occlusion, blood flow ceases beyond the blockage

Cardiac muscle has little or no blood flow

The overall process is called myocardial infarction

After the onset of MI, small amounts of collateral blood begin to seep into the infarcted area

Progressive dilation of local blood vessels

In later stages, the vessel walls become highly permeable and leak fluid

Cardiac muscle tissue becomes edematous

Subendocardial infarction and systolic contraction

slide44

In the common heart attack a thrombus form in a coronary artery.

Death of more than 1/3 of the left ventricle will lead to severe heart failure.

Acute Myocardial Infarction

Infarction

causes of death after coronary occlusion
Causes of Death After Coronary Occlusion

1) Decreased cardiac output

2) Damming of blood in the pulmonary edema

3) Fibrillation of the heart

4) Rupture of the heart

causes of death after coronary occlusion1
Causes of Death After Coronary Occlusion

1) Decreased cardiac output (Systolic stretch and cardiac shock)

Systolic stretch

Incapable heart to pump sufficient blood into the peripheral arterial tree

Coronary shock, cardiogenic shock, cardiac shock or low cardiac output failure

Cardiac shock occurs when >40% of the LV is infarcted

Death occurs in 85% of patients once they develop cardiac shock

causes of death after coronary occlusion2
Causes of Death After Coronary Occlusion

1) Decreased cardiac output (Systolic stretch and cardiac shock)

causes of death after coronary occlusion3
Causes of Death After Coronary Occlusion

2) Damming of blood in the body’s venous system

Acutely reduced cardiac output leads to diminished blood flow to the kidneys

The kidneys fail to excrete enough urine

This adds to progressively to the total blood volume and congestive symptoms

Development of pulmonary edema

causes of death after coronary occlusion4
Causes of Death After Coronary Occlusion

3) Fibrillation of the ventricles after myocardial infarction

Sudden ventricular fibrillation

Four factors into tendence for the heart to fibrillate:

a) Acute loos of blood supply to the cardiac muscle and increased K ions in the extracellular space

* irritability of cardiac muscle

b) Ischemia of the muscle causes “injury current”

* ischemic muscle cannot completely repolarize

c) Powerful sympathetic reflexes develop after massive infarction – irritability increases

d) Cardiac muscle weakness causes the ventricles to dilate excessively.

* This increases the pathway length for impulse conduction

causes of death after coronary occlusion5
Causes of Death After Coronary Occlusion

4) Rupture of the infarcted area

Dead heart muscle bulges outward with each contraction

Systolic stretch becomes greater and the heart may rupture

Loss of blood into the pericardial space and development of cardiac tamponade

stages of recovery from acute myocardial infarction
Stages of Recovery from Acute Myocardial Infarction

Small or large ischemic area

Replacement of dead muscle by scar tissue

After a few days to three weeks, most of the nonfunctional muscle becomes functional again or die

Fibrous tissue begins developing among the dead fibers, ischemia stimulates growth of fibroblasts

slide52

Prolonged ischemia of the heart leads to myocardial infarction. Cells begin to die approximately 20 min after the onset of a coronary occlusion and killing is complete after 6 hr.

A heart slice with a fresh infarct

recovery from mi
Recovery from MI

Value of rest in treating myocardial infarction

Effect of exercise or emotional strain

Function of the heart after recovery from MI

Occasionally a heart that has recovered from a large MI returns almost to full functional capability

More frequently its pumping capability is permanently decreased below that of a healthy heart

Cardiac reserve – reduction to 100%

  • Pain in coronary heart disease
    • Feeling the heart
    • Ischemic cardiac muscle often causes pain sensation
    • Histamine, kinins, cellular proteolytic enzymes, lactic acid etc
angina pectoris
Angina Pectoris

Progressive constriction of coronary arteries, cardiac pain, angina pectoris

It appears when the load on the heart increases

Usually felt beneath the sternum and often referred to left arm, shoulder and neck

Exercise or emotional stress increases angina

Treatment

Vasodilator drugs

Nitroglycerin and other nitrate drugs

Beta adrenergic blockers – inhibition of sympathetic activity of the heart

Propranolol

surgical treatment of coronary disease
Surgical treatment of coronary disease

Coronary angiography

Coronary angioplasty

Aortic coronary bypass surgery

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