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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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.
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 .
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
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.
Right and left coronary arteries
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.
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.
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.
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
Epicardial vs subendocardial CBF (intramyocardial pressure)
Epicardial arteries in the outer surface supply most of the muscle
Subendocardial arterial plexus is beneath the endocardium
Sol koroner arter
Sağ koroner arter
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
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
Betareceptorsarevasodilatory (more in theintramusculararteries)
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
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 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
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 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.
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.
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.
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
Death of more than 1/3 of the left ventricle will lead to severe heart failure.
Acute Myocardial Infarction
1) Decreased cardiac output
2) Damming of blood in the pulmonary edema
3) Fibrillation of the heart
4) Rupture of the heart
1) Decreased cardiac output (Systolic stretch and cardiac shock)
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
1) Decreased cardiac output (Systolic stretch and cardiac shock)
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
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
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
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
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
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%
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
Nitroglycerin and other nitrate drugs
Beta adrenergic blockers – inhibition of sympathetic activity of the heart
Aortic coronary bypass surgery