1. CORONARY CIRCULATION

3. 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.

4. Anatomy
The myocardium is supplied by left and right coronary arteries that originate from the root of the ascending aorta immediately above the aortic valve.
The right coronary artery generally supplies the right heart, whereas the left coronary artery supplies the left.
The arteries course over the heart’s surface and then dive down through the muscle layers. The vasculature is notable for numerous collaterals connecting adjacent arteries and also for the presence of precapillary sphincters .

5. 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 5

6. Regulation At rest, the coronary circulation receives 5% of CO.
Cardiac muscle extracts 70% of available O2 from blood, and it has a very low capacity for anaerobic metabolism, much like the brain.
This O2 dependence means that any increase in work must be matched by an increase in coronary flow, achieved entirely through local control mechanisms.

7. Local controls:
Coronary resistance vessels are exceptionally sensitive to adenosine. Local control mechanisms allow for a fourfold to fivefold increase in coronary flow when CO increases, a phenomenon called coronary reserve.
2. Central controls:
Coronary resistance vessels are innervated by both branches of the ANS, but their influence is overridden by local controls.

8. Coronary Circulation
Right and left coronary arteries 8

9. External Heart: Anterior View

10. External Heart: Posterior View

11. Coronary Circulation: Arterial Supply

12. Coronary Circulation: Venous Supply

14. Coronary reserv

15. Precapillary sphincters
Precapillary sphincters comprise single smooth muscle cells wrapped around the inlets to individual capillaries . They contract and relax with changes in local metabolite concentrations and function as on/off switches to capillary flow.

16. When CO is minimal, most sphincters are contracted (“off”), and flow is inhibited. They relax intermittently
as local metabolite levels rise but again contract when the increased flow washes the metabolites away.
At rest, only a small proportion (20%) of sphincters is relaxed, and capillaries are actively perfused, but the pattern of capillary flow shifts continually (vasomotion).
When cardiac workload increases, levels of metabolic waste products rise, and the sphincters spend a much greater percentage of time in the “on” position. At maximal levels of CO, all sphincters are open all the time, and coronary flow rises to maximal levels also.

17. Vasomotion and basis of coronary reserve

18. Extravascular compression
Blood flow through most systemic vascular beds follows the aortic pressure curve, rising during systole and falling during diastole.
Flow through the left coronary artery drops sharply during systole and then rises sharply with the onset of diastole. This unique flow pattern occurs because ventricular myocytes collapse the arterial supply vessels as they contract (extravascular compression).
The effect is felt strongest during early systole because aortic pressure, the main force maintaining vascular patency, is at a low point. During diastole, the compressive forces are removed, and blood surges through the musculature at peak rates.

19. Left coronary blood flow.

20. 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 20

21. Extravascular compression in the left ventricular wall
Extravascular compression in the left ventricular wall. LV= left ventricle; P= pressure.

23. 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 23

24. Aort kapağı
Sol koroner arter
Sağ koroner arter

25. 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 25

26. Nervous Control of Coronary Blood Flow
Autonomic nerves can affect the CBF both directly and indirectly
Direct stimulation of coronary blood vessels
Indirect effects result from secondary changes in CBF caused by increased or decreased activity of the heart
Direct effects of nervous stimuli on coronary vasculature
Parasympathetic fiber distribution is not great
There is more sympathetic innervation of coronary vessels
Constrictor receptors are alpha adrenoreceptors (more epicardial)
Beta receptors are vasodilatory (more in the intramuscular arteries) 26

27. 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 27

28. 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 28

29. 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 29

30. 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 ( micrometre in diameter)
This collateral circulation may delay appearance of ischemic heart symptoms 30

31. Collaterals:
Collaterals are vessels that connect adjacent arterioles. They are usually constricted in a healthy heart, but, if a supply vessel becomes occluded, they dilate in response to rising metabolite levels.
Flow through collaterals may prevent infarction if the occluded vessel is small. In time, these channels enlarge to provide near-normal flow to the ischemic area.

32. Flow interruption
Because the ventricular myocytes extract such high levels of O2 from the blood, a delicate balance exists between myocardial workload and coronary supply. If the balance is disturbed, then myocytes become
ischemic and infarcted. Most commonly, this occurs due to atherosclerosis and coronary artery disease.

33. Atherosclerosis:
Atherosclerotic lesions appear at an early age in the populations of most Western countries. They evolve to become complex plaques of lipids, hypertrophied myocytes, and fibrous material. Plaques enlarge at the expense of the vascular lumen and impair blood fl ow. This causes an imbalance between coronary supply and myocardial demand, resulting in ischemia.
Ischemic myocytes release large quantities of vasoactive compounds, such as adenosine, but vasodilators have no effect on plaque.
As the O2 deficit continues, the myocytes release lactic acid, which stimulates pain fibers within the myocardium and causes angina pectoris.

41. Coronary angiography

42. Coronary angioplasty

43. 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 43

44. Acute Myocardial Infarction
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

45. 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 45

46. 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 46

47. Causes of Death After Coronary Occlusion
1) Decreased cardiac output (Systolic stretch and cardiac shock) 47

48. 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 48

49. 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 49

50. 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 50

51. 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 51

52. Prolonged ischemia of the heart leads to myocardial infarction
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

53. 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 53

54. 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 54

55. Surgical treatment of coronary disease
Coronary angiography
Coronary angioplasty
Aortic coronary bypass surgery 55