You are on page 1of 52

Circulation

Coronary Circulation & IHD

Coronary Circulation & IHD


The normal and pathological physiology of the Coronary circulation is one of the most important subjects in medicine.

Coronary Arteries

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 chambers of the heart.
4

Coronary Arteries
The Right & the Left Coronary arteries arise at the root of the Aorta, from the two Aortic sinuses just above the Aortic valve.

Coronary Arteries
The Left Coronary artery supplies the anterior and left lateral portions of the heart

Coronary Arteries
The Right Coronary artery supplies: Most of the Right Ventricle as well as Most of the posterior part of the Left Ventricle.
7

Cardiac Veins
Most of the Coronary venous blood from the Left Ventricle returns to the Right Atrium by way of the Coronary sinus (about 75 % of the total venous return)

Cardiac Veins
The remaining 25 % 30 % of the blood returns through two different pathways;

Cardiac Veins
Most of the coronary venous blood from the right ventricle returns by the small Anterior Cardiac veins directly to the Right Atrium.

10

Cardiac Veins
The rest returns directly to the various chambers of the heart through the various small Thebesian veins.

11

Phasic Coronary Blood Flow During Cardiac Cycle

12

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.

13

Blood Supply At The Different Levels Of The Myocardium


The squeeze is the maximum in the subendocardial layer. The squeeze is the least in the epicardial layer of the myocardium.

14

Blood Supply At The Different Levels Of The Myocardium

Intramural vessels

15

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.
16

Blood Supply At The Different Levels Of The Myocardium


The subendocardial layer of the myocardium: Always repolarizes last, even in health, causing an upright T wave. Most susceptible to infarction

17

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)
18

Control Of Coronary Blood Flow


Sympathetic supply Epicardial vessels have mostly receptors. Intramural arteries have mostly receptors.

19

Control Of Coronary Blood Flow


Sympathetic supply Hence, there is a greater possibility of sympathetic stimulation causing vasoconstriction. However, the local metabolic factors always have an overriding effect

20

Cardiac Muscle Metabolism


Under resting conditions Cardiac tissues get about 225 ml of blood; about 5 % of the Cardiac output. Under resting conditions, 70 - 80 % of O2 is extracted from the blood flowing in the Coronary arteries. Hence during times of extra needs, the increase in blood flow is the prime means of meeting the increased demands.
21

Cardiac Muscle Metabolism


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 of lactic acid are liberated.

22

Cardiac Muscle Metabolism


95 % of the energy derived thus is used for the synthesis of ATP. The energy stored in the ATP is used for muscle contraction. The ATP is broken down to ADP AMP Adenosine Adenosine is reabsorbed and reutilized.
23

Cardiac Muscle Metabolism


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 of 2 % per hour.

24

Ischemic Heart Disease


Most common cause of deaths in the Western Culture 35 % of the people in the USA die suddenly as a result of Acute Coronary occlusion or Fibrillation of the Heart. Others die as a result of progressive weakening of the pumping mechanism of the Heart

25

Ischemic Heart Disease


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.

26

Ischemic Heart Disease


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).

27

Ischemic Heart Disease


Soon the atheromatous plaques protrude into the lumen of the artery and cause a degree of occlusion. This causes slowing of the blood flow.

28

Ischemic Heart Disease


If the surface endothelium gets eroded, platelets get deposited on the rough surface laid bare Thrombus formation. Occasionally, muscular spasm at the edge of the atheromatous plaque may result in Secondary Thrombus formation.

29

Ischemic Heart Disease


Soon the thrombus may break off and head downstream Embolus formation. The embolus may go and lodge at the opening of the distal branch of the artery.

30

Ischemic Heart Disease


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.

31

Collateral Circulation
In the normal heart, there are communications between the smaller branches of the Coronaries.

32

Collateral Circulation
When sudden occlusion occurs in one of the larger Coronary arteries, the small anastomoses dilate and compensate for the loss of blood supply.
33

Collateral Circulation
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.

34

Collateral Circulation
In larger ischemic areas or where the collaterals do not or cannot compensate the loss, there is death of the myocardium Myocardial infarction.

35

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.

36

Myocardial Infarction
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.

37

Myocardial Infarction
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.

38

Myocardial Infarction
Normal resting cardiac muscle is supplied 8 ml of O2 / 100 gms of muscle / min. For survival, the myocardial cell needs just 1.3 ml of O2 / 100 gms of muscle / min. (15 30 % of the normal resting supply)

39

Myocardial Infarction
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.

40

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

41

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.
42

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.

43

Fibrillation Of The Heart


Causes of Ventricular Fibrillation:
(in the first 10 mins or during the 2nd hour onwards).

Rapid depletion of intracellular K+ ions. Ischemic part can generate abnormal impulses (Current of Injury). Powerful Sympathetic stimulation. Cardiac muscle weakness resulting in dilatation of the heart Circus movement.
44

Circus Movement

45

Initiation & Propagation Of Fibrillation

46

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 right atrium.

47

Stage Of Recovery From Acute Myocardial Infarction

48

Pain In Coronary Disease


Pain is felt due to increased levels of: Lactic Acid Histamine Kinins Proteolytic enzymes Which stimulate the nerve endings of the cardiac muscle.
49

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.

50

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.

51

Angina Pectoris
Treatment: Rest Oxygen Vasodilator drugs (Nitroglycerine) Beta blocker (Propranolol) Surgical treatment (Aortic Coronary Bypass, Coronary angioplasty)
52