Archive for the ‘ L1-Physio Coronary Circulation ’ Category

L1- Physiology of Coronary Circulation

HEART

-70ml/beat, 7200 l/day

-35 million beats /year, 2.5 billion beats/life

The work of the heart in one life is equivalent to lifting 30 tons to the Mount Everest

Myocardial O2 Demand

• The cardiac muscle always depends on aerobic oxidation of substrates even during heavy exercise

•Therefore, The cardiac muscle has the highest O2 uptake (VO2) compared to other tissues of the body(12-15 volume%; 7-9mlO2/100gm/min)

•This is achieved by a dense network of capillaries, all is perfused at rest (no capillary reserve)

& by maximal extraction of O2 from RBCs (almost no O2 extraction reserve)

What determines Myocardial O2 Demand?

•The direct factor is Left Ventricular Work (ventricular contraction to eject blood)

•VO2 is increased by an ↑ in;

1.Afterload

2.Contractility

3.Heart rate

4.Preload*

How this affects Coronary blood flow?

•The fact that there is no O2 reserve for cardiac muscle makes the increase in blood flow is the alternative for an extra need for O2

•Thus, any restriction in flow → increased risk of tissue damage

•The increased flow is due to functional hyperaemia which explains the major role of local metabolic factors in regulating coronary circulation

Physiological Anatomy of Coronary Circulation

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•Coronary Blood flow is provided by Lt. & Rh coronary arteries originating from root of aorta behind the aortic cusps

•These 2 large arteries give rise to

Large Epicardial Coronary Arteries (EPCA) encircling the surface of heart

Intramyocardial Coronary Arteries (IMCA) penetrating into deeper layers of heart

•The Coronary arterial tree gives rise to millions of capillary blood vessels that nourish the myocardium.

•The coronary arteries are having small anastomotic connections (end arteries)

•Therefore, risk of tissue damage is greater if arterial occlusion occurs.

Coronary Venous drainage:

– Coronary sinus draining ~90% of Lt ventricle into Rh atrium

– The bsian veins +arterioluminal veins draining rest of myocardium into all cardiac chambers

•Lt CA (6/7 of flow)

-Supplies Lt ventricle, Lt atrium & anterior part of septum

Rh CA (1/7 of flow):

-supplies Rh atrium, ventricle, post.part of septum.

Picture2

Coronary Arterial Tree

Picture3

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Special Features of Coronary Circulation

-At rest, Coronary BF

= 5% of CO

=250ml/min

=60-80ml/100gm/min

-During exercise ↑ by 3-4 times (coronary vasculature has a high vasodilator reserve capacity)

Coronary Bl. Flow is Phasic

•Total Coronary flow is greater during diastole

•Therefore, The most crucial factors for perfusing coronary arteries are

  1. aortic pressure
  2. duration of diastole

•An ↑in HR, with diseased CA, will shorten diastolic period & CBF → anginal pain

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•The lowest coronary flow (even retrograde flow may occur) occurs during isometric contraction phase (systole)

•The greatest flow occurs during isometric relaxation phase (the only circulation in which flow occurs during diastole)

•Perfusion of arteries supplying Rh ventricle is less affected by contracting myocardium because tension developed in Rh ventricle is always lower than that in Lt ventricle

Picture8

•The myocardial cells contain large amounts of myoglobin; a pigment that can carry O2 acting as O2 store

•It is saturated with O2 at very low O2 tension

•Releases its O2 during systole when blood flow is reduced thus ensuring continuous supply of O2 to myocardium

Regulation of Coronary Circulation

  1. Intrinsic; (Local Regulatory)
  2. Extrinsic; Neuro-Humoral Control

I- Intrinsic Regulation (Metabolic)

The marked increase in coronary blood flow following an occlusion of coronary flow led to the concept that:

•A metabolic link exists between myocardial O2 demand and the level of coronary blood flow

•Thus,

↑O2 demand →↑Bl.Flow

↓O2 demand→ ↓flow

Picture9

This Metabolic link may be:

•Hypoxia itself has a direct relaxant effect

•Or hypoxia leads to release of:

  1. Adenosine; a degradation product of AMP, accumulated
  2. Lactate & H+
  3. PG I2

All come to stimulate Nitric oxide (atherosclerosis) release from endothelium leading to vasodilatation → ↑CBF

Mediators of Intrinsic Local Regulation of C.Bl. Flow

•Adenosine is the most important VD metabolite linking O2 supply with O2 demand in cardiac muscle

•It is formed from dephosphorylation of AMP, the product of hydrolysis of ATP & ADP

•Its formation ↑during hypoxia & ↑O2 consumption

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•Thus, in coronary circulation, the metabolic theory of intrinsic regulation is the dominant whereas in cerebral circulation both the myogenic & metabolic interplay to  autoregulate cerebral blood flow

II- Extrinsic Regulation

Nervous

1- Sympathetic stimulation

Direct Effect:

α1-adrenorecptor mediated VC

β2-adrenoreceptor-mediated mild VD

Indirect:

β1mediated ↑ HR → ↑metabolic activity → accumulation of vasodilator metabolites → VD

The Net Effect:  VasoDilation → ↑ Coronary Bl. Flow

2- Parasympathetic stimulation

Direct

cholinergic mediated moderate VD → ↑Coronary Bl. Flow

Indirect

↓HR → ↓metabolic activity → ↓O2 demand → ↓coronary Bl.Flow

The net result is VC → ↓coronary Bl.Flow

3- Anrep’s Reflex

•↑VR → atrial stretch → vagal stimulation → coronary VD → ↑CBF

•Important during muscle exercise

4- Gastro-coronary Reflex

Heavy meals → gastric distension → reflex coronary VC → ↓CBF

•Anginal Pain may be related to eating heavy meal

Hormonal

•Norepinephrine, Epinephrine, thyroxin → coronary dilation

•Angiotensin & vasopression → coronary constriction.

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