Properties of Special Circulation Flashcards

1
Q

Describe the structure of the coronary circulation.

A
  • Two coronary arteries originate from the left side of the heart, at the root of the aorta, just as it exits the ventricle.
  • Cardiac veins carry blood with a poor level of oxygen from the myocardium to the right atrium.
  • Most of the blood in the coronary veins returns through the coronary sinus.
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2
Q

Describe the special requirements and the special structural features of the coronary circulation.

A
  • SPECIAL REQUIREMENTS: -
    • needs a high basal supply of O2 (20 times as much as resting skeletal muscle)
    • increased O2 supply in proportion to increased demand / cardiac work
  • SPECIAL STRUCTURAL FEATURES: -
    • high capillary and fibre density
    • large surface area for O2 transfer
    • Both of the structural features give rise to shorter diffusion distances. Diffusion time is proportional to distance2 so O2 transport is fast.
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3
Q

Describe the special functional features of the coronary circulation (during normal activity and during increased demand).

A
  • DURING NORMAL ACTIVITY: -
    • high blood flow (10 times the flow per weight as compared to the rest of the body)
    • relatively sparse sympathetic innervation
    • high NO released, leading to vasodilation
    • high O2 extraction (75%) - the average of the body is 25%.
  • DURING INCREASED DEMAND: -
    • the coronary blood flow increases in proportion to demand
    • the production of vasodilators (adenosine, K+, acidosis) out-compete the relatively low sympathetic vasoconstriction
    • circulating adrenaline also dilates coronary vessels due to the abundance of β2-adrenoreceptors (adrenaline is usually a vasoconstricter acting on alpha-1 but remember in coronary arteries and skeletal muscles due to increased abundance of beta-2 receptors they cause vasodilation).
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4
Q

Describe how 75% of the oxygen is unloaded to the myocardium during normal activity (Bohr shift).

A
  • The coronary sinus blood returning to the right atrium from the myocardial tissue has a greater carbon dioxide content due to the high capillary density, high surface area and small diffusion difference.
  • The high CO2 and low pH (so more H+ due to carbonic acid) shifts the oxygen dissociation curve to the right.
  • This means that the haemoglobin has less affinity for the oxygen, and more O2 is given up to the myocardial tissue.
  • Thus, the myocardium is able to extract 75% of the oxygen as opposed to the typical 25% in other tissues.
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5
Q

Why can an increased O2 demand not rely on the increase of O2 extraction?

A
  • Extraction is already near the max in cardiac muscle during normal activity.
  • Therefore, to provide more O2 during demand, we must increase BLOOD FLOW.
  • Myocardium metabolism generates metabolites to produce vasodilation and increase blood flow (myocardium hyperaemia).
  • Examples include adenosine, produced by ATP metabolism.
  • Others include increases in pCO2, H+ and K+ levels.
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6
Q

Human coronary arteries are functional end-arteries. Describe how this can contribute to ischaemic heart disease.

A
  • (An end artery is an artery that is the only supply of oxygenated blood to a portion of tissue. The blockage of one coronary artery generally results in death of the heart tissue due to lack of sufficient blood supply from the other branch.).
  • Coronary arteries are functional end-arteries, and therefore, decreased perfusion can produce major problems.
  • It means that the heart is very susceptible to sudden or slow obstruction.
    • SUDDEN: can be due to acute thrombosis, producing a myocardial infarction.
    • SLOW: can be caused by an atheroma (sub-endothelium lipid plaques), causing the chronic narrowing of the lumen, producing angina. Heart systole also obstructs blood flow.
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7
Q

What are some of the effects of thrombosis in coronary vessels on the heart?

A
  • eg. total occlusion of left anterior descending coronary artery
  • Occlusion leading to obstruction of blood flow to anterior (front) left ventricle – myocardial infarction
    • ischemic tissue, acidosis, pain (stimulation of nociceptive C-fibres that cause excessive pain)
    • impaired contractility
    • sympathetic activation
    • arrhythmias - as the affected part of the heart does not conduct electrical activity properly.
    • cell death (necrosis)
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8
Q

What is an angiography?

A

Radiography of blood or lymph vessels, carried out after injection of a radiopaque substance into the vessels.

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9
Q

Describe how angina can be a problem during increased activity.

A
  • In a normal heart, the resistance is low in the large coronary artery, and high in the arterioles.
  • During exercise, metabolic vasodilation of the arterioles reduces the total resistance.
  • This means that there is increased blood flow to meet the increased O2 demands.
  • In a heart with an angina, there is stenosis in the large coronary artery, increasing the resistance.
  • This means that metabolic hyperaemia (the increased blood flow that occurs when tissue is active) occurs at rest, so that the blood flow meets the O2 needs.
  • During exercise, arterioles will further dilate to reduce resistance, but the total resistance is still too high to dominate the stenosis.
  • This means that the O2 demand cannot be met, and angina develops.
  • Can lead to the activation of the nociceptive C fibres leading to pain.
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10
Q

We know that coronary blood flow is obstructed during systole. List some other mechanical factors that will reduce coronary flow.

A
  • Blood only able to pass through the heart in diastole. Ventricle relaxes so aortic pressure > ventricular pressure so blood moves from aorta and around the heart.
  • Mechanical factors reduce coronary flow:-
    • shortening of diastole (eg. high heart rate)
    • increased ventricular end-diastolic pressure (eg. heart failure)
    • reduced diastolic arterial pressure (eg. hypotension, aortic regurgitation)

[In most tissues, blood flow peaks during ventricular systole due to increased pressure in the aorta and its distal branches. Flow through the coronary vessels, however, is seemingly paradoxical and peaks during ventricular diastole. This unusual pattern is a result of external compression of coronary vessels by myocardial tissue during systole. When the ventricles relax during diastole, the coronary vessels are no longer compressed, and normal blood flow resumes.]

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11
Q

List some special properties of cutaneous circulation (skin circulation).

A
  • defence against the environment
  • Lewis triple response to trauma (increased blood flow)
  • temperature regulation
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12
Q

Describe special structural features of cutaneous circulation.

A
  • ARTERIO-VENOUS ANASTOMOSES (AVAs):
    • They are direct connections of arterioles and venules which exposes the blood to regions of high surface area.
    • This serves as a way to reduce body heat, etc.

This is done by:-

  • SYMPATHETIC VASOCONSTRICTOR FIBRES:
    • They release NA, acting on α1-adrenoreceptors.
  • SUDOMOTOR (anything that stimulates the sweat glands) VASODILATOR FIBRES:
    • There is acetylcholine acting on the endothelium to produce NO.
    • This is driven by temperature regulation nerves in the hypothalamus.
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13
Q

Describe the effect of cold ambient temperature on the skin blood flow.

A
  • In the beginning, there is COLD-INDUCED VASOCONSTRICTION.
  • This allows the body to conserve heat.
  • Sympathetic nerves react to local cold by releasing noradrenaline, which binds to local α2-adrenoreceptors on vascular smooth muscle in the skin.
  • They bind NA at lower temperatures than α1-adrenoreceptors.
  • After some time, there is PARADOXICAL COLD VASODILATATION.
  • This is caused by paralysis of sympathetic transmission.
  • Long-term exposure can lead to oscillations of contract/relax.

(So prolonged cold on the skin. If you hold your hand in ice water, it eventually goes red….this is because of paradoxical cold vasodilatation.)

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14
Q

How does increased core temperature (caused by exercise, etc) affect cutaneous circulation?

A
  • There is increased cutaneous perfusion with increased core temperatures.
  • Increased core temperatures stimulate warmth receptors in the anterior hypothalamus.
  • This causes: -
    • SWEATING caused by increased sympathetic activity to sweat glands, mediated by acetylcholine (vasodilation).
    • VASODILATATION caused by increased sympathetic sudomotor activity, such that acetylcholine acts on the endothelium to produce NO, which dilates the arterioles in extremities.
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15
Q

List some other functional specialisations of the cutaneous circulation.

A
  • BAROREFLEX/RAAS/ADH-STIMULATED VASOCONSTRICTION OF SKIN BLOOD VESSELS:-
    • The blood is directed to more important organs/tissues during the loss of blood pressure following haemorrhage, sepsis, acute cardiac failure, etc.
    • This response is mediated by sympathetic vasoconstrictor fibres, adrenaline, vasopressin and angiotensin II.
    • It is responsible for the pale, cold skin of a patient in shock.
  • EMOTIONAL COMMUNICATION :-
    • For example, blushing (sympathetic sudomotor nerves)
  • RESPONSE TO SKIN INJURY :-
    • The Lewis triple response
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16
Q

Describe the sequence of events that leads to the expression of the Lewis triple response.

A
  • There is a trauma on the skin.
  • This is recognised by C fibres (nociceptive afferent fibres); C fibre axon reflex mediates the flare to trauma.
  • C fibre (nociceptive afferent) goes to spinal cord to brain. Collateral axons of nociceptive afferent can also fire to produce a local response. Axon collateral releases substance P to degranulate mast cells to release histamine.
  • Histamine dilates vessels in the skin to send more immune cells there.
  • This accounts for the triple response.
  • The triple response is: -
    • local redness at the site
    • local swelling (wheal)
    • a spreading flare
17
Q

Due to the complexity of the cutaneous circulation, there are instances where special problems can arise. Describe some of these problems.

A
  • PROLONGED OBSTRUCTION OF FLOW BY COMPRESSION:
    • This is severe tissue necrosis.
    • It’s found mostly at the heels, buttocks and other weight-bearing areas.
    • It can be avoided by shifting position.
  • POSTURAL HYPOTENSION / OEDEMA DUE TO GRAVITY:
    • Often, standing for long periods of time in hot weather will decrease the central venous pressure (hypotension) and increase the capillary permeability (oedema).
    • This causes you to feel faint.