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.

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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
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4
Q

Describe how 75% of the oxygen is unloaded to the myocardium during normal activity.

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 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

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
  • ischaemic tissue, acidosis, pain (stimulation of C-fibres)
  • impaired contractility
  • sympathetic activation (causing constriction)
  • arrhythmias
  • cell death (necrosis)
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8
Q

Describe how atheroma 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 atheroma, there is stenosis in the large coronary artery, increasing the resistance. This means that metabolic hyperaemia 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.

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9
Q

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

A
  • shortening of diastole (eg. high heart rate)
  • increased ventricular end-diastolic pressure (eg. heart failure)
  • reduced diastolic arterial pressure (eg. hypotension, aortic regurgitation)
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10
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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11
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.

SYMPATHETIC VASOCONSTRICTOR FIBRES:
They release NA, acting on α1-adrenoreceptors.

SUDOMOTOR 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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12
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.

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13
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
- 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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14
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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15
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.
There is an increased delivery of immune cells and antibodies to the site of damage to deal with the invading pathogens, so the axon reflex caused mast cell degranulation, which releases histamine at the site of trauma. This accounts for the triple response.

The triple response is:

  • local redness at the site
  • local swelling
  • a spreading flare
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16
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.

17
Q

What is a Pressure Sore?

A

O2/nutrients so close but diffusion is too slow