Properties of Special Circulation Flashcards
What are the 5 special circulations?
→ Cerebral → Pulmonary → Skeletal Muscle → Renal → GI
What are the 3 characteristics to consider with special circulations?
→ Special requirements are met by circulation
→ Special structural or functional features of the circulation
→ Specific problems relating to that circulation
Where do the two coronary arteries originate from?
→ The left side of the heart at the beginning (root) of the aorta just after it exits the left ventricle
Where do cardiac veins carry deoxygenated blood?
→ From the myocardium to the right atrium
Where does most of the blood of the coronary veins return to?
→ Returns through the coronary sinus
What are the special requirements of the coronary circulation?
→ Needs a high basal supply of O2
→ 20 x that of skeletal muscle
- High capillary density
- Large surface area for O2 transfer
- Together these reduce diffusion distance to myocytes….diffusion time is proportional to distance squared – so O2 transport is fast.
Why does the coronary circulation have a high capillary density?
→ Large surface area for O2 transfer
→ Reduces the diffusion distance to the myocytes
→Cardiac muscle contains high numbers of fibres and capillaries
giving rise to shorter diffusion distances.
Skeletal fibre diameter=50um capillaries=400/mm2
Cardiac muscle fibre diameter= 18um
capillaries 3000/mm2
What is diffusion time proportional to?
→ Distance squared
What is the blood flow of the coronary circulation during normal activity?
→ High blood flow
→ x10 of the flow per weight of the rest of the body
What is the sympathetic innervation like in the coronary circulation?
→relatively sparse
What is O2 extraction like during normal activity?
→ High nitric oxide released leading to vasodilatation so:
High O2 extraction 75%
→ average in the body 25%
How does the production of vasodilators change during increased demand?
→ Production of vasodilators out-compete relatively low sympathetic vasoconstriction
Why does adrenaline dilate coronary vessels?
→ Abundance of Beta 2 adrenoreceptors
How is 75% of the oxygen able to be unloaded to the myocardium during normal activity?
→ Coronary sinus blood returning to the right atrium from myocardial tissue has a greater CO2 content due to high capillary density, surface area and small diffusion
→The high CO2 and low pH has shifted the curve to the right
→Hb has less affinity for O2 and more O2 is given up to myocardial tissues.
Increased 2,3 DPG indicates lots of metabolic activity
How does increased O2 requirement produce increased blood flow?
→Extraction is near maximum during normal activity
→ To provide more O2 during demand blood flow must increase
→ Myocardium metabolism generates metabolites to produce vasodilation which increases blood flow eg. Adenosine, produced by ATP metabolism and is released from cardiac myocytes. Also, increases in pCO2, H+, K+ levels.
Describe ischaemic heart disease
→Coronary arteries are functional end-arteries and therefore decreased perfusion produces major problems
→The heart is very susceptible to sudden and slow obstruction
What does sudden ischaemic heart disease produce?
→ acute thrombosis
→ Myocardial infarction
What can lead to slow ischaemic heart disease?
→ Atheroma
→ Chronic narrowing of lumen - produces angina
→ Systole obstructs coronary flow because only diastole that blood moves through the heart
What does occlusion of the Left Anterior Descending Coronary Artery in thrombosis lead to?
→ obstruction of blood flow to anterior left ventricle
What does myocardial infarction lead to?
→Ischemic tissue →Acidosis →Pain (stimulation of C-fibres) →Impaired Contractility →Sympathetic activation →Arrhythmias →Cell death (necrosis)
In a normal heart what is the resistance like?
Resistances are in series - they add together
R=low in large coronary artery R=high in arterioles
During exercise what happens to the resistances in a normal heart?
→Metabolic vasodilation of arterioles
→reduces total R
→Increased blood flow to meet increased O2 demands
→Total R reduced
What is the resistance like in the heart of someone with angina (Resting) ?
→Stenosis in large coronary artery →Increases resistance →Metabolic hyperaemia occurs at rest, so blood flow meets needs R=high in large coronary artery R=low in arterioles
What is the resistance like in the heart of someone with angina (exercise) ?
→During exercise, arterioles further dilate to reduce resistance
→total resistance is still too high due to dominance of stenosis
→O2 demand cannot be met, so angina develops
What are the mechanical factors that reduce coronary flow?
→Shortening diastole
E.g. high heart rate
→Increased ventricular end-diastolic pressure
E.g. heart failure (aortic stenosis, stiffening of ventricle)
The ventricle is not relaxed
→Reduced diastolic arterial pressure
E.g. hypotension
Aortic regurgitation
Reducing diastolic window as result of fast heart rate means less time for perfusing the heart
What are the special properties of cutaneous circulation?
→Defence against the environment
→Lewis triple response to trauma (increased blood flow)
How is temperature regulated?
→Blood flow delivers heat from body core
→Radiation (proportional to skin temperature)
→Conduction to skin – convection from skin (skin temperature)
→Sweating (latent heat of evaporation)
→Skin temperature can rage from 0C to 40C (briefly) without damage
→Poikilothermic rather than homeothermic
What does skin temperature depend on?
Skin blood flow
Ambient temperature
What is the function of Arterio-Venous Anastomoses (AVAs)?
→Direct connections of arterioles and venules expose blood to regions of high surface area
→Convection, conduction, radiation, evaporation
What do sympathetic vasoconstrictor fibres do?
→ Release noradrenaline acting on alpha 1 receptors
Situations to conserve heat- close down capillaries and bypass them through anastomoses and then back through the veins
What do sudomotor vasodilator fibres do and what are they driven by?
→ AcH acting on endothelium to produce NO
→ Driven by temperature regulation nerves in the hypothalamus
What are the special functional features of the cutaneous circulatory system?
→Responsive to ambient and core temperatures
→Help heat loss
→Increased ambient temperature causes vaso- and venodilation
→Help to conserve heat
→Decreased ambient temperature causes vaso- and venoconstriction
What happens in severe cold?
→Severe cold causes “paradoxical cold vasodilation”
→Core temperature receptors in the hypothalamus control sympathetic activity to skin and hence skin blood flow
What is cold-induced vasoconstriction and what is the reason for it?
→Conserve heat
→Sympathetic nerves react to local cold by releasing noradrenaline
→binds to α2 receptors on vascular smooth muscle in the skin
→α2 receptors bind to noradrenaline at lower temperatures than α1 receptors
What is paradoxical cold vasodilation for and what does long term exposure to it cause?
→Protects against skin damage
→Caused by paralysis of sympathetic transmission
→Long-term exposure leads to oscillations of contraction/relaxation
What happens with increased cutaneous perfusion?
→Stimulate warmth receptors in anterior hypothalamus causing :
Sweating
Increased sympathetic activity to sweat glands mediated by acetylcholine
Vasodilation:
Increased sympathetic sudomotor activity such that acetylcholine acts on endothelium to produce NO
NO dilates arterioles in extremities
Where is blood directed to following loss of BP?
Blood directed to more important organs/tissues during loss of BP following haemorrhage, sepsis, acute cardiac failure
What is blood redirection mediated by?
→Mediated by sympathetic vasoconstrictor fibres + adrenaline + vasopressin + angiotensin II
Responsible for pale cold skin of patient in shock.
What happens if you warm up the body quickly during haemorrhage?
→During a haemorrhage, warming up the body too quickly may reduce cutaneous vasoconstriction and be potentially dangerous
→Blood flows to the skin and not to the vital organs
What happens during emotional communication?
Blushing (sympathetic sudomotor nerves)
What happens in response to skin injury?
The Lewis triple response
What are the three stages of the Lewis Triple Response?
→Local redness
Site of trauma
caused by capillary vasodilation.
→Flare, a redness in the surrounding area due to arteriolar dilation mediated by axon reflex.
→Wheal, exudation of extracellular fluid from capillaries and venules due to increased vascular permeability
Increased delivery of immune cells & antibodies to site of damage to deal with invading pathogens
What mediates the flare to trauma?
C-fibre axon reflex mediates the flare to trauma
What happens at the site of damage regarding pathogens?
Increased delivery of immune cells & antibodies to the site of damage to deal with invading pathogens
What happens during prolonged obstruction of flow by compression and how are they avoided?
Severe tissue necrosis
→Bed sores
→Heels, buttocks, weight bearing areas
Avoided by…
Shifting position / turning causing reactive hyperaemia (on removal of compression)
High skin tolerance to ischemia
As soon as you move, those areas will undergo reactive hyperaemia and build of metabolites
What is postural hypotension and what are the symptoms?
→Often standing for long periods in hot weather will decrease central venous pressure (hypotension)
→As well as increased capillary permeability (oedema)
Starling’s law, less stretch, less perfusion to the brain
→You feel faint, rings of fingers can be tighter
When does the blood flow through the heart wall?
When the heart is contracting during systole, blood is not flowing through the cardiac muscle when the heart relaxes, the residual pressure in the aorta will force blood through coronary arteries
What is metabolic hyperaemia?
Active hyperemia is the increase in organ blood flow (hyperemia) that is associated with increased metabolic activity of an organ or tissue
Reactive hyperemia is the transient increase in organ blood flow that occurs following a brief period of ischemia
