Pressures and Flows in the Systemic Circulation Flashcards
Define systolic blood pressure
The pressure exerted against the arterial wall during ventricular systole
Measured at the point where the pulse sound is first heard where the sphygmomanometer pressure is reduced from starting pressure (usually around 180mmHg)
Define diastolic blood pressure
The pressure being exerted against the arterial wall during ventricular diastole
Measured at the point at which the pulse disappears
Define mean arterial pressure
How is it calculated?
The average arterial pressure during one cardiac cycle
Calculated by:
- MAP = SBP + 2(DBP) / 3
What are baroreceptors?
What are the different types?
Where are the most important ones located?
Receptors that detect stretch within blood vessels
Located throughout vascular tree
2 types:
- High pressure= arterial
- Low pressure= venous and right side of heart
Most important ones located in the carotid sinus and the aortic arch
Describe the mechanism of action of arterial baroreceptors
What is their role?
Continuous feedback loop
Continuously fire with arterial stretch during ventricular systole
Vital role to compensate in sudden reduction in blood pressure:
- Decreased BP causes decreased firing rate
- Reflex via medulla acts to increase BP by:
- Increased sympathetic activity:
- Increases cardiac output and systemic vascular resistance
- Decrease vagal activity:
- Increases cardiac output
- Increased sympathetic activity:
Describe the mechanism of action of venous baroreceptors
Where are they found?
Unresponsive to arterial baroreceptors
Predominantly in atria, ventricles and pulmonary arteries
Respond to volume changes and cause either vasoconstriction or vasodilation
- Increased volume = vasodilation
- Causes increased renal excretion by inhibiting release of ADH from posterior pituitary and reduces renal sympathetic outflow
What are chemoreceptors?
Receptors stimulated by a change in their immediate environment. Stimulated by:
- Hypoxia
- Hypercapnia
- pH change
Causes increased sympathetic stimulation of heart and peripheral vasculature via medullary centres to increase cardiac output and blood pressure.
Affect the respiratory and cardiovascular system
Why does pulse pressure increase moving peripherally from the aorta to the arteries?
Increasing vessel wall rigidity
Aorta has high elasticity so can absorb some of the pressure frm ventricular systole without increasing aortic pressure.
How can veins respond to rapid alterations in blood volume?
How do they alter cardiac output?
Can accommodate up to 25% blood loss by venoconstriction
Can accommodate up to 500ml rapid infusion by venodilation
Modify cardiac output by modifying venous return
What provides resistance to venous flow?
Fixed structures such as first rib, the neck (subject to atmospheric pressure which is higher than venous)
What does local perfusion control?
Delivery of oxygen to tissues
Delivery of nutrients, e.g. glucose, amino acids, fatty acids
Removal of CO2 from tissues
Removal of H+ from tissues
Maintenance of appropriate ion concentrations in tissues
Transport of hormones e.t.c to tissues
Which acute mechanisms control local perfusion?
Vasodilation: from either hypoxia or vasodilators released.
Nutrient deficiencies
Vasoconstriction: from either myogenic mechanism (stretch placed on vessel wall induces constriction) or metabolic theory (high blood pressure washes away vasodilator substances)
Nitric Oxide: released by endothelial cells in response to stress of extra blood flow. Activates cGMP-dependent protein kinase which causes vasodilation.
- Stress on small arterioles initiates release of NO from larger vessels upstream to ensure adequate perfusion to match increased demand.
Endothelin: causes local vasoconstriction, released from damaged endothelium. Prevents blood loss
What is chronic local control?
Control of the amount of blood vessels supplying a tissue
Which mechanisms control chronic local perfusion?
Lack of oxygen in tissues causes release of angiogenic growth factors which stimulate increased vascularity to a level which is adequate for tissue requirement.
Describe neural blood pressure control
Afferents to vasomotor centres in medulla:
- Direct stimulation: CO2, hypoxia
- Excitatory inputs:
- Pain pathways and muscles
- Carotid and aortic chemoreceptors
- Cortex via hypothalamus
- Inhibitory inputs:
- Lungs
- Carotid, aortic and cardiopulmonary chemoreceptors
- Cortex via hypothalamus
What type of nerves innervate blood vessels?
Cholinergic: fibres travel with sympathetic nerves
- Vasodilators: no constant tone
Noradrenergic: on all vessels
- Vasoconstrictors: constant tone
What does sympathetic innervation to the cardiac muscle cause?
Positive ionotropy and postitive chronotropy
(Increases speed and force of contraction of the heart muscle)
(In constant opposition with vagal innervation)
How do sympathetic and parasympathetic nerves control BP?
- Adrenalin and noradrenalin
- Secreted by sympathetic nerves which also stimulate their release from the adrenal medulla (control with both local and systemic secretion)
- Noradrenaline= vasoconstriction
- Adrenaline= vasoconstriction and can also vasodilate, e.g. coronary arteries.
Which hormones are involved in the control of blood pressure?
- Atrial natriuretic peptide
- Anti-diuretic hormone
- Adrenalin and noradrenalin
- Kinins
- Renin-angiotensin system
How does the renin-angiotensin system affect BP?
- Renin-angiotensin system
- Potent vasoconstrictor at arterial level
- Increases total peripheral resistance
- Constricts renal afferent and efferent arterioles reducing renal blood flow and increasing sodium and water retention
- Stimulates ADH secretion
- Increases thirst
How does anti-diuretic hormone (vasopressin) affect BP?
- Synthesised in hypothalamus and released from posterior pituitary in response to afferent baroreceptor stimulus.
- Potent vasoconstrictor
- Can reduce renal blood flow and GFR
- Increases water permeability of the collecting duct luminal membrane by inserting protein channels for water reabsorption.
How does histamine affect BP?
Released from mast cells
Potent vasodilator
Can cause oedema
How do kinins affect blood pressure?
What are they activated and inactivated by?
Kallikrien: activated by tissue inflammation or maceration. Acts on alpha2 globulins to produce Kallidin which is modified to produce bradykinin.
- Inhibited by kallikrien inhibitor
Bradykinin is a vasodilator and increases vascular permeability
- Inactivated by carboxypeptidase
How does atrial natriuretic hormone affect blood pressure?
Activation of stretch receptors in cardiac muscle cells causes release of ANP.
Causes renal excretion of sodium and water
Increases GFR by dilating afferent and constricting efferent arterioles
Inhibits renin secretion and aldosterone release.
Which factors cause vasoconstriction?
- Local factors:
- Low temperature
- Autoregulation
- Local hormones:
- Endothelin
- Serotonin
- Circulating hormones:
- Noradrenaline
- Adrenaline
- Angotensin II
- Neuropeptide Y
- Vasopressin
- Neural control:
- Increased noradrenergic vasomotor stimulation
Which factors cause vasodilation?
- Local factors:
- CO2
- Hypoxia
- Potassium
- Adenosine
- Lactate
- Increased temp
- Decreased pH
- Local hormones:
- Nitric oxide
- Kinins
- Circulating hormones:
- Atrial natriuretic peptide
- Substance P
- Histamine
- VIP
- Adrenaline in skeletal muscle and liver
- Neural factors:
- Decreased noradrenergic vasomotor stimulation
- Activation of cholinergic discharge dilator fibres to skeletal muscle
