Pressure and flows in the systemic circulation Flashcards
Define systolic BP and how it is measured
Systolic BP refers to the pressure being exerted on the arterial wall during ventricular systole.
Measured at the point when first pulse sound is heard as pressure is released from approx. 180mmHg
Define diastolic BP and how it is measured
Diastolic BP refers to the pressure being exerted on the arterial wall during ventricular diastole.
Measured when pulse sounds can no longer be heard as pressure is released.
Define mean blood pressure and how it is calculated
The average arterial pressure during one cardiac cycle.
MAP = SBP + 2DBP /3
What is the function of baroreceptors?
Baroreceptors are pressure receptors located throughout the vascular tree that detect stretch within blood vessels.
Receptors in the arterial tree detect high pressure whilst receptors in the venous tree and right atrium detect low pressure.
[Most important arterial receptors found in the carotid sinus and in the aortic arch]
What is the function of chemoreceptors and where are they found?
Chemoreceptors respond to changes in the environment in which they are located (e.g. hypoxia, hypercapnia or pH changes)
Oxygen receptors are found in the carotid body and decreased oxygen levels cause hyperventilation and vasodilation.
Carbon dioxide receptors are found in the medulla and decreased CO2 levels cause hypoventilation and vasoconstriction.
Describe how pressure changes as it moves along vascular tree
Increased pressure in the systemic circulation (with fluctuations). This pressure starts to decline significantly as it enters into arterioles and then into the venous system.
Slight increase in pressure as blood enters the right side of the heart and leaves via the pulmonary arteries and arterioles before decreasing as it passes through capillaries, venules and the pulmonary veins before entering the left side of the heart.
What factors influence how blood flows through your veins?
- Valves prevent back flow
- Fixed obstructions provide resistance (e.g. 1st rib)
- Local and central factors influencing calibre
How do lymphatics circulate?
Enter by one way valves between endothelial cells
Flow is both passive and peristaltic (aided by skeletal muscle contraction)
Bacteria removed as fluid travels through lymph nodes
What mechanisms are involved in the control of BP?
Hormonal control
Nerve innervation
Cardiac innervation
What mechanisms are involved in the control of acute local perfusion?
Changes in diameter of valves in arteries or capillaries:
Vasodilation:
- Vasodilator substance theory (release of vasodilators from hypoxic tissue e.g. ADP)
- Oxygen demand theory (relaxation of muscles due to surrounding hypoxic tissue)
- Stress of extra blood flow through vessels causes the release of Nitric Oxide which results in activation of cGMP-dependent protein kinase which causes vasodilation.
Vasoconstriction:
1. Endothelin - vasoconstrictor released from damaged endothelium to prevent excessive blood loss from traumatised vessels
What mechanisms are involved in the control of chronic local perfusion?
An increase or decrease in the number of blood vessels supplying the tissue.
Lack of oxygen/ nutrients in tissues causes release of angiogenic growth factors which stimulate increased tissue vascularity to match tissue requirement.
What impact does sepsis have on the cardiovascular system?
- Hyperdynamic circulation
- Local factor vasodilation
- Relative hypovolaemia
- Increased tissue oxygen demand
- Decreased cardiovascular supply
How is acute sepsis managed?
The sepsis 6:
- High flow oxygen
- Broad spectrum abx (e.g. ceftriaxone)
- IV fluid
- Blood cultures
- Serum lactate
- Urine output (hourly)
What hormones influence control of BP?
Adrenaline/ Noradrenaline RAAS ADH Atrial Natriuretic Hormone Local mediators Kinins
How does adrenaline and noradrenaline influence BP?
Secreted by sympathetic nerves which also stimulate their release from the adrenal medulla.
Dual control - local and systemic secretion of mediators.
Noradrenaline is a vasoconstrictor.
Adrenaline can be a vasodilator.
What impact does Angiotensin II have on BP?
Vasoconstrictor
Reduces renal blood flow by constricting afferent and efferent arterioles in nephrons(thus increasing sodium and water retention)
Increases thirst and water intake
Stimulates ADH secretion
Inhibits renin secretion (via negative feedback)
How does ADH influence BP?
- Decreased plasma volume detected by baroreceptors which decrease firing in response.
- Decreased baroreceptor firing initiates ADH release from the posterior pituitary.
- ADH increases water permeability in the cortical collecting ducts by inserting aquaporin channels (thus increasing water reabsorption and increasing blood volume)
How does Atrial Natriuretic Hormone influence BP?
Stretch receptors in cardiac atrial cells stimulate the release of ANP which leads to increased renal excretion of sodium and water (thus reducing BP).
Increases filtration pressure in glomerulus (by dilating AA and constricting EA)
Inhibits secretion of renin and therefore release of aldosterone (inhibition of RAAS)
How do local mediators work to control BP?
Histamines - produced in response to allergic tissue inflammation - vasodilator, increases permeability
Ions:
Calcium - vasoconstrictor (due to action on smooth muscle)
Magnesium - vasodilator
H+ and CO2 - vasodilators
What are kinins and what is their relevance in controlling BP?
Small polypeptides split from alpha2-globulins in the plasma or tissue fluids by proteolytic enzymes
Example: Kallikrein
- Kallikrein activated by tissue maceration or inflammation
- Acts on a2-globulins to create Kallidin
- Modified to form bradykinin
- Bradykinin causes arteriolar vasodilation and increases vascular permeability
How do arterial baroreceptors respond to a decrease in arterial pressure?
Baroreceptors are constantly firing with arterial wall stretch during systole.
Sudden drop in pressure causes decreased firing of baroreceptors, this initiates a reflex via the medulla which increases sympathetic activity and decreases vagal (parasympathetic) activity to increase pressure (by increasing cardiac output and systemic vascular resistance, SVR)
How does Aldosterone act to increase BP?
Via RAAS in response to low BP - increases reabsorption of sodium in renal cortical collecting duct
Increases production of proteins in collecting duct (e.g. Na+ and K+ channels)
Increases Na+ reabsorption from gut, sweat and salivary glands (in response to a low BP)
[Increased sodium reabsorption = increased water reabsorption]
Where is the carotid sinus located?
Just superior to the bifurcation of the internal and external carotids (at base of internal carotid)
How does pulse pressure change as blood moves towards the peripheries?
Pulse pressure increases due to increased vessel wall rigidity
Why is control of local perfusion important?
- Delivery of oxygen and nutrients to tissue
- Removal of CO2 and H+ from tissue
- Maintenance of ion concentration
- Transport of hormones/ regulatory substances
How does Nitric Oxide affect perfusion?
Nitric Oxide is a vasodilator, released by endothelial cells in response to sheer stress of extra blood flow.
Works by activating cCMP-dependent protein kinase.
[Stress on arterioles causes release of NO upstream to ensure adequate perfusion to meet metabolic demand]
How does Endothelin affect perfusion?
Endothelin is a vasoconstrictor, released by damaged endothelium to prevent excessive blood loss from traumatised vessels.
How does the nervous system aid blood pressure control?
Afferent fibres to the vasomotor centre
Innervation of blood vessels and the myocardium
Sympathetic stimulation causes positive inotropism and chronotropism
What do inotropic agents do?
Positive inotropic agents increase muscular contraction whilst negative inotropic agents weaken muscular contractions
What is chronotropism?
Interfering with heart rate
[e.g. a positive chronotrope increases HR]
