Cardiovascular Physiology 5 Flashcards
Imagine an artery splitting into 4 arterioles, how would constriction in one arterioles affect the others?
When vessel B constricts, resistance of B increases and flow through B decreases. Flow diverted from B is divided among the lower resistance vessels A, C and D
What are the other factors affecting blood flow, aside of constriction?
- myogenic control
- active hyperemia
These are 2 local mechanisms
Outline myogenic autoregulation of blood flow- organs
- Increase in blood pressure leads to increased afferent arterioles stretch
- Increased afferent arterioles stretch leads to non-specific cation channels open
- Non-specific cation channels open leads to depolarization
- Depolarization lead to calcium channels to open
- Afferent arteriole contracts as a result of calcium channels opening
Outline how active hyperemia locally regulates blood flow
- Increased tissue metabolism leads to release of metabolic vasodilators into ECF
- Increase release of metabolic vasodilators into ECF cause the arterioles to dilate
- Arteriole dilation decreased resistance
- Decreased resistance leads to increased blood flow
- Increased blood flow cause blood flow to match metabolism
What are the major local factors that contribute to vasodilation to match flow with metabolic demand?
-decreased oxygen, increased carbon dioxide, increased protons, increased potassium
Adenosine and nitric oxide (NO)
Describe the structure of the artery
Thick wall( mean diameter =4 mm)(mean wall thickness= 1 mm)
Increased elastic tissue; ‘compliance’
Describe the structure of the arteriole
Thin diameter( mean diameter= 30 um)(mean wall thickness= 6 um) lots of smooth muscle; major resistance vessels & control blood flow to organs
Describe the structure of a capillary
Leaky epithelium; exchange of nutrients and gases
Describe the structure of a venue
Thin diameter
Describe the structure of a vein
Large diameter(mean= 5 mm), some muscular coating, compliant, sympathetic control
How does ventricular relaxation and contraction affect pressure and direction
Ventricular contraction- ventricle contracts, semilunar valve opens, and aorta and arteries expand and store pressure in elastic walls
Ventricular relaxation- isovolumeric ventricular relaxation occurs, semilunar valve shuts, preventing flow back into ventricle, and elastic recoil of arteries sends blood forward into rest of circulatory system
Why does arterioles pressure fall?
- Arterial pressure does not drop to zero because of arterial compliance
- Pressure drop is greatest at arterioles. This is the site of greatest resistance (60%).
- Pressure drops progressively from capillaries to veins
What is mean arterial pressure?
Is the driving force that keeps the blood moving forward continuously through the blood vessels
MAP= diastolic pressure+ 1/3(systolic -diastolic pressure ) or (pulse pressure)
Fluid flows only if…
If there is a positive pressure gradient
No pressure gradient= no flow
Flow depends on difference(triangle) in P, not absolute P
Explain the mathematical relationship of 🔼 P in cardiovascular flow
Blood flows from high P to low P
Flow inversely proportional to 🔼P/R(resistance )
- R inversely proportional to radius, viscosity & length
Factors affecting blood flow
Blood pressure is recorded as: systolic pressure/diastolic pressure
This varies with CO & peripheral resistance (PR)
CO= SV * HR
Peripheral resistance= 8nl/pir^4 or 1/r^4
n= viscosity l=length r=radius
NB: if the radius of 1cm is doubled, the resistance would decrease 16 fold
What is the relationship of CO and resistance ?
Mean arterial pressure inversely proportional to CO * resistance
What is meant by flow and viscosity?
Flow refers to the distance, a fixed volume of blood travels in a given period of time
Velocity is the measure of how fast blood flows past a point
Velocity of flow is faster in a narrow section & slower in a wider section
-It is inversely proportional to the cross sectional area
What is the relationship between flow and cross sectional area in the cardiovascular system?
As total cross sectional area through arterioles & capillaries increases, flow rate decreases. The reduced flow rate in capillaries is suited for fluid exchanges
How is capillary exchange adapted diffusion, transcytosis and bulk flow ?
Endothelial cell junctions allow water and small dissolved solutes to pass. Also has transocytosis vesicles
Diffusion occurs between endothelial cell junctions
- Diffusion rate of small molecules and gases determined by concentration gradient
- Larger molecules are transported via ‘transcytosis’. Brings large molecules across endothelial cells.
Bulk flow occurs as a balance filtration & absorption. Determined by balance of hydrostatic and colloid osmotic forces. ‘Starling forces’
Describe the application of starling forces
Net pressure= hydrostatic pressure- colloid osmotic pressure
Hydrostatic pressure Pcap forces fluid out of the capillary
Colloid Osmotic pressure of proteins within the capillary pulls fluid into the capillary
Pcap= capillary hydrostatic pressure
pi sign= colloid osmotic pressure
Net flow out of capillaries= 3 L a day
Amount of blood going through an artery a day= 7200 L/day
Explain the effect of starling forces and capillary exchange
Capillary hydrostatic pressure (Pcap) decreases along the length of the capillary from arterial (~32 mm Hg) to venous (15 mm Hg) side
- it is an outward force that favors filtration
- interstitial fluid hydrostatic (Pif) pressure is negligible and considered to be zero
Capillary colloid osmotic pressure (pi sign cap) is produced by the large plasma proteins present in the capillaries which are not present in the ISF.
-it is relatively constant along the length of a capillary
- it is an inward force and favors absorption’s (~25 mm Hg)
- Interstitial Colloid Osmotic pressure (pi cap) pressure is negligible and considered to be zero
NET PRESSURE= (Pcap-Pif)+ (pif-picap)
A net pressure calculation shows net filtration is higher than net absorption, what does this indicate
Excess fluid (~3 liters a day) is lost to into ISF at capillary beds
Excess fluid is returned to cardiovascular systems via the lymphatic system into venous system
What is the relationship between capillaries and lymph vessels
- Excess fluid is returned to cardiovascular system via the lymphatic system and eventually into the venous system
- Alterations in hydrostatic pressure, oncotic pressure & lymph flow will disrupt this balance
What assists in venous return?
- Skeletal muscle pump: contraction of skeletal muscle compresses veins and forces blood toward heart via one at valves
- Respiratory pump: chest expansion during inspiration creates negative pressure which ‘sucks’ more blood from abdomen via inferior vena cava
- Sympathetic nerve stimulation: during baroceptor reflex & constriction of veins allows for increased venous return & imcreased CO
Summarize baroceptor reflex activity with the autonomic nervous system
Sympathetic response:
-SA node; myocardium, conduction, vasculature
Parasympathetic response:
-SA node
Outline the response of pacemakers to the sympathetic nervous system
Cardiovascular control center in Medulla oblangata—>sympathetic neurons(NE)—> B1-receptors of autorhythmic cells—> Na+ and Ca+ influx —> rate of depolarization —> heart rate
How does the myocardium respond to the sympathetic nervous system?
Epinephrine and norepinephrine bind to B1 receptors that activate cAMP second messenger system resulting in phosphorylation of voltage gated Ca+ channels and phospholambian
Phosphorylated voltage gated Ca2+ channels : open time increases, leading to mode calcium ion entry from ECF. This leads to increased Ca2+ stores in ER and THUS increased Ca2+ released
Phosphorylated phospholambian: increased Ca2+-ATPase on SR this leads to two things: to increased Ca2+ stores in ER and THUS increased Ca2+ released(more forceful contraction as well as Ca+ removed from cytosol faster which leads to shortened Ca+-troponin binding time(shorter duration of contraction)
What is the sympathetic response to vasvulature?
Arterioles diameter is controlled by tonic release of norepinephrine by a-receptor
There is a change in signal rate- increased norepinephrine release onto a-receptors result in increased tonic signal rate
Decreased norepinephrine release onto a-receptors causes blood vessel to dilate
Outline the parasympathetic response of pacemakers
Cardiovascular control center in medulla oblangata activates parasympathetic neurons (ACh)
- Muscuranic receptors of autorhythmic cells cause an increase in potassium efflux, : Ca2+ influx
- Hyperpolarizes cell and rate of depolarization leads to decreased heart rate
Explain the negative feedback of decreased mean arterial blood pressure upon standing
Decreased mean arterial blood pressure upon standing—> decreased firing of carotid and aortic bark receptors activates cardiovascular control center in medulla
This increases sympathetic out put and decreases parasympathetic output
Increased sympathetic output leads to increase force of ventricles and causes vasoconstriction on arterioles and veins. Vasoconstriction increases peripheral resistance and increases blood presssure. Increased ventricle force of contraction increases CO. This increases blood pressure
Decreased parasympathetic output causes SA node to increase heart rate, and also cause ventricle to increase force of contraction, both of these increase CO. INCREASED CO, increases blood pressure
What factors determine mean arterial blood pressure?
Blood volume
Effectiveness of the heart as a pump
Resistance of the system to blood flow
Relative distribution of blood between arterial and venous blood vessels
What factors affect blood volume?
Fluid intake and fluid loss
Fluid loss may be passive or regulated by kidney (RAS)
What factors determine the effectiveness of the heart as a pump (cardiac output)?
Heart rate
Stroke volume
What is determined by resistance of the system to blood flow?
Determined by diameter of the arterioles
What factors determine the relative distribution of blood between arterial and veinous blood vessels?
Determined by diameter of the veins
