Flashcards in Cardiovascular Regulation Deck (43):
The movement and the forces of the heart during contraction
End diastolic volume
the amount of blood within the ventricles after complete relaxation (diastole)
End systolic volume
The amount of blood found within the ventricles (remaining) after a complete contraction
the amount of blood taken away from the heart (pumped) per heartbeat (EDV-ESV)
How much of the blood that is pumped from the heart (precentage) - calculated by SV/ EDV
the degree of stretching that can be produced by the heart in order to acoomodate the blood during ventricular dialstole. it is directly proportional to the EDV - the higher the preload, the higher the end diastolic volume will be.
is the tension created by the ventricular systole - enough to be be able to open the semi lunar valves.
Stoke volume x heartrate
Stoke volume is dependent on
the end diastolic volume - end systolic volume
What two factors increase the preload? (starlings law)
The venous filling time and the venous return
what does preload do?
increases energy of contraction - more preload, more stronger contraction.
allows stretching of the myocytes to increase the area for the blood to fill the ventricles.
what 3 factors affect the end systolic volume?
The preload - the amount of stretching of the myocytes, allows more volume of blood in which then increases the tension of the myocytes - as more the filling of the ventricles, more myocyte tension generated thus more force of contraction.
The Contractibility - the ability and the force within the left ventricles in order to contract the heart with a certain amount of preload - autonomic intervention and hormones.
The Afterload - the amount of tension created by the contraction, enough to open up the semilunar valves.
what is the pressure in the aorta? what is the pressure in pulmonary artery
what happens if the afterload increases but the preload remains the same?
Stroke volume will decrease as the heart contractions are too rapid to be able to remove all the blood from the atria.
Factors that increase contractility? POSITIVE INOTROPIC AGENTS
Beta adrenergic agonists, neurtotransmitters, sympathetic hormones,
Factors that decrease contractility?
parasymathetic hormones and neurotransmitters, beta blockers, vrampril, calcium channel blockers, muscarininc agonists, increase in pottasium, increase in anoxia or acidosis.
Factors that influence heartrate?
Autonomic regulation, hormones
where is the cardiovasular control centre
where does it receive its information from (cardiovascular centre)
the baroreceptors, proprioreceptors, chemoreceptors, which are brought by the glossophyrengeal nerve into the Medulla.
The higher centres of the brain such as the crebral cortex and hypothalumus.
where does the info go from the medulla?
the sympathetic chain which branches off the spinal chord into the throacic region into the cardiacc plexus. (ACCELERATOR)
the parasympathetic branch which goes from the medulla oblongata directly (VAGUS)
What does the vagus nerve do?
decreases contractility of the heart
decreases stroke volume.
what does the accelerator nerve do?
opp to vagus
The cardiovasucular centre contains a vasomotive centre and a cardiac centre - what regions are in the cardiac centre and what do they do?
Cardioacceleratory centre - increases heartrate and spontaneous depolarisations of the SA node.
Cardioinhibitory centre - decreases heartrate and spontaneous depolarisations of the SA node,
Why does homestasis control the CVS
in order to maintain enough perfussion into tissues and allow enough blood flow.
tissue perfussion is influenced by
what are the homestatic mechanisms in order to perfuse to tissues
How is blood flow autoregulated within tissues?
Precapillary sphincters in the metarterioles which cause the perfusion of the blood within the tissues.
what are the local vasodialators?
low carbon dioxide
histamine and other proinflamatory agents
thromboxanes - released by platelets cause vasoconstriction at wound site.
endothelines - released by damaged endothelial cells
what happens when precapillary sphincters contract?
blood flow to the capllaries decreases
vasomotive centre contains two poplulation of blood vessels cells - which are most abundant
vasoconstriction - mpst abundant
vasodialtion - least abundant
where are vasocontriction cells found
coronary, skin and internal organs
where are vasodialation cells found
skeletal muscles and brain
what do vasoconstrction cells do
vasocontrict the blood vessels around organs due to sympatheitc stimulation of the alpha 1 adrenergic receptors in the smooth muscle cells.
what do vasodialation cells do
relax smooth muscles
cholinergic (ACh) causes nitric oxide to be released.
nitroxidergic release nitric oxide and target smooth muscles directly.
found in carotid sinus and the aortic sinus - detect stretching of aorta and the carotid arteries - regulate blood pressure in the brain and the rest of body.
atrial or bainbridge reflex
baroreceptors in atria - detect degree of stretch, causing thbaroreceptros to take the signals through the glossophyrengeal nerve to the MO - stimlation of cardioinhibitory centre - if blood pressure high (more venous return) and inhibition of the cardioacelatory centre. also the vasomotive centre inhibits vasoconstriction.
increased pxygen leads to vasocontrcition therefore mechanism allows VASODIALATION
decreased oxygen and increased co2, pH leads to vasodilation therefore mechanism allows VASOCONSTRICTION
what does ADH do?
Released from posterior pituitary gland causing the retaining of water from the kidneys and also vasocontriction in order to increase BP.
Released when blood volume is low, BP is low, osmotic potential is low, angeotensin 2 is present.
released when BP is low.
Released from juxtaglomerullar cells
renin is released from the kidneys and it binds with the angiotensinogen from the liver which creates angiotensin 1. angiotensin 1 reacts with ACE enzyme from lungs creating angiotensin 2.
what does angitensin 2 do?
releases ADH causes retention of sodium and pottasium and water
stiumlates thirst - more water drank - increased blood volume
stimulates CO and vasoconstriction
increase in blood viscosity
increase in blood volume
increase in RBC production
increase in oxygen carrying capacity and vasoconstriction.
RELEASED IN LOW PPO2 AND LOW BP