Cardiovascular system Flashcards
3 principle components of CVS
heart
blood
blood vessels
what other systems impact the function of the CVS
endocrine
nervous
kidneys
2 loops of CVS
systemic
pulmonary
systemic loop
blood from heart to body to heart
blood leaves left ventricle via aorta which branches to form systemic arteries that branch to form the microcirculation (arterioles, capillaries, venules)
venules form veins which form into 2 large vessels: inferior vena cava and superior vena cava
inferior vena cava
collects blood from below heart
superior vena cava
collects blood from above heart
what is the function of the pulmonary system/loop
carries oxygen-poor blood to the lungs and back to the heart
blood leaves ventricle via pulmonary trunk which divides into pulmonary arteries
at the lungs there are arterioles, capillaries, venules, veins and blood returns to the left atrium via 4 pulmonary veins
2 categories of arteries
muscular
conduit/elastic
how is pressure in blood vessels measured
mm of mercury (Hg)
flow
volume moved, mm/min
definition for resistance
how difficult it is for blood to flow between 2 points at any given pressure difference
3 factors affecting resistance
blood viscosity (volume, number of erythrocytes)
total blood vessel length
blood vessel diameter (relaxed vessels decrease resistance, vasoconstricted vessels increase resistance)
vein vs artery
few layers of smooth muscle and connective tissue, few elastic layers, wider lumen
arteriole vs vein vs capillary
lumen endothelium smooth muscle cells
endothelium connective tissue
endothelial cells
elastic arteries
closer to heart
eg aorta
Large lumen vessels (low resistance) that contain more elastin
than the muscular arteries
pressure reservoirs
expand and contract (recoil) as blood is ejected by the
heart. This allows blood flow to be continuous.
muscular arteries
deliver blood to specific organs (mesenteric artery, renal artery etc.).
They have proportionally the most smooth muscle and are very active in vasoconstriction.
These arteries can play a large role in the regulation of blood pressure.
factors effecting pressure
volume
compliance (degree of stretch)
volume effecting pressure
Only about 1/3 of stroke volume
leaves arteries during systole
Rest of stroke volume remains in the arteries during systole, distending them, and raising the arterial pressure
After ventricular contraction, artery recoils passively, and blood
continues to be driven into arteriole
systolic blood pressure
Maximal arterial pressure reached during peak ventricular ejection
diastolic blood pressure
Minimal arterial pressure reached just before ventricular ejection
pulse pressure
difference between systolic and diastolic blood pressure
what are arterioles controlled by
neural, hormonal and local chemicals
arteriole function
control minute-to-minute blood flow in capillary beds
contraction diverts blood flow away from the tissues
dilation increases blood flow to the tissues
impact blood pressure
intrinsic tone
basal level of contraction of arterioles
how is smooth muscle in arterioles regulated
autonomically by local or extrinsic control
how to decrease flow to tissues
increase resistance by vasoconstriction
keep pressure constant
how to increase flow to tissues
increase pressure
or vasodilate to reduce pressure
local control of arteriolar resistance
metabolism increases: oxygen dec, carbon dioxide, potassium ions, nitric oxide, hydrogen ions, adenosin increase
causes vasodilation, reduces resistance, increases blood flow
extrinsic control of resistance
hormones
sympathetic nerves
examples of hormones controlling resistance of arterioles
Epinephrine – vasodilates or constricts
depending on the tissue
Angiotensin II – constricts most arterioles
Vasopressin – constricts most arterioles
3 types of capillary
continuous
fenestrated
sinusoidal
continuous capillary
found in skin, muscle, most
common kind, have tight junctions.
fenestrated capillary
more permeable —
intestines, hormone-producing tissues, kidneys
sinusoidal capillary
only one with an incomplete
basement membrane; these are found in the liver,
bone marrow and lymphoid tissues
how do capillaries grow and develop
angiogenesis
VEGF
angiogenic factor released by vascular endothelial cells
what does blood flow through the capillaries depend on
other vessels in the microcirculation
eg, vasodilation of arterioles causes increased capillary flow
metarteriole
supplies some capillaries
can be damaged by high blood pressure
precapillary sphincter
site at which a capillary exits from a metarteriole
surrounded by a ring of smooth muscle that relaxes and contracts in responses to local stimuli
why is blood flow through capillaries slow
to maximise time for substance exchange across capillary wall
what is blood velocity dependent on
cross-sectional area of the blood vessel type
smaller diameter reduces speed
pressure difference between veins and right atrium
veins (10-15 mmHG) and the right atrium (0 mmHG)
major functions of veins
act as low pressure conduits returning blood to heart
maintain peripheral venous pressure
factors determining venous pressure
volume of blood in veins
compliance of walls- their walls are very thin and compliant (low pressure)
how is unidirectional flow maintained in veins
valves
factors that can increase venous pressure
increase activity of sympathetic nerves to veins
increase blood volume
increase inspiration movements
increase skeletal muscle pump
effect of increase in venous pressure
increase in venous return
atrial pressure increases
end-diastolic ventricular volume increases
stroke volume increases
cardiac output
amount of blood pumped out of each ventricle in one minute.
It is the product of heart rate (HR) and stroke volume (SV)
stroke volume
difference between end diastolic volume and the end systolic volume
Volume of blood pumped from the left ventricle per beat.
SV = EDV − ESV
myocardium
muscular wall of
the heart formed from cardiac
muscle cells
epicardium
fixes inner layer of
pericardium to heart
pericardium
muscular sack enclosing heart
atrioventricular septum
muscular wall separating the ventricles
pulmonary semi lunar valve
blood from right ventricle to pulmonary trunk
aortic semi lunar valve
blood from left ventricle into aorta
Chordae tendinae
fasten AV valves to the papillary muscles
papillary muscles
limit movement to prevent backward flow of blood
bicuspid valve
2 fibrous cusps at left AV valve
tricuspid valve
right Av valve
3 fibrous cusps
how is permeability of capillaries determined
water filled interellular clefts
intercellular clefts are gaps between adjacent cells in endothelium
cardiac muscle cells
1-2 centrally located nuclei
striated
adjacent cells connected by intercalated disks
gap junctions essential for electrical stimulation
large mitochondria
node cells-automaticity
desmosomes
conducting system of the heart
cells with specialised features for heart excitation
in electrical contact with cardiac muscle cells via gap junctions
initiates the heartbeat and helps spread the impulse rapidly throughout the
heart
control of increase in heart rate
sympathetic nervous system-innervates entire heart muscle and node cells
releases norepinephrine which binds to beta-adrenergic receptors on cardiac muscle cells
control of decrease in heart rate
parasympathetic nervous system
innervates node cells
release acetylcholine which binds to muscarinic receptors
epinephrine
hormone released from adrenal medulla
binds to same receptors as norepinephrine with same effects
how are action potentials transmitted through heart
gap junctions between myocardial cells
transmission/path of depolarisation
sinoatrial node
atrial muscle cells
through internodal pathway via gap junctions to
AV node
bundle of His
left and right bundle branches
left and right perkinje fibres
ventricular muscle cells
signal delay at AV node
allows atria to contract and completely fill the ventricles before they contract
purkinje fibres and papillary muscles
purkinje fibres supply papillary muscles, signalling them to contract before the rest of the atria to help prevent backflow through valves
P wave on ECG
depolarisation wave from the SA node to the AV node. Atria contract
0.1 second after P wave starts
QRS complex on ECG
ventricular depolarisation and precedes ventricular contraction
T wave
ventricular repolarisation
effect of atrial fibrillation on ECG
electrical impulses in atria fire chaotically
what is stroke volume influenced by
volume of blood in ventricles, sympathetic nervous system, pressure heart is pumping against
effect of decreased heart rate on SV and CO
SV decreases
CO maintained by increasing HR again
positive chronotropic factors
increase HR
negative chronotropic factors
decrease HR
frank starling mechanism
The ventricle contracts forcefully more
during systole when it has been filled to a greater degree during diastole (more venous return)
length-tension relationship. The greater the end diastolic volume, the more the muscles are stretched, and thus the greater the contraction
contractility
The strength of a contraction at any given end-diastolic volume
Norepinephrine acts on beta-adrenergic receptors to increase ventricular contractility
Plasma epinephrine also increases contractility
effect of increased contractility
increased stroke volume due to a more complete ejection of the end-diastolic volume
mean arterial pressure calculation
(in terms of pressure)
Diastolic pressure + 1/3 (Systolic pressure − diastolic pressure)
mean arterial pressure calculation
(in terms of CO)
Cardiac Output × Total Peripheral Resistance
TPR is dependent on vasculature
mean cardiac output equation
stroke volume x heart rate
where heart rate dependent on +/- chronotropic factors and sympathetic or parasympathetic activity
mean stroke volume equation
end diastolic volume - end systolic volume which are dependent on frank starling mechanism and contractility
arterial baroreceptors
respond to short term changes in arterial pressure; nerve endings are highly sensitive to stretch or distortion (degree of stretching is directly proportional to blood pressure)
can adapt to long term changes
response of baroreceptors to increase in mean arterial pressure
increase frequency of action potentials
response of baroreceptors to decrease in mean arterial pressure
decrease frequency of action potentials
what receives impulses from baroreceptors
medullary cardiovascular centre in medulla oblongata
input from baroreceptors determines frequency of action potentials from the CV centre
events after baroreceptors increase frequency of action potentials
decrease sympathetic outflow to heart, arterioles and veins and increase parasympathetic outflow to heart
decrease in arterial pressure-hormonal response
increase concentrations of angiotensin II and vasopressin which causes arterioles to constrict and increase arterial pressure again
renin-angiotensin system
intra-renal baroreceptors detect changes in stretching with lower blood volume–>increase production of renin
what happens within hours of blood loss
Compensatory movement of
interstitial fluid into the capillaries
to increase plasma volume (redistribution of fluid)
also: increase in thirst, decrease in salt and water excretion
what happens within days of blood loss
Replacement of cells:
erythropoiesis
haematopoiesis
key concept of diuretics
increase excretion of sodium and
water, decreasing cardiac output with no
change in peripheral resistance
