Cardio Flashcards
Why do humans require a circulatory system?
Transportation of materials to allow exchange between cells of the body and the external environment
overall design of cardiovascular system
series of tubes (blood vessels), filled with fluid (blood), and connected to a pump (heart)
- closed circuit
- operates by pressure differences
pulmonary circulation
oxygen depleted blood from right heart to lungs
systemic circulation
oxygen rich blood from left heart to rest of body
arteries
take blood away from heart
veins
return blood to heart
two main components of blood
plasma and cells
blood plasma
mostly water
red blood cells
contain hemoglobin which plays important role in transporting oxygen (erythrocytes)
white blood cells
immune function (leukocytes)
platelets
blood clotting
split off from megakaryocytes
flow of blood in the cardiovascular system
- directly proportional to pressure gradient
- inversely proportional to resistance to flow
Pouiselle’s Law
resistance is proportional to: length x viscosity x radius^4
-small changes in radius lead to big changes in resistance
what part of hemoglobin binds oxygen
iron
three ways carbon dioxide can be transported
1) bind with hemoglobin
2) form bicarbonate ions (what most does)
3) dissolved in plasma
erythropoieten
hormone produced in the kidneys and can induce RBC production
4 chambers of heart
R and L atria: receive blood
R and L ventricles: eject blood
base of heart
the top, round
apex of heart
bottom, point of cone
aorta
receives blood from left ventricle to send to systemic arteries
pulmonary vein
receives blood from veins of the lungs and sends to left atrium
vena cavae (superior and inferior)
receive blood from systemic veins and send to right atrium
pulmonary trunk (artery)
receives blood from right ventricle and send to lungs
what path does blood take
Systemic veins –> RA–> RV–> PA–>Lungs–>PV –>LA–> LV –> Systemic arteries
systole
ventricular contraction
- AV valves close to prevent backflow into atria
- semilunar valves open
- pushing blood into aorta
diastole
ventricular relaxation
- semilunar valves closed to prevent backflow into ventricles
- mitral valve (bicuspid) open
- allow ventricles to fill with blood
electrical signal pathway in heart
SA node –> Atria–> AV Node –> Bundle of His–> Bundle Branches–> Ventricles
mechanical contraction
electrical signal is stimulus for coordinated mechanical contraction of atria then ventricles
how are electrical signal and mechanical contraction linked?
an increase in cytosolic calcium levels within cardiac contractile cells
contractile cells
- sarcomeres
- generate tension that causes muscle contraction
autorhythmic cells
- initiate electrical signal for contraction a SA node
- smaller than contractile cells
- no sarcomeres
excitation-contraction coupling
occurs through cytosolic calcium
-contracts when Ca is high (systole)
SA node
- pacemaker of the heart
- AV node and purkinje fibers can act as pacemaker is SA node not functioning
autorhythmic action potentials
- unstable membrane potentials
- depolarization is due to calcium channels opening
Funny channels
allow sodium to enter and depolarize cell
calcium channels in autorhythmic cells
T-type open first
L-type open second
contractile cell action potentials
- depolarization due to sodium entry
- repolarization due to potassium exit
- plateaus due to calcium entry in the cell preventing tetanus
why do we have long refractory period in cardiac muscle
to prevent tetanus and allow ventricles to refill
P wave
atrial depolarization
QRS complex
wave of ventricular depolarization
T wave
ventricular repolarization
atrial repolarization
part of QRS complex, occurs at same time as ventricular depolarization
PR segement
corresponds to delay at AV node
ST segment
time between ventricular depolarization and repolarization
excitation-contraction coupling in contractile cells
1) AP from adjacent cell depolarizes membrane
2) Ca influx triggers more release of Ca from SR
3) Ca binds to troponin to initiate contraction
4) relaxation when Ca unbinds troponin and is pumped back into SR
ventricular diastole
ventricles filling (includes atrial systole) LA pressure > LV pressure
isovolumic contraction
ventricles contract without change in volume
LA pressure < LV pressure < Aortic pressure
ventricular ejection
SL valves open and blood in ejected into PA/aorta
LV pressure > Aortic pressure
isovolumic relaxation
ventricles relax without change in volume
LA pressure < LV pressure < Aortic pressure
S1
“lubb” 1st heart sound
occurs when AV valves close
S2
“dub” 2nd heart sound
occurs when SL valves close
timing of mechanical and electrical events
electrical events followed by mechanical
- depolarization followed by contraction
- repolarization followed by relaxation
cardiac ouput
volume of blood ejected by each ventricle in one minute
-product of heart rate and stroke volume
stroke volume
amount of blood ejected from ventricle in each heart beat
End diastolic volume - End systolic volume
ejection fraction
percentage of EDV ejected during each contraction
regulation of heart rate
initiated at SA node and modulated by ANS
parasympathetic branch
slows heart rate
sympathetic branch
increases heart rate
parasympathetic neurons
- release ACh that binds to muscarinic receptors
- K out, Ca in
- hyperpolarize cell and decrease rate of depolarization
- slow HR
sympathetic neurons
- release NE that binds to beta-1 receptors
- Na and Ca influx
- increase rate of depolarization
- speed up HR
stroke volume regulation
- length of muscle fibers at beginning of contraction: increased length as muscles stretch
- contractility: more Ca released and able to bind to troponin to generate greater force of contraction
Frank Starling Law of the Heart
- stroke volume is proportional to end diastolic volume
- EDV = “preload” determines length of muscle fibers prior to contraction
- “the heart pumps the blood it receives”
EDV is determined by
Venous return:
- skeletal muscle pump
- respiratory pump
- constriction of veins
ionotropic agent
any chemical that affects contractility
positive ionotropic effect
epinephrine and norepinephrine
negative ionotropic effect
beta blockers and calcium channel blockers
phospholamban
regulates activity of sarcoplasmic ATPase pump
arteries and arterioles
take blood away from heart
- elastic walls
- thick layers of vascular smooth muscle
- constriction and relaxation to influence blood distribution
capillaries
facilitate exchange of materials between blood and tissue
venules and veins
take blood back to heart
- thin walls of vascular smooth muscle
- constriction can increase venous return
determinant of blood flow
blood flows if there is a pressure gradient
high to low pressure
determinants of blood pressure
flow x resistance
blood flow follows a pressure gradient that is highest in the aorta/large arteries and moving to arterioles and lowest in the veins
resistance
inversely proportionally to radius^4
proportional to length and viscosity (usually stay same)
what regulates arteriole diameter
vascular smooth muscle
- vasoconstriction
- vasodilation
small changes in radius have big changes in resistance
decrease radius –> decrease flow
increase radius –> increase flow
local control
matches tissue blood flow with the metabolic needs of a given tissue
ex) adenosine in hypoxic cells can increase blood flow to match metabolism
sympathetic reflexes
to maintain arterial pressure and regulate blood distribution for homeostatic needs
ex) NE release on alpha receptors
hormones
either directly or by altering ANS
ANS regulating HR
SNS and PNS innervation influence rate of SA node depolarization
- SNS release NE to increase HR
- PNS release ACh to decrease HR
ANS regulating stroke volume
SNS innervation
- NE and E from adrenal medulla influence contractility
- SNS mediated venoconstriction
SNS influences arteriolar resistance
-tonic release of NE maintains muscle tone
alpha: vasoconstriction of GI and kidneys
beta 1: pos. ionotropy and increased HR
-Epi release from adrenal medulla
beta 1: pos. ionotropy and increased HR
beta 2: vasodilation
baroreceptor reflex
ensure adequate perfusion of the brain and heart by maintaining sufficient mean arterial blood pressure
mean arterial blood pressure determinants
blood volume, effectiveness of heart as a pump, resistance, and relative distribution of blood (between arteries and veins)
drop in BP
increased SNS/decreased PNS
increased HR and SV
vasoconstriction
elevated BP
increased PNS/decreased SNS
decreased HR and SV
vasodilation
continuous capillaries
endothelial cells form continuous lining with leaky junctions; muscle, connective tissue, neural tissue (most common type)
fenestrated capillaries
large pores between endothelial cells; kidneys and intestines
velocity of blood flow
slowest at capillaries, but they have greatest surface area
capillary exchange
diffusion: small dissolves gases and solutes
bulk flow (paracellular pathway)
vesicles: larger solutes
bulk flow
mass movement as a result of hydrostatic or osmotic pressure gradients
absorption
fluid movement into capillaries
- net absorption at venous end
- caused by colloid osmotic pressure
filtration
fluid movement out of capillaries
- net filtration at arterial end
- caused by hydrostatic pressure
lymphatic system
returns fluids and proteins filtered out of the capillaries to circulatory system
edema
excess fluid in the interstitial space
causes of edema
1) inadequate drainage of lymph
2) blood capillary filtration exceeds absorption
adjustments of cardiovascular system during exercise
- increased cardiac output
- increased central venous pressure (venous return)
- decreased systematic vascular resistance
baroreceptor reflex during exercise
CNS modifies and resets to a higher control point to avoid bradycardia
adjustments to cardiovascular system during hypotension caused by an abrupt change in body posture or blood loss
sudden change to standing can cause hypotension (which triggers baroreceptor reflex)
-short term response by baroreceptor and long term response by hormones
stenotic valves
-narrowing of valve opening
-increased resistance to flow
-increased velocity of flow
heart murmur when valves should be open
insufficient valves
-valve leaflets do not completely seal when valve should be closed
-causes regurgitation of blood
heart murmur when valves should be closed
heart failure
diminished contractility
- rightward shift on SV vs. EDV curve (to maintain SV)
- Poor pump function can ultimately cause pulmonary/systemic edema
Atherosclerotic Vascular Disease
causes: stenosis of artery
consequences: increased vascular resistance
treatment: bypass surgery or angioplasty
hypertension
causes: any factor that increases blood volume, CO, or TPR
consequences: Kidneys are complicit in ”allowing” chronic elevation in BP
treatment: target reductions in blood volume or TPR
