day 12 - cardiovascular system Flashcards
heart (def)
organ that pumps blood and creates pressure in vascular system
arteries + arterioles (def)
vessels that carry blood away from heart
capillaries (def)
vessels that allow for gas/nutrient exchange with tissue(s)
veins + venuoles (def)
vessels that carry blood toward the heart
blood is made up of: (super basic)
liquid and cells
components of blood:
- plasma
- hematocrit
plasma (def)
liquid portion of blood
what is plasma made up of
small ions, amino acids, glucose, horomones, etc
hematocrit (def)
percent of blood composed of cells (not liquid)
what makes up hematocrit
primarily red blood cells
also white blood cells, and platelets
red blood cells (func)
have hemoglobin which transports O2
white blood cells (func)
important for immune function
platelets (func)
important for blood clotting
normal college-age person has hematocrit levels around…
~42% for males
~38% for females
what makes blood viscus
hematocrit
what/in which situations can/is your blood more viscus
dehydrated or use of erythropoietin (EPO) to make more red blood cells
main functions of cardiovascular system (3)
1) transports O2 and nutrients to tissue(s)
2) removes CO2 and metabolic byproducts from tissue(s)
3) regulates body tempurature
how does the cardiovascular system regulate body tempurature
1) blood gains heat when it flows through/by working muscles and transports that heat to skin as blood is circulated away from heart + out toward perifery
2) increased circulation post exercise helps body cool off faster (cool down/walk)
systemic circuit
left side (L ventricle) of the heart pumps oxygen-rich blood out of aorta to body via arteries and returns oxygen-poor blood from body to right side of hear (R atrium) via veins
pulmonary circuit
right side (R ventricle) of heart pumps oxygen-poor blood to lungs via pulmonary arteries and returns oxygen-rich blood from lungs through pulmonary veins
what artery/arteries carry DO2/oxygen-poor blood
pulmonary arteries
going from heart to lungs to get oxiginated
what vein/veins carry oxiginated blood
pulmonary veins
going from lungs to heart to get pumped out to body
cardiac output (Q) def.
total amount of blood ejected from heart per minute (L/min)
heart rate (HR) def.
number of heart beats/contractions per minute (bpm)
stroke volume (SV) def.
amount of blood ejected by heart per beat (mL/beat)
equation for cardiac output (Q)
Q = HR * SV
“normal” blood pressure
<120 and/or 80mmHg
high (stage 1) blood pressure
> 130 and/or 90mmHg
how is blood pressure expressed/recorded
systolic/diastolic blood pressures
systolic pressure is the BLANK number
first/top
systolic blood pressure (def)
pressure generated in aorta/arteries due to hearts ventricular contraction
systole (def)
ventricular contraction of the heart
diastolic blood pressure is the BLANK number
second/bottom
diastolic blood pressure (def)
pressure in aorta/arteries during heart’s ventricular relaxation/filling period
diastole (def)
heart’s ventricular relaxation/filling period
central command theory (def)
initial signal sent to drive cardiovascular system, comes from higher brain centers in medulla oblongada
fined tuned by/with feedback
what gives feedback to the cardiovascular system
1) chemoreceptors in arteries (aorta, corotid)
2) mechanoreceptors in muscles + heart (myocardium)
3) baroreceptors in arteries (aorta, corotid)
4) thermoreeptors in CNS and muscles
VO2 MAX is BLANK times more than VO2 at rest
10-20x
Q MAX is BLANK times more than Q at rest
4-8x
hypertension (def)
high blood pressure
true/false the heart can generate its own action potentials
true
if not controlled by parasympathetic NS, beats at ~100bpm
SA node (func)
generates action potential in heart
AV node (func)
gets action potential from SA node cascade + slows SA node a bit
decrease in HR
- via vagus nerve, acetylcholine
ACh onto SA node = slows, AV node slowed slightly as well
increase in HR
- via cardiac accelerator nerves
increases HR AND contractile force (contractility)
uses norepinephrine (excitatory)
factors affecting HR at REST
1) age: HRmax decreases with age
2) biological sex: HR in females averages 5-10 bpm faster than adult males
3) posture: HR tends to increase by ~10bpm when going from sitting to standing
4) injection of food: HR (resting and exercise) goes up after eating as internal metablic work rate increases
5) emotion: anxiety/stress can cause increase in resting + exercise HR
6) body temp: HR is positivly related to body tempurature
main factors effecting stroke volume
1) end diastolic volume (EDV)
2) total periferal resistance
3) strength of ventricular contraction
end diastolic volume (def)
highest volume of blood in the ventricle (more blood u can fit into heart = more blood you can pump out)
how does end diastolic volume affect stroke volume
- greater ventricular filling results in more ventricular stretch and a more forceful contraction when valve(s) open (water balloon getting stretched)
what influences end diastolic volume (EDV)
venous return (more return = more blood pushed in and out of heart)
what influences rate of venous return
1) venoconstriction – via smooth muscle sympathetic reflex
2) skelital muscle pump – rhythmic skelital muscle contractions force blood in extremities toward the heart
3) respiratory pump: increased rate + depth of breathing promotes blood flow toward the heart
total periferal resistance (def)
pressure heart has to pump against to eject blood into systemic circuit
if you have hypertension, this pressure is higher so you cant get as much blood out per beat (stroke volume is less)
contractility (def)
strength of ventricular contraction (increased contractility = increased stroke volume)
circulating norepi + epi cause direct sympathetic stimulation of heart myocardium
more minor factors that affect stroke volume at rest
1) posture: blood pools in lower extremidies/toward gravity, can decrease venous return and thus SV
2) size of heart: larger, stronger heart muscle can contract with more force
3) non-pathalogical cardiac hypertrophy
cardiac hypertrophy (def)
increase in number of contractile proteins (actin + myosin) in heart tissue/cells
pathalogical cardiac hypertrophy (def)
disease (chronic hypertension) induced increase in the thickness of the heart walls, with a decrease in chamber size
non-pathalogical cardiac hypertophy (def)
exercise-induced increase in thickness of hear walls with an increase in chamber size
how can VO2 increase 10-20x from rest to max, but Q only increases 4-8 times from rest to max
during exercise, more O2 is utilized per L of blood
concentration of O2 in working muscle cells goes down (being used to make ATP) so the driving force for O2 into the cells increases and O2 enters cells)
SV plateaus around BLANK for most people
~40% VO2 MAX
SV plateaus around BLANK for highly trained atheletes
60% VO2 MAX
cardiac output increases due to:
1) increased HR
2) increased SV
3) oxygen uptake by muscle cells increases (more O2 pulled out per L of blood)
factors that effect strength (2)
neural adaptivity + hypertrophy
hyponutremia (def)
low blood-salt levels
redistribution of blood flow during exercise
- increased bloodlflow to working skelital muscles, skin (cooling), heart
- reduced bloodflow to less active organs, but none are reduced to near zero
when looking at redistribution of bloodflow info, you should use relative or absolute numbers
ABSOLUTE ALWAYS
how does increased bloodflow to skeletal muscles actually work
- withdrawl of parasympathetic vasoconstriction (veins open up)
- autoregulation by CNS:
a) bloodflow increases to meet metabolic demands of tissue
b) chemoreceptors (CO2, lactate)
c) mechanoreceptors (GTOs, muscle spindles)
a BLANK CHANGE in HR occurs at the start of exercise
rapid increase in HR
does HR platoe in steady state?
yes, just like VO2
HR recovery (to rest) after exercise depends on
1) duration and intensity of exercise
2) body temp, epinephrine in system
3) training state of subject (untrained = slower, trained = faster)
does heart rate immediatly return to rest after exercise
NO
its like EPOC but with heartrate
variables in HR response to exercise (4)
1) intensity: relative to workrate, positive relationship btwen HR and instensity
2) mod of exercise: static vs dynamic activity + speed of movements
3) duration: HR usually plateaus at low to moderate intensity
4) emotional influence: HR is increased with anxiety/fear (plays much less of a role in HR when exercising than resting HR)
CV (cardiovascular) response to prolonged exercise, particuraly in hot + humid environments
- rising body temp leads to increased bloodflow to skin (vasodialation) and prolonged sweating
- dehydration can occur, causing loss of blood plasma
- gradual decrease in SV can occur due to plasma loss to sweat
- cardiac output (Q) maintained by CV control centers (in medulla)
- gradual increase in HR even at low to moderate intensity
cardiovascular/O2 drift (def)
HR, breathing rate, and VO2 rise slowly over time
HR variability (def)
the time between heart beats (during sleep)
high HR variability is considered BLANK
HEALTHY
low HR variability is considered BLANK
UNhealthy
low HR variability can be a sign/symptom of BLANK
overtraining sydrome
sympathovagal balance (def)
balance between SNS and PNS
balance between SNS and PNS is called
sympathovagal balance
