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End Diastolic Volume
volume of blood in the left ventricle after diastole (fully filled)
EDV value at rest
125 mL
End systolic volume
volume of blood left in the left ventricle after systole (a full contraction, will be less than EDV)
ESV value at rest
42 mL
Stroke volume
volume of blood pumped out of the heart in one beat
SV value at rest
82 mL
length of cardiac cycle at rest
0.8 ms
four primary determinants of cardiac output
prelaod
afterload
heart rate
contractility
preload definition
stretch of the myocardium
factors affecting preload (4)
frank starling
q/blood volume/venous tone
filling time/HR
muscle pump/respiratory pump
frank starling mechanism
more stretch = greater contraction
higher EDV = higher SV
cardiac output equation
Q = HR x SV
Q value at rest
5-6 L/min
afterload
resistance the ventricle must overcome to eject blood
endurance exercise increases volume/pressure load
volume
resistance exercise increases volume/pressure load
pressure
valsalva maneuver
forced expiration against a closed glottis
collapses veins, decreased venous return, decreased SV, decreased BP
phase 1 valsalva
brief rise in arterial pressure due to rise in intrathoracic pressure pressing on aorta
no change in HR
phase 2 valsalva
arterial pressure low due to continued strain and compression of veins; lowers venous return
HR increases due to baroreceptors increasing sympathetic tone
phase 3 valsalva
strain released; brief drop in pressure as venous return restored
phase 4 valsalva
arterial pressure returns to baseline and overshoots
sudden return of blood increases preload and SV
HR slows and pressure returns to normal
contractility definition
strength of contraction independent of preload
contractility is affected by
positive inotropes and negative inotropes
positive inotropes
sympathetic stimulation and catacholamines via calcium influx and CICR
negative inotropes
acidosis, hypoxemia, reduced sympathetic drive
systolic pressure
peak pressure during ejection
diastolic pressure
lowest pressure during ventricular filling
pulse pressure
systolic pr - diastolic pr
mean arterial pressure (MAP)
average driving pressure for blood flow in systemic circulation
Cardiovascular drift
during prolonged exercise, HR rises and SV declines while Q is maintained
At higher intensities, SV plateaus or declines but Q is maintained. Why?
continued rise in HR
Cardiovascular endurance training adaptations
lower HR
improved Ca handling and contractility
increases SV
What percent of blood flow can be redistributed to muscle during exercise?
85%
Poiseuille’s law
small changes in vessel radius produce large changes in resistance/flow
3 solutions to central conflict during exercise
large increase in Q
vasoconstriction in inactive vascular beds
rise in blood pressure set point
baroreceptor location
carotid sinus and aortic arch
myogenic response
autoregulation
responds to changes in vascular pressure and stretch to constrict vessels
local in muscle
sympatholysis
autoregulation
overrides vasoconstriction in response to rising metabolite levels
local in muscle
myogenic response
senses changes in stretch and tell the control center to increase sympathetic tone
4 mechanisms that support venous return during exercise
muscle pump
respiratory pump
sympathetic venoconstriction
increased blood volume
how much can endurance training increase blood volume by
300-500 mL in a few days
cardiovascular triage
protects brain and coronary blood flow during exercise
fick equation
VO2 = Q x A-VO2 diff
resting value for AVO2 diff
5.6 vol%
maximal value for AVO2 diff
16 vol%
why does stroke volume plateau while HR rises?
shortened filling time decreases EDV
structural and functional adaptations from endurance training
increased LV mass
increased LV volume
increased blood volume
increased calcium handling
increased stroke volume
why does systolic pressure rise during exercise?
increase in Q
why does diastolic pressure stay the same or decrease during exercise?
decrease in TPR
minute ventilation
volume of air breathed each minute
alveolar ventilation
volume of air participating in gas exchange
dead space ventilation (ADS)
air in the conducting zone not participating in gas exchange
4 factors that contribute to pulmonary gas exchange
tissue area
diffusion coefficient
difference in partial pressure`
tissue thickness
OH Curve
arterial PO2 can fluctuate without large drops in saturation
at lower PO2, there is a larger unloading of O2 to tissues
Bohr effect
hemoglobin’s affinity for oxygen decreases in response to lower pH and higher levels of CO2
enhances oxygen delivery to tissues
what 3 things affect the oxyhemoglobin dissociation curve?
low pH
2,3 DPG concentration
body temperature
three mechanisms of CO2 transport in the blood
carbonic anhydrase-bicarbonate ions
chloride shift
haldane effect
haldane effect
CO2 unloading in the lungs