week 12 Flashcards
what is the formula for calculating Q (cardiac output)?
Q = 100 x (VO2 / [CaO2 - CvO2])
define cardiac output (Q)
the volume of blood pumped out of the left ventricle in 1 min (L/min)
Q = HR x SV
define heart rate (HR):
the number of cardiac cycles or beats per min (beats/min or bpm)
define stroke volume (SV)
the volume of blood pumped out of the left ventricle in one heart beat (mL)
define venous return (VR)
the volume of blood coming back into the heart in 1 min (not always equal to Q)
how can we increase cardiac output (Q)?
increase HR
increase SV
increase HR and increase SV
define diastole and end-diastolic volume (EDV)
diastole: the relaxation phase when cardiac filling occurs
EDV: the amount of blood in the ventricles at the end of diastole - what is in the ventricle at the end of filling
define systole and end-systolic volume (ESV)
systole: contraction phase, when cardiac ejection occurs
ESV: amount of blood in the ventricle at the end of systole - at the end of ejection
how do we calculate SV
EV = EDV - ESV
how do we increase SV
increase EDV
decrease ESV
what is an ejection fraction and how do we calculate it
proportion of blood in the ventricle that is ejected with each beat
EF = SV/EDV x 100 (in %)
copy down the first slide on page 5 of cardiac output
why is Q one of the most important determinants of VO2 max and of endurance performance?
- the ability to match Q to metabolic demands has huge implications for health and general function
- training adaptations to Q have implications for both performance and for health
to understand what happens to Q during acute and chronic exercise, we need to know what happens to HR, EDV, and ESV and WHY
copy down first slide on page 6 of cardiac output!!!
what is HR regulated by?
HR is regulated by the autonomic nervous system (ANS)
- cardioacceleratory (SNS) and cardioinhibitory (PSNS) centers in the medulla
- direct innervation of SA node by accelerator nerve and vagus nerve - increases or decreases firing rate
- HR can be increased via increased SNS outflow, decreased PSNS outflow, or both
what is the balance of SNS/PSNS outflow from the cardiovascular control center influenced by?
- mvmt via motor cortex + proprioceptors
- emotions via hypothalamus
- body temp via hypothalamus
- metabolic activity in muscles via metaboreceptors
- circulating O2, CO2, and H+ via chemoreceptors
- arterial BP via baroreceptors
- venous return via RA stretch receptors
what influences a persons resting HR?
genetics, age and endurance training status
what is the typical resting HR and what is it called when someone is below or above that?
typical resting HR: 60-100 bpm
lower: bradycardia
higher: tachycardia
what determines a persons HR max?
genetics and age
what is SV influenced by
preload, contractility and afterload
define preload
amount of stretch in ventricle/muscle cells
preload is more or less synonymous with EDV
define contractility
the amount of force produced during contraction (at a given period)
contraction force is established by contractility of muscle fibers and is enhanced when cells are stretch towards optimum length by higher preload
define afterload
force opposing ventricular ejection (what the heart needs to overcome to pump blood into the aorta)
what determines ESV
ESV is determined by the balance between the force of contraction and the force the heart is pumping against (afterload). ESV will be lower with increased contraction force and decreased afterload
copy down first slide on page 9 of cardiac output
what are some factors that influence contractility
movement, emotions, body temp, local metabolites, arterial BP, venous return, SNS/PSNS outflow, etc…
accelerator and vagus nerves also innervate the myocardium therefore factors that influence SNS/PSNS outflow from the medulla also influence contractility
SNS - increased contractility = + inotropic effect
PSNS - decreased contractility = - inotropic effect
what are some factors that influence preload?
the same factors that affect SNS outflow from medulla also trigger release of E/NE into bloodstream
this causes venoconstriction throughout body
which increases venous BP b/c the same amount of fluid is now squeezed into smaller vessels
this squeezing encourages blood to flow back to the heart, increasing VR. VR influences preload
which is more or less synonymous with EDV
venous BP is also influenced by blood volume b/c the more fluid in a vessel, the higher the pressure. blood volume influences arterial BP for the same reason.
venous return is enhanced by the skeletal muscle pumps b/c muscle contractions helps pump blood back towards the heart. valves prevent backflow
preload is also influenced by the amount of time available to get blood into the ventricle which is determined by HR
what is the main determinant of afterload
BP is the main determinant of afterload
BP is influenced by vascular resistance (= resistance encountered by blood flowing through vessels)
increased VR = increased afterload
decreased VR = decreased afterload
VR is influenced by length of blood vessels, viscosity of blood, and diameter of blood vessels. Vessel diameter is the only one we can cahnge in the short term
what effect do vasodilation and vasoconstriction have on VR
vasodilation: decreased VR
vasoconstriction: decreased VR
copy down second slide on page 11 of cardiac output
what are metabolites and what do they do
metabolites are products of metabolism like CO2, H+ and La-
they cause vasodilation in the vascular beds where they appear
write down and memorize second slide on page 12 of cardiac output
copy down both slides on page 15 of cardiac output
what are the two plausible theories that explain cardiovascular drift
- driven by increased HR
- HR increases
- since Q is regulated, SV decreases to maintain Q
HR increases over time bc
- increased body temp
- hypothalamus signals cardioacceleratory center
- SNS outflow to SA node
- driven by decreased SV
- SV decreases
- since Q is regulated, HR increases to maintain Q
SV drops over time bc
- thermoregulatory response
- increased skin blood flow to dump heat
- eventual dehydration
- due to sweat lost and resp losses
