circulatory system Flashcards
2 major adjustments to BF during exercise
- inc CO…move more blood out of heart/min
- blood flow redistribution to active tissues
SA node
sets heart rate at rest
resting heart rates of diff ppl
avg = 70bpm
trained = 60bpm
elite athletes = 50bpm
what determines heart rate at rest vs at exercise
at rest:
- ventricles eject 2/3 volume
- HR 70-75bpm
- SA node determines rate
at exercise:
- HR max abt 180bpm
- dec cardiac cycle, short phases
- HR steadily inc w exercise, indicates intensity
if HR is low for high workload, indicates heart efficiency
PNS and SNS during exercise
initial HR increase: due to PNS withdrawal
- rest to 100bpm (SA node)
- PNS fibres release Ach, which causes hyperpolarization…makes it harder to depolarize
- PNS slows HR, so withdrawal causes initial inc
continued HR increase: from SNS activity
- cardiac accelerator nerves allow SNS to inc HR
max HR calc
220 - age in yrs (+/- 12_
= 208 - (0.7 x age)
heart rate variability
standard deviation of peak to peak interval over period of time
sympathovagal balance: balance b/w PNS and SNS
wide variation = healthy
- low HRV = predictor of CV morbidity and mortality
- patients w CVD have low HRV
myocardial cells
contract tgt to generate enough force
- act as single unit
greater force of contraction = more blood pumped
stroke volume
volume of blood pumped by ventricles/beat
SV = EDV - ESV
EDV: end diastolic vol, volume in ventricles at end of diastole
ESV: end systolic volume
what determines stroke volume
- EDV: found by frank and starling…aka pre-load
- as ventricle stretched, SV inc bcs inc actin-myosin overlap
- venous return: amount of blood returning to blood, alters EDV - vascular resistance: aortic pressure, aka afterload
- ability of vascular system to receive SV
- as resistance dec, SV inc
- arteriole vasodilation will dec afterload, makes it easier for arterial system to receive blood - contractility: force of heart contraction
- altered by circulating SNS catecholamines (NE and E)
- inc NE/E will inc contractility…inc SV
- also inc EDV
what affects EDV
- vasoconstriction: inc pressure on venous system, pumps blood
- muscle pump: musc contract and send blood to heart
- respiratory pump: pressure in veins less than in lungs, blood moves down gradient to heart
effects of exercise
inc EDV, dec ESV
inc BF
increases SV until PLATEAUS at 40-60% vo2max
- endurance athletes can have stroke vol 2000ml/beat
cardiac output
Q/CO = HR X SV
in L/min
reflects functional capacity of CV system
amount blood pumped/beat
what regulates blood flow in capillaries
scphincter constriction/relaxation
- opens capillaries to inc BF
factors affecting it:
1. driving force of increased local BP, intrinsic neural control
2. local metabolites
how is arterial blood pressure expressed
systolic BP/diastolic BP
i.e. 120/80
pulse pressure
SBP - DBP
i.e. 120 - 80 = 40
MAP
mean arterial pressure
- avg pressure during cardiac cycle
MAP = DBP + 0.33(SBP - DBP)
equation doesn’t work during exercise bcs based on timing of cardiac cycle
how is blood pressure regulated
short term:
1. SNS
2. baroreceptors: on aorta and carotid artery
- info sent to CVCC/cardiovascular centre
- inc BP results in dec afferent info (dec Q)
- dec BP increases afferent info (inc Q)
long-term:
- via volume control in kidneys
- stimulate to either retain/increase BV, or remove blood volume
- Q helps maintain BP, which drives blood flow
blood o2 carrying capacity
o2 rich blood: 20g/100ml
= 2000g of o2/L (bcs Q measured in L/min)
o2 depleted blood = 150g/L
- we don’t use much o2 at rest
- have large capacity to inc a-v o2 difference
each gram carries 1.34ml of o2
a-v o2 difference
arteriovenous o2 difference
measures amt o2 taken up by tissues from blood
fick principle
vo2 determined by amount of blood pumped from lungs and amount extracted from lungs
VO2 = Q x a-v o2 difference
FUNDAMENTAL CONCEPT
must convert to L/min
what impacts blood flow
- viscosity
- length
- radius: dec radius will inc resistance
BF = delta P/R
poiseulle’s law
shows that radius affects blood flow the most
vasodilation/constriction of smaller arterial BVs are mechanism to regulate regional BF
- arterioles greatest resistance
even small change can have large impact
redistribution of blood flow
inactive tissues need less o2, whereas active need more
- inc Q, body “knows” where to redirect
local metabolites begin vasodilation of active tissues to inc CO
at rest: Q mainly to liver, kidneys, musc
84% to musc during exercise
- heart gets more Q, though relative amount
- brain gets more Q, though lower relative to normal
always 4-5L in body, though amount PUMPED can inc w exercise
emotional influence on exercise
if emotionally charged, inc BP and HR bcs of inc SNS activity
does not impact peak HR/BP
- exercising lowers HR as emotion reduced and focus on activity
rest to exercise to recovery
rapid inc in Q and HR w/in seconds
if work rate constant and below lactate threshold, will steady state
recovery depends on intensity, duration, fitness
cardiovascular drift
progressive inc in HR and dec of SV
- when exercise is prolonged and in heart
insufficient venous return dec EDV
- compensates by inc HR to deal w low SV
drifts up to 20bpm
- why HR not good target
- work harder to reach lower values
classic explanation: blood flow goes to skin for cooling
new explanation: if increase b-receptor action, no drift bcs keeps HR suppressed
- w drugs
incremental exercise and arm work
HR and BP recovery b/w increments
avf HR is misleading bcs impacted by rest periods
- depends on fitness, duration, intensity
arm work > leg work
- more SNS activity
- vasoconstriction during arm work keeps more blood volume in upper body
double product/rate pressure product
HR x SBP
indicates work of the heart
- inc linearly w intensity
what causes inc o2 supply
increased blood flow during exercise
- ONLY inc BF causes this
effect of body position
blood pools into lower body when standing
if lying down, more BF in system
- dec HR, inc SV
- dec hydrostatic load
resistance exercise
vascular compression, inc total peripheral resistance and dec musc perfusion
to restore BF, must inc SNS, Q, MAP
acute CV strain dangerous to ppl w heart disease
central command theory
motor signal from w/in brain, changes at onset of exercise bcs of centrally generated CV motor system
signals set general pattern of CV response
fine tuning of blood flow/CV
heart and muscle mechanoreceptors
chemoreceptors
baroreceptors
sudden death in exercise
unexpected natural death w/in 6h of exercise
- 30% cardiac
- less than 20/yr
kids:
- genetic anomalies
- myocarditis/heart inflammation
- lethal cardiac arrhythmia
adults
- coronary artery disease
- cardiomyopathy
protection of endurance exercise
regular exercise is cardio protective
- dec indicidence of MI and inc survival from heart attack
exercise dec damage from heart attack
