Chapter 9 - exam 2 Flashcards
What are the purposes of the cardiorespiratory system
1) transport O2 and nutrients to tissues
2) remove CO2 waste from tissues
3) regulation of body temperature – w/i circulatory system
What are the two major adjustments of blood flow w/ exercise
1) increased cardiac output: Q=HR*SV
2) restriction of blood flow from inactive organs to active muscle
– respiratory steal == redirect blood flow from legs to lungs to maintain respiratory
– thermoregulation == increase blood to periphery to decrease temp
What are the 4 valves of the heart
Mitral valve (Left AV), Aortic semilunar valve, pulmonary semilunar valve, Tricuspid valve (Right AV)
Explain the pulmonary circuit and its functions
- right side of the heart
- pump deoxygenated blood to the lungs via pulmonary arteries
- return oxygenated blood to the left side of the heart via pulmonary veins
Explain the systemic circuit and its functions
- left side of the heart
- pumps oxygenated blood to the whole body via arteries
- returns deoxygenated blood to the right side of the heart via veins
What biomaterials make up plasma
- it is the liquid portion of blood
- contain ions, proteins, hormones
What are the different types of cells that are within blood
RBC: contain hemoglobin to carry oxygen
WBC: important in preventing infection
Platelets: important in blood clotting
What is the equation for hematocrit
hematocrit = height of RBC/Total Height
What is hematocrit
percentage of blood that is composed of packed RBCs
What is blood flow and how is it effected
- directly proportional to the pressure difference b/t the two ends of the system
- inversely proportional to resistance
What is the equation for blood flow
blood flow = change in pressure / resistance
if you have greater resistance is there lower or higher blood flow
lower blood flow
explain pressure and what it is proportional to
proportional to difference between the MAP and the right atrial pressure (change in pressure)
When measuring pressure, explain the movement of blood
deoxygenated blood goes into the Right Atrium and oxygenated blood leaves from the left ventricle
What is diastole
relaxation period ** mitral and tricuspid valves open when Ventricular pressure < atrial pressure
- ventricles fill with blood
- pressure in ventricles low
- Filling with blood from atria
What is systole
contraction phase ** aortic valve and pulmonary (semilunar) valve open when ventricular P > aortic P
- pressure in ventricles rise
- blood ejection in pulmonary and systemic circulation
Explain the time during systole and diastole during rest vs exercise
AT REST: diastole is longer than systole (HR is slower)
AT EXERCISE: both systole and diastole are shorter – systole longer than diastole (HR higher)
Explain one stroke volume
When the atrium is filling up the ventricles = “preload”
End diastolic volume = 100mL in the ventricles
–> systolic volume = 60mL in blood vessels and pump through body
–> End systolic volume (left over in ventricles) = 40mL at end of ventricular contraction [w/ squeezing movement not perfect and some blood stay in ventricles]
how do you calculate stroke volume
difference between end-diastolic volume (EDV) and end-systolic volume (ESV)
Explain the pathway of drawing the Left-ventricular pressure-volume loop
1) isovolumetric contraction = ventricles contract with no corresponding volume change
2) ventricular ejection = as pressure increases, blood is ejected into the aorta
3) isovolumetric relaxation = ventricles relax with no corresponding volume change
4) ventricular filling = atrial contraction forces small amount of blood into ventricles
Define cardiac output and the equations that solve for cardiac output
Q = amount of blood pumped by the heart each minute
Q = HR * SV
- HR (beats/min)
- SV (mL/beat) = amount of blood ejected in each beat
cardiac output depends on what two factors
training state and sex
Explain the initial stimulus that regulates cardiac output and what is the physiological response to both and result
1) high activity of sympathetic nerves to the heart –> increased SV due to stimulation of ventricular myocardium + increased HR due to stimulation of SA node ==== increase cardiac output
2) decreased activity of the parasympathetic nerves to the heart –>
increased HR due to stimulation of SA node ==== increase cardiac output
What nervous system regulates HR and SV
Autonomic nervous sytem –>
Vagus nerve (parasympathetic) – goes to SA and AV nodes Cardiac nerve (sympathetic) – goes to SA node, AV node, and ventricular myocardium
What 2 things regulate the HR
1) parasympathetic nervous system –> via vagus nerve === inhibit signal from SA or AV to slow HR
2) Sympathetic NS –> via cardiac accelerator nerves, increase HR by stimulating SA and AV nodw
how does Ach decrease HR
stimulates mAch Receptors
What is released that increases the HR by stimulating Beta1-ADR
catecholamines release (NOREPI)
- because + ions are rushing in === causes depolarization of the cell == easier to generate action potential
- on Beta 1 == cause vasodilation
the initial increase in HR at the onset of exercise (up to 100pbm) is due to what
parasympathetic withdrawal — allow sympathetic to take over
After 100bpm what causes increases the HR w/ exercise
sympathetic outflow
How can body temperature influence HR during exercise and why
if you have a high core body temp you will have an increase in HR
- b/c the heart works harder to maintain perfusion pressure
men who have a higher blood volume have a higher/lower SV and higher/lower HR
higher SV and lower HR
Explain HR Variability
- variation in time b/t heart beats
- measured at the R-R time interval (resting HR from peak to peak) using ECG tracing
What is the difference between wide and low variation in resting HRV (HR variability)
- WIDE variation = good index of “healthy” balance b/t SNS and PNS - time b/t beaks constantly changing
- LOW variation = imbalance in autonomic regulation –> good predictor of cardiovascular dysfunction
– sympathetic SN taking over – too much stress and cause cardio issues
What diseases promote decrease in HR variability
- depression
- hypertension
- heart disease = Myocardial infarction
- physical inactivity
What are the three ways that stroke volume is regulated
1) end-diastolic volume (EDV)
2) Average aortic BP
3) strength of ventricular contractility (intropy)
How does EDV effect SV
volume of blood in ventricles at the end of diastole (“preload”) – more preload = more blood in ventriclesi
more stretch on ventricles –> cause more contractility == Frank-Starling Mechanism.
if you have a high EDV = “preload” what happens to SV
increase in SV
Explain the Frank-Starling mechanism
-greater EDV results in more forceful contraction === b/c of stretch in ventricles
—> more stretch = more optimal position for contraction and more blood out means more blood in
*** at rest is the optimal position
- depend on venous return –> more forceful contraction
Venous return is increased by what 4 factors
1) Venoconstriction: smooth muscle in blood vessels use SNS to vasoconstrict and pump more blood
2) Skeletal muscle pump
3) Respiratory Pump
4) Frank Sterling Law
How does skeletal muscle pump effect venous return to the heart
- rhythmic skeletal muscle contractions force blood in the extremities towards the heart == push blood up through valves into the heart
- one-way valves in veins prevent blackflow of blood
How does respiratory pump effect venous return to the heart
- changes in thoracic pressure pulls blood towards the heart
–> w/ inhalation the diaphragm contracts and changes the pressure in the lungs and moves the blood up
–> exhalation gets blood to go down into the heart
The filling time of the heart is affected by what two factors
1) heart rate = if you have a high HR then you will have a lower filling time and lower preload
2) body position
How is your end diastolic volume effected by body position
STANDING: lower stroke volume (blood pools in legs)
SUPINE: higher stroke volume (blood evently distributed in veins –> increased central venous pressure –> increased end-diastolic volume –> increased SV –> increased pulse pressure
If you are lying supine for long periods what happens to. your body to decrease the central pressure increase
begins to decrease the amount of RBCs to decrease the blood volume so the pressure is lower
How does the average aortic blood pressure regulate SV
pressure in the ventricles must overcome the pressure and pump against to open the valve and eject blood (“afterload”)
Explain what afterload is
the pressure the ventricles must pump against to eject blood during contraction
- amount of resistance the heart must overcome to overcome to open the aortic valve and push the blood volume into systemic circulation
- afterload is represented by the knot at the end of the balloon –> to get air out, the balloon must work against that knot
Explain what preload is
left ventricular end-diastolic pressure == amount of ventricular stretch at the end of diastole
- heart loading up for the next big squeeze of ventricles during systole
- blow air into the balloon and it stretches — the more air you blow in the greater the stretch
Is stroke volume directly or indirectly proportional to the afterload
inversely proportional
If you have lower afterload what happens to the stroke volume
if you have less afterload and the same pressure there will be more blood flow because the “door” is open longer and easier for the blood to leave
With a low end systolic volume and low ventricular pressure what type of SV does it create?Afterload?
increased SV
How does the strength of ventricular contractility (intropy) effect SV
if you have higher contractility it increases SV == enhanced by:
1) circulating epinephrine and norepinephrine
2) direct sympathetic stimulation of the heart
What type of stimulation causes ventricular contractility
sympathetic stimulation
- more or less intropy
= less binding of catecholamines = not as forceful contraction
= more binding of catecholamines = more Ca2+, KK into cell for muscle contraction
if you have higher inotropy (ventricular contractility) how does it effect SV
increase SV
For the LVP diagram how does the graph shift from control for increased preload, increased afterload, and increased intropy
- higher preload shifts RIGHT
- higher afterload shifts UP: higher venous return
- higher inotropy shifts LEFT: more forceful contraction
What is the initial stimulus for regulation of SV
- high venous return and high sympathetic activity or epinephrine
How does high venous return and high sympathetic activity or epinephrine effect the ventricle and contractility
in the ventricle it increases end-diastolic volume and increases contractility causing an increase in SV
–> ALSO: less arterial pressure (afterload)W
what are the factors that regulate cardiac output
Q = HR * SV
HR: parasympathetic inhibit and sympathetic nerves promote
SV: sympathetic nerves and Frank-starling (increase stretch) causes increase contraction strength, increase in end-diastolic volume – MAP (afterload) inhibits stroke volume
How does the left-ventricular diagram change with exercise
overall increases size of the diagram on all sides except the bottom
High SV during exercise due to:
- high EDV (preload)
- high ventricular contractility (inotropy)
What is the Fick Equation
VO2 = Q * (a-v)O2 difference
what is the effect of exercise on oxygen demand on muscles
with exercise - oxygen demand by muscles during exercise is 15-25x greater than at rest
What is the difference between hemoglobin and myoglobin
hemoglobin: anywhere in blood flow within the body
myoglobin: only found within muscle cells and transport oxygen w/i muscles
What two factors allow increased O2 delivery during exercsie
1) increased cardiac output
2) redistribution of blood flow: from inactive orans to working skeletal muscle
Up to 40-60% of the VO2 max cardiac output is effected due to what
- increased HR
- increased SV
highQ =highHR * highSV
if an individual is exercising at a VO2 max greater than 40-60% cardiac output is effected by what
an increase in HR because SV BEGINS TO PLATEAU
How do you predict Max O2 uptake using submax HR values
use predicted Hr max and values from submax HR exercise to predict VO2max
if an individual has a greater aerobic capacity will they have a higher or lower VO2 max
higher VO2 max
With untrained individuals how does SV change during exercise
- at high HR, filling time is decreased == cause SV plateau at around 40% of VO2max
- decrease in EDV and SV
How does SV change during supine and upright exercise
Supine position: higher SV and have overall higher volume of output (EDV higher in supine - no pooling in legs)
Upright position: lower SV
How is blood redistributed during exercise
- more blood flow to skeletal muscle: less now to liver, kidney, GI tract (inactive organs)
- O2 consumption high if easier to breathe = VO2 max does not change only submax VO2 changes
** easier to breathe = more blood flow to legs
redistribution of blood flow during exercsie is dependent on what
metabolic rate
- use local regulation to move blood flow to certain areas
Explain local (auto regulation) of blood flow during exercise
- control blood fow by increase in metabolites (ie. nitric oxide == vasodilation), prostaglandins (made at sights of inflammation) , ATP, adenosine…)
- work together to promote vasodilation and increase blood flow to working muscles
What does nitric oxide do for blood flow
is vasodilator (found in beets) better blood flow during exercise
how does the (a-v) o2 difference change during exercise
higher A-V difference
- increase during exercise due to higher O2 uptake in tissues
– used for oxidative ATP production
** is muscle consumes high O2 = larger gradient of O2 to move from arteries into tissue.
How does the arterial O2 consumption change during exercise
CaO2 (arterial) –> stays constant
How does the venous O2 consumption change during exercise
As you consume more O2 the venous content has less O2
** you want to increase oxygen consumption if youre exercising more
- slide 80
What is the emotional influence on a heart
- higher HR and BP in emotionally charged environment b/c increase in SNS activity
- increase pre-exercise HR and BP
Explain what happens to the heart at the transition from rest to exercise
at oneset of exercise:
- rapid in crease in HR, SV, and Cardiac output
- plateau in submax (below lactate threshold) exercise
Explain HR and Q during graded exercise
- increases linearly w/ increasing work rate
- reaches plateau at 100% VO2 max
What happens to BP with graded exercise
MAP increases linearly
- systolic BP increases
- diastolic BP remains fairly constant
