Cardiac Physiology Pt. II Flashcards
Cardiac output
• How to ensure the right amount of blood is pumped
• Determined by total tissue blood flow
• How to ensure the right amount of blood is pumped
CO=____
• Brain - \_\_\_\_% • Heart - \_\_\_\_% • Spleen a lot, kidneys muscles, skin use a lot • CO = HR x SV ○ Amount of blood that leaves heart with each cycle, times number of cycles per minute
HR x SV
14
4
Cardiac output = O2 need
- Cardiac output increases with body’s consumption of ____
- Sum of total body factors to control blood flow
- Tight curve – very well ____• O2 consumption in blue; cardiac output (L/min per L2, area) in red
○ Relationship between both
§ Drives the amount of blood that’s needed
oxygen
regulated
Cardiac output – decreases with ____
• Declining activity and declining ____
• Cardiac Index – ____
• Peaks at age \_\_\_\_ > declines with age (muscle mass, activity, etc.)
age
muscle mass
CO/area
10
Measuring heart rate
• EKG ____ interval
• Pulse
– ____
– phone – gym
R-R
manually
Heart rate
• Normalheartrateatrest ________ bpm
• Maximum =____ bpm-age
60
60
100
200
Compare max heart rate with refractory periods
Can drugs you give as dentists change this RRP?
• How does HR compare to refractory periods? ○ ERP > minimum duration of \_\_\_\_; won't be able to initiate another AP in that amount of time
ventricular contraction
Stroke volume
Stroke Volume=
____ – End Systole Volume
In typical male, =120 ml-50 ml=70 ml
SV = EDV – ESV EF = SV / EDV
* End diastolic volume - end systolic volume * How do you measure this?
end diastole volume
Measuring stroke volume
• Estimate ventricle volumes from ____
– Subtract volume of the blood ESV from EDV
• Fick’s principal O2 consumption
• Can measure using an echocardiogram ○ Measure volume in chambers, and do the subtraction • Can use Ficks - \_\_\_\_ is a close measure of your cardiac output ○ Can measure changes in \_\_\_\_
echocardiogram
O2 consumption
SV
Calculating cardiac output CO=HRxSV
- Volume of blood being pumped by the heart per unit time
- CO(L/min)=HR(beat/min) x SV (L/beat)
- 70 beats/m x 70 ml/beat = 4900 ml/min ~ ____ L/min
5
Cardiac output
Cardiac factors:
____
____
Coupling factors:
____
____
heart rate
myocardial contractility
preload
afterload
The P-V Loop
• A > mitral valve \_\_\_\_ (end diastolic volume) • B > isometric \_\_\_\_ (aortic valve \_\_\_\_) • C > end systolic (aortic valve \_\_\_\_) • D > isovolumetric \_\_\_\_ ○ One loop of this curve = one heart beat • If stop the heart from contracting at all > removing the Ca++ (add EGTA to remove any excess Ca++) and inject solution > takes more to get it contracting (during diastolic) • Systolic pressure curve is much \_\_\_\_ slope > add Ca++ to keep the LV contracted all the time > constant \_\_\_\_ ○ Properties are different then when relaxed; much smaller volume to get base line pressure, and increase the volume > pressure fills up much more \_\_\_\_ than in the relaxed in the state (diastolic)
closes contraction opens closes relaxation
steeper
contraction
rapidly
The P-V Loop
Ejection fraction = ____/Peak Vol
50ml/100 ml = 50%
• Curve allows you to get the SV, and the ejection fraction (how efficient the pumping heart is)
stroke volume
Modeling stroke volume with pressure-volume curve
- Opening and closing of valves
- Isovolumetric relaxation and contraction
- Tan area = ____
- Stroke volume =EDV-ESV
i.e. when to valves open and close
• Tan area = external work output; energy that your heart is using ○ Isovolumetric relaxation > \_\_\_\_ isn't changing; same with the isovolumetric contraction > no change in \_\_\_\_
external work output
volume
volume
Factors affecting HR and SV – the simple version
HR: autonomic innervation \_\_\_\_ fitness levels \_\_\_\_
SV: heart size \_\_\_\_ gender \_\_\_\_ duration of contraction \_\_\_\_ afterload(resistance)
hormones
age
fitness levels
contractility
preload (EDV)
Cardiac output affected by intrinsic and extrinsic factors
• Intrinsic factors
– Preload: amount ventricles are ____ by contained blood, EDV
– Afterload: ____ exerted by blood in the large arteries leaving the heart
• Extrinsic factors – Neural – Hormonal – Ionic – Temperature
• Preload ○ Amount by which ventricles are stretched by blood they contain ○ Larger end \_\_\_\_ volume > the more stretched • Afterload ○ What does the heart have to pump against • Important in normal \_\_\_\_ (making CO matches needs of body), and the factors that can influence CO
stretched
back pressure
diastolic
regulation
Effect of increasing muscle length on force & velocity
• Relationship bt force and velocity ○ Speed at which you can contract is increased by \_\_\_\_ to a certain point § Increasing the \_\_\_\_ of muscle > allows you to alter load-velocity relationship
load
length
Degree of sarcomere overlap underlies Frank-Starling law
Greater ____ increases amount of tension that can be developed, up to a point
• Sarcomere overlap (higher degree, A) > signal to contract > you're not going to get a lot of movement because you're almost completely overlapped • As you increase the \_\_\_\_ between sarcomeres > gain more when you trigger a contraction > overly stretched and cannot engage the contact • Length of sarcomere is \_\_\_\_ to the tension you will develop ○ Reasoning behind the Frank-starling law
stretch
distance
proportional
Frank-Starling law and preload
- Preload, or degree of stretch of cardiac muscle before contraction controls ____
- Greater ____, greater force
- If SV ↑, HR can ____
- Slower heart beat, exercise increase venous return, ↑ stretch, preload, contraction
- Ventricle is stretched at beginning > greater opportunity to generate force > greater ability to overlap and create force > trigger contraction
- Increase SV > same amount of blood in circulation with a lower ____ > exercisers have larger volume of blood in ventricle > circulate same amount of blood with a lower HR; makes the heart more ____ because you’re extending the cross bridge opportunities > move more blood due to better contraction > lower ____
stroke volume
stretch
decrease
HR
efficient
RHR
Preload - volume of blood in heart at the end of diastole (EDV)
- The preload determines the stretch and ____ of the cardiac sarcomeres
- This determines the ____ of thick and thin filaments and the force generating potential
- ____ doesn’t change, just greater contraction
- Heart more efficient• Extreme athletes are extending their stroke volume
○ Pump same amount of blood through system with fewer cycles
○ Determines length of cardiac sarcomeres > greater force contraction when it happens
○ Increased EDV > stretched amount of blood you can have there
length
overlap
systole
Modeling stroke volume with pressure-volume curve
- ____=B-A
- If lower HR, more blood in ____, more stretch• Lower the HR > more blood in ventricle > more stretch > more cross-bridges > a larger contraction
SV
ventricle
• Increased afterload is not good because it increases the ____ that the ventricle has to work against
pressure
Afterload: load heart must eject blood against
- Afterload ~ ____ (σ)
- Related to ____ law Tension=P x r
- ~____• Afterload is proportional to the pressure > allows to see how increasing resting BP will make your heart work harder
ventricular wall stress
laplace’s
aortic pressure
Increased afterload increases ventricular pressure for given volume
- If aortic pressure higher, aortic valves open and close at ____ pressure
- Decreased ____
- Heart less efficient• Need to have a higher pressure before you can open the aortic valve
○ Increased pressure is required to open valve because there is an increased aortic pressure
• Volume of the heart is larger at the point at which valves snap back shut
○ Fighting against higher aortic pressure, the valves will snap back at a higher pressure because the afterload has to work against the aortic pressure
○ Decrease SV > heart will have to beat more in order to circulate more blood through tissues
§ Because LV is working against a larger amount of pressure!
higher
stroke volume
Afterload: effect of decreasing arterial pressure
- Decreasing arterial pressure allows more rapid ____, bigger effect on end systolic volume, EDV-ESV=SV
- ____ valve opens with less ventricular pressure, more blood ejected, ____ ESV• Rapidly reduce arterial pressure > look at LV volume > as arterial pressure decreases, the ESV decreases (also smaller EDV, but not that much)
○ The difference between top and bottom of curves is getting bigger
○ Aortic valve can open with less ventricular pressure
• Shift ESV to the left much more than EDV > ____ decreased
○ Lowering blood pressure is good for your heart
ejection
aortic
lower
SV
Loading and stroke volume
- Increased preload increases ____
- ____
- Increased afterload decreases ____
- ____
stroke volume
stretch
stroke volume push
Neural control of cardiac output • Parasympathetic nerves ↓ – \_\_\_\_: Chronotropy – \_\_\_\_: dromotrophathy • Sympatheticnerves↑ – \_\_\_\_ – \_\_\_\_ – \_\_\_\_: inotropy
• Para > decrease HR (chronotropy), and conduction velocity (dromotropy) ○ Little effect on contractility; most of their effect is on \_\_\_\_ • Symp > increase HR and conduction velocity, but also the contractility (increase \_\_\_\_, and can speed relaxation)
HR
conduction velocity
HR
conduction velocity
contractility
timing
Signaling paths to alter myocyte contraction
- NE and epi – net rise in ____
- Increases contraction
- Positive inotropic effect
- ACh, Adenosine net decrease• Contraction is driven by Ca++
○ First rely on Ca++ into cell, and then Ca++ release from SR > cross-bridge cycle in muscles
• How to alter this Ca++
○ Epi/Ne > B1/B2 receptors > ____ > inc cAMP > PKA > stimulates ____ channels
• Parasymp signalling
○ M2/A1 by Ach > ____ > decrease in cAMP > less PKA activation > reduction in ____ influx
• Reduce contractility of cardiac muscle:
○ Inhibit this pathway via ____ > block beta receptor > reduce cAMP, PKA and dec Ca++ influx
Ca++
Gs
Ca++
Gi
Ca++
beta blockers
Modulation of cardiac output by neural stimulation
- Sympathetic increases – max ____
- Normal baseline increased by ____
- Combination of HR and SV
- Parasympathetic decreases – max ____• Balance between para and symp
• Give maximum symp stimulation > 2x CO (large amounts of epi)
○ Beating, contractility, etc.
• Basic ____ > normally symp enhanced
• Block completely > ____% reduction
• If increase parasymp > decrease normal CO by 50%
2x
sympathetic
1/2x
tone
20
Parasympathetic innervation
slows heart rate
• via Vagi to tissue near SA, AV node
- ACh released
- Increases permeability to ____
- Hyperpolarization EXPLAIN
• Decreases rate of SA beats
– Further from threshold – ____ takes longer
• Decreases excitability of AV node
– ____ can’t excite nodal fibers
• Strong vagal stimuli can stop heart beat
• Purkinje start beating after ____ sec -
____ – keeps you alive
• Ach from parasymp > increase permeability to K+ in pacemaking cells > hyperpolarization • Na+ leaking that drives PM potential to threshold takes longer • Going to take longer to coordinate the electrical signaling from atria to ventricular chambers • Ventricular escape ○ In this case, parasymp innervation prevents stimulation from coming from SA and AV node > pacemakers in \_\_\_\_ keep the heart beating; lose a lot of contractility of \_\_\_\_, but keeps you going
K+ leak atrial fibers 20 ventricular escape
purkinje fibers
atrium
Sympathetic innervation increases heart rate
- Releases norepinephrine– acts a ____ receptors
- Increases permeability to ____, Na+
- In SA node, more ____, less time for lead to get to threshold
- In AV node, more ____ excitation of bundles• Top: normal resting SA node resting potential
○ Leaking Na+ bring to threshold, then Ca++ then K+ repolarizes
• When have parasymp stimualtion > Ach opens up K+, hyperpolarize resting membrane potential > takes more leaking to bring to threshold > slows the AP rate
• When have symp stimulation > more depolarized ____, and don’t need much leaking now > alter the amount of time to reach threshold
• SA node drives this, but can modulate rate at which signal is transmitted through the bundles; by acting on AV node can speed up ____ of going atrium into ventricles
b1 adrenergic
Ca++
depolarized
efficient
baseline
transmission
Sympathetics and Contractility
Increased contractility by NE is a positive ____ effect; for a given LV pressure, greater ____
• Increase in Ca++ with contractility, for a given end diastolic pressure > you can increase contractility and work > because have more Ca++ coming in > more cycling of contraction
inotropic
contraction
Norepinephrine increases ventricular contractility
- Eject more blood for given ____ – more forceful
- Shifts ____ aspect of PV curve
- Increases ____• Add epi
○ Contractility (systolic curve) > adding more Ca++ > more pressure generated for a given ____
§ For a given amount of pressure, more blood can be cycled through
§ Valves stay longer until longer > eject more ____
EDV
systolic
stroke volume
blood
Contraction decreases in heart failure
- Weaker muscle in ____, dilated cardiac myopathy
- Decreases ____ PV relationship
- Needs increased ____ gives a boost
- Increased EDV, working much harder than it should, increases failure• Weaker muscles > contract less for a given change in volume
○ In order to generate more force > stretches out the ____
○ Boost from increasing the preload
○ Shift to ____ > makes the heart work harder
fibrosis systolic preload ventricular volume right
Hormones modulate
cardiac output
- Cardiac responses to “Fight or flight
- Epinephrine (NE 10-20%) – ____
- Increases HR by depolarizing ____,
- Conductivity by depolarizing ____
- Contractility by increasing ____ entry to myocytes.• Increases conductivity and contractility
adrenal medulla
SA node
AV node
Ca++
Lidocaine usually co-injected with epinephrine
• Inject lidocaine > include epi > make sure that you can maintain in the area you need pain relief > \_\_\_\_ vessels ○ Activates beta receptors > increase \_\_\_\_ and \_\_\_\_ of myocardial contraction > lead to \_\_\_\_ and excessive stimulation • Increase HR > shifting and depolarizing the resting potential
constrict
rate
force
arrhythmia
Potassium, calcium and the heart
- Increased Ca2+ - ____ contraction, decreased Ca2+ - ____,
- Increased extracellular potassium (K+) concentration ____ resting membrane potential long term
- Muscle in sustained contraction, no ____
- Both usually well controlled by body, watch when administer
- Too much K+ in EC solution > depolarize resting membrane potential consistently
- Must be able to contract AND relax
spastic
flaccid
depolarizes
pumping
Potassium chloride stops the heart
• Induce sleep, relax muscles and inject KCl and kill ○ Depolarizes membrane potential to point where you can't stop the \_\_\_\_
contraction
Temperature modulates cardiac output • \_\_\_\_ ↑ HR and strength of contraction. • \_\_\_\_ ↓HR and strength of contractions. • If really chill heart, stops \_\_\_\_ • Employed during \_\_\_\_ surgery
• Slow the heart down during open heart surgery
hyperthermia
hypothermia
beating
open heart
Hormones modulate cardiac output
• Thyroid hormone – \_\_\_\_, – Longer lasting than \_\_\_\_, NE – T3 enters cardiocmyocytes, leads to \_\_\_\_ changes – Somewhat controversial – Cause or effect
• High thyroid > oxygen demand > increase \_\_\_\_ for given change in volume > burn a lot of \_\_\_\_, but a lot of \_\_\_\_ on heart
tachycardia adrenaline transcriptional contractility calories stress
Baroreceptors are stretch receptors
- Baroreceptors – stretch receptors activated by change in ____
- In ____ - close to aorta so clear readout
- Relatively short term, but rapid and ____
- Important to keep blood flowing to the ____
- Close to aorta > very accurate measure of pressure coming out of aortic arch
- Huge help ____, when you’re on two feet you need blood to the head
blood pressure carotid sinus bidirectional head evolutionarily
Baroreceptors change heart rate to maintain correct arterial pressure
- If suddenly stand up, decreased arterial pressure sensed by baroreceptors pressure
- Decreased BR firing increases ____, decreases ____ activity
- Raises ____
- Raise ____• Decreased vagal activity in the medulla (very primitive) > increase CO, and small effect on vascular resistance
• Decrease in vagal activity > how does it increase CO?
○ Increase your ____ and contractility against ____
• Sympathetic activity > how does it increase CO?
○ Increase ____, contraction, and increase efficiency of ____ signal from atrium to ventricles
sympathetic
vagal
cardiac output
systemic vascular resistance
HR
AV node
HR
transmitting
Baroreceptors also respond to high BP
increased BP > increased firing freq. > decreased ____ & inhibit vasoconstriction, increased ____, decreased preload
HR
preload
Bainbridge Effect (Atrial Reflex)
Triggers Bainbridge Reflex Pump more
* Only really works in dogs or women after they give birth * Example of how feedback system works * Increase a large amount of \_\_\_\_ > diff in systolic and diastolic changes quickly > adaptation very quickly in response to the \_\_\_\_ of the vessels
ventricular volume
stretching
How does Atrial Pressure change?
• Atrial pressure increases when ventricular contraction is ____.
– Can provide feedback to block ____
– Can trigger ____ to increase HR
• Right atrial pressure increases when there is increased ____.
– Mobilization of ____ if needed.
– Achieved through ____ stimulation of venous ____ contraction.
low
venous return
bainbridge reflex
venous return
venous reserve
sympathetic
smooth muscle
