Cardiac Physiology Pt. II Flashcards Preview

BS V, Module I > Cardiac Physiology Pt. II > Flashcards

Flashcards in Cardiac Physiology Pt. II Deck (44)
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1
Q

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
A

HR x SV
14
4

2
Q

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
A

oxygen

regulated

3
Q

Cardiac output – decreases with ____
• Declining activity and declining ____
• Cardiac Index – ____

• Peaks at age \_\_\_\_ > declines with age (muscle mass, activity, etc.)
A

age
muscle mass
CO/area
10

4
Q

Measuring heart rate

• EKG ____ interval
• Pulse
– ____
– phone – gym

A

R-R

manually

5
Q

Heart rate
• Normalheartrateatrest ________ bpm
• Maximum =____ bpm-age

A

60
60
100
200

6
Q

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
A

ventricular contraction

7
Q

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?
A

end diastole volume

8
Q

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 \_\_\_\_
A

echocardiogram
O2 consumption
SV

9
Q

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
A

5

10
Q

Cardiac output

Cardiac factors:
____
____

Coupling factors:
____
____

A

heart rate
myocardial contractility

preload
afterload

11
Q

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)
A
closes
contraction
opens
closes
relaxation

steeper
contraction
rapidly

12
Q

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)
A

stroke volume

13
Q

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 \_\_\_\_
A

external work output
volume
volume

14
Q

Factors affecting HR and SV – the simple version

HR:
autonomic innervation
\_\_\_\_
fitness levels
\_\_\_\_
SV:
heart size
\_\_\_\_
gender
\_\_\_\_
duration of contraction
\_\_\_\_
afterload(resistance)
A

hormones
age

fitness levels
contractility
preload (EDV)

15
Q

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
A

stretched
back pressure
diastolic
regulation

16
Q

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
A

load

length

17
Q

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
A

stretch
distance
proportional

18
Q

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 ____
A

stroke volume
stretch
decrease

HR
efficient
RHR

19
Q

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
A

length
overlap
systole

20
Q

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
A

SV

ventricle

21
Q

• Increased afterload is not good because it increases the ____ that the ventricle has to work against

A

pressure

22
Q

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
A

ventricular wall stress
laplace’s
aortic pressure

23
Q

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!
A

higher

stroke volume

24
Q

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
A

ejection
aortic
lower
SV

25
Q

Loading and stroke volume

  • Increased preload increases ____
  • ____
  • Increased afterload decreases ____
  • ____
A

stroke volume
stretch
stroke volume push

26
Q
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)
A

HR
conduction velocity

HR
conduction velocity
contractility
timing

27
Q

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
A

Ca++

Gs
Ca++

Gi
Ca++

beta blockers

28
Q

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%
A

2x
sympathetic
1/2x

tone
20

29
Q

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
A
K+
leak
atrial fibers
20
ventricular escape

purkinje fibers
atrium

30
Q

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
A

b1 adrenergic
Ca++
depolarized
efficient

baseline
transmission

31
Q

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
A

inotropic

contraction

32
Q

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 ____
A

EDV
systolic
stroke volume
blood

33
Q

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
A
fibrosis
systolic
preload
ventricular volume
right
34
Q

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
A

adrenal medulla
SA node
AV node
Ca++

35
Q

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
A

constrict
rate
force
arrhythmia

36
Q

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
A

spastic
flaccid
depolarizes
pumping

37
Q

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 \_\_\_\_
A

contraction

38
Q
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
A

hyperthermia
hypothermia
beating
open heart

39
Q

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
A
tachycardia
adrenaline
transcriptional
contractility
calories
stress
40
Q

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
A
blood pressure
carotid sinus
bidirectional
head
evolutionarily
41
Q

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
A

sympathetic
vagal
cardiac output
systemic vascular resistance

HR
AV node
HR
transmitting

42
Q

Baroreceptors also respond to high BP

increased BP > increased firing freq. > decreased ____ & inhibit vasoconstriction, increased ____, decreased preload

A

HR

preload

43
Q

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
A

ventricular volume

stretching

44
Q

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.

A

low
venous return
bainbridge reflex

venous return
venous reserve
sympathetic
smooth muscle