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BMS200 > Week 5, Lecture 1 > Flashcards

Week 5, Lecture 1 Flashcards

1
Q

which ventricle pumps more blood per minute

A

left ventricle

The left ventricle pumps more blood per minute than the right ventricle. Although both ventricles pump the same volume of blood over time, the left ventricle is responsible for pumping oxygenated blood to the entire body, which requires a greater force and pressure. In contrast, the right ventricle pumps deoxygenated blood to the lungs, which is a shorter distance and requires less pressure. So, while their output is equal in volume, the left ventricle works harder overall due to the demands of systemic circulation.

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2
Q

what is the flow of blood through the heart

A

deoxygenated from vena cava –> RA –> tricuspid valve –> RV –> pulmonary valve –> pulmonary circulation (blood to lungs to get oxygen)

oxygenated blood returns through pulmonary veins –> left atrium –> mitral valve –> left ventricle –> aortic valve –> aorta (oxygenated blood to the body)

Deoxygenated Blood Entry: Blood that is low in oxygen returns to the heart from the body through two large veins: the superior vena cava (from the upper body) and the inferior vena cava (from the lower body).
Right Atrium: The deoxygenated blood enters the right atrium, a chamber at the top right side of the heart.
Tricuspid Valve: When the right atrium contracts, blood flows through the tricuspid valve into the right ventricle.
Right Ventricle: The right ventricle pumps the deoxygenated blood through the pulmonary valve into the pulmonary arteries.
Pulmonary Circulation: The pulmonary arteries carry the blood to the lungs, where it picks up oxygen and releases carbon dioxide.
Oxygenated Blood Return: The now oxygen-rich blood returns to the heart through the pulmonary veins.
Left Atrium: The oxygenated blood enters the left atrium.
Mitral Valve: The left atrium contracts, pushing blood through the mitral valve into the left ventricle.
Left Ventricle: The left ventricle, which has the thickest walls to generate high pressure, pumps the oxygenated blood through the aortic valve into the aorta.
Systemic Circulation: The aorta distributes the oxygen-rich blood to the rest of the body.

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3
Q

what are the 2 things that force a cardiomyocyte generates with each systole depends on

A
  1. PRELOAD
    overlap between actin and myosin during diastole
  2. INOTROPY
    amount of calcium available to bind troponin
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4
Q

what is inotropy

A

AKA contractility
Amount of calcium available to bind to troponin

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5
Q

factors that increase inotropy

A

HR, SNS, cortisol, TSH

▪ Increased sympathetic nervous system
stimulation
▪ Increased heart rate (“loads” more calcium in the SR during relaxation)
▪ Things that increase SNS effectiveness – thyroid hormone, cortisol, etc.

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6
Q

what is preload

A

ventricular filling

Preload is the filling pressure of the heart at the end of diastole.

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7
Q

preload vs afterload

A

google

Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling. Afterload is the force or load against which the heart has to contract to eject the blood.

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8
Q

positive ionotriopic agents (i.e. increase contractility)

A

certain hormones (e.g., epinephrine) and drugs (e.g., digitalis), can increase the force of contraction, leading to increased sarcomere shortening.

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9
Q

what do positive ionotropic agents do to sarcomere length

A

increase sarcomere shortening because of increases contraction force

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10
Q

negative ionotropic agents

A

reduce the force of contraction, which can be associated with reduced sarcomere shortening.

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11
Q

what increases force development

A

good overlap of actin and myosin

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12
Q

right atrium pressure tracing

A, C, X, V, Y waves

A
  • A Wave – Atrial contraction (atrial systole)
  • C Wave – Bulging of tricuspid
  • X Wave – Atrial relaxation (atrial diastole)
  • V Wave – Passive filling of the atria (ventricular systole)
  • Y Wave – Emptying of atria into the ventricles with the opening of AV valves (early diastole).
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13
Q

isovulmetric

A

there is a change in pressure, but no change in volume

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14
Q

are the valves open or closed if isovolumetric

A

closed

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15
Q

systole vs diastole

A
  • Systole – when the chamber applies pressure work to blood through contraction
  • Diastole – when the chamber no longer applies pressure work to blood through contraction
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16
Q

wiggers diagram good to show that

A
  • The Wiggers diagram is a good way to illustrate that the ventricle cannot:
    ▪ eject blood into the great artery until its pressure is greater than that in the artery
    ▪ accept blood from the atria unless its pressure is less than that in the atria
  • Valves ensure that blood only flows one direction despite the large changes in ventricular pressure
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17
Q

rapid ventricular slowing vs. slower filling

what is rapid ventricular filling because of?
what is rapid ventricular filling aka?

A
  • Rapid ventricular filling is due to the rapid expansion of the ventricle and the drop in volume that ensues
    ▪ Also known as passive filling, and it is responsible for 80% of ventricular filling at rest
    ▪ Passive filling takes time – decreased with increased heart rates
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18
Q

what does aorta pressure oscillate between>

A

around 80-120

Aortic pressure oscillates between systolic and diastolic pressure

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19
Q

what happens when the aortic valve closes? what’s the notch called in between?

A
  • After the aortic valve closes, a secondary wave can be seen
    ▪ The division between these two waves is known as the dicrotic notch

2 waves with dicrotic notch in between

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20
Q

what is the most accurate marker or aortic valve closeure

A

dicrotic notch

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21
Q

what is the 2nd wave from in aortic pressure curve

A

▪ The secondary wave is thought to be formed by the elastic recoil of the aorta against a closed aortic valve
▪ Likely also partially impacted by complex vibrations due to the “weird” shape of the aorta

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22
Q

S3 and S4 sounds in phonocardiogram- are they healthy?

A

s3 can be heathy, s4 bad

  • S3–oftenfoundinhealthy young adults and children
    ▪ New emergence is usually pathological in adults (often indicator of myocardial ischemia)
    ▪ Blood enters a non- compliant or “not-fully- relaxed” ventricle during rapid filling
  • “Kentucky”(eeisS3)
  • S4 – usually pathologic
    ▪ Ventricle “straining” as the atria contract and “force” blood into a non-compliant ventricle
  • “Tennessee”(TennisS4)
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23
Q

how does right and left heart differ

A

right heart has lower ventricle pressure and pulmonary artery pressure is way less than aorta on left side

atrium is relatively similar

  • Note the lower pressures that develop in the right ventricle and pulmonary arteries
  • Pulmonary artery pressure is ~ 25/7 mm Hg
  • Slightly lower atrial pressures in the right vs. left
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24
Q

RV vs LV pressures

A

RV= 25/4
LV= 120/8

bottom number= end diastolic pressure

25
Q

RA vs LA for ventricular filling (as atrial contraction ends)

A

RA= 4
LA= 8

26
Q

aorta vs pulmonary artery

A

aorta- 120/80
PA= 25/10

27
Q

end diastolic volume and end systolic volume

A
  • End diastolic volume (EDV) – the volume in the ventricle at the end of diastole
  • End systolic volume (ESV) – the volume in the ventricle at the end of systole
28
Q

wiggers diagram approximate volume of end systolic and end diastolic volumes

A

EDV= 120
ESV= 50

29
Q

what is stroke volume? formula?

A

the volume ejected with each heartbeat

▪ SV = EDV – ESV

30
Q

what is cardiac output?

formula?

A

the volume ejected by each systole X heart rate

▪ CO = SV X HR

31
Q

ejection fraction? formula?

A

is the proportion of EDV that is ejected each beat

▪ EF = SV/EDV = (EDV – ESV)/EDV

32
Q

what corresponds to preload

A

EDV (end diastolic volume) [[the volume in the ventricle at the end of diastole]]

33
Q

what is the optimal preload

A

greater force of contraction due to optimal overlap of actin and myosin in sarcomeres

34
Q

what are the 3 things that stroke volume is impacted by

A
  1. preload
  2. contractility (ionotropy)
  3. afterload
35
Q

what is ionotropy/ contractility dependent on

A

dependent on calcium handling within the cardiomyocyte – intrinsic ability

36
Q

what is afterload

A

the pressure that the heart must overcome to eject blood into the great arteries.

37
Q

what facctors increase afterload (how much pressure to overcome to eject blood into great arteries)

A

aorticstenosis,elevatedblood pressure

38
Q

what is one of the major factors that determines delivery of oxygen and nutreints to tissues

A

cardiac output

and vascular tone in tissue receiving blood

39
Q

what is measured as an “estimate” of heart function in heart failure?

A

ejection fraction (proportion of EDV ejected each beat)

40
Q

what is the pressure volume loop of the ventricle helpful to measure

A

▪ Total workload of the heart (ventricle)
▪ Contractility
▪ Compliance of the heart itself
▪ Basic hemodynamic parameters
* EDV * ESV * SV

41
Q

what is the systolic pressure curve vs diastolic pressure curve in the ventricular pressure volume loop

A
  • Systolic pressure curve – with a given volume, pressure generated during systole is recorded
  • Diastolic pressure curve – The pressure is recorded during diastole for the specified volume
42
Q

pressure volume loop diagram with definitions SLIDE 27

A

xx

43
Q

what is the majority of work done by the ventricle? minority?

A

pressure-volume work

The minority of cardiac work is due to actually ejecting blood from the ventricle into the artery (kinetic energy)

44
Q

what happens if you increase afterload (the pressure the heart must overcome to eject blood into the great arteries)

A

decrease SV and ejection fraction

decrease stroke volume (volume ejected with each heart beat) and ejection fraction (the proportion of EDV ejected each beat)

increases myocardial oxygen demand more than ionotropy –> hypertension is energetically expensive

45
Q

what is afterload technically determined by

A

tension

technically determined NOT by the systolic blood pressure, but by the tension that the ventricle needs to develop to open the aortic valve

46
Q

Laplace law and afterload

A

Laplace law for wall stress

increase pressure or radius then wall tension increases

increase thickeness then wall tension decreases

47
Q

what happens when you increase preload (the filling pressure of the heart at the end of diastole.)

A

increase stroke volume (more blood to send out)

48
Q

what happens to stroke volume if decreases contractility/ ionotropy

A

lower stroke volume as inotropy decreases
▪ As it decreases, then the amount left at the end of systole also decreases…
* Representing a decrease in ejection fraction

49
Q

what is a normal ejection fraction

A

> 50%

50
Q

increased venous return…

A

increased venous return→increased preload→ increased stroke volume… but also a slight increase in afterload as the wall tension increases (increase in pressure)

51
Q

increased afterload…

A

afterload increases→decreased stroke volume→ increased preload→a new “steady state” with slightly elevated preload but a greater increase in afterload

52
Q

inotropy increases…

A

inotropy increases→increased stroke volume→ decreased volume left after systole→a slightly lower preload

53
Q

effect on cardiac output:

▪ Catecholamines?
▪ Parasympathetic stimulation?
▪ Stretching of the ventricles?
▪ Isolated increases in heart rate (chronotropic and inotropic)?
▪ Increases or decreases in central blood volume?
▪ Increases or decreases in systolic blood pressure?

A

increases
decrease
increase
increase
increase BV = increase
increase systolic BP = increase

54
Q

what is the treppe effect

A

accumulation of calcium in the SR as HR increases

  • Notenoughtimeto “remove” calcium from the cell across the plasmalemma
55
Q

SNS impacts

A

increase cardiac output
increase heart rate
increase force contraction

56
Q

what is the most determinant of cardiac ouput

A

preload and venous return to the heart

▪ As the heart delivers more blood to peripheral tissues, then venous return increases
▪ Force of contraction will also increase as preload increases
▪ This will eventually be limited by the increase in afterload that
occurs as blood pressure rises

57
Q

cardiac output in each ventricle?

A
  • Cardiac output must be equal between the left and right ventricles for multiple reasons:
    ▪ Proper tissue perfusion & oxygen delivery
    ▪ Preventing pulmonary congestion and systemic hypoperfusion
58
Q

ventricle relations

A
  • PRELOAD OF ONE VENTRICLE DEPENDS ON THE CARDIAC OUTPUT OF THE OTHER.

BMS200 (19 decks)

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