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CV 2 > Cardiac Cycle > Flashcards

Cardiac Cycle Flashcards

1
Q

What is the driving force of the cardiac cycle?

A

pressure gradient

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2
Q

What ensures unidirectional flow?

A

one-way valves

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3
Q

Source of normal heart sounds

A

valve closures

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4
Q

what is the contraction phase called?

A

systole (to contract– ventricles are ejecting)

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5
Q

what is the relaxation phase called?

A

diastole (to expand- ventricles are filling)

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6
Q

purpose of the muscle contractions of papillary muscles

A

keep the valve closed

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7
Q

What makes the lub sound?

A

tricuspid and mitral valves closing

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8
Q

What makes the dub sound?

A

semilunar valves closing

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9
Q

one cardiac cycle: 2 parts

A

relaxation –> contraction

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10
Q

two parts of diastole

A

ventricular filling and isovolumetric relaxation (phases 1 and 4)

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11
Q

two parts of systole

A

Isovolumetric contraction, ejection (phases 2, 3)

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12
Q

comparative durations of diastole and systole

A

at 75 bpm cardiac cycle is 800 ms

300 ms systole

500 ms diastole

Increasing the HR impacts the relative time

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13
Q

Cardiac cycle (4 phases)

A

ventricular filling

isovolumetric contraction

ventricular ejection

Isovolumetric relaxation

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14
Q

Phase 1: ventricular filling

A

atrial pressure is slightly higher than ventricular pressure (–> passive ventricular filling) Atrial pressure goes up during atrial contraction–> final ventricular filling (P wave)

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15
Q

Phase 2: ventricular contraction

A

pressure builds in ventricle, A-V valve slams shut (first hear sound) Dramatic pressure building, volume in the (left) ventricle stays the same (isovolumetric) until it exceeds the pressure in the aorta

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16
Q

Phase 3: ventricular ejection

A

stroke volume is ejected, ventricular volume decreases. As myocytes begin to relax (= repolarization) –> semilunar valve slams shut (second heart sound)–> phase 4

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17
Q

Phase 4: isovolumetric relaxation

A

volume stays the same, and as pressure drops, the A-V valve opens again

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18
Q

How the cycle of the heart is different on the right vs the left

A

Right heart pumps into pulmonary circulation, and pulmonary artery’s pressure is significantly lower than the aorta’s. Also, less time spent in contraction and relaxation because there is a lower peak pressure to build up to / fall from. Slight difference in outflow velocity because of the different pressures.

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19
Q

How does cardiac output compare between chambers?

A

Always the same amount; otherwise we would get backup.

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20
Q

3 tips of right-sided heart catheterization

A

RA, RV, and pulmonary wedge (left atrial pressure, wedged into small pulmonary artery)

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21
Q

what is the function of right ventricular wall thickness?

A

Push out same amount of volume against greater pressure

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22
Q

What is stroke volume?

A

The volume of blood that is ejected in one beat/ contraction. THe difference between end-diastolic volume and end-systolic volume. SV= EDV - ESV

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23
Q

What is ejection fraction?

A

Percent of the end-diastolic volume that was ejected in one beat. EF= SV/ EDV Normal range is 50-55%

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24
Q

What is the dicrotic notch

A

disturbance on the aortic pressure line when the semilunar valve closes

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25
Q

Sounds of the heart

A

S1- lub- closure of mitral/ tricuspid valves S2- dub-closure of aortic and pulmonary valves OS- opening snap (opening of a stenotic mitral valve) S3- 3rd heart sound- diastolic filling gallop or ventricular or protodiastolic gallop S4- 4th heart sound- atrial sound that creates an atrial or presystolic gallop

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26
Q

S1

A

Left ventricular contraction begins just before right, mitral valve closes just before tricuspid valve. Minimal difference in timeing; unusual to hear a split S1 (M1, T1)

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27
Q

S2

A

Right ventricular ejection is longer vs left ventricular ejection Aortic valve closes before pulmonary valve due to greater downstream pressure. Pulmonary valve opens first and closes last (lower downstream pressure) –> normal physiological splitting of S2 heart sound (A2, P2)

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28
Q

timing of semilunar valve openings

A

Right ventricle has shorter isovolumetric contraction Does not require as much pressure to open the pulmonary semilunar valve for ejection Pulmonary valve opens just before aortic valve

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29
Q

timing of AV valve openings

A

Right isovolumetric relaxation is shorter than left (green) Lower peak pressure from which to decrease Tricuspid valve opens before the mitral valve Right ventricular filling before left

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30
Q

Effect of inspiration on right side of the heart

A

Relatively negative intrathoracic pressure  greater VR to RA/RV  increased EDV  greater RV ejection volume Additional time for RV ejection delays pulmonary valve closure (P2) more Enhances physiological splitting of S2

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31
Q

Effect of inspiration on left heart

A

Relatively negative intrathoracic pressure  retention of blood in dilated pulmonary v.v.  reduced VR to LA/LV  decreased LV EDV & ejection Less time for LV ejection accelerates aortic valve closure (A2) more Enhances physiological splitting of S2

32
Q

Abnormal heart sound: S3

A

Early diastole, after S2 During rapid ventricular filling phase Normal in younger people Often indicates volume overload associated w/ heart failure “Gallop” S1, S2 + S3 and/or S4 Protodiastolic gallop: S1- S2 - S3 (“Ken-tuck-y”)

33
Q

Abnormal heart sound: S4

A

S4: Late diastole, just before S1 Associated with unusually strong atrial contraction Indicative of pathology, ventricular wall stiffness and decreased compliance associated with hypertrophy “Gallop” S1, S2 + S3 and/or S4 Presystolic gallop: S4 - S1- S2 (“Ten-nessee”)

34
Q

Heart Murmurs

A

Sound generated by turbulent flow through heart

35
Q

structural issues leading to heart murmurs

A

Thickening of valve leaflets Narrowing (stenosis) of valve openings Holes in chamber walls or septae between chambers

36
Q

Hemodynamic issues leading to heart murmurs

A

decreased viscosity: anemia

37
Q

Venous Pulse

A

•Systemic veins:

Pressure waves independent of arterial pressure waves

•Contributions to venous pulse:

  1. Retrograde action of the heartbeat during cardiac cycle
  2. Respiratory cycle
  3. Contraction of skeletal muscles
38
Q
A

Effects of cardiac cycle on jugular venous pulse

  • a wave: RA contraction
  • c wave: RV pressure in early systole

(bulging of tricuspid valve into RA)

  • v wave: RA filling (tricuspid closed)
  • Increase pressure subsequent to y minimum à

occurs as VR continues with reduced ventricular filling

39
Q

Jugular Venous pulse: clinical correlates of a waves (RA contraction)

A
  • Large a waves: Tricuspid Stenosis, Right Heart Failure
  • Cannon a waves: 3 °, Complete Heart Block (AV dissociation)
  • No a waves: Atrial fibrillation
40
Q

clinical correlates of jugular venous pulse (c wave)

A

RV pressure in early systole (tricuspid bulging)

41
Q

clinical correlates of jugular venous pluse- v wave

A

RA filling (tricuspid closed)

•Large v wave (c-v wave): Tricuspid regurgitation

42
Q

Jugular Pulse: Effect of Respiratory Cycle

A

Inspiration

  • Negative jugular v. pressure
  • ↓ intrathoracic pressure (thoracic vessels & RA)

–↓ RA & VC pressure –> dilation à

↓ resistance –> ↑ flow

–↑ VR from head & upper extremities

43
Q

L.E. Venous Pressure: Effect of Skeletal Muscle Contraction “Muscle Pump”

A
  • Standing: Venous pooling –> pressure rises in foot
  • Walking: Pumping action of muscles on leg v.v. + unidirectional venous valves limit retrograde flow

–Promotes VR & decreases venous pressure in foot

–Each step: small oscillation & net decrease in foot pressure

44
Q
A

1–> 2 Isovolumetric contraction (aortic valve opens at end)

2–> 3 Ejection (at 3 we are at end systolic volume) (aortic valve closes at end)

3–> 4 isovolumetric relaxation (mitral valve opens at end)

4–> 1 ventricular filling (mitral valve closes at end)

45
Q

Work

A

pressure x change in volume

W= p delta V

  • Pressure-volume component: Aortic pressure & change in volume (SV: EDV – ESV)
  • Does not factor acceleration imparted to blood for ejection (kinetic energy) or energy expended during isovolumetric contraction (tension heat)
46
Q

Tension Heat

A

= Major Energy (ATP) Cost (heart not doing work but using a lot of ATP)

(T): Ventricular wall tension

Major determinant: Afterload

(Δt): Time in Systole

(k): Converts T · Δt into units of energy

TENSION HEAT:

  • Maintenance of isometric tension –> ATP splitting –> heat
  • Greatest energy cost
  • Splitting ATP during Isovolumetric Contraction
  • Isometric: no “work” without movement
47
Q

Ventricular Wall Tension

A

•Ventricular wall tension/stress: Tangential force acting on myocardial fibers; Force acting to pull fibers apart

–Energy expended to oppose wall stress

•3 major determinants of myocardial O2 demand:

–Ventricular wall tension

–Heart rate

–Contractility (inotropic state)

–(Minor: basal metabolism, electrical depolarization)

48
Q

Approximation of wall tension by laplace’s relationship

A

•Wall tension (σ) is related to transmural pressure (P), radius (r), and wall thickness (η)

–σ = P x r/ 2h

•Directly proportional to:

–Systolic ventricular pressure (P)

–Radius of ventricular chamber (r)

•

•Inversely proportional to:

–Ventricular wall thickness (η)

•

49
Q

Cardiac output

A

Volume of blood pumped by the ventricles per minute (ml/min or L/min)

–Common indicator of cardiac function

–Normal = ~ 5 L/min at rest

  • 7,200 L/day and 210,240,00 L in 80 years
  • Not including exercise, which increases 5-6xs in an average person
50
Q

Cardiac Index

A

–Common indicator of cardiac performance: CO normalized for body size

–Cardiac index: L/min/m2

•Normal reference range: 2.8 – 4.2

51
Q

Preload

A

–Sarcomere length prior to contraction

–Relates to ventricular filling: ventricular stretch at end of diastole (EDV)

Positive impact on stroke volume

–Isometric tension: isovolumetric contraction phase

–↑ Preload –> ↑ SV

52
Q

Afterload

A

–Relates to pressure which contracting fibers must oppose for ejection

–Direct measure: maximum systolic ventricular pressure

–Indirect estimate: MAP

–↑ afterload –> ↑ ESV –>↓ SV

negative impact on stroke volume (SV)

–Isotonic tension: ejection phase

53
Q

Contractility (Inotropy)

A

–Force generation independent of preload

–Influenced by autonomic input

positive impact on stroke volume

54
Q

Pre-Load: Frank Starling Law of the Heart

A

Length-tension relationship for cardiac m.

Initial fiber length is important determinant of work performed by heart

KEY: Degree of ventricular filling prior to contraction (EDV = preload) is an important determinant of force generated with contraction

55
Q

Greater Pressure with Greater Filling

A

•End-diastolic volume (EDV/LVEDV) is proportional to initial fiber length (passive stretch)

–Parallels initial portion of passive tension of L-T curve

•Systolic pressure is proportional to tension production of fibers

–Parallels ascending portion of active tension of curve L-T curve

56
Q

Proposed mechanisms for increased amount of stretch on cardiac myocytes

A

Calcium is related.

FYI:

  • Increased regulatory protein affinity to Ca2+ (Troponin C)
  • Stretch-activated Ca2+ channels on the sarcolemma

–Increases Ca2+ influx: increases Ca2+ -induced- Ca2+ release from SR

Increases sensitivity of RYR receptors to Ca2+ influx

57
Q

Frank starling curve for systolic failure

A

Failing” heart: Flatter curve

  • For a given EDV or Pressure: ↓ SV (and CO) vs. normal
  • Increased EDV remaining after systole in an impaired heart results in insignificant increase in SV despite increase in LV end-diastolic pressure
58
Q

Cardiac Cycle: effects of prelaod

A

•Velocity of myocardial contraction is directly related to Preload

–↑ preload, ↑ shortening velocity

–↑ Ejection fraction

59
Q
A
60
Q

Cardiac cycle: effects of afterload

A

•Velocity of myocardial contraction inversely related to Afterload

–↑ afterload, ↓shortening velocity

–↓ Ejection fraction

•Key: ↑ Afterload –> greater proportion of systole spent in isovolumetric contraction phase

–> ↓ SV and ejection fraction

–> ↑ ESV (BAD)

61
Q

myocyte contractile phases of systole

A

•Myocyte contractile phases (systole):

–Isovolumetric contraction:

isometric contraction (pressure generated to open aortic valve)

–Ejection phase: isotonic contraction

62
Q

Contractility/Inotropy

A

Think changes in calcium levels, autonomic regulation!

•Contractility = Contractile strength independent of preload (i.e., sarcomere length/end-diastolic volume)

–↑ contractility –> ↑ SV

  • ↑ Contractility: shifts Starling curve up & left for a given EDV
  • ↓ Contractility: shifts curve down & right for a given EDV
  • Intrinsic factor of cardiac performance

–Rate of pressure development during ejection (Δ P/ Δ t)

•Velocity of ejection

–Impacts slope of end-systolic pressure-volume relationship (ESPVR)

•Autonomic input influences [Ca2+]i à contractility

63
Q

Contractility and ESPVR (End-systolic pressure-volume relationship)

A

•↑ Contractility –> ↑slope of ESPVR

64
Q

3 Factors influencing SV

A

SV = EDV - ESV

  1. EDV relates to preload
  2. ESV relates to afterload
  3. Inotropy: ↑ SV by ↓ ESV

(independent of EDV)

65
Q

Venous Return and Cardiac Output

A

•Venous return (VR) to right side of heart must equal output of left side of heart

–Normal steady state: VR = CO

  • If CO ≠ VR: blood would accumulate in the thorax OR be removed from the thorax
  • If LV output = 6 L/min and RA return = 5 L/min: blood would shift to periphery

–Peripheral edema

66
Q

Cardiac Function Curve

A

Cardiac output as a function of Right Atrial Pressure (red line)

•Same relationship as Frank Starling Law

–

  • ↑ RAP
  • ↑ Ventricular filling
  • ↑ EDV
  • ↑ SV
  • ↑ CO
67
Q

commonly used variables as indicators of cardiac function

A

Stroke Volume (SV)

Cardiac Output (CO, Q)

Cardiac Index (CI)

68
Q

commonly used variables as indicators of ventricular filling (preload)

A

End Diastolic Volume (EDV)

End Diastolic Pressure (EDP)

Central Venous Pressure (CVP)

Left Atrial Pressure/Right Atrial Pressure (LAP/RAP)

Pulmonary capillary wedge pressure (PCWP)

69
Q

Vascular Function Curve: venous return, cardiac INPUT

A

•Relates to pressure gradient which favors venous return

–↓ RAP –> ↑ VR

–↑ RAP –> ↓ VR

•As RAP becomes more negative: ↑ VR driving force (ΔP = CVP - RAP)

70
Q

Slope of vascular function curve determined by…

A

compliance and resistance of vessels

71
Q

plateau of vascular function curve

A

indicates most negative RA that can still allow for VR

-At more negative values: large central veins collapse, inhibiting VR

–Plateau ~ RAP of -1 mmHg)

72
Q

venous return and right atrial pressure

A

•Right Atrial Pressure:

depends on VR; determines extent of ventricular filling (and vice versa)

•At normal CO of 5 L/min:

RAP = 0 - 2 mmHg

–RAP ↓ as CO ↑ (drawing blood from right heart)

•VR = CO at equilibrium

73
Q

Interaction of cardic and vascular function curves

A
  • Equilibrium: Intersection of cardiac and vascular function curves
  • Steady state:

VR = CO and CO = VR

–CO and VR depend on RAP

–RAP depends on CO and VR

•Intrinsic compensation to transient changes

Dynamic state of equilibrium in healthy system

74
Q
A

aortic stenosis (pressure in left ventricle very high)

75
Q
A

heard during diastole, atrial pressure is higher than expected to eject across stenotic mitral valve

76
Q
A

aortic regurgitation

77
Q
A

mitral insufficiency (hear it during systole)

CV 2 (3 decks)

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