Cardiac Cycle

Front 1

valve closure and opening order

Back 1

atrial systole -> mitral valve closed, tricuspid valve closed, pulmonary valve opened, aortic valve opened -> ventricular systole -> aortic valve closed, pulmonary valve closed, tricuspid valve opened, mitral valve opened -> ventricular diastole ---- closing occurs L before R, opening occurs R before L ---- this is because R has longer ejection time b/c less contractile and has more filling time b/c more compliant

Front 2

cardiac cycle phases

Back 2

after atrial systolic ejection, first phase is isovolumetric relaxation (12-16 msec) which occurs from SL valve closure to AV valve opening (due to atrial P > ventricular P), there is rapid ventricular P decline during this stage due to myocardial active state termination; second stage is diastolic filling (150-800 msec), which occurs from AV valve opening to AV valve closing (due to ventricular P > atrial P); third stage is isovolumetric contraction (10 msec, beginning 40 msec after electrical ventricular systole begins), which occurs from AV valve closure to SL valve opening (due to ventricular P > great vessel P), there is rapid ventricular P rise during this stage due to incr. of myocardial active state; fourth stage is systolic ejection (250-280 msec), which occurs from SL valve opening to SL valve closure)

Front 3

ventricular diastolic filling pattern

Back 3

majority of filling occurs in beginning when compliance is maximal; the filling rate declines as the ventricle fills, until the "a kick" near the end due to atrial systole which increases filling rate for a short time prior to AV valve closure

Front 4

ventricular diastolic filling pressures

Back 4

quick spike in P at beginning as most filling occurs; slow but steady rise in mid (less flow, but also less compliance so P increases at a significant rate), large spike at end corresponding to "a kick" of atrial systole (again, large P increase b/c compliance low at this point)

Front 5

why is atrial systole shorter than ventricular systole?

Back 5

b/c atrial AP duration is shorter than atrial systole

Front 6

systole vs diastole lengths in cycle

Back 6

2/3 of total cycle length is diastole, 1/3 systole; when HR incr systole % incr and diastole % decr

Front 7

atrial systole vs ventricular systole timing

Back 7

atrial systole occurs 120-160 msec before ventricular systole

Front 8

AV valve opening mech

Back 8

passive, due to higher P in atria than ventricle

Front 9

AV valve closure requirements (4)

Back 9

passive movement of valve leaflets toward atria driven by ventricular P; contraction of circumference of valve annulus by ventricular myocardium; contraction of papillary muscles to control position of valve leaflets; contraction of ventricular myocardium to control papillary muscle position ---> lots of things can go wrong to make AV valve incompetent

Front 10

SL valve opening and closing mech

Back 10

both are passive; SL valves generally competent unless valve annulus dilated

Front 11

phospholamban

Back 11

normally inhibits SERCA, thus making it harder for myocyte to relax; can be phosphorylated by PKA (through SNS pathway -> Ga -> cAMP -> PKA), which causes it to dissociate from SERCA and for SERCA to upregulated (incr ability for relaxation, as well as incr Ca released during AP)

Front 12

requirements for competence of SL valve

Back 12

appropriate valve annulus diameter, appropriate leaflet geometry

Front 13

ways valves can be dysfunction

Back 13

regurgitation if they fail to close properly, stenosis if they fail to open properly

Front 14

arterial pressure waveform

Back 14

three phases: rapid upstroke at onset of ventricular systole due to ejection into aorta, rounded peak in mid-late systole due to decay of ventricular ejection, this peak ends with dicrotic notch due to SL valve closure, then gradual decay of P during diastole as blood runs into peripheral vasculature

Front 15

determinants of arterial P waveform (3)

Back 15

ejection rate into great vessel, great vessel compliance, reflected P waves

Front 16

atrial pressure waveform

Back 16

A wave = positive deflection in atrial P due to atrial contraction just before end of ventricular diastole; X descent = at onset of ventricular systole due to atrial relaxation; V wave = positive deflection during ventricular systole due to atrium filling from venous system w/ closed AV valve; Y descent = negative deflection at onset of ventricular diastole as atria rapidly empty into ventricles

Front 17

when is LV pressure the lowest?

Back 17

in early diastole as the mitral valve opens

Front 18

normal vs athersclerotic pulse wave timing

Back 18

in normal arteries, the reflection site is 80 msec from aortic valve, pulse wave velocity is 5 m/sec, and so wave reaches reflection site at 160 msec and back to valve in 320 msec (arrives back in early diastole, incr diastolic P and thus augmenting coronary artery flow); in aged arteries, pulse wave velocity incr to 12 m/sec, so reflected wave arrives back at valve in 135 msec (during systole - incr systolic P and pulse P)

Front 19

why is right side diastolic P less than L side diastolic P?

Back 19

b/c R side is more compliant than left, so higher LA pressure is needed vs RA pressure

Front 20

normal pressures: RA, RV, PA, PCW/LA, LV, AO

Back 20

RA mean 0-5 mmHg; RV 25/5; PA 25/10 (15); PCW/LA mean 5-12 mmHg; LV 120/12; AO 120/80 (95)

Front 21

importance of aortic P

Back 21

provides perfusion to drive systemic circulation (can't be too low), also constitutes LV afterload (can't be too high)

Front 22

importance of LA P, what happens if too high/too low

Back 22

this P generates LVEDP (may have lung edema b/c LA needs to be high to generate high LVEDP for pathologically low LVEF), and is also the P that pulm capillaries are exposed to --- if too high, can cause pulmonary edema, if too low, can cause inadequate LV preload -> inadequate CO

Front 23

importance of RA P, what happens if too high/too low

Back 23

overall measure of pt's intravascular volume and hydrational state; if too high get peripheral edema, if too low get inadequate RV preload -> inadequate CO

Front 24

causes of heart sounds (2)

Back 24

rapid acceleration/deceleration of blood (valve openings/closings, ventricular filling gallops); turbulent (high velocity) blood flow in cardiac murmers and vascular bruits

Front 25

how to detect vibrations

Back 25

feel up to 50 Hz, hear from 20 - 20,000 Hz

Front 26

normally audible heart sounds

Back 26

S1 - AV closure (mitral then tricuspid); S2 - SL closure (aortic then pulmonary) - these sounds bracket systole, and thus interval between S1 and S2 (systole) should be shorter than the interval between S2 and S1 (diastole) b/c diastole is longer than systole (2/3 of cycle vs 1/3 of cycle at rest); as HR incr interval between S2 and S1 should shorten more than interval between S1 and S2

Front 27

change in splitting w/ respiration

Back 27

w/ inspiration, RA fills more and LA fills less, so tricuspid closes later and mitral closes earlier -> this increases the splitting heard in S1; ditto RV ejects more and LV ejects less w/ inspiration, so pulmonary closes later and aortic closes earlier -> this increases the splitting heard in S2

Front 28

S3: due to, timing, indicates

Back 28

rapidly early ventricular filling; occurs 160 msec after S2; low frequency therefore not normally audible in adults (indicates accentuated early ventricular filling or disordered diastolic compliance)

Front 29

S4: due to, timing, indicates

Back 29

accentuated late diastolic filling due to atrial contraction; occurs 100 msec before S1; low freq so not normally audible in adults (indicates abnormal diastolic compliance and accentuated atrial filling)

Front 30

murmur types

Back 30

systolic, diastolic, continuous

Front 31

systolic murmur: when, cause (3)

Back 31

between S1 and S2; associated w/ ventricular ejection: outflow tract obstruction (i.e. aortic stenosis), AV valve regurgitation, interventricular communication

Front 32

diastolic murmur: when, cause (2)

Back 32

between S2 and S1; associated w/ ventricular inflow: SL valve regurgitation, AV valve obstruction

Front 33

continuous murmur: cause

Back 33

PDA (blood continuously flows from aorta -> PA)

Front 34

diastolic force-length relationship: due to, linearity, result

Back 34

due to compliance of myocardium in inactive state (more force req to stretch to greater lengths); det by titin and other non-contractile components of sarcomere; not linear -> myocardium becomes stiffer as it lengthens (maintains sarcomere length between 1.65 microns and 2.2 microns); this means that while achieving modest diastolic volume doesn't require great filling P, the filling P required to achieve larger diastolic volumes is considerably greater

Front 35

end-systolic force-length relationship: due to, linearity, result

Back 35

determined by contractile elements (myofilament proximity, inotropic state); reasonably linear; longer sarcomere = more force it can generate; in response to given afterload, muscle can only shorten to length predetermined by this end-systolic F-L relationship (if it is already at that length at end diastole, then it won't be able to shorten at all -> isometric contraction, no ejection)

Front 36

heart enlargement and LePlace

Back 36

tension = P x r / t; as heart enlarges, the same P generates increased tension on wall -> makes it harder for large hearts to eject in systole (hearts will increase thickness as compensatory technique for lowering wall tension); in diastole, LePlace means that same diastolic P will stretch myocytes more (incr tension) when heart is larger

Front 37

how does SV change w/ diff preloads and afterloads?

Back 37

larger preloads = larger SV; larger afterloads = smaller SV

Front 38

how does increasing inotropy change the end-systolic F-L relationship?

Back 38

moves it up and to the left, so that a given preload and afterload will generate a greater SV

Front 39

what determines LVEDV? (2)

Back 39

end-diastolic P (preload), diastolic F-L relationship (compliance)

Front 40

what determines LVESV? (3)

Back 40

peak aortic systolic P (afterload), end-systolic F-L relationship (how small CAN a fiber get when pushing against a given afterload?), inotropic state (changes end-systolic F-L relationship)

Front 41

during systole, what occurs to wall force and pressure?

Back 41

F = P x r; throughout first third of systole, P rises and r drops; r drops more than P rises, and thus F drops continuously throughout systole --- this means that ejection is "self-reinforcing", in that the decrease in radius during ejection contributes to decreased wall tension opposing the remainder of ejection

Front 42

when is peak wall force in systole?

Back 42

at onset of ejection (when ventricle at max EDV)