Cardiac Cycle Flashcards
1
Q
What is the driving force of the cardiac cycle?
A
pressure gradient
2
Q
What ensures unidirectional flow?
A
one-way valves
3
Q
Source of normal heart sounds
A
valve closures
4
Q
what is the contraction phase called?
A
systole (to contract– ventricles are ejecting)
5
Q
what is the relaxation phase called?
A
diastole (to expand- ventricles are filling)
6
Q
purpose of the muscle contractions of papillary muscles
A
keep the valve closed
7
Q
What makes the lub sound?
A
tricuspid and mitral valves closing
8
Q
What makes the dub sound?
A
semilunar valves closing
9
Q
one cardiac cycle: 2 parts
A
relaxation –> contraction
10
Q
two parts of diastole
A
ventricular filling and isovolumetric relaxation (phases 1 and 4)
11
Q
two parts of systole
A
Isovolumetric contraction, ejection (phases 2, 3)
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
13
Q
Cardiac cycle (4 phases)
A
ventricular filling
isovolumetric contraction
ventricular ejection
Isovolumetric relaxation
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)
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
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
17
Q
Phase 4: isovolumetric relaxation
A
volume stays the same, and as pressure drops, the A-V valve opens again
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.
19
Q
How does cardiac output compare between chambers?
A
Always the same amount; otherwise we would get backup.
20
Q
3 tips of right-sided heart catheterization
A
RA, RV, and pulmonary wedge (left atrial pressure, wedged into small pulmonary artery)
21
Q
what is the function of right ventricular wall thickness?
A
Push out same amount of volume against greater pressure
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
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%
24
Q
What is the dicrotic notch
A
disturbance on the aortic pressure line when the semilunar valve closes
25
Sounds of the heart
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
26
S1
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)
27
S2
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)
28
timing of semilunar valve openings
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
29
timing of AV valve openings
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
30
Effect of inspiration on right side of the heart
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
31
Effect of inspiration on left heart
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
Abnormal heart sound: S3
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
Abnormal heart sound: S4
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
Heart Murmurs
Sound generated by turbulent flow through heart
35
structural issues leading to heart murmurs
Thickening of valve leaflets Narrowing (stenosis) of valve openings Holes in chamber walls or septae between chambers
36
Hemodynamic issues leading to heart murmurs
decreased viscosity: anemia
37
Venous Pulse
•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
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
Jugular Venous pulse: clinical correlates of a waves (RA contraction)
* Large a waves: Tricuspid Stenosis, Right Heart Failure
* Cannon a waves: 3 °, Complete Heart Block (AV dissociation)
* No a waves: Atrial fibrillation
40
clinical correlates of jugular venous pulse (c wave)
RV pressure in early systole (tricuspid bulging)
41
clinical correlates of jugular venous pluse- v wave
RA filling (tricuspid closed)
•Large v wave (c-v wave): Tricuspid regurgitation
42
Jugular Pulse: Effect of Respiratory Cycle
Inspiration
* Negative jugular v. pressure
* ↓ intrathoracic pressure (thoracic vessels & RA)
–↓ RA & VC pressure --\> dilation à
↓ resistance --\> ↑ flow
–↑ VR from head & upper extremities
43
L.E. Venous Pressure: Effect of Skeletal Muscle Contraction “Muscle Pump”
* 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
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
Work
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
Tension Heat
= 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
Ventricular Wall Tension
•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
Approximation of wall tension by laplace's relationship
•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
Cardiac output
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
Cardiac Index
–Common indicator of cardiac performance: CO normalized for body size
–Cardiac index: L/min/m2
•Normal reference range: 2.8 – 4.2
51
Preload
–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
Afterload
–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
Contractility (Inotropy)
–Force generation independent of preload
–Influenced by autonomic input
positive impact on stroke volume
54
Pre-Load: Frank Starling Law of the Heart
Length-tension relationship for cardiac m.
## Footnote
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
Greater Pressure with Greater Filling
•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
Proposed mechanisms for increased amount of stretch on cardiac myocytes
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
Frank starling curve for systolic failure
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
Cardiac Cycle: effects of prelaod
•Velocity of myocardial contraction is directly related to Preload
–↑ preload, ↑ shortening velocity
–↑ Ejection fraction
59
60
Cardiac cycle: effects of afterload
•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
myocyte contractile phases of systole
•Myocyte contractile phases (systole):
–Isovolumetric contraction:
isometric contraction (pressure generated to open aortic valve)
–Ejection phase: isotonic contraction
62
Contractility/Inotropy
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
Contractility and ESPVR (End-systolic pressure-volume relationship)
•↑ Contractility --\> ↑slope of ESPVR
64
3 Factors influencing SV
**SV = EDV - ESV**
1. EDV relates to preload
2. ESV relates to afterload
3. Inotropy: ↑ SV by ↓ ESV
(independent of EDV)
65
Venous Return and Cardiac Output
•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
Cardiac Function Curve
Cardiac output as a function of Right Atrial Pressure (red line)
•Same relationship as Frank Starling Law
–
* ↑ RAP
* ↑ Ventricular filling
* ↑ EDV
* ↑ SV
* ↑ CO
67
commonly used variables as indicators of cardiac function
Stroke Volume (SV)
Cardiac Output (CO, Q)
Cardiac Index (CI)
68
commonly used variables as indicators of ventricular filling (preload)
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
Vascular Function Curve: venous return, cardiac INPUT
•Relates to pressure gradient which favors venous return
–↓ RAP --\> ↑ VR
–↑ RAP --\> ↓ VR
•As RAP becomes more negative: ↑ VR driving force (ΔP = CVP - RAP)
70
Slope of vascular function curve determined by...
compliance and resistance of vessels
71
plateau of vascular function curve
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
venous return and right atrial pressure
•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
Interaction of cardic and vascular function curves
* 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
aortic stenosis (pressure in left ventricle very high)
75
heard during diastole, atrial pressure is higher than expected to eject across stenotic mitral valve
76
aortic regurgitation
77
mitral insufficiency (hear it during systole)
