Exam 6 - Cardiac Cycle / Starling Curve Flashcards
When are all valves closed
- Isovolumic contraction and relaxation
Relationship of SV in ventricles
- should be equal in a healthy person
Duration of cardiac cycle
- Obtain HR
- Take inverse of HR
- Multiply by 60 to get duration of 1 cardiac cycle
1 Hz
- 1 beat per minute
Time in systole and diastole
- 1/3 in systole
- 2/3 in diastole
Length of systole
- starts with A-V valve closure (isovolumic contraction)
- ends with semi-lunar valve closure (isovolumic relaxation)
- atrial contraction happens during systole
Length of diastole
- starts with semi-lunar valve closure (isovolumic relaxation)
- ends with closure of A-V valves (isovolumic contraction)
- as HR increases…time spent in diastole decreases
- both get shorter but diastole is sacrificed more - most of time spent in diastole is passive filling
Atrial kick contribution
- 30% of the filling
- 20% of the actual SV
At what HR is time spent in each phase switched
200 bpm
Problems filling and ejecting can lead to….
- Heart failure
Aortic Stenosis
- effects systole
- isovolumic contraction pressure would increase
Aortic Insufficiency
- effects diastole
- Aortic valve doesn’t close all the way at dicrotic notch
Mitral stenosis
- effects diastole
Mitral insufficiency
- effects systole
- more pressure in atria during systole
Hypertrophy
- thickening of heart wall
Dicrotic notch
- Aortic valve closing
- closes when there is no more forward flow through aorta
What keeps Aortic valve open at end of systole
- KE of blood flow
A wave on wigger diagram
- atrial contraction
- atrial kick
- small increase in atrial and ventricular pressure
C wave on wigger diagram
- AV (mitral) valve closing and bulging into atrium
V wave on wigger diagram
- atrial filling increases atrial pressure
- falls when mitral valve opens and releases blood into ventricle
S1 heart sound
- beginning of systole (isovolumic contraction)
- mitral and tricuspid valves slam shut
- valves closing, vibrations, blood recoil….all cause noise
- heard over apex of heart
S2 heart sound
- beginning of isovolumic relaxation
- aortic and pulmonary valve slam shut
- PA after A because A has bigger pressure gradient - heard near end of t-wave
S3 and S4
- not normally heard
- heard during diastole
- when heard it creates gallop rhythm
- S3 heard in heart failure….S4 associated with atrial contraction
Left vs Right atrial and ventricular pressures
- Left should be higher
Palliative surgery
- alleviates symptoms
Corrective surgery
- fixes problems permanently
Arterial-Venous O2 difference
- 25% (100% arterial - 75% venous)
- Heart takes 75% of the 100…25% left for body
- Heart functions under aerobic only
- if low O2….increase coronary blood flow (1:1 O2/flow ratio)
Hypoxia
- lack of O2
Ischemia
- lack of blood flow
Diameter effect on velocity
- if diameter decreases….velocity increases
Types of heart work
- Pressure work: work needed to open semilunar valves
- work that builds up pressure
- EXTERNAL work
- 99% of total work - Volume work: work needed to eject blood
- KE of blood flow
- 1% of work….but can increase up to 50% w/ aortic stenosis
Work output of heart
- Pressure work + Volume work
- amount of energy converted to work by heart for each beat
- Increase in preload / afterload will increase work by heart
- area under curve = stroke work output
Minute work output
- Stroke work output x HR
Total energy output of heart
- Heart external work (area under cure) + PE
- PE is work the heart could do if it were able to contract all the way to empty ventricle
Work load of Left vs Right side
- Right side is 1/6th of left
- due to pressure difference…PVR is much lower than SVR
- also uses 1/6th of the O2
Energy efficiency of heart
- ATP used by heart turned into heat and work
- 20-25% efficient
- can go as low as 5-10% with heart failure
Diastolic pressure
- Pressure at end of Diastole
- Created by resting stretch
- exponential curve shape due to compliance
- high compliance at beginning….lower at end - optimal preload is 120-170ml…after that you get too big of increase in diastolic pressure
Max ventricle pressure generation
- 250-300 for LV
- 60-80 for RV
Stroke volume
- EDV-ESV
Ejection fraction
- SV/EDV
- Normal is 50-70% (AHA)
- 40% can be indicative of heart failure
O2 consumption in diastolic phase
- still happens…just less than systolic phase
Tension developed during isometric contraction
- enough to overcome afterload
Relationship of stroke volume and fiber shortening
- directly proportional
Ejection vs shortening
- As muscle fibers shorten….ejection occurs
- Even though pressure increases due to ejection…radius of ventricle gets smaller (shortening) so overall tension decreases
Normal CO
- 5 L/min
- changes based on moment to moment needs
- HR x SV
- CO is passive….meaning venous return dictates CO
Factors that change HR
- Sympathetic tone
- Parasympathetic tone (dominant controller of HR)
Factors that will change SV
- Intrinsic contractility (preload, resting stretch/tension) (+)
- After-load (-)
- Extrinsic contractility
Preload and SV relationship
- Increases preload increases distance fibers can shorten
- 1 mmHg change in preload changes volume by 25 mls
- changing EDV does not change ESV
- no change in extrinsic contractility
Afterload and SV relationship
- increase in afterload will increase ESV
- increase in afterload will decrease SV
- 1 mmHg change in afterload changes SV by 0.5 ml
- pressure change in preload affects SV more than afterload - EDV does not change but ESV does
- Afterload is normally controlled tightly so normally wont see this
Extrinsic contractility and SV relationship
- increased sympathetic tone moves peak tension curve up and left
- each fiber able to generate more tension at any given length
- SV increases because fibers can shorten more than normal
- ESV is decreased
How increased contractility looks on graph
- ESV moves left
- same systolic pressure at lower systolic volume
- increased slop of extrinsic line
If only pre-load changes…
- EDV changes proportional to preload change
- fiber length changes same way (resting stretch) - ESV does not change
- SV changes proportional to preload change
- ability of fibers to shorten changes too
If only after-load changes
- EDV does not change
- resting fiber length does not change - ESV changes (proportional to after-load change)
- SV changes (inversely proportional to after-load change)
If only extrinsic contractility changes
- EDV does not change
- ESV changes (inversely proportional to contractility change)
- SV changes (proportional to contractility change)
Estimation of contractility
- End systolic pressure / End systolic volume
- can use PA to measure systolic pressure
Volume pressure curves only show changes in what?
- Stroke volume
- assuming no change in HR
Maximum Cardiac Outputs
- Max Para / No Symp: 7.5
- No Para / No Symp: 10-11
- No Para / Normal Symp: 12.5
- No Para / Max Symp: 24-25
Effects of parasympathetic on CO
- Lower HR (negative chronotropic)
Effects of sympathetic on CO
- Increase HR (positive chronotropic)
- Increase SV (positive inotropic)
Effects of arterial pressure on CO
- arterial pressure is AFTER-LOAD
- more after-load will decrease SV
Effects of filling pressure on CO
- Filling pressure is PRE-LOAD
- more pre-load will increase SV
Energy production by the heart
- 70-90% from fatty acids
- 10-30% from lactate and glucose
- fetal cells use more lactate and glucose until few weeks old
Myoglobin
- protein in heart cells that binds with O2
- not as strong as hemoglobin
O2 consumption by heart
- remember heart uses 75% of available O2
- of the O2 it consumes….
- 25% used for basal metabolism… no contraction
- 75% used for muscle contraction
- 50% for x-bridges
- 25% for pumping calcium
Pressure work O2 consumption
- 50% of overall cardiac O2 use
- largest consumer of O2
- major determinant is after-load
Volume work O2 consumption
- only 0.5% of overall cardiac O2 use
- Pressure is more costly in energy than volume
