Lec 14-15 Cardiac Cycle Flashcards
How do preload and afterload affect cardiac output?
- high preload = increased cardiac output
- higher afterload = decreased cardiac output
How does Ca affect contraction strength?
small ca induced ca release [CICR] –> weak contraction
large CICR –> strong contraction
What two things does contraction strength depend on?
- Ca release
2. initial length [preload]
2 factors in force-length relation in intact heart?
- ventricular filling from veins/atria pre-stretches the ventricles [preload]
- ventricles must contract against existing arterial pressure [afterload]
When are LVP and aortic pressure closest?
at their peak, just at end of QRS is ST interval
LVP still > than aortic pressure
What causes mitral valve to open? to close?
open: LAP > LVP
close: LVP > LAP
What changes to pressure and volume between mitral valve closure and aortic valve opening?
- LVP gets bigger, volume stays the same = isovolumic contraction
What causes aortic valve to open? to close?
opens: when LVP > aortic pressure
closes: aortic P > LVP
What is happening to pressure and volume in left ventricle during ejection?
- pressure and volume both changing
What kind of relaxation in LV after aortic valve closes?
isovolumic relaxation
- volume is flat, pressure changes
What is first heart sound? and second?
first: closing AV valves [QRS wave]
second: closing aortic and pulmonary valves [just after T wave]
3 important principles illustrated by wiggers diagram?
- atrial P is low, Ventricular/aortic P is high
- valves only open when upstream P > downstream P
- heart sounds correspond to discrete events
Where are the 4 valves located [and names]
AV valves
tricuspid: RA –> RV
mitral [bicuspid]: LA –> LV
semi-lunar valves
pulmonary: RV –> pulm artery
aortic: LV –> aorta
Why are valves so important?
ensure unidirectional blood flow
4 phases of PV loop [including valve events]
MV closes 1. isovolumic contraction Aortic V opens 2. ejection Aortic V closes 3. isovolumic relaxation MV opens 4. diastolic filling
How to get SV [stroke volume] from EDV and ESV?
SV = EDV - ESV
How to get EF [ejection fraction] from SV and EDV?
EF [ejection fraction] = SV/EDV
What is the EDPVR? linear or non-linear?
- end-diastolic pressure-volume relationship
- nonlinear
- defines the lower boundary for end-diastolic P-V point of PV loop
What does the slow of the EDPVR mean?
on P-V graph: x axis = V, y axis = P
flatter = more compliant
steeper = less compliant
What does EDPVR nonlinearity mean?
low volume: small slope, ventricle compliant, easy to fill
high volume: large slope, ventricle stiff, difficult to fill
What is the ESPVR? linear or non-linear?
- end-systolic pressure-volume relationship
- linear
What do EDPVR and ESPVR do together?
define boundaries within which PV loop sites
independent of preload and afterload
Do EDPVR/ESPVR depend on preload and afterload?
No, they are independent
What is the preload? Two common ways to measure it? What point is it on PV loop?
- the load imposed on ventricle at end of diastole
- measured as end-diastolic volume [EDV] or end-diastolic pressure [EDP]
- the bottom right corner on PV loop
With constant afterload and contractility, how does preload affect SV and arterial BP?
increased preload –> increased SV and arterial BP
What is frank starling curve [x and y axes]? what relation does it show?
x axis: LVEDP or LVEDV or right atrial pressure or venous pressure
y axis: stroke volume or CO
it shows that increased preload –> increased output
What 2 things increase preload?
- fluid retentions [in advanced heart failure]
- constriction of veins
What 2 things decrease preload?
- blood loss
- dilation of veins
What is afterload? Common way to measure it?
- mechanical load of ventricle during ejection
- normally determined by arterioles
- Commonly measured at TPR
What is equation for TPR?
TPR = MAP/CO
What are 2 effected of increased TPR when constant preload and contractility?
- increased pressure
- decreased SV
What 3 things can increase afterload?
- temporary constriction of arterioles
- chronic hypertension
- aortic stenosis [valve narrowing or blockage]
What 1 thing decreases afterload?
dilation of arterioles
What will negative inotropic agent do to ESPVR?
ESVPR will have less steep slope
What will positive inotropic agent do to ESPVR?
ESVPR will have steeper slope
What is Ees? what changes it?
- slope of ESPVR
- its the index of ventricular contractility
- inotropic drugs change it –> pos inotropic drugs increase it, negative inotropic drugs decrease it
What 3 things increase contractility?
- B adrenergic stimulation in ventricle
- increased plasma Ca
- increase in muscle mass [physiological hypertrophy]
What 4 things decrease contractility?
- B adrenergic receptor blockers
- Ca channel blockers
- decreased energy supply [ischemia or hypoxia]
- decreased muscle mass [MI]
Does increased SV indicate an increase in contractility?
- NOPE – Not by itself
What 3 things things can increase SV?
- increased contractility
- increased preload
- decreased afterload
What is clinical contractility index?
ejection fraction [EF]
What is equation for ejection fraction?
EF = SV/EDV SV = stroke volume, EDV = end diastolic v
Does afterload affect EF?
Yes, significantly
Does preload affect EF?
yes minorly
does contractility affect EF?
yes!
