9 HF- pressure volume loops Flashcards
How do you calculate cardiac output?
CO = HR x SV
What are 3 major determinants of stroke volume?
- contractility
- preload
- afterload
How is cardiac output a function of preload?
- The more a normal ventricle is distended during diastole, the greater the amount of blood ejected during the next contraction
- Frank-starling relationship
- Higher preload= higher SV
- preload measured as EDV/EDP (indicates degree of stretchin at the end of diastole)
How do you calculate wall stress?
- Law of LaPlace
- σ = P x r / 2h
- P=ventricular pressure, r=ventricular radius, h=ventricular wall thickness
- Wall stress rises in response to higher pressure load (HTN) or increased chamber size (e.g. dilated LV)
- Increased wall thickness is a compensatory mechanism to reduce wall stress
Describe afterload
- The resistance the ventricle must overcome to empty its contents
- Formally defined as the ventricular wall stress that develops during systolic ejection
- Estimated by the LaPlace relationship
What affects the contractility of the heart?
Contractility accounts for changes in myocardial force for a given set of preload and afterload conditions
**dependent on chemical and hormonal influences
Describe a pressure-volume loop
How does changing preload affect the pressure-volume loop?
Increased preload= increased EDV
(ESV stays the same so SV increases as well)
How does a change in compliance affect the pressure-volume loop?
Increased compliance= decreased slope (more stretch results in less pressure for the same EDV)
How does changing afterload affect the pressure-volume loop?
- Increased afterload increases pressure generated during ejection
- More work expended to overcome resistance to eject
- ESV is greater but EDV stays the same
- increased afterload= decreased SV (EDV-ESV)
- ESPVR= end systolic pressure volume relationship (linear)
How does a change in contractility affect the pressure volume loop?
- Slope of the ESPVR line is a function of contractility
- Increased contractility= steeper slope
- Therefore the ventricle empties more completely as contractility increases, resulting in a smaller ESV (thus, increased SV)
What factors affect ESV?
ESV depends on the afterload and contracitliy, but NOT preload
What are the 3 main pathophysiological reasons for heart failure?
Reduced EF:
- Impaired ventricular contractility
- Increased afterload
Preserved EF:
- Impaired relaxation and filling
Describe heart failure with reduced ejection fraction
- Ventricle has diminished capacity to eject blood because of impaired contractility or pressure overload
- Loss of contractility from:
- myocyte destruction
- abnormal myocyte function
- fibrosis
- Pressure overload= increased resistance to outflow= impaired ejection fraction
Describe heart failure with preserved ejection fraction
- usually abnormalities in diastolic function
- impaired early relaxation
- increased wall stiffness
- possible causes:
- acute ischemia
- hypertrophy
- fibrosis
- restrictive cardiomyopathy
- pericardial diseases
How can frank starling mechanisms worsen heart failure?
- Normally, body increases EDV to increase SV
- However, in heart failure an increase in EDV cannot significantly increase SV and instead causes pulmonary congestion
- Heart failure= severely depressed contractile function
How does neurohormonal activation affect heart failure?
- Activation results in…
- Symp/RAAS/antidiuretic activation
- increases peripheral vascular resistance (maintaining perfusion of organs during reduced CO)
- promotes Na/water retention -> increases vascular volume -> increases preload -> maximizes CO (frank-starling)
- Initially benefitial, but continued activation ultimately proves harmful
