CAM201 Lecture Notes - Lecture 8: European Cooperation In Science And Technology, Inotrope, Vasodilation

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8 Jun 2018
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Learning Objectives
Understand and identify key features of the PV loop
Describe how preload, afterload and contractility interact with each other
Define and explain the differences between systolic and diastolic HF
Understand how myocardial function changes in HF and the adaptive changes that follow
Understand the adaptations in chronic volume and pressure overload leading to HF
Pressure and Volume in LV
1. Mitral valve closes
Isovolumic contraction
Aortic valve still closed
2. Aortic valve opens
Ejection: rapid at first then slows down as pressure in aorta increases
3. Aortic valve closes
Isovolumic relaxation
Mitral valve still closed
4. Mitral valve opens
Passive ventricular filling - rapid at first then slows down
Atrial contraction: active filling
Pressure Volume (LOOP) in LV
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Ends systolic pressure volume relationship (ESPVR)
Describes the maximum pressure that can be generated for any given LV volume in a
fully contracted ventricle
This slope is really a measure of contractility
The steeper the slope the greater the inotropic state and the more pressure that can be
generated
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End diastolic pressure (EDPVR)
Describes the pressure for any given amount of volume in a fully relaxed ventricle
This slope is really the inverse of compliance (stretching of ventricle to accommodate
blood volume)
The steeper the slope the less compliant the ventricle (its stiffer)
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Document Summary

Pressure and volume in lv: mitral valve closes. Isovolumic contraction: aortic valve still closed, aortic valve opens, ejection: rapid at first then slows down as pressure in aorta increases, aortic valve closes. Isovolumic relaxation: mitral valve still closed, mitral valve opens, passive ventricular filling - rapid at first then slows down, atrial contraction: active filling. What happens if venous return increases: an increase in venous return increases end diastolic volume (preload) of lv, esv and edv pressures are barely affected. Increased preload results in increased sv via frank-starling mechansim: this is o(cid:374)ly if (cid:271)oth afterload a(cid:374)d (cid:272)o(cid:374)tra(cid:272)tility are u(cid:374)(cid:272)ha(cid:374)ged (cid:449)hi(cid:272)h does(cid:374)"t ge(cid:374)erally happen in reality. What happens if aortic pressure changes: a decrease in aortic pressure will decrease afterload, a decreased afterload will result in increased sv. Increase in contractility (positive inotropy) increases slope of espvr: any given ventricular volume, the ventricle can generate more pressure. Increased sv: decrease in contractility will reduce slope of espvr and reduces stroke volume.

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