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Left ventricular volume50 100 150 200

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StrokeWork

Stroke work = Stroke volume x MAP

PreloadDenition: stress (tension) inwall of ventricle @ end diastole

Increases passive lling curve

+Preload will:+Stregth contraction+Velocity contraction+extent of sortening+Stroke volume (thus CO)

AfterloadDened: stress (tension) inwall of ventricle @ during systole

Decreases dP

+Afterload will:- Velocity of shortening- Extent shortening- Stroke volume- Cardiac output

Compliance = dV/dPSmall decrease in compliance

leads to large decrease in ventricular lling (hypertrophy)

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ESPVR line is made by ploting one individuals End systolic volume at two dierent afterloads-interestingly this line is the max strength of isovolumetric contraction with increased preload-increased inotropic state increases the slope and shifts graph to the left.

3 molecular mechanisms for increased inotropic stateNPE or NE from sympathetic bind to B-adgrenergic receptors G-protein coupled receptors to AC --> increase cAMP which increases PKA activityPKA phospohorylates 1) Calcium channels: increase sensitivity =more trigger calcium 2) PLB: decrease inhibition on SERCA so quicker resequastration 3) Troponin-I, whic decreases troponin Cs anity for Ca at low levels so it can be resequestered faster. Cardiac glycosideslike "digitalis" or "oubain" improve heart failure --X Na/K-ATPase decreases Na gradient for Na/CaX. -This extra Ca can be taken into the SR to an extent and a new steady state of inux and eux is reached

Preload shifts velocity curve to rightY-intercept remains the same

increased inotropic state increases Vmaxas well as Fmax