Cardiovascular lecture 1: the heart as a pump week 3 Flashcards Preview

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What is the effective (absolute) refractory period (ERP)? What is the relative refractory period (RRP)? Explain what channels in cardiac myocytes lead the cardiac AP to have such a long refractory period and why cardiac APs cannot summate. 

ERP: defines the time period before another AP of any kind can be evoked. Note that in cardiac muscle, the muscle has begun to relax before the ERP is over and even more so after the relative refractory period. During the RRP, another AP can be evoked but it will be weak and will conduct slowly. 

As we know, the cardiac AP is much longer than in other cell types due to the L-type Ca2+ current that flows during the plateau and drives Vm toward Eca (120) mV. This is balanced by delayed rectifier K+ currents that work to bring Vm toward Ek (-95mV). As a result of the plateau, the ERP is extremely long. While Vm is depolarized, Na channel inactivation gates remain closed (remember these gates open upon repolarization). The channel doesnt begin recovering from inactivation until repolarization begins after the plateau phase. They begin to recover during the RRP but not completely. 

In skeletal muscle, the refractory period is relatively short and so repeated APs can be fired well before relaxation begins. No tetanic summation of cardiac muscle twitches is possible bc the duration of the AP is essentially the same as the duration of the twitch-cardiac muscle is nearly relaxed before another AP can be fired. 


What 3 factors change the force of contraction? 

1. length of fibers at time of contraction: Frank-Starling effect

2. afterload

3. contractility (IS)


How does the Frank-Starling effect impact force development? By what mechanisms is this though to possibly occur? What factors determine contractility? How is this different from contractility?

Increased lenght of myofibers results in increased force development. This is different from increased contractility, which is an increase in force developed at the same muscle length. The Frank-Starling effect increases EDV (preload) so does not effect inotropic state (fibers stretch more, can fill more, and contract with more force). Anything that is not considered preload or afterload is inotropic state. A change in IS is completely independent from changes in fiber length and is distinct from the Frank-Starling effect, which is an inherent property of the muscle in the absence of extrinsic factors. IS is effected by [Ca2]i, number of functional myocytes, and coronary artery supply. 

The increase in force with an increasing length (Frank-Starling effect) may result from:

1. a change in the lateral spacing btwn thick and thin filaments such that greater force developement is achieved. 

2. increased myofilament Ca2+ sensitivity


Why is the effect of afterload on SV limited? What is this phenomenon called?

homeometric autoregulation: Increased afterload → increased end systolic volume 
→ increased end diastolic volume → Frank-Starling

Increased stretch also causes the release of angiotensin II and endothelin that increase the inward flux of Ca2+: positive inotropic effect: also counters effects of 
increased afterload



Consider the attached pressure volume loop. If the aortic valve is insufficient, where will point A be relative to point B? Point C relative to point D?

aortic insufficiency:

point B goes to the right of A. pressure in aorta is greater than in ventricles so blood flows into ventricles
C moves to the left of D: when aortic valve should be closed, blood leaks from the insufficient valve into the lower pressure ventricle and increases ventricular volume 


What is the physiologically predominant determinat of CO?

Bc HR varies over a wider range, when the body wants to increase CO it largely looks towards HR. Also, when the sympathetic NS increases both SV and HR, the effect on HR dominates. 


Of the determinants of SV, which is the most potent?

Increased EDV stretches the ventricular walls and increases the length of the cardiac muscle fibers. This causes increased force of contraction (Frank-Starling effect) and thus increased SV. 


What effect does increased wall tension have on a normal heart and a diseased heart? (hint: Law of LaPlace)


Explain the reason for the shift in this curve with NE.

When left ventricular EDV (LVEDV) increases, this increased end diastolic pressure and distends the ventricular walls. This stretches the ventricular msucel and an increase in the force of contraction results as noted in the figure. This manifests itself on the whole heart level as an increase in SV. 

Increasing the IS of cardiac muscle (NE) results in greater ventricular output at any level of left ventricular fills. Increased IS is represented by an upward shift of the Starling curve, reprsented as stroke volume (eq to force development) vs left ventricular end diastolic pressure (equivalent to muscle length)


Explain the reason for the shift in the ESPVR line in the attached pic with increased IS. (also answer what this line is). Which way does the graph shift in dilated cardiomyopathy and why?

As a heart beats over time, there are tiny shifts in the parameters that determine the force of contraction at every beat. For example, preload is never exactly the same on a beat-to-beat basis. End systolic pressures will fall along this line dependent upon the preload in th system. A higher preload will result in a higher ESP bc force of contraction increases. A lower preolad will result in a lower ESP bc force of contraction decreases. In each case, the end systolic pressure falls somewhere on the diagonal line.

If there is an increase in IS, the line shifts. Compared to the normal muscle, ESP increases and ESV decreases (i.e. SV increases) for the same preload (i.e. same initioal filling. 

The graph shift down and to the right for a pt with dilated cardiomyopathy due to negative inotropic state. 



True or false: Inotropic state often serves to maintain CO when preload is decreased.