Physiology: Cardiac Cycle Flashcards Preview

Cardiology Exam IV > Physiology: Cardiac Cycle > Flashcards

Flashcards in Physiology: Cardiac Cycle Deck (22):

Phase II correlates to the influx of Ca++ into the myocytes. How does this affect contraction ?

Ca++ is the molecule that regulates contraction by its binding to Troponin.

This can be shown on the Ventricular pressure diagram. Pressures begin to rise during Phase II because the influx of Ca++ initiates contraction.


How is Calcium brought into the cytosol to initiate contraction ?

2 mechanisms

1. L-Type Ca++ Channels in the Sarcolemma
Opened due to AP going along the sarcolemma.
2. Ca++ Induced Ca++ release from the Sarcoplasmic Reticulum

Ca++ from L-Type enters and activates the ryanodine receptor. this will lead to Ca++ release from the SR into the cytosol.


What is the fate of Ca++ after contraction

Majority is transported back in to the SR via an SERCA ATPase (phospholamban inhibits this transporter--> increased Ca++ in cytosol)
Remainder is pumped into the Interstitium via a Na/Ca++ antiporter.

Note this antiporter is substrate dependent and can switch polarity depending on which is more plentiful
Made possible by the Na/K+ ATPase


What is the effect of CCB's on force of contraction ?

The use of CCB's will lead to decreased force of contraction due to decreased Ca++ that will enter the cell to cause Ca++ induced Ca++ release.


What is the effect of hypercalcemia on contraction of heart muscle ?

Hypercalcemia will lead to INCREASED force of contraction because more Ca++ will enter the cell when DHP channels are opened. This will lead to more Ca++ induced Ca++ release.

The opposite is true for hypocalemia


What is the effect of High Intracellular Na+ on the Na+/Ca++ exchanger at the cell membrane ?

high intracellular Na+ will cause a reverse in polarity of this exchanger so that sodium will be taken out of the cell whilst Ca++ is brought into the cell.


Effects of Beta Agonists

Increase contractility
(positive inotropy)
•Increase relaxation rate (positive lusitropy)
•Increase heart rate
(positive chronotropy)
•Increase conduction velocity (positive dromotropy)


Why will an early premature contraction cause a more significant loss in contractility as compared to a late premature contraction ?

Early premature will lead to a decreased force of contraction due to low [ca++] in the cell compared to normal contraction and less stimulus to release [Ca+] from the SR

still partly refractory


How much time is spent in systole and diastole respectively

Systole: 1/3
Diastole: 2/3


Describe the activity of valves in atrial systole

Mitral open
Aortic Closed


Describe the activity of valves in isovolumetric contractions

All valves are shut


Describe the activity of valves in rapid ejection

aortic is open and mitral is closed


Describe the activity of valves in isvolumetric relaxation

all closed


Describe the activity of valves in rapid filling

mitral open aortic closed


What is occuring at S1

AV valves are closing going into isovolumetric contraction


Aortic and peripheral pressures remain equal from ...

opening of aortic valve until the closing of the aortic valve (S2)


What causes the dicrotic notch ?

dicrotic notch is when blood bounces off of closed aortic valve leading to turbulence. Prior to this Aortic BP is greater than ventricular but valve is not closed yet for some reason leading to slowed ejection at the end. This unusual closing is due to differential in kinetic energy of blood (momentum, inertia, velocity blah blah)



atrial contraction



beginning of right ventricular contraction


x descent

after atrial contraction; reverse pressure;
floating of AV valve upward



prior to mitral valve open (venous return)


y descent

mitral valve opens