Heart phys Flashcards
Time delay between electrical excitation and contraction of heart muscle?
~100ms
What specifically does calcium bind to to induce cross-bridge cycling?
TnC domain of troponin, inhibiting TnI which is causing TnT to hold tropomyosin over the myosin binding site on the actin filament
Thus tropomyosin is moved and the myosin binding site on actin is exposed
In the resting state, what are the myosin heads of cardiac muscle bound to?
ATP
What does binding of myosin heads to actin cause (what is this called)?
Cross bridge formation hydrolyses ATP to ADP + Pi
What happens during the power stroke?
ADP and Pi are released, and the myosin heads tilt, shortening the sarcomere
What causes myosin heads to release from actin? How might you remember this?
Binding of ATP
Rigor mortis only occurs because their is no ATP to relax the muscles
Which phase of the ECG does hypokalaemia affect most?
What kind of problems does hypokalaemia cause?
What does hypokalaemia do to resting membrane potential?
Repolarisation
Ventricular ectopic complexes, atrial tachycardias, Long QT, flattened T wave
Hyperpolarises
Why does hyperkalaemia decrease excitability and hypokalaemia increase excitability?
Hyper - causes slightly more depolarised resting membrane potential, increasing probability that VGNaCs will spontaneously open, decreasing the concentration of VGNaCs available to open when stimulated by an action potential, raising the threshold potential, requiring a higher stimulation to excite the cell
Hypo - causes slightly more hyperpolarised resting membrane potential, decreasing probability that VGNaCs will spontaneously open increasing their availability when action potential arrives, effectively reducing threshold potential and increase excitability
Hyperkalaemia effects of T wave, QT and action potential duration and how?
Higher e[K+] increases open probability of VGKCs
Therefore, faster repolarisation, causing larger T wave, shorter QT and shorter action potential
