Chapter 2 Characteristics of cardiac muscle cells Flashcards
There are 3 general types of such transmembrane protein structures that are involved in ion movement across the cell membrane:
(1) ion channels (2) ion exchangers (3) ion pumps
There exists one membrane potential called the potassium equilibrium potential at which the electrical forces tending to pull K + into the cell exactly balance the concentration forces tending to drive K + out. EXPLAIN HOW THIS HAPPENS
a cell that (1) has K + more concentrated inside the cell than outside, (2) is permeable only to K + (i.e., only K + channels are open), and (3) has no initial transmembrane potential. Because of the concentration difference, K + ions (positive charges) will diffuse out of the cell. Meanwhile, negative charges, such as protein anions, cannot leave the cell because the membrane is impermeable to them. Thus, the K + efflux will make the cytoplasm at the inside surface of the cell membrane more electrically negative (deficient in positively charged ions) and at the same time make the interstitial fluid just outside the cell membrane more electrically positive (rich in positively charged ions). K + ion, being positively charged, is attracted to regions of electrical negativity. Therefore, when K + diffuses out of a cell, it creates an electrical potential across the membrane that tends to attract it back into the cell. When the membrane potential has this value, there is no net movement of K + across the membrane. With the normal concentrations of approximately 145 mM K + inside cells and 4 mM K + in the extracellular fluid, the K + equilibrium potential is roughly −90 mV (more negative inside than outside by nine hundredths of a volt).
A stable membrane potential?
A stable membrane potential that lies between the sodium and potassium equilibrium potentials implies that there is no net current across the membrane. This situation may well be the result of opposite but balanced sodium and potassium currents across the membrane.
Under resting conditions, both electrical and concentration gradients favor the entry of Na + and Ca 2 + into the resting cell. WHY?
Under resting conditions, most heart muscle cells have membrane potentials that are quite close to the potassium equilibrium potential. Thus, both electrical and concentration gradients favor the entry of Na + and Ca 2+ into the resting cell.
True/F: norepinephrine has no effect on resting length-tension relationship of the cardiac muscle
True. Nepi causes increased shortening by changing the final but not the initial muscle length associated with afterload contractions.
T/F: norepi will increased the fractional shortening oat any given resting length
True
The cellular mechanism of the effect of norepi on contractility is mediated by which receptor?
beta 1 adrenergic receptor
What are the effects of norepi to 1) inotrope 2) chronotrope 3) lusitrope 4) dromotrope
positive inotrope, positive chronotrope, positive lusitrope, positive dromotrope
T/F: parasympathetic activith have a small negative inotropic effect on the heart
True
What is the major determinant of preload?
The extent of diastolic filling of the ventricle (increase in ventricular volume - increased in ventricular circumference - increase in the length of the cardiac muscle cells)
What is the major determinant of afterload?
arterial blood pressure (increase in tension of individual cardiac muscle cells in the wall causes an increase in intraventricular pressure)
Elaborate the law of Laplace
T = P x r T: total wall tension P: intraventricular pressure r: radius Tension depends on both intraventricular pressure and its internal radius
What are the effects of sodium channel blockers on PR interval, duration of QRS complex?
prolong depolarization (phase 0), increase PR interval, widen QRS complex
What are the effects of calcium channel blockers on the rat of the firing of SA nodal cells? On the rate of conduction of the action potential through the AV node? on myocardial contractility?
reduce the firing rate of SA node, decrease rate of conduction on the AV node, decrease contractility
What are the effects of potassium channel blockers on action potential duration? on refractory period?
prolong plateau phase, increase QT interval (ventricular systole), prolong effective refractory period
