Chapter 2 & 4 Flashcards
*Small changes in extracellular potassium ion concentrations have major effects on cell membrane potentials.
What will happen to the potassium equilibrium potential of cardiac muscle cells when interstitial [K] (ie, [K],) is elevated?
The potassium equilibrium potential will become less negative because a lower electrical potential is required to balance the decreased tendency
for net K* diffusion out of the cell (Eck* = (-61.5 mV) log (K), /K),).
*Small changes in extracellular potassium ion concentrations have major effects on cell membrane potentials.
What effect will this have on the cells’ resting membrane potentials?
Because the resting membrane is most permeable to K’, the resting membrane potential is always close to the K’ equilibrium potential. Lowering the absolute value of the K* equilibrium potential will undoubtedly also lower the absolute resting membrane potential (ie, depolarize the cells).
*Small changes in extracellular potassium ion concentrations have major effects on cell membrane potentials.
What effect will this have on the cells’ excitability?
Two things can happen when the resting membrane potential is decreased:
(1) the potential is closer to the threshold potential, which should increase excitability; and
(2) the fast sodium channels become inactivated, making the cell less excitable.
Thus, small increases in (K, may increase excitabil-ity, whereas large increases in (K, decrease excitability.
There are several classes of drugs that are useful for treating various cardiac arrhythmias. Identify the primary effects of each of the following classes of drugs on cardiac myocyte characteristics:
a. What are the effects of sodium channel blockers on the PR interval of the ECG?
On the duration of the QRS complex?
Sodium channel blockers delay the opening of the fast sodium channels in cardiac myocytes. This will slow the rate of depolarization during the action potential (phase 0), which will in turn slow conduction velocity.
This results in a prolongation of the PR interval and a widening of the
QRS complex.
There are several classes of drugs that are useful for treating various cardiac arrhythmias. Identify the primary effects of each of the following classes of drugs on cardiac myocyte characteristics:
What are the effects of calcium channel blockers on the rate of firing of SA nodal cells? On the rate of conduction of the action potential through the AV node? On myocardial contractility?
Calcium channel blockers slow the firing rate of SA nodal cells by blocking the calcium component of the diastolic depolarization. They will reduce the rate of rise of the AV nodal cell action potential (which is largely due to calcium entry into the cells) and slow the rate of conduction through the AV node. In addition, calcium channel blockers will decrease the amount of calcium made available to the contractile machinery during excitation-contraction coupling and thus will decrease the tension-producing capabilities of the cardiac muscle cell.
There are several classes of drugs that are useful for treating various cardiac arrhythmias. Identify the primary effects of each of the following classes of drugs on cardiac myocyte characteristics:
What are the effects of potassium channel blockers on action potential duration? On refractory periods?
Potassium channel blockers inhibit the delayed increase in potassium permeability that contributes importantly to the initiation and rate of repolarization of the cardiac myocyte. This prolongs the duration of the plateau phase of the action potential, prolongs the QT interval of the ECG, and prolongs the effective refractory period of the cell.
Very high sympathetic neural activity to the heart can lead to tetanic concentration of the cardiac muscle. True or false?
False. It is true that increase in sympathetic activity will increase the heart rate (a positive chronotropic effect). However, the electrical refractory period of cardiac cells extends throughout the duration of the cell’s con-traction. This prevents individual twitches from ever occurring so closely together that they could summate into a tetanic state.
An increase in which of the following (with the others held constant) will result in an increase in the amount of active shortening of a cardiac muscle cell?
a. preload
b. afterload
c. contractility
The correct answers are a and c. Increase in preload increases the amount of shortening by increasing the starting length of the muscle, whereas increase in contractility increases the amount of shortening from a given starting length. Increase in afterload limits the amount of shortening because of increase in tension requirement. (See Figures 2-9 and 2-10.)
What happens when an intervention promotes early activation of the “delayed rectifier” K* channel (I«) in a cardiac muscle?
a. The resting potential is increased (hyperpolarized)
b. The action potential duration is decreased.
c. The action potential amplitude is decreased.
d. The action potential conduction velocity is increased.
e. The absolute refractory period is prolonged.
B, because activation of this channel initiates repolarization (phase 3 of the action potential).
Action potential conduction velocity in cardiac muscle tissue is influenced by all of the following except:
a. cell diameter
b. resting membrane potential
c. extracellular potassium concentration
d. rate of rise (phase 0) of the action potential
e. duration of the plateau phase (phase 2) of the action potential
E, because changes in the configuration of the action potential at any given site after the initial rising phase have no influence on the conduction from cell to cell.
The primary route of removal of [Ca’*) from the sarcoplasm during relaxation of a cardiac muscle cell is by:
a. active transport out of the cell
b. passive exchange with extracellular sodium
c. active transport into the sarcoplasmic reticulum
d. trapping of calcium by troponin in the myofilaments
e. passive movement out of the cell via L-type calcium channels
C, because normally about 80% of the transient increase in cytoplasmic calcium during a contraction is retrapped into the SR.
A decrease in atrioventricular nodal conduction velocity will
a. decrease the heart rate
b. increase the P-wave amplitude
c. increase the PR interval
d. widen the QRS complex
e. increase the ST-segment duration
C, Increase the PR interval
The P wave on lead aVR of the normal electrocardiogram will be
a. an upward deflection
b. a downward deflection
c. not detectable
d. highly variable
The correct answer is B.
According to the standard ECG polarity conven-tions, the P, R, and T waves will normally all be downward deflections on lead aVR.
If the R wave is upright and equally large on leads I and aVF, what is the mean electrical axis of the heart? Is it within normal range? Which lead(s) will have the smallest R-wave amplitude?
According to the electrocardiographic conventions, the electrical axis is at
45 degrees and falls within the normal range (in the patient’s lower-left quadrant). The smallest amplitude deflection will occur on the lead to which the electrical axis is most perpendicular. Lead III and lead aVL are both within 15 degrees of being perpendicular to 45 degrees and therefore will have equally small deflections.
What is the definition of cardiac “ejection fraction”?
a. stroke volume expressed as a percent of cardiac output
b. the ratio of the end-systolic volume to the end-diastolic volume
c. the ratio of the end-diastolic volume to the end-systolic volume
d. the ratio of the stroke volume to the end-diastolic volume
e. the ratio of the time spent in systole to the time spent in diastole
D, The ratio of the stroke volume to the end-diastolic volume
