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Cardiovascular physiology > Chapter 3 > Flashcards

Chapter 3 Flashcards

1
Q
  1. How is the electrical potential measured in an individual cell?
A

a. By inserting a microelectrode into the cell and measuring the electrical potential in mV inside the cell relative to the outside of the cell

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2
Q
  1. Define resting membrane potential (Em).
A

a. Em is determined by the concentrations of positively and negatively charged ions across the cell membrane, the relative permeability of the cell membrane to these ions, and the ionic pumps that transport ions across the cell membrane.

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3
Q
  1. What is typical resting membrane potential of a ventricular myocyte in millivolts?
A

a. -90mV

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4
Q
  1. What are the most important ions involved with determining the membrane potential?
A

a. Na+, K+, Ca++

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5
Q
  1. What is the single most important ion involved with determining the membrane potential?
A

a. K+

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6
Q
  1. What are the intracellular and extracellular concentrations of K+, Na+, and Ca++ in a typical cardiomyocyte at a resting membrane potential of -90Mv?
A

a. K+ in: 150 mM / out: 4mM
b. Na+ in: 20mM / out: 145mM
c. Ca++ in: 0.0001mM / out: 2.5mM

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7
Q
  1. What is a chemical gradient?
A

a. Concentration difference

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8
Q
  1. The concentration differences across the cell membrane for these ions are determined by what?
A

a. The activity of energy-dependent ionic pumps and the presence of impermeable negatively charged proteins within the cell that affect the passive distribution of cation and anions

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9
Q
  1. Explain how concentration gradients of ions across a cell membrane affect membrane potential.
A

a. K+ diffuses down its chemical gradient and out of the cell because its concentration is much higher inside than outside the cell. As K+ diffuses out of the cell, it leaves behind negatively charged proteins, thereby creating a separation of charge and a potential difference across the membrane (- inside the cell relative to outside). The membrane potential that is necessary to oppose the outward movement of K+ down its concentration gradient is termed the equilibrium potential for K+

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10
Q
  1. What is an equilibrium potential?
A

a. The potential difference across the membrane required to maintain the concentration gradient across the membrane.

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11
Q
  1. What is the equilibrium potential for K+?
A

a. -96mV

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12
Q
  1. Define net electrochemical force.
A

a. Net driving force. Ex: Because the equilibrium potential for K+ is -96mV and the measured resting membrane potential is -90mV a net electrochemical force acts of the K+ causing it to diffuse out of the cell

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13
Q
  1. If the Em = -90mV, what is the net electrochemical driving force for K+?
A

a. +6mV

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14
Q
  1. What is the equilibrium potential for Na+?
A

a. +52mV

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15
Q
  1. If the Em = -90mV, what is the net electrochemical driving force for Na+?
A

a. -142mV

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16
Q
  1. What is the equilibrium potential for Ca++?
A

a. +134mV

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17
Q
  1. If the Em = -90mV, what is the net electrochemical driving force for Ca++?
A

a. -224mV

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18
Q
  1. Explain how the electrical and chemical forces work collectively to determine the movement of ions.
A

a. Membrane permeability for an ion determines the movement of an ion being driven by a net electrochemical force. Because this ion movement represents an electrical current it is common to speak in terms of ion conductance.

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19
Q
  1. Why would there be little movement of and ion even when there is a large electrochemical force acting on the ion?
A

a. At rest for Na+ even though there is a large electrochemical force driving sodium movement into the cell, at rest the permeability of the membrane to Na+ is so low that only a small amount of Na+ leaks into the cell

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20
Q
  1. What is ion conductance?
A

a. The ion current divided by the net voltage (net electrochemical force) acting on the ion

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21
Q
  1. How are ion permeability and conductance related?
A

a. An increase in membrane permeability for an ion results in an increase in electrical conductance for that ion.

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22
Q
  1. Write an equation that relates Em to the relative conductances and equilibrium potentials of K+, Na+, and Ca++.
A

a. Em = g’K(Ek)+g’Na)+g’Ca(Eca)

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23
Q
  1. In a cardiac cell, how much do the individual ion concentrations change when ions cross the cell membrane during depolarization and repolarization?
A

a. They change very little

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24
Q
  1. Why is the Em close to the EK?
A

a. Because g’K is high in the resting cell, while g’Na and g’Ca are low

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25
Q
  1. Why do Na+ and Ca++ contribute little to the resting membrane potential?
A

a. Th low relative conductance of Na+ and Ca++ multiplied by their equilibrium potential values causes those ions to contribute little to the resting membrane potential

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26
Q
  1. How do changes in conductance of the different ions change the membrane potential, such as during an action potential?
A

a. When g’Na increases and g’K decrease (as occurs during a ventricular AP) the membrane potential becomes more positive (depolarized) because the sodium equilibrium potential has more influence on the overall membrane potential. Similarly, a large increase in g’Ca particularly when g’K is low, will also result in depolarization

27
Q
  1. How is the conductance of some ion channels influenced by the concentration of the ion?
A

a. The maintenance of these concentration gradients requires the expenditure of energy (ATP) coupled with ionic pumps. Ex: Na+ constantly leaks into the resting cell, and K+ leaks out. Moreover whenever an AP is generated, additional Na+ enters the cell and additional K+ leaves.

28
Q
  1. With an action potential, in general, how many ions move across the sarcolemmal membrane?
A

a. Relatively small amount

29
Q
  1. Diagram, describe, and explain in detail the sarcolemmal ion pumps and exchangers.
A

b. These pumps maintain transmembrane ionic gradients for Na+, K+, and Ca++. Na+ and Ca++ enter the cell and K+ leaves the cell down their electrochemical gradients through ion specific channels. Na+ is actively removed from the cell by the electrogenic Na+/K+-ATPase pump, which brings two K+ into the cell for every 3 Na+ that are pumped out. Ca++ is removed by an electrogenic Na/Ca++ exchanger that exchanges 3 Na+ for every 1 Ca++. Ca++ is also removed by an ATP-dependent electrogenic Ca++ pump

30
Q
  1. Which of these requires ATP in order to function?
A

a. Na+/K+-ATPase (NKA) pump, ATP-dependent Ca++ pump

31
Q
  1. Define the term electrogenic.
A

a. An ion pump that generates a net charge flow as a result of its activity

32
Q
  1. What is the function of phospholemman?
A

a. A regulatory protein associated with the NKA, inhibits the pump activity

33
Q
  1. What are the two general types of ion channels?
A

a. Voltage gated channels: open and close in response to changes in membrane potential and receptor gated channels: open and close in response to chemical signals operating through membrane receptors

34
Q
  1. Diagram and describe the general structure of sodium channels in cardiomyocytes.
A

b. In the resting (closed) state the m-gates (activation gates) are closed although the h-gates (inactivation gates) are open. Rapid depolarization to threshold opens the m-gates (voltage activated), thereby opening the channel and enabling sodium to enter the cell. Shortly thereafter, as the cell begins to repolarize, the h-gates close and the channel becomes inactivated. Toward the end of repolarization, the m gates again close and the h gates open. This brings the channel back to its resting state

35
Q
  1. What are the 3 primary states of the fast sodium channel?
A

a. Open, closed, inactivated

36
Q
  1. Explain the transition between each state and the factors that contribute to these transitions.
A

a. The more a cell is depolarized, the greater the number of inactivated sodium channels. At a membrane potential of about -55mV, virtually all fast sodium channels are inactivated. If a myocyte has a normal resting potential but then undergoes slow depolarization, more time is available for the h-gates to close as the m-gates are opening

37
Q
  1. How would the fast sodium channel response change when the resting membrane potential is partially depolarized or slowly depolarized?
A

a. More time is available for the h-gates to close as the m-gates are opening. This causes the sodium channel to transition directly from the resting (closed) state to the inactivated (closed) state. The result is that there is no activated open state for sodium to pass through the channel, effectively abolishing fast sodium currents through these channels

38
Q
  1. What factors determine the amount of sodium that passes through sodium channels when a cardiac cell undergoes depolarization?
A

a. The amount of sodium (the sodium current) that passes through sodium channels when a cardiac cell undergoes depolarization depends upon the number of open sodium channels, the duration of time the channels are in the open state, and the electrochemical gradient driving the sodium into the cell

39
Q
  1. What is an action potential?
A

a. APs occur when the membrane potential suddenly depolarizes and then repolarizes back to its resting state

40
Q
  1. What is the action potential duration in a typical ventricular cardiac myocyte, and how does this compare to other muscles and nerves?
A

a. Typical nerve: 1-2ms
b. Skeletal muscle cell: 2-5ms
c. Ventricular: 200-400ms (cardiac myocyte)

41
Q
  1. What cell types exhibit the “fast response” action potential?
A

a. Atrial and ventricular myocytes, and Purkinje fibers

42
Q
  1. Do nonpacemaker cells have a true resting membrane potential?
A

a. Yes, it remains near the equilibrium potential for K+ because gK, through inward rectifying potassium channels is high relative to gNa and gCa in resting cells

43
Q
  1. Define phase 4 and describe in detail the events that are involved with this phase.
A

a. Non pacemaker cells have a true resting membrane potential that remains near the equilibrium potential for K+. The resting membrane potential is very negative during phase 4 (about -90mV) because potassium channels are open. K+ conductance and K+ currents are high.

44
Q
  1. Define phase 0 and describe in detail the events that are involved with this phase.
A

a. When these cells are rapidly depolarized to a threshold voltage of about -70mV there is a rapid depolarization that is caused by a transient increase in fast Na+ channel conductance through fast sodium channels. This increases the inward directed depolarizing Na+ currents that are responsible for the generation of these fast response action potentials

45
Q
  1. Define phase 1 and describe in detail the events that are involved with this phase.
A

a. Represents an initial repolarization that is caused by the opening of a special type of transient outward K+ channel, which increases gK+ and causes a short lived hyperpolarizing outward K+ current.

46
Q
  1. Define phase 2 and describe in detail the events that are involved with this phase.
A

a. However, because of the large increase in slow inward gCa++ occurring at the same time and the transient nature of Ikto, the repolarization is delayed and there is a plateu phase in the action potential. The inward calcium movement is through long lasting calcium channels that open up when the membrane potential depolarizes to about -40mV.

47
Q
  1. Define phase 3 and describe in detail the events that are involved with this phase.
A

a. Repolarization occurs when gK+ increases along with the inactivation of Ca++ channels (decreased gCa++). Therefore, the AP in non pacemaker cells is primarily determined by relative changes in fast Na+, slow Ca++, and K+ conductances and currents

48
Q
  1. What is the absolute refractory period?
A

a. The cell is refractory (unexcitable) to the initiation of new action potentials

49
Q
  1. What is the purpose/benefit of the absolute refractory period?
A

a. The ERP acts as a protective mechanism in the heart by limiting the frequency of action potentials and therefore contractions that the heart can generate. This enables the heart to have adequate time to fill and eject blood. The long ERP also prevents the heart from developing sustained, tetanic contractions like those that occur in skeletal muscle

50
Q
  1. What is the relative refractory period?
A

a. At the end of the ERP the cell is in its relative refractory period. Early in this period suprathreshold depolarization stimuli are required to elicit actions potentials.

51
Q
  1. Do pacemaker cells have a true resting membrane potential?
A

a. no

52
Q
  1. What cell types exhibit the “slow response” action potential and where are they located?
A

a. Pacemaker cells. The depolarizing current of the AP is carried primarily by relatively slow inward Ca++ currents (through L type calcium channels) instead of by fast Na+ currents. These are normally found in the SA and AV nodes of the heart

53
Q
  1. What is overdrive suppression and what mechanisms are involved with this?
A

a. Pacemaker cells in the AV node and ventricular conduction system’s firing rates are driven by the higher rate of the SA node because the intrinsic pacemaker activity of the secondary pacemakers is suppressed by a mechanism (overdrive suppression). This mechanism causes the secondary pacemaker to become hyperpolarized when driven at a rate above its intrinsic rate.

54
Q
  1. Describe the action potentials observed in the specialized conducting cells of the His-Purkinje system
A

a. They display fast response action potentials and also have intrinsic pacemaker activity that is normally supporessed. Nonpacemaker AP are triggered by depolarizing currents from adjacent cells, whereas pacemaker cells are capable of spontaneous action potential generation

55
Q
  1. Explain the pacemaker current.
A

a. In the repolarized state, a pacemaker current or funny current has been identified. This depolarizing current involves a slow inward movement of Na+

56
Q
  1. What is the intrinsic depolarization rate of the SA node?
A

a. 100-110 depolarizations per minute

57
Q
  1. What is vagal tone and when is it most active?
A

a. At low resting heart rates vagal influences are dominant over sympathetic influences

58
Q
  1. How do autonomic nerves alter SA node firing rate?
A

a. Heart rates can vary between 50-200. These changes in rate are controlled by autonomic nerves acting on the SA node. At low resting heart rates, vagal influences are dominant over sympathetic influences. This is termed vagal tone.

59
Q
  1. Define positive chronotropy and negative chronotropy.
A

a. An increase in heart rate is a positive chronotropic response (or positive chronotropy) whereas a reduction in heart rate is a negative chronotropic response

60
Q
  1. What are the mechanisms by which autonomic nerves alter the rate of pacemaker firing
A

a. Autonomic influences alter the rate of pacemaker firing primarily by changing the slope of phase 4, which determines the time required for phase 4 to reach threshold

61
Q
  1. How could these mechanisms increase or decrease the slope of phase 4?
A

a. Sympathetic activation of the SA node increases the slope of phase 4, increasing pacemaker frequency (positive chronotropy)

62
Q
  1. What neurotransmitter is released by the vagus nerve at the SA node?
A

a. Acetylcholine

63
Q
  1. What is the effect of vagal stimulation at the SA node?
A

a. Vagal stimulation releases acetylcholine at the SA node, which decreases the slope of phase 4 by inhibiting funny currents thereby causing the pacemaker potential to take longer to reach threshold and slowing the rate (negative chronotropy)

64
Q
  1. What nonneural mechanisms can alter pacemaker activity?
A

a. Circulating catecholamines (epinephrine and norepinephrine) cause tachycardia by a mechanism similar to norepinephrine released by sympathetic nerves

Cardiovascular physiology (2 decks)

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