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Cardiopulmonary Renal > Cadiac Action Potential > Flashcards

Cadiac Action Potential Flashcards

1
Q

What means that the Cardiomyocyte has a resting membrane potential of about 90 mV?

A

The potential inside the cardiomyocyte is 90 mV more negative than the potential in the extracellular fluid on the outside of the cardiomyocyte

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2
Q

What determines the membrane potential?

A

Concentration of (+) and (-) charged IONS across the membrane

The relative permeability of the cell membrane to these IONS

Ionic pumps that transport IONS across the membrane

K+, Na+, Ca2+, Cl-

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3
Q

What is the k+ ion concentration in and out of a cardiomyocyte?

A

K+

Inside- 140 mEq/L
Outside-4 mEq/L

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4
Q

What is Na+ concentration inside and outside the cardiomyocyte?

A

Inside- 10 mEq/L

Outside- 142 mEq/L

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5
Q

What is the Ca2+ inside and outside the cardiomyocyte?

A

Inside- 0.0001 mEq/L

Outside- 2.4 mEq/L

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6
Q

What is the Cl- inside and outside a cardiomyocyte ?

A

Inside-4 mEq/L

Outside- 103 mEq/L

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7
Q

What is the K+ concentration ratio of the cardiomyocyte?

A

K+ inside/ outside= 35.0

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8
Q

What is the Na+ concentration ratio of the cardiomyocyte ?

A

Na+ inside/ outside = 0.1

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9
Q

Why do we have those large concentration gradients of K+ and Na+ across cell membrane ?

A

The sodium potassium pump (ATPase)

3 Na+ to the outside for each 2 K+ to the inside

Concentration gradient inside/outside

Electrogenic pump

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10
Q

What is the function of the tandem pore domain?

A

This is the K+ leak channel

K+ can leak even in a resting cell

May also leak Na+ slightly

BUT

It is 100 times more permeable to K+ than to Na+

Diffusion potential —> large K+ concentration gradient
Strong tendency for extra numbers of K+ ions to diffuse outward they carry positive electrical charges to the outside and electronegativity inside because of negative anions

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11
Q

What is the significance of diffusion potential ?

A

When diffusion potential across the membrane exactly opposes the net diffusion of a particular ion through the membrane is called: Nernst potential fir that ion

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12
Q

Describe the origin of the normal resting membrane potential

A

Resting membrane potential is determined by the passive movement of several ions
-Contribution of the K+ diffusion potential MOST IMPORTANT

-Contribution of the Na+ diffusion
When membrane is permeable to several different ions, the resulting membrane potential can be calculated using:
Goldmann-Hodgkin-Katz equation

Contribution of the Na+/K+ pump
It is an electrogenic pump, so it adds -4 mV to the resting membrane potential

RMP= -90mV

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13
Q

What cardiac muscles generate non-pacemaker action potentials?

A
  • atrial myocyte
  • ventricular myocyte
  • Purkinje fiber
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14
Q

What are the sodium channels characteristics and their gating?

A

Fast Na+ (INa)—> gating: voltage—> characteristics: phase 0 of myocytes

Slow Na+ (If)—> gating: voltage and receptor—> contributes to phase 4 pacemaker current in SA and AV nodal cells

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15
Q

What are the calcium channels, their gating and their characteristics?

A

L-type (ICa)—> gating: voltage—> characteristics: slow inward, long lasting current : phase 2 of myocytes and phases 4 and 0 of of SA and AV nodal cells

T-type(ICa)—> gating: voltage—> characteristics: transient current; contributes to phase 4 pacemaker current in SA and AV nodal cell

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16
Q

What are the 5 potassium channels and their gating and character?

A

Inward rectifier(Ik1) —> gating: voltage—> characteristics: maintains negative potential in phase 4: closes with depolarization; it’s decay contributes pacemaker currents

Transient outward(Ito)—> gating: voltage—> characteristics: contributes to phase 1 in myocytes

Delayed rectifier (Ikr)—> gating: voltage—> characteristics: phase 3 repolarization

ATP- sensitive (Ik, ATP) —> gating: receptor—> characteristics: inhibited by ATP, opens when ATP decreases

Acetylcholine activated (Ik, ACh)—> gating: receptor—> characteristics: activated by acetylcholine; GI-protein coupled

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17
Q

What determines flow of ions across the ventricular myocyte?

A

Direction of current flow is determined by the electrochemical gradient fir that ion AND conductance. Note: there are no large changes in ionic concentrations

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18
Q

At resting potential and repolarization, what ion decides the membrane potential of a ventricular myocyte?

A

K+

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19
Q

In depolarization, what ions determine the potential of a ventricular myocyte?

A

Ca2+(+123) & Na+(+67)(closest to Na+)

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20
Q

Describe phase 0 of a cardiac action potential from a ventricular myocyte

A

Depolarization > threshold triggers opening of voltage-gated Na+ channels (rapid opening of activation or m gate opens)
—> Na+ rapidly enters cell

—> Cell depolarizes , inside becomes +ve and approaches ENa. Two events prevent depolarization to ENa.

Na inactivation process starts (inactivation or h gate closes as Vm less negative)

Membrane starts to repolarize

Also: Cell depolarizes , inside becomes +ve and approaches ENa. Two events prevent depolarization to ENa.—> depolarization of cell triggers the opening of voltage-gated K+ channels (repolarization), this leases to outward flow of K+ i (to)

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21
Q

What are the function of gap junctions?

A

Are regulated pores that allow for exchanging chemical and electrical information

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22
Q

Describe the events of phase 1 of cardiac action potential from a ventricular myocyte cell

A

Initial rapid repolarization due to Na+ inactivation and outward flow of K+ (i to)

Meanwhile, the voltage-gated L-type Ca2+ (L=long lasting) channels have finally opened in response to the depolarization of phase 0. (Start to open bat about - 40 mV, can be phosphorylated B-agonists to increase inotrope—> inward Ca2+ current—>

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23
Q

Describe phase 2 of a cardiac action potential from a ventricular myocyte cell

A

Plateau phase

Inward flow of Ca2+ (iCa)

Inward flow of Ca2+ slows down the repolarization due to the outward K current (Ito)

Membrane potential is “held” at about 0mV for a prolonged period (about 150 ms)

At the end of the plateau phase- Ca2+ channels start to close and another set of Kc channels (delayed rectifiers) start to open—> K+flow out Ik

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24
Q

Describe phase 4 of cardiac action potential from a ventricular myocyte cell

A

Resting phase

Ca2+ channels closed
Small background Na+ current. Membrane less perm. to Na+, done by ib
Small k+ current. Inward rectified K current (ik1). Membranous permeable to K+. Major determinant of resting potential. Depolarization decreases conductance

Both of these are counterbalanced by the Na+/K+ ATPase pump

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25
Q

Describe phase 3 of cardiac action potential from a ventricular myocyte cell

A

Rapid repolarization due to outward K+ current Ik through the delayed rectifier channels.

Slow repolarization

  • not propagated
  • several potassium channels

This leads to membrane potential returns to the resting levels

26
Q

Whaat is card8aac action potential due to?

A

Action potential due to:

  • electrochemical gradient
  • conductance (wh8ch channels are open)

Channel conductance:
Downward= inward current(iNa)
Upwards= outward current

Transient outwards (slow, fast) i to

Delayed rectifiers (slow, fast) ik

Resulting membrane potential ik1

27
Q

What is the absolute refractory period(ARP) of the cardiac action potential?

A

Depolarization block of voltage gated Na+ channels. Requires repolarization for inactivated h-gate to be reset (Hodgkin-Huxley model-m and h gates).
-No stimulus of any magnitude evokes propagated response (infinite threshold)

28
Q

What is the relative refractory period (RRP) of the cardiac action potential?

A

Stimulus above normal threshold generates a response (re-entry circuits pathology)

29
Q

Give an advantage and disadvantage: long refractory period in cardiac muscle prevents tetanic contractions

A

Advantage- no tetanus. Heart cannot fill if in continuous and max contracted state

Disadvantage- ectopic currents-heart beat arises from fibers outside SA node. Can render the heart refractory to normal signal from SA node

30
Q

Describe the duration of the ARP

A

During the phases 0,1, 2, and part of phase 3, the cell is refractory (unexcitable)

During the ARP, stimulation of the cell dies not produce new, propagated action potentials

ARP acts as a protective mechanism in the heart by limiting the frequency of action potentials and there fore contracts that the heart can generate, enabling the heart to have adequate times to fill and eject blood

The long ARPalso prevents the heart from developing sustained, tetanic contractions like those that occur in the skeletal muscle

31
Q

Describe the duration of relative refractory period

A

At the end of the ARP the cell is in its RRP

Early in this period suprathreshold depolarization stimuli are required to elicit action potentials

Because not all the sodium channels have recovered to their resting state by this time, action potentials generated during RRP have a decreased phase 0 slope and lower amplitude

32
Q

What accounts for the long refractory period of cardiac action potential ?

A

This sustained sodium channel inactivation, combined with activation of calcium channels and the delay in opening of potassium channels, accounts for the long plateau phase and the long cardiac refractory period, which lasts until the end of phase 3 (repolarization)

33
Q

Describe the Antiarrhythmic class I(sodium channel blockers)

A

During the phases 0, 1, 2, and. Part of phase 3, the cell is refractory(unexcitable)

During the ARP, stimulation of the cell does not produce new, propagated action potentials

ARP acts as a protective mechanism in the heart by limiting the frequency of action potentials and therefore contractions that the heart can generate, enabling the heart ti have adequate times to fill and eject blood

The long ARP also prevents the heart from developing sustained, tetanic contractions like those that occur in the skeletal muscle

34
Q

Why are there time delays between SA & AV?

A

SA before AV (sets pace; overdrive suppression-hyperpolarization of other pacemakers)

Delay between Atrial and Ventricular contraction- due to AV node

35
Q

Summarize the conduction system of the heart

A
  • Heart rate initiated by SA node (ANS modulate HR)
  • depolarization of myocytes spread via gap junctions -synctium
  • Special system for rapid conduction of depolarization through heart (especially ventricles)- conducting system
36
Q

What are the advantages of the conduction system?

A
  • control timing of contraction

- Control which regions contract

37
Q

What is the ordered contraction of the heart ?

A

SA node—> intermodal branches—> AV node (a major site of ANS regulation)—> bundle of His—> Purkinje fibers

Ordered contraction of heart
-Atria first- allowing time to fill ventricle

-Ventricles- contract septum, then apex to base. (Efficient ejection of blood)

38
Q

What conducts the fastest?

A

Bundle branches= Purkinje about equal to AV bundle>atrial myocard> ventricle myocard> SA node> AV node

OR

  1. Electrical conduction system> 2. Myocardium > 3. Nodes
39
Q

Why is the AV node the only normal electrical pathway between the atria and the ventricle ?

A

Only normal path for depolarization is through AV node

Atria electrically isolated from ventricles by fibro-adipose tissue (cardiac “fibrous skeleton”)

Abnormal paths- Bundle of Kent—> Wolf-Parkinson-White syndrome (pre-excitation )

40
Q

What are the advantages and disadvantages of delayed electrical contact of AV node?

A

Advantages-

  • allows time to contract before ventricles contract
    • atria-topping up ventricles (about 10% at rest, 40% during exercise)

Atrial tachyarrhythmias may not be transmitted to the ventricles- safeguarding the ventricles

Disadvantages of delay- low safety factor for transmission

-discuss pathologies of conduction system later

41
Q

What is the only electrical contact between atria and ventricles ?

A

AV node

42
Q

Summarize the progression of wave of depolarization through the heart

A
  1. Depolarize atria
  2. Depolarize septum from left to right
  3. Depolarize anteroseptal region of myocardium toward the apex
  4. Depolarize bulk of ventricular myocardium, from endocardium to epicardium
  5. Depolarize posterior portion of base of the left ventricle
  6. The ventricles are nor depolarized
43
Q

What are the rates of each part of the conduction system ?

A

SA node: 60-75 bpm(normal sinus rhythm)

AV node: 50 bpm

Bundle of His: 40 bpm

Purkinje fibers: 15 bpm

However, HR is set by the fastest- the SA node.
So, AV cannot drive HR under normal conditions

-SA node primary pacemaker—> overdrive suppression. Leads to hyperpolarization of other pacemaker sites

44
Q

Where is the SA node located?

A

Located within the posterior wall of the right atrium

Primary pacemaker site of the heart

45
Q

Where is the AV node located?

A

Located at the base of the right atrium within the triangle of Koch, a region defined by the following landmarks:

The coronary ostium, tendon of Todaro, and the septal leaflet of the tricuspid valve

Other pacemaker cells exist within the ventricular conduction system

46
Q

Why the firing rate of all the pacemaker cells are drive by the higher rate of Sinoatrial node?

A

Overdrive suppression

47
Q

What is overdrive suppression?

A

This mechanism causes the secondary pacemaker to become hyper polarized when driven at a rate above its intrinsic rate

Hyperpolarization occurs because the increased action potential frequency stimulates the activity of the electrogenic Na/K ATPase pump as a result of enhanced entry of sodium per unit time into these cells

If the SA node become depressed, or it’s action potential fail to reach secondary pacemakers, overdrive suppression ceases, which permits a secondary site to take over as the pacemaker for the heart. When this occur, this new pacemaker is called an ectopic foci

48
Q

Describe the events of phase 4 of action potentials from the SA node

A

Pacemaker potential

(Slower diastolic potential ) due to
inward Na+ current i f
Inward Ca2+ current i Ca

Na channels are “funny”-they open when membrane is relatively polarized or at rest (unusual)

Pacemaker potential unstable

I f channels open—> inward Na+ current —> depolarization —>. Open T-type Ca2+ channels T=transient—> iCa—> more depolarization

49
Q

Describe the events of phase 0 of the action potential from the SA node

A

Phase 0

Rapid depolarization

ICa L-type

When depolarization reaches threshold (-40 mV) L-type Ca2+ channels open. i f channels are now closing.

As Ca2+ channels start closing, K+ channels start opening in response to the depolarization

50
Q

Describe the events of phase 3 of the action potential of the SA node

A

Repolarization due to closure of Ca2+ channels

Opening of K+ channels—>. As the membrane becomes more and more repolarizes the Na+ i f channels start to open again

51
Q

Describe the events of phase 4 of SA node action potential

A

Pacemaker potential

Na+ i f channels open and membrane starts to SPONTANEOUSLY depolarize again

Repolarization opens the Na+ i f channels

52
Q

What are the characteristic features of SA node action potential?

A

Unstable resting potential

No plateau phase

Upstroke of action potential (phase 0) is due to inward Ca2+ current (not Na+). Upstroke slower than in ventricular AP

53
Q

What are the sympathetic and parasympathetic of the SA node?

A 
Sympathetic:
Increased activity:
-increased slope phase 4 AP
-increased SA node firing
-decreased vagal tone 
Parasympathetic 
Vagal tone dominant resting heart 
Increased activity:
-hyperpolarized 
-decreased slope phase 4 AP
54
Q

What are the effects of sympathetic and parasympathetic influence on AV node?

A

Sympathetic: increased conduction velocity

Parasympathetic: decreased conduction velocity

55
Q

What are the influences of parasympathetic and sympathetic influence on atrial myocyte ?

A

Sympathetic: innervated-increased atrial inotropy

Parasympathetic: innervated-decreased inotropy

56
Q

What are the sympathetic and parasympathetic affects on ventricle myocyte?

A

Sympathetic-little innervation (gap-junctions synctium)

Parasympathetic- little innervation

57
Q

What are the effects of parasympathetic stimulation on the SA node?

A

ACh causes a slower rate of rise of the pacemaker potential leading to decreased heart rate

Hyperpolarize and decreased ion channel activation

58
Q

How does acetylcholine slow heart rate?

A

Acetylcholine activates muscuranic M2 receptors

One way:
Activates G proteins (GBy)—> opens KACh channel—> increases K conductance—> hyperpolarization of SA node—> prolongs phase 4 of SA node—> slows heart rate

Other way:
Activates G proteins (Gia)—> decreased Adenylate cyclase—> decreased cAMP—> decreased PKA—> decreased activation of i f and I Ca channels —> slows rate of spontaneous depolarization of SA node—> prolongs phase 4 of SA node—> slows heart rate

59
Q

Summarize the effect of sympathetics on heart rate

A

Norepinephrine increases rate of depolarization in phase 4

60
Q

Give the pathway of sympathetics affecting heart rate

A

Norepinephrine (B1 agonist)—> activates cardiac B1 receptors—> increased cAMP—> phosphorylation of if(funny) and iCa channels—> increased if and I Can (increased probability of opening)—> increased rate of depolarization —> increased heart rate

61
Q

What are the indirect effects of the SNS on the heart?

A

Relaxation: cardiac relaxation also increased with Catecholamine mediated increase HR(alllows heart ti beat faster)

  • catecholamine-induced Ca2+ uptake into SR —> increase rate of relaxation (rem9ves phosphorylation inhibition of SERCA)
  • results in positive lusitropy

Calcium levels: Bowditch effect - increases HR, increases inotropy (similar Digixin mode of action)
Short version: rapid HR—> calcium clearance from cytoplasm not keep up —> increases intracellular Ca2+

Leads to positive inotropy

Cardiopulmonary Renal (35 decks)

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