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CV exam 1 AP > Action Potential,Resting Membrane Potential and Conduction System (Montemayor) > Flashcards

Action Potential,Resting Membrane Potential and Conduction System (Montemayor) Flashcards

1
Q

what are the types cardiac cells

A

contractile cells - perform mechanical work

autorhythmic cells- initiate action potentials

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2
Q

automaticity of the heart?

A

self stimulating AP

cyclic depolarization of autorhythmic cells independent of neural input

Specialized cells in atria & ventricles initiate electrical activity required for mechanical contraction (heartbeat)
Located mainly in nodal tissues or specialized conducting fibers [Conduction System]

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3
Q

what is the order and timing of electrical events in the heart.

A 
SA node
inter-atrial pathway
AV node
Common AV bundle  (bundle of his)
R and L bundle branches
Purkinje fibers
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4
Q

what is the functional syncytium

A

myocytes contract as a single unit due to gap junctions

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5
Q

what is the location and function of the SA node

A

right atrial wall just inferior to opening of superior vena cava

primary PACEMAKER (80-100 bpm)
rate of reaching threshold is fastest and drives the heart rate

initiates impulse that is normally conducted throughout the left and right atria

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6
Q

what is the location and function of the AV node

A

floor of the right atrium immediately behind the tricuspid valve and near the opening of the coronary sinus

***connects atira to ventricular conducting system

receive impulse from the SA node and delays relay of the impulse to the bundle of HIs allowing time for the atria to empty their contents into the ventricles before the onset of ventricular contraction

40-60 bpm

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7
Q

location function of bundle of his

A

Superior portion of interventricular septum

receives impulse from AV node and relays it to right and left bundle branches

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8
Q

where is the location and what is the function of right and left bundle branches

A

interventricular septum

receives impulse from bundle of His and relays it to Purkinje fibers

RBB–> direct continuation of bundle of His—> down right side of IV septum

LBB–> thicker than RBB, perforates IV septum
splits–> thin anterior division and thick posterior division

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9
Q

function and location of Purkinje fibers

A

arise from RBB and Anterior and Posterior LBB
spread out over subendocardial surfaces of R and L ventricles

receives impulse from bundle branches and relays it to ventricular myocardium

FASTEST CONDUCTION VELOCITY and largest diameter cardiac cells (increase diameter and decrease internal resistance)

30-40 bpm

rapid activation of endocardium layer–> epicardium layer and then –> Apex–> base

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10
Q

what is the cause of bradycardia

A

SA nodal failure

this leads to unmasking of slower, latent pacemakers in the AV node or ventricular conduction system

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11
Q

how does the SA node get the impulse to the right atrium?

A

internodal pathway (anterior, middle and posterior)

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12
Q

how does the SA node get the impulse to the left atrium

A

anterior interatrial myocardial band (Bachmann’s bundle)

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13
Q

what is the AV junction and what are the regions

A

AN region-transitional zone between atrium and the node ***

N region- midportion of the AV node
NH region- nodal fibers merge with bundle of his

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14
Q

why is there a delay between atrial and ventricular excitation? AV nodal delay

A

so there is time for filling !

adequate filling time during diastole of the ventricles

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15
Q

how does the AV nodal delay occur

A

because the AN region has a longer conduction path

the N region has a slower conduction velocity

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16
Q

how does the heart prevent atrial fibrillation or flutter

A

decremental conduction
increase in stimulation frequency actually causes a decrease in conduction velocity

this limits the rate of conduction to the ventricles from accelerated atrial rhythms

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17
Q

what can lead to Ventricular bradycardia

A

AV block- so the AV node is essentially knocked out

results in distal pacemaker sites generating the ventricular rhythm –> secondary pacemaker sites have a lower intrinsic rate than the SA node

purkinje fibers –> 20-40 bpm (slow)

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18
Q

what is Wolff Parkinson white syndrome

A

**May result in reentry and is a cause of supraventricular (above ventricles) tachyarrythmias **

Alternate path around AV node (Bundle of Kent)
(accessory conduction pathway)
AP conducted directly: atria –> ventricle

Faster than normal AV nodal pathway

Ventricular depolarization is generally slower than normal

Accessory depolarization path does not follow normal path of purkinje fibers

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19
Q

what are the steps in AP conduction (location wise)

A

AV node –> bundle branches

IV septum depolarized L–> R

Anteroseptal region depolarizes

myocardium depolarizes from endocardium –> epicardium

depolarization spreads from apex –> base via Purkinje fibers

ventricles are fully depolarized

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20
Q

why is there early contraction of the IV septum

A

rigid: anchor point for ventricular contraction

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21
Q

why is there early contraction of the papillary muscles

A

prevents prolapse of atrioventricular valves during ventricular systole

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22
Q

why is there depolarization from apex to base

A

allows efficient emptying of ventricles into aorta and pulmonary trunk at the base

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23
Q

what are the fastest conductors of the conduction system of the heart?

A

purkinje fibers (due to larger diameter and lower internal resistance)

bundle branches

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24
Q

what are the slowest conductors of the conduction system of the heart?

A

AV node
SA node

small diameter–> increased resistance

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25
Q

where does cardiac muscle store calcium

A

ECF and SR

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26
Q

what is characteristic of cardiac muscle

A

striated
mononucleated
intercalated disks (gap junctions (low resistance))
T-tubules and SR (Ca stores in ECF and SR)***

Ca 2+ regulation of contraction: binds troponin

Relatively slow speed of contraction***

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27
Q

Biomarkers of myocardial injury?

A

Troponin (cTnT, cTnl)

CK -MB

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28
Q

what is the functional sycytium

A

Cardiac

cells contract in synchrony

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29
Q

what are intercalated disks

A

connect cardiac cells through mechanical junctions and electrical connections

desmosomes- mechanical, so cell doesn’t pull apart when it contracts

Gap junctions -electrical connection (low resistance) allowing AP propagation

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30
Q

what is one way a widening of the QRS complex can happen (in terms of the functional syncytium)

A

Ventricular depolarization that spreads only cell to cell via gap junctions results in the widening of the QRS complex (PVC’s, Ventricular Tachycardia)

group of cells firing in their own rate, taking longer than normally would see

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31
Q

do the atria and ventricles contract as separate units?

A

YES

each form a functional syncytium

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32
Q

what is the all or non law for the heart and how is this different than skeletal muscle?

A

all cardiac cells contract or NONE do
no variation in force production via motor unit recruitment (as can be done in skeletal muscle)

this is due to the functional syncytium and conduction system

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33
Q

what is contractility in terms of the heart

A

increased force contraction is modified by altering sympathetic NS input (increasing Ca2+ permeability)

so it is INDEPENDENT of initial fiber length or preload

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34
Q

what is the role of extracellular Ca in cardiac contraction

A

influx of extracellular Ca is REQUIRED for additional Ca release from the SR

Release of Ca2+ from SR is also required

this is called Ca induced (Ca dependent) Ca release from the SR through Ca release channels RYR (ryanodine receptors)

amount of Ca from ECF alone is too small to promote actin-myosin binding

Ca influx from ECF triggers Ca release from SR

Ca release channels remain open longer

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35
Q

what channels does Ca use to get in from the ECF

A

from ECF via voltage gated L type Ca channels during long plateau phase of cardiac muscle AP

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36
Q

how does relaxation of cardiac muscle occur

3 things

A

Removal of Ca to the ECF

  • 3Na-1Ca antiporter
  • Sarcolemmal Ca2 pump

Sequestering Ca into the SR
SERCA

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37
Q

how does the Sarcolemmal 3Na 1Ca antiporter work

A

moves ca against large gradient

na higher in the ECF, so uses the Na gradient to power Ca2+ removal

*** if the Na concentration in the ECF is abnormal this pump might not work properly

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38
Q

how does the sarcolemmal Ca2 pump work

A

uses ATP to extrude Ca from cell against gradient

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39
Q

How does the SERCA pump work

A

Ca back in the SR

regulated by phospholamban

b-adrenergic mediation of phosphorylation increases SERCA activity

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40
Q

is there tetanus in cardiac muscle

and what pumps are contributing to the cardiac muscle either having or not having tetanus

A

NO (unlike skeletal muscle)

cardiac muscle cannot increase force of contraction through tetanus

AP is so long, can’t sum twitches, long refractory period

GOOD b/c tetanus would be fatal because effective pumping would be inhibited

**Primarily due to activation of voltage gated L type Ca channels and slow delayed K channel opening **

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41
Q

what is the difference between the pacemaker cells and non pacemaker cells in terms of resting membrane potential

A

pacemaker cells have no resting potential -just have a maximum diastolic potential (spontaneous slow depolarization phase)

nonpacemaker cells have a true resting potential (-80 to -90mV)

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42
Q

which ions have the greatest impact on resting membrane potential and describe the primary distribution

A

K- high inside
Ca- very high outside compared with inside
Na- very high outside compared with inside

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43
Q

what is the K+ contribution to the RMP

A

resting cell membrane is relatively permeable to K+ (much more than Na and Ca)
LEAK CHANNELS
hyperkalemia –> depolarize the membrane

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44
Q

what is the Na contribution to the RMP

A

Because gNa is so small in the resting cell, changes in ECF (na) do not significantly affect Vm

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45
Q

what is the main contributor to the peak value of the upstroke of the AP (of non-pacemaker cells

A

Na

change in the ECF concentration of Na can change the amplitude of the AP

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46
Q

why does AP propagation require careful timing?

A

to synchronize ventricular contraction to optimize ejection of blood

initiation time, shape and duration of AP’s are distinct for cells of varied function within cardiac regions

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47
Q

APs characterized by slow rate of depolarizing upstroke …

A

SA and AV nodes

48
Q

AP’s characterized by fast rate of depolarizing upstroke

A

Atrial myocytes, purkinje fibers and ventricular myocytes

49
Q

2 main types of cardiac action potentials

A

fast

  • higher amplitude
  • faster conduction velocity

slow (sa nodes and av nodes)

  • no true resting membrane potential
  • maximum diastolic potential is less negative than starting point of the fast response
  • lesser amplitude
50
Q

fast vs slow resting membrane potential

A

more negative in fast

51
Q

fast vs slow threshold potential

A

slow - reach threshold at -40

fast - reach threshold at about -70 mV

52
Q

what contributes to how fast an AP is propagated

2 things

A

AP amplitude and upstroke slope

53
Q

in which AP (slow or Fast) tissue type is conduction block more likely to happen

A

in slow response tissue b/c it is slower

54
Q

what are the 4 major time dependent and voltage gated currents

A

Na
-rapid depolarizing phase in atrial, ventricular, and Purkinje fibers

Ca
-“rapid” depolarizing phase in the SA node and AV node
primarily responsible for plateau phase of fast-response AP’s
Triggers contraction in all contractile cardiomyocytes

K
-repolarizing phase in all cardiomyocytes

Pacemaker funny current
-pacemaker activity (slow depolarization phase) in SA and AV nodal cells and sometimes Purkinje fibers

55
Q

what is going on at phase 0 for slow and fast

UPSTROKE

A

slow
due to Ca current inward

fast
due to both Na and little bit of Ca influx

56
Q

what is going on at phase 1

early rapid partial repolarization

A

only associated with fast responses

activation of minor K+ current (transient)

inactivation of Ina and Ica (likely T-type Ca 2+ channels)

57
Q

what is going on in the plateau phase

A

continued influx of Ca2+ countered by small K+ current

Small, remaining Na+ current possible and a minor membrane current due to the Na-Ca exchanger)

58
Q

what is going on in phase 3

FINAL repolarization

A

depends on K current in cells (so K efflux)

59
Q

what is going on in phase 4

electrical diastolic phase

A

changes in K Ca and funny current produce pacemaker activity in SA and AV nodal cells

Atrial and ventricular muscle have no time-dependent currents during phase 4 (this is when there is no inward or outward flux of K, Na or Ca)

60
Q

Na + role

A

Ventricular m., atrial m., and Purkinje fibers have many voltage-gated Na+ channels and a large Na+ current (INa)

closed at negative resting potentials and rapidly activate when membrane depolarizes to threshold

Na influx mainly responsible for rapid upstroke of AP (phase 0)

partial role in the early repolarization of the AP (phase 1)

Within the range of positive voltages, a very small INa remains: prolongs plateau phase (phase 2)

61
Q

what does the magnitude of the Na current impact?

A

impacts regenerative conduction of AP’s

depolarization induced by na current activates both na current in adjacent cells and other currents in the same cell (Ca and K)

62
Q

what are L-type Ca channels

A

long -lived

63
Q

what are the T-type Ca channels

A

transient

64
Q

what is the role of Ca2+ in slow type tissue

SA nodes and AV nodes

A

contributes to pacemaker activity (gradual ) phase 4

influx contributes to upstroke (phase 0) (major contribution)

Ca is smaller than Na current
-this is obvious with the slower upstroke of Nodal cells versus atrial and ventricular mm.

65
Q

why are AP’s in nodal cells smaller?

A

slower conduction velocity because the smaller ca current depolarizes adjacent cells more slowly

66
Q

what is the role of Ca in fast type tissue

ventricular, atrial and purkinje fibers

A

smaller Ca influx during phase O but larger contribution from Na

activated more slowly than voltage gated sodium channels (b/c they have more positive voltage they need to be activate dat) and close more slowly

67
Q

what is the major contributor to the prolonged plateau phase in fast type tissue

A

L-type Ca channels

Ca entering through L type Ca channels activates the release of Ca from the SR by calcium-induced Ca release in atrial and ventricular mm

68
Q

what is potassiums role

A

the slow, delayed current of K contributes to the relatively long cardiac Ap’s

the K current is responsible for repolarization at the end of the ap in both fast and slow types (phase 3)

slowly activates with depolarization and does not inactivate

69
Q

what is happening with the K current at negative diastolic voltage in SA and AV nodes

A

K current decreases at this voltage contributing to the pacemaker activity

decreasing K+ efflux promotes depolarization

70
Q

what happens in phase 0 of fast type

A

upstroke, spike, overshoot

beings with depolarization opens voltage gated Na channels –> rapid Na influx, minor contributor is slower Ca influx and K efflux

inactivation gates kick in more slowly as it passes threshold

also note ECF Na affects AP amplitude

71
Q

what happens with hypernatremia?

A

it affects the maximum upstroke

with increase in ECF na there is a larger AP amplitude (the peak of the AP increases )

72
Q

what happens in phase 1 of fast type

A

early repolarization

primarily due to K efflux via K(transient) channels

Na influx SLOWS as majority of Na channels inactivate
Delayed Ca influx (plateau) phase begins

73
Q

what happens with 4-aminopyridine (K+channel blocker)

A

the notch in phase 1 is less prominent b/c there is probably not as much K+ efflux

74
Q

what happens in phase 2 of fast type ?

A

primarily due to slow Ca2 influx (L-type)

slow efflux continues

contributes to longer duration of Cardiac AP **

75
Q

what happens in phase 3 of fast type

A

rapid repolarization due to K efflux

na and ca channels are CLOSED

76
Q

what happens if K+ channels are blocked

A

the AP duration will increase

delayed repolarization

77
Q

what happens in phase 4 of fast type

A

resting membrane potential

fully polarized state of resting cardiac cell

membrane will remain polarized until reactivated by another stimulus

78
Q

what is unique about the atrial muscle AP

A

has 3 time/voltage dependent currents (na k ca)

AP duration SHORTNER in ATRIAL vs. ventricular: due to greater efflux of K+ during plateau phase ***

no pacemaker activity

79
Q

what is unique about Ventricular muscle AP

A

3 time/voltage dependent currents (na k ca)

no pacemaker activity

rapid upstroke

plateau phase is prolonged (ca current activates SR ca release for contraction)

AP duration varies among ventricular cells: differences in the delayed rectifier K+ current

80
Q

what is conduction velocity

A

how quickly an AP can be conducted to an adjacent cell

81
Q

what does conduction velocity depend on

A

Amplitude of the AP
-greater amplitude can more effectively depolarize adjacent membrane

Rate of change of potential during phase 0

  • slope of depolarization
  • if depolarization is too gradual it may not produce depolarization in adjacent membrane
82
Q

what two things CAN impact AP amplitude

A

RMP (Vm) and Na (ECF) outside cell

Normal AP: depolarization is so fast inactivation gates do not tend to close until end of phase 0 BUT
If a partial depolarization of RMP occurs gradually, inactivation gates have time to close

If many Na+ channels are already inactivated, only a fraction are open for Na+ influx during phase 0
Decreases amplitude & slope of depolarization –> slows conduction velocity

83
Q

what is the problem with hyperkalemia

A

SLOWS CONDUCTION VELOCITY

may cause cell to be in a persistent slightly depolarized state and this can cause Na channels to be in inactivation state. so the amount of Na channels available for sodium influx to respond to an AP will be LESS therefore smaller influx of Na and lower slope of phase 0 and a lower amplitude –> decrease conduction velocity

at high enough K ECF Vm is depolarized to inactivate majority of fast Na channels and the fast-response AP’s begin to look like slow -response AP’s

84
Q

what happens with blood flow reduction and ischemia of heart (Coronary artery disease)

A

decrease metabolic substrates powering Na+/K+-ATPase (the NaK pump)

Impairment: Excess intracellular Na+ and excess extracellular K+

Elevated [K+]o can result in rhythm disruption

85
Q

what happens with MI in terms of ECF K concentration

A

Infarcted cells release intracellular K+ stores causing increase in ECF K

86
Q

what is the effective (absolute) refractory period

A

After initiation of fast response AP, the depolarized cell is no longer excitable until the cell is partially repolarized

Time during which a subsequent electrical stimulus (of any size) has no effect

from phase 0 to mid phase 3

***it is due to the fact that Na and Ca are largely inactivated by depolarization (inactivation gates)

87
Q

what is the relative refractory period

A

fiber is not fully excitable until complete repolarization

Before repolarization is complete, another AP may be initiated if stimulus is strong enough

ICa, INa: inactivation gates open with repolarization
Phase 3: repolarization with increased IK (efflux)

88
Q

what are the various outcomes with initiation of AP during relative refractory period at different times?

A

AP characteristics vary based on Vm at time of stimulation

The later in the relative refractory period the greater the amplitude and slope of upstroke (greater the conduction velocity)

this is because there are more fast Na channels recovered from inactivation as repolarization proceeds during phase 3

89
Q

why is the refractory period important in cardiac muscle

A

It prevents sustained tetanic contraction

  • Relaxation of cardiac muscle: mainly during AP phase 4
  • Tetanus would result in sustained contraction & interfere with normal intermittent contractions that promote effective pumping (adequate filling)

Safety measure
-limits extraneous pacemakers from triggering ectopic (out of place) beats which would reduce pump efficiency

90
Q

what is ectopic foci and what does it cause

A

generate AP’s that do not follow normal conduction pathway

myocytes take longer to depolarize cell-to-cell via gap junctions

cause premature contractions

91
Q

what does a ventricular ectopic foci look like on EKG

A

wide QRS

92
Q

what are the possible causes of ectopic foci

A

Local areas of ischemia

Mildly toxic conditions can irritate fibers of the A-V node, Purkinje system, or myocardium (ex: various drugs, nicotine, or caffeine, alcohol)

Calcified plaques irritating adjacent cardiac fibers

Cardiac catheterization: mechanical initiation of premature contractions

93
Q

what are afterdepolarizations

A

Abnormal depolarizations of cardiac myocytes that interrupt phase (2), 3, or 4 of the AP

the earlier the more detrimental

94
Q

what can afterdepolarizations cause?

A

tachycardia

May increase pacemaker activity of existing pacemakers, induce pacemaker activity in Purkinje fibers, or in ventricular myocytes

May trigger extra systole (PVC)

Series of extra systoles (3+) –> ventricular tachycardia (can lead to ventricular fibrillation

can set up an oscillatory repolarization

95
Q

what happens with an Early Afterdepolarization (EAD)

A

Increased frequency of abortive APs

Abnormal depolarization late phase 2 or phase 3
Phase 2 interruption: augmented Ca2+ channel opening

Phase 3 interruption: Na+ channels open or delayed inactivation

Ex: Long QT Syndrome –> Torsades de Pointes

96
Q

what happens with delayed afterdepolarizations (DAD)

A

Ap generation during phase 4 depolarization before another AP would normally occur

elevated Ca2+ (digoxin toxicity)

97
Q

how does the timing of premature depolarization determine clinical consequence?

A

late in RRP or after full repolarization–> little consequence

early in RRP likely slowed conduction of the early impulse

REENTRY is more likely to occur
fibrillation may develop –> inefficient contractions can lead to death

98
Q

what is reentry

A

abnormal impulse conduction may re-excite myocardial regions through which an impulse has already passed

CIRCUS movements

responsible for many arrhythmias –> fibrillation

requires UNIDIRECTIONAL BLOCK

need at whatever location, need the region where the signal reenters in the improper way to enter in area where it is out of the refractory period

99
Q

what is global reentry

A

Macro reentry

between atria and ventricles BACKWARDS

can cause Supraventricular tachycardia (SVT)

Wolff-Parkinson-White syndrome

100
Q

what is local reentry

A

Microreentry

within the atria or ventricles

cause atrial or ventricular tachycardia

101
Q

Requirements for Reentry

A

Partial depolarizaiton of a conduction pathway

unidirectional block

timing: reentrant current must occur beyond ERP

102
Q

how can alterations in autonomic input promote or block reentry

A

if you have sympathetic activation of AV node and ventricular conduction pathways then you increase conduction velocity and decrease ERP

if you have vagal activation of AV node you decrease conduction velocity and increase ERP

103
Q

3 factors promoting reentry in pathological cardiac conditions ***

A

lengthened conduction pathway

  • commonly occurs in dilated heart chambers
  • atrial fibrillation due to atrial enlargemnet associated with valve lesions or ventricular failure

decreased conduction velocity (slope and amplitude)
-Purkinje system block, ischemia, hyperkalemia

reduced refractory period

  • can occur in response to various drugs
  • epinephrine
104
Q

what is the result of circus movements?

A

fibrillation

105
Q

what does an external automated defibrillator do

A

strong high voltage alternating current can promote a “re-set” by putting all cells into refractoriness at once STOPPING fibrillation

106
Q

what are some characteristics of Slow response AP’s that is different from Fast-response

and what is the key one??

A

No true RMP
-Slow depolarization (pacemaker potential)** KEY

Less steep AP upstroke (phase 0)
-Minimal INa contribution

No early repolarization (phase 1)

Absent or less distinct plateau (phase 2)

Gradual repolarization (phase 3)

Less negative Vm during “rest” (~ − 60/65 mV) (phase 4)

Less IK, less negative Vm (retain intracellular +); funny current mainly Na+ influx

107
Q

firing frequency of pacemaker cells can be altered how?? 3 things

A

Depolarization rate (altering ion currents)

Vm during phase 4 (starting point)

threshold

108
Q

what is in charge/responsible for the slow diastolic depolarization (phase 4) in slow response AP’s

A 
Funny current  (non-specific cation channel)
-inward (mainly Na) activated during HYPERpolarization

increase Ca influx

decrease K efflux

109
Q

what is the funny current

A

opens at progressively more negative voltages

slow activation near end of depolarization (phase 3)

activated when Vm reaches -50 mV (as repolarizing)

***activation increases with increasingly negative Vm

mainly Na influx

110
Q

what is the role of calcium current in slow AP response

A

contributes to slow diastolic depolarization

activate near end of phase 4

influx of Ca increases rate of depolarization to threshold

MAJOR CONTRIBUTOR to AP upstroke (phase 0)

111
Q

what would happen to slow response Ap’s if ECF Ca is changed

A

Increase–> increase amplitude and upstroke

Decrease –> exact opposite

112
Q

what is the role of K is the slow AP response

A

major current contributing to REPOLARIZATION

K current opposes Funny and Ca currents during phase 4

K efflux gradually decreases during phase 4 which helps DECREASE the opposition to ca and funny currents allowing threshold to be reached again

113
Q

How does hyperkalemia affect heart rate

A

increase in ECF K –> leads to decrease in HR

changes in driving force for K efflux

slows phase 4 depolarization

increases AP duration in nodal cells

delay in reaching hyperpolarization voltage required to activate funny current that is needed to start the slow depolarization

114
Q

what effect does an AP evoked in the RRP have in slow response refractory periods?

how is the recovery time to full excitability in slow response compared to fast response AP’s

A

AP evoked EARLY have small amplitudes and shallow upstrokes
***Results in slower conduction velocity and can lead to conduction blocks

AP evoked later have progressively increasing amplitudes and upstroke slopes

**Recovery of full excitability is slower than in fast response AP’s

115
Q

which pacemaker rate is faster. SA or AV

A

SA

so if SA node fails, AV node can take over pacemaker role to drive HR

and if both SA and AV nodes fail than purkinje fibers take over

116
Q

what does tetrodotoxin do?

A

blocks fast Na channels –> fast response fiber can generate slow response

Purkinje fibers can exhibit both fast-response and slow response AP’s

117
Q

what do purkinje fibers do?

A

have 4 time/voltage dependent currents

typically exhibit fast response AP’s and rapidly conduct AP’s due mainly to I na

slowest intrinsic pacemaker rate

CV exam 1 AP (12 decks)

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