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Cardiovascular and Pulmonary > Cardiovascular Systems Physiology and Pathophysiology II > Flashcards

Cardiovascular Systems Physiology and Pathophysiology II Flashcards

1
Q

Cardiac APs are initiated within nodal tissues and are conducted through the bundle branches to the

A

Myocardium

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2
Q

What channels enable inward Ca2+ and Na+ (funny current) and outward K+ in the SA node?

-Pacemaker Potentials

A

T-type Ca2+ channels, Na+ HCN channels, and K+ channels

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3
Q

To begin one pacemaker cycle, a gradual depolarization is enabled by

A

Inward Ca2+ and Na+ and outward K+

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4
Q

During the gradual depolarization, the membrane potential creeps upward, becoming less negative and reaching around

A

-55 mV

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5
Q

What happens at around -55 mV?

A

T-type Ca2+ channels are increasingly activated

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6
Q

The increasing activation of T-type Ca2+ channels in a pacemaker potential produces a rapid upstroke in

A

Action potential

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7
Q

HCN and Ca2+ channels are inactivated, shutting down If, and thus allowing repolarization via K+ efflux at about

A

0 mV

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8
Q

Repolarization leads to a brief period of hyperpolarization which is necessary to reactivate

A

HCN channels

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9
Q

In a cardiomycete depolarization-repolarization plateau potential (different from pacemaker potential) phase 0 is dependent upon

A

Na+ influx

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10
Q

The rapid, Na+ dependent depolarization of cardiac muscle is followed by phase 1, which is a

A

Transient K+ dependent repolarization

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11
Q

On the sarcolemma, the Na+ dependent AP also activates

A

Votage gated- Ca2+ channels (Type L)

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12
Q

Increased intracellular Ca2+ stimulates the release of
Ca2+ via activation of

-called calcium induced calcium release

A

Ryanodine receptors within SR

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13
Q

Elevations in sarcoplasmic Ca2+ from extracellular (via type L channels) and intracellular (from the SR) sources is represented by phase 2 which is the

A

Plateau phase

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14
Q

To complete the cycle of cardiac muscle AP, phase 2 is followed by phase 3 which is a

A

Rapid K+ dependent repolarization

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15
Q

Phase 4 of the plateau potential is a

A

Slight efflux of K+

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16
Q

Type L channels are very interesting proteins. Not only are they voltage-gated, but they are also functionally coupled to

A

Type B1 and B2 adrenergic receptors and Cholinergic-muscarinic (ACh) receptors (type M2)

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17
Q

Because of this complex triad motif, the fundamental activation of type L channels is dependent upon the

A

Na+ induced AP

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18
Q

Also, the L type Ca2+ channel activity is modulated by

A

Catecholamines and ACh

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19
Q

The predominant beta adrenergic isoform expressed in a healthy heart, and are coupled to the stimulation of the G protein-adenylyl cyclase-dependent production od cAMP and PKA signalling cascades

A

B1 receptors

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20
Q

This signal transduction pathway activates L channels; thus, promoting

A

Ca2+ influx

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21
Q

Also facilitate L channel activation but activation of this receptor can also induce lusitropy

A

B2 receptors

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22
Q

Increased rate of relaxation that is medicated by mobilization of Gi protein dependent signaling

A

Lusitropy

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23
Q

An increase in the dominance of cardiac B2 activity plays a role in the pathogenesis of certain forms of

A

Heart failure

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24
Q

Activated in the presence of elevated sacoplasmic Ca2+ concentrations

A

Troponin C

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25
Q

Binds Ca2+ and causes a conformational change in the troponin-tropomyosin complex that reveals the myosin binding sites within actin

A

Troponin C

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26
Q

Increased PKA signaling induces a triple response in cardiac myocytes. These responses are

A
  1. ) Activation of type L channels
  2. ) Phospholamban is phosphorylated by PKA
  3. ) PKA mediates the phosphorylation of troponin I
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27
Q

Intracellular protein with a stimulatory effect on SERCA, which cause rapid re-sequestration of Ca2+ into the SR

A

Phospholamban

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28
Q

Reduces the affinity of troponin C for Ca2+

A

Activated (phosphorylated) troponin I

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29
Q

Causes an increase in the rate of cardiac pumping by causing changes in intracellular Ca2+

A

Adrenergic activation of cAMP/PKA signaling

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30
Q

Binds to and activates cholinergic M2 receptors, which interrupts the activation of type L channels and slows cardiac muscle contractility

A

ACh

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31
Q

The primary intrinsic cardiac pacemaker; as directed by ANS input, it controls increases and decreases in HR based upon metabolic demand

A

The SA node

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32
Q

In absence of other mediation, the SA node fires to cause approximtely

A

80-100 beats per minute

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33
Q

The chronic component of the SA node and decreases the rate of SA node firing

A

PSNS

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34
Q

The PSNS sets the basal (resting) HR by suppressing the frequency of

A

SA node AP

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35
Q

Preganglionic fibers of the PSNS originate within the medulla in the

A

DMV and NA

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36
Q

Preganglionic PSNS fibers travel via the right and left vagus, and synapse with post-ganglionic fibers within the heart, very near the

A

SA and AV nodes

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37
Q

The SA node is mainly innervated by fibers from the

A

Right vagus nerve

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38
Q

What effect would an increase in right vagal PSNS activity have?

A

Decreased SA node firing

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39
Q

SA nodal tissue contains voltage-dependent (T-type) Ca2+ channels that are:

  1. ) Activated by?
  2. ) Suppressed by?
A
  1. ) Adrenergics

2. ) ACh

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40
Q

These specialized T-type Ca2+ channels contain two gates (f and d), that when open enable Ca2+ influx and depolarization of the

A

SA node

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41
Q

What happens to the f and d gates upon membrane depolarization?

A
  1. ) f gates gradually close

2. ) d gates gradually open

42
Q

The optimal membrane voltage for maximal percent open f and d gates is approximately

A

-40 mV

43
Q

As f gates close, Ca2+ current diminishes, but at this time there is a stimulation of an

A

Outward K+ current

44
Q

The repolarization that is induced by K+ efflux stimulates the influx of

A

Na+ through HCN channels (the pacemaker current)

45
Q

The cycle of Na+ influx, slow Ca2+ influx, K+ outflux, and Na+ influx through HCN channels is a self perpetuating mechanism and is identified as a

A

Pacemaker current

46
Q

Activates ligand-gated K+ channels; in so doing, driving membrane potential more negative and inducing a slower depolarization

A

ACh

47
Q

This occurs via the ACh-mediated activation of Type 2 cholinergic-muscarinic receptors (CM2) within the

A

SA node

48
Q

In response to CM2 activation by ACh, the βƴ subunit of specific G proteins are coupled to the activation of

A

Outward rectifying K+ channels

49
Q

Outward IK+ essentially clamps membrane potential

near the equilibrium potential for K+, and in so doing Impedes depolarization, slows SA nodal firing, and thus

A

slows HR

50
Q

Activation of PSNS fibers suppresses both the slow inward Ca2+ current and If; thereby, lowering the rate of rise of the pacemaker current and dampening the

A

Rate of SA firing

51
Q

Increase the rate and magnitude of SA nodal APs by augmenting the inward Na+ (If) and Ca2+

A

SNS neurotransmitters

52
Q

Demonstrates the same general phases as are observed in ventricular myocytes

A

Atrial myocyte depolarization

53
Q

What has a shorter duration, the plateau phase of an atrial AP or a ventricular AP?

A

Artial AP

54
Q

Performs intrinsic pacemaker and key interface functions between the atria and ventricles

A

AV node

55
Q

The only electrical connection between the atria and ventricles

A

AV node

56
Q

A healthy AVnode will only allow unidirectional conduction of AP from the atria to the

A

His bundle

57
Q

In the absence of normal regulatory mechanisms, the AV node independently will fire at approximately

A

40-50 beats per minute

58
Q

The main difference between the AV nodal AP and the SA nodal AP is that the AV nodal AP also has slow

A

L-type Ca2+ channels

-SA node only has T-type (which AV also has)

59
Q

The presence of slow (L-type) Ca2+ in addition to

type T Ca2+ channels, enables the phenomenon of

A

AV nodal delay (long time interval between AV nodal APs)

60
Q

Type-L Ca2+ channel antagonists which are specific for the type-L Ca2+ channels expressed in the heart

A

Diltiazem and verapamil

61
Q

What effect do diltiazem and verapamil have on AV conduction?

A

Slow AV conduction and have a negative inotropic effect

62
Q

The relatively slower pacemaker ability of the AV node is accounted for by considering that relative to the SA node, the AV node has a much slower generation of the

A

Funny current (Na+ influx from HCN)

63
Q

The AV node is innervated by post-ganglionic PSNS fibers from the

A

Left vagus nerve

64
Q

Therefore, an increase in left PSNS vagal activity would be correlated with a

A

Decrease in frequency of AV nodal APs

65
Q

The bridge between the AV nodal relay and the ventricular myocardium

A

The His-Purkinje system

66
Q

Work with the AV node to ensure optimal relay of conduction between the atria and ventricles

A

His fibers

67
Q

Fast conducting tracts that coordinate ventricular contraction

A

Purkinje fibers

68
Q

Conduction via a normal His-Purkinje system leads to so-called

A

Narrow complex QRS

69
Q

That is, conduction via normal His-Purkinje system results in the duration of the QRS complex being

A

Less than 120 msec in duration

70
Q

The characteristics of His-Purkinje APs resemble those generated within the myocardium, with the addition of a very slow

A

Phase 4 pacemaker current (If)

71
Q

In the event of a complete block in AV nodal relay, there can be a generation of an escape pacemaker of approximately

A

20-40 bpm

72
Q

The AV node is functionally coupled to the

A

Central bundle of His

73
Q

The central bundle divides into the right and left bundle branches, which in turn give rise to the

A

Purkinje fibers

74
Q

The Purkinje network itself has an intrinsic pacemaker activity that can support approximately

A

15-20 bpm

75
Q

Purkinje fiber AP is similar to that previously described in SA and AV nodal tissue, with the exception of a

A

Predominant phase 1 and an intermediate phase 2

76
Q

The characteristics of the Purkinje AP enable a relatively long

A

Refractatory period

77
Q

This long refractatory period serves as a buffer/modulator in response to

A

Rapid atrial induced APs

78
Q

The refractatory period of Purkinje fibers is inversely correlated with

A

HR

79
Q

Under basal conditions, impulses are modulated within the SA node by the

A

PSNS

80
Q

Upon generation of SA nodal AP, the signal spreads radially through the atrial myocardium to the

A

AV node

81
Q

From the AV node, signals are relayed through the bundle of His to the right and left bundle branches, downward, to the apex region of the

A

Ventricles

82
Q

From there, APs are propagated upward via the

A

Purkinje fiber network

83
Q

This induces a highly coordinated depolarization (contraction) of ventricular myocardium from

A

Apex to base

84
Q

Mistiming of depolarization which can occur without noticeable disruption of the normal cardiac cycle; however serious ones can be fatal

A

Arrhythmias

85
Q

The phenomenon of reentry, which results from premature stimulation of previously activated myocardial fibers can cause

A

Tachyarrhythmias

86
Q

Can be caused by a unidirectional block of conduction of the cardiac AP with slowed conduction through the reentry path

A

Reentry

87
Q

In order for reentry to occur, a region of fibers within the conduction pathway must have an abnormally short

A

Refractatory period

88
Q

Travel in proximity to the PSNS efferents along the right and left vagus nerves to the heart

A

Post-ganglionic SNS fibers

89
Q

Dissociate from the vagal tracts and accompany the coronary blood vessels through the myocardium

A

SNS fibers

90
Q

What do the following SNS fibers do>

  1. ) SNS fibers from right vagus nerve
  2. ) SNS fibers from left vagus nerve
A
  1. ) Increase HR

2. ) Increase contractile force of myocardium

91
Q

Electrical activity of the heart is measured via the

A

Electrocardiogram (ECG)

92
Q

An ECG is based upon the principle of

-can be mathematically represented by a vector

A

Electromotive force (EMF)

93
Q

Divided by distinct wave segments (P, QRS, and

T) that directly reflect the electrical events occurring in specific regions of the myocardium at a given moment in time

A

Electrocardiograph

94
Q

The ECG tracing is divided in boxes. Reading horixzontally, the boxes indicate

A

Time (each small box (1mm) = 0.04 seconds)

95
Q

The ECG tracing is divided in boxes. Reading vertically, each 1mm box indicates

A

Voltage

  • upward is positive
  • downward is negative
96
Q

The net voltage for a given waveform is simply the difference between

A

Upward and downward deflection

97
Q

Upward deflections within the ECG represent a depolarization wave moving toward a

A

Positive eletrode

98
Q

Downward deflections within the ECG represent a depolarization wave moving

A

Away from positive electrode

99
Q

Repolarization waves moving away from a positive

electrode will also induce

A

Upward deflections

100
Q

Thus, in the normal heart, the deflections of R and T waves in a given lead should be

A

Matched

Cardiovascular and Pulmonary (25 decks)

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