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1 STEP Uworld cardio > Conduction system > Flashcards

Conduction system Flashcards

1
Q

How long lasts paroxysmal AF and persistent AF?

A

Paroxysmal - resolves within 7 days

Persistent - lasts longer than 7 days

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2
Q

What induces (2 factors) development of AFib? Those factors predisposes to ……..

A

Both structural and electrical conduction changes.

Predisposes to initiation and maintenance of electrical reentrant circuits and/or ectopic foci

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3
Q

2 factors that induce atrial remodeling.

A

Age-related myocardial changes;

Atrial enlargement from heart disease (HTN, MS)

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4
Q

The structural component of atrial remodeling likely involves comorbidities that lead to chronic ……………. and ……………

A

Chronic atrial stretching and dilation

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5
Q

How CAD can induce AFib?

A

CAD –> ischemia –> LV dysfunction –> consequent left atrial dilation

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6
Q

What are 2 factors that induce AFib by conduction system alterations?

A

Age-related changes and previous AF

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7
Q

What (1) facilitates propagation of the arrhythmia?

A

Conduction system changes during AF

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8
Q

What is the common location of electrical foci?

A

Pulmonary veins

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9
Q

What is the strongest risk factor for AFib?

A

Age-related changes

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10
Q

Apart from age-related changes, what other changes of what structure strongly increase risk for AFib?

A

left atrial dilation. Risk increase all comorbidities, that cause left atrial dilation - HTN, HF, MS

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11
Q

AFib 2 main ECG changes

A

Varying R-R intervals = irregularly irregular rhythm

Fibrillary waves present, but no P waves

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12
Q

What is a typical cause of AV nodal reentrant tachycardia?

A

An abnormal pathway in the AV node

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13
Q

What population is most commonly affected AV nodal reentrant tachycardia?

A

Young patients with normal heart

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14
Q

In what 2 diseases can develop cardiac autonomic neuropathy?

A

Parkinson disease;

Poorly controlled DM

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15
Q

What is impaired in cardiac autonomic neuropathy?

A

Sympathetic cardiac response

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16
Q

Manifestation of cardiac autonomic neuropathy? (2)

A

Exercise intolerance and orthostasis

BUT not contribute to cardiac arrhythmia

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17
Q

Conduction system fibrosis often related to ……

A

age

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18
Q

Conduction system fibrosis is a primary contributor to …………. including ……… and ……….

A

bradyarrhythmias, including sinus bradycardia (eg sick sinus syndrome) and AV block

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19
Q

Enhanced sinoatrial node automaticity causes ……….. (1)

A

sinus tachycardia

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20
Q

Sinus tachycardia is caused by ………………

and bradyarrhythmias by ………………..

A

Enhanced sinoatrial node automaticity;

Conduction system fibrosis

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21
Q

During AFib, electrical signals in the SA node are suppressed by ……………

A

widespread disorganized electrical activity throughout the atria

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22
Q

What drug therapy is recommended in AFib? Why?

A

Long-term anticoagulation;

due to significant risk of systemic thromboembolism

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23
Q

What are 3 factors contribute to thrombus development in AF?

A

Left ventricle enlargement;
Blood stasis - due to ineffective atrial contraction
Atrial inflammation and fibrosis - exerts a procoagulant effect

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24
Q

Approximately 90% of left atrial thrombi are found within the ……………….. in patients with nonvalvular AF

A

left atrial appendage

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25
Q

Atrial thrombus can embolize to ……. (3)

A

brain –> stroke;
acute limb ischemia;
acute mesenteric ischemia

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26
Q

LV thrombus develops in ………. (2)

A

LV aneurysm or severe LV systolic dysfunction

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27
Q

Prosthetic valve thrombosis can occur with ……….. (2)

A

bioprosthetic or mechanical mitral valves in patients without adequate anticoagulation.

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28
Q

How often occurs thrombosis of pulmonary veins or aortic sinus?

A

Rare

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29
Q

Aortic sinus is called ……

A

Sinus of Valsalva

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30
Q

Is thrombus due to AFib more often occurs in left or right atrial appendage?

A

In left

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31
Q

A right atrial thrombus poses risk of embolization to the ………….

A

Pulmonary circulation

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32
Q

Cardiac impulses normally originate in the ………….

A

SA node

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33
Q

SA node ……………… delivers an electrical impulse to the surrounding ………………, which carries the action potential to the ………………. at a rate of ………………

A

Depolarization; atrial myocardium; AV node; 1,1m/sec

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34
Q

Speed of conduction in the ………. is the slowest at a rate of …………

A

AV node; 0,05m/sec

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35
Q

The delay in the AV node allows …………..

A

the ventricles to completely fill with blood during diastole

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36
Q

From the AV node, the action potential enters the …………….

A

His-Purkinje system

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37
Q

Impulses travel the fastest through the ………… at the rate of ………..

A

Purkinje fibers (2.2 m/sec)

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38
Q

Why s needed fast impulse in Purkinje?

A

It ensures that the ventricles contract in a bottom-up fashion (necessary for efficient propulsion of blood into the pulmonary artery and aorta).

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39
Q

From the Purkinje fibers, the action potential is transmitted to the ……………, where it travels at a rate of …….. m/sec.

A

ventricular myocardium;

0.3 m/sec.

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40
Q

Ventricular myocardium gets action potential from ………….

A

From the Purkinje fibers

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41
Q

Points 1-2-3-4 are arranged in order of increasing conduction speed (not conduction time), as follows

A

1 - AV node 0,05 m/sec

  1. Ventricular muscle 0,3 m/sec
  2. Atrial muscle 1,1 m/sec
  3. Purkinje system 2,2 m/sec
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42
Q

Conduction speed of the ……….. muscle is faster than that of the ……….. muscle.

A

atrial muscle is faster than ventricular muscle.

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43
Q

PSVT originates ……….. or ………. the ………… node

A

At or above AV node

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44
Q

What is the most common type of PSVT?

A

AV nodal reentrant tachycardia (AVNRT)

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45
Q

AV nodal reentrant tachycardia most commonly occurs in ………….. (patients population)

A

Young patients (eg age <40 y/o)

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46
Q

Patients with AVNRT have ……………….. AV nodal conduction pathways:

A

2 distinct

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47
Q

Description of both pathways participating in AVNRT mechanism.

A

Fast pathway - long refractory period

Slow pathway - short refractory period

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48
Q

………………………….. occurs while the fast pathway is still refractory [AVNRT]

A

Premature atrial contraction (PAC)

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49
Q

If the fast pathway is no longer refractory by the time the PAC reaches the bottom of the slow pathway, the impulse may travel back up the fast pathway, creating a ……………. with rapid conduction of impulses to the ventricles

A

Reentrant circuit

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50
Q

How forms reentrant circuit in AVNRT?

A

PAC –> if fast pathway is no longer in refractory period - impulse goes up to within the fast pathway + other impulse down to AV node –> ventricles

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51
Q

ECG of AVNRT? (4)

A

No P waves
Narrow QRS
Tachycardia (>15/min)
Regular rythm

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52
Q

What is the most common pediatric arrhythmia?

A

SVT

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53
Q

What is heart beat rate in children SVT?

A

> 220/min

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54
Q

How persistent tachycardia affect ventricular diastole?

A

Ventricular diastole shortens –> less time for ventricular relaxation and filling

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55
Q

How shortened ventricular diastole affect ventricle? (2) Effect on SV and CO?

A

Less time for ventricular relaxation and filling –> decreased SV and CO –> hypotension and poor peripheral perfusion

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56
Q

How manifest SVT in infants due to persistent tachycardia?

A

Altered - letargic, poor feeding

Signs of HF - tachypnea, crackles, hepatomegaly

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57
Q

How SVT changes peripheral vascular resistance?

A

Tachycardia –> short diastole –> low SV and CO –> decreased perfusion –> compensatory increase in peripheral vascular resistance

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58
Q

In SVT - hypertention or Hypotension?

A

hypotension - short diastole leads to low SV and CO

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59
Q

Where originate conduction abnormalities in cardiac ischemia? Those abnormalities leads to —–>

A

In ischemic areas of the LV free wall.

It leads to ventricular tachycardia

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60
Q

What is an arrhythmic abnormality in ischemic myocardium?

A

Monomorphic ventricular tachycardia

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61
Q

Monomorphic VT may occur in what 2 comorbidities?

A

myocardial ischemia and LV systolic dysfunction

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62
Q

ECG of monomorphic VT? (4)

A

No P waves
Regular (constant R-R intervals)
Tachycardia (>100)
Wide QRS (>0,12 sec)

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63
Q

Why in monomorphic VT is regular?

A

because arrhythmia originates below AV node

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64
Q

How is called the most common location of AFib?

A

Ectopi foci in pulmonary vein ostia

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65
Q

ECG of AFib?

A

No P waves (truly absent)
Iregularly irregular rythm (varying R-R intervals)
narrow QRS

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66
Q

What main reason of sick sinu syndrome?

A

Degeneration of SA node. Therefore it is common in age > 65

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67
Q

ECG of sick sinus syndrome? (3)

A

Sinus bradycardia;
Sinus pauses (delayed P waves)
Sinus arrest

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68
Q

Sick sinus syndrome may develop episodes of tachycardia. It is similar to ………….. (disorder), but there are normal ………….

A

Similar to PSVT, but normal P waves

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69
Q

SA node is responsible for …………

A

Initiating normal cardiac conduction

70
Q

Impaired signaling from the sinoatrial node can markedly slow the rate of …………, leading to ………………..

A

Ventricular contraction, leading to reduced CO

71
Q

What is the reason of dyspnea, fatigue, lightheadedness, presyncope, and syncope in sick sinus syndrome?

A

Impaired signaling from SA –> slow rate of ventricular contractions –> reduced CO

72
Q

Sinus pauses refer to ……..

A

Delayed P waves

73
Q

Sinus arrest refers to ……

A

Dropped P waves

74
Q

What is a type of polymorphic VT?

A

Torsades de pointes

75
Q

How to describe ECG changes in torsades de pointes?

A

QRS complexes that oscillate in height and position

76
Q

What is the pathophysiology of torsades de pointes?

A

Delayed repolarization of ventricular cardiomyocytes

77
Q

Reentrant circuit in atrial flutter involves ……….

A

Cavotricuspid isthmus

78
Q

What shows ECG in flutter?

A

Saw-tooth flutter waves
QRS - regular or irregular - depends on how consistently flutter waves are conducted through the AV node.
rate: aprox 300/min

79
Q

How is called accessory conduction pathway in WPW?

A

bundle of Kent/accessory bypass tract

80
Q

Bundle of Kent (accessory conduction pathway connects ………………… and ……….

A

Atria to the ventricle

81
Q

Bundle of Kent allows electrical impulses to bypass …………………..

A

the AV node

82
Q

Bypass of AV node allows ……………………. of the ventricles

A

Preexcitation (early exctation)

83
Q

3 changes of ECG in WPW?

A

Short PR interval (<0,12s);
Wide QRS
Delta wave - slurred and broad initial upstroke of the QRS complex

84
Q

Manifestation (combination of ECG and symptoms) in WPW?

A

WPW pattern on ECG + presence of symptomatic arrhythmia

85
Q

What is the most common arrhythmia that occurs in WPW?

A

Atrioventricular reentrant tachycardia

86
Q

AVRT symptoms (4)

A

Intermitent palpitations, sensating of racing heart, lightheadness or syncope

87
Q

2 ways how WPW can manifest. What are both ECG?

A

WPW pattern on ECG + asymptomatic

WPW pattern on ECG + symptomatic [symptoms due to AV reentrant tachycardia] = cia jau WPW syndrome

88
Q

In LQTS genetic mutations in …………….. lead to …………

A

Genetic mutations in K channels lead to decreased outward potassium flow –> prolonged action potential

89
Q

Manifestation of torsades de pointes? (4)

A

Recurrent palpitations, syncope, seizures, SCD

90
Q

Unprovoked syncope in a previously asymptomatic young person may result from a …………..

A

Congenital QT prolongation syndrome

91
Q

What are 2 important congenital syndromes that cause QT prolongation?

A

Jervell and Lange-Nielson syndrome;

Romano-Ward syndrome (more common)

92
Q

What type of arrhythmia is torsades de pointes?

A

ventricular tachyarrythmia [polymorphic ventricular tachycardia].

93
Q

Long QT + deafness =?

A

Jervell and Lange-Nielsen syndrome

94
Q

Long QT but no deafness =?

A

Romano-Ward syndrome

95
Q

QT interval prolongation –> ventricular arrhythmias, which include …….. (2)

A

Torsades de pointes and ventricular fibrillation

96
Q

Mutation in either ………. on …………… cause brugada syndrome

A

Cardial sodium or L type calcium channels

97
Q

ECG in Brugada? (2)

A

Pseudo right bundle branch block

ST-segment elevation in leads V1-V3

98
Q

Third-degree (complete) AV block involves a total lack of communication between the atria and ventricles due to …………………

A

AV node dysfunction

99
Q

Third-degree (complete) AV block involves a total lack of communication between the …………. and ………. due to AV node dysfunction

A

Atria and ventricle

100
Q

Total AV node dysfunction can occur due to …….. (2)

A

Ischemia
Infiltrative disease
Infection
Age-related fibrosis with cellular degeneration

101
Q

When there is total AV block, where originates impulse?

A

Intrinsic pacemaker of the His bundle or ventricle is triggered –> junctional or ventricular escape rhythm

102
Q

ECG on total AV block?

A

Dissociation of P waves and QRS complexes

103
Q

What initiates P waves and QRS complexes in complete AV block? what are the rates?

A

P waves - SA node (~74/min)

QRS - His bundle of ventricles (~45/min)

104
Q

How is called rythm that creates QRS in total AV block?

A

Junctional or ventricular escape rhythm, which originates in His bundle or ventricles

105
Q

Slow ventricular rate in complete AV block leads to …………….., which manifest as ………… (4)

A

Reduced CO –> dyspnea, fatigue, lightheadedness, syncope

106
Q

What is a management of complete AV block?

A

permanent pacemakers

107
Q

Conduction through the interventricular septum mostly involves the …………………… and ……………….. branches

A

Left and right bundle branches

108
Q

QRS complex is widened in bundle branch block due to ……………….

A

Impaired synchronization of ventricular depolarization

109
Q

Resting potential is determined largely by membrane permeability to …………… when in the resting state

A

K+ ions

110
Q

The resting potential of cardiac myocytes is approximately …………….

A

-90mV

111
Q

Resting potential of skeletal myocytes is approximately …………..

A

-75mV

112
Q

The highly negative resting potential of cardiac myocytes reduces ………………….. as a larger stimulus is needed to excite the cells.

A

the risk of arrhythmias

113
Q

Phase is called ……….. and occurs during ………………

A

Resting potential;

diastole

114
Q

Phase 0 is called ………….

A

Rapid depolarization

115
Q

Rapid depolarization is ……. phase

A

0

116
Q

Resting potential is ………… phase

A

4

117
Q

Rapid depolarization occurs when ………………

A

Voltage-gated Na channels open and Na ions rush into the cell

118
Q

Phase 1 is called ………..

A

initial rapid repolarization

119
Q

Initial rapid repolarization is …….. phase

A

1

120
Q

In initial rapid repolarization ……………….

A

Occurs rapid closure of Na channels

121
Q

What ions participate in plateu phase? What channels opens and what closes?

A

Opening of L-type Ca

Closure of some K

122
Q

Plateu is …………phase

A

2

123
Q

Phase 2 is called ……….

A

plateu

124
Q

Phase 3 is called ……….

A

late rapid repolarization

125
Q

Late rapid repolarization is ……… phase

A

3

126
Q

What channels open and what close in phase 3?

A

Closure of Ca

Opening of K –> efflux

127
Q

Efflux of K+ from the cell ………………………… (effect on MP)

A

Restores the membrane resting potential

128
Q

What are 3 ions in action potential in cardiac cycle?

A

Incr. permeability to Na and Ca;

Decr. permeability to K

129
Q

Automaticity of cardiac pacemaker cells is …………..

A

Slow spontaneous deloparization at regular intervals

130
Q

How is called 0 phase in cardiac pacemaker cells?

A

Upstroke

131
Q

What is depolarization threshold in cardiac pacemaker cells in upstroke phase?

A

-40mV

132
Q

What is happens in cardiac pacemaker cells in upstroke phase 0?

A

opening of voltage gated L type Ca –> influx of Ca into cell

133
Q

How is called phase 3 in cardiac pacemaker cells?

A

Repolarization

134
Q

What happens in cardiac pacemaker cells in phase 3?

A

Closure of L type Ca in conjunction with the opening of K –> efflux of K from the cell

135
Q

How is called phase 4 in cardiac pacemaker cells?

A

Pacemaker potential

136
Q

Pacemaker potential in cardiac pacemaker cells is …… phase

A

4

137
Q

Phase 4 in cardiac pacemaker cells begins when ………..

A

At the end of repolarization starts slow influx of Na+

138
Q

What happens to K when starts phase 4 in cardiac pacemaker cells?

A

Slow influx of Na and at the same time slow decrease in K+ efflux, because K channels continue to close

139
Q

At what voltage in phase 4 in cardiac pacemaker cells open T type Ca channels?

A

-50mV

140
Q

At what voltage in phase 4 in cardiac pacemaker cells open L type Ca channels?

A

-40mV

141
Q

What 2 substances reduce the rate of spontaneous depolarization in cardiac pacemaker cells? What phase?

A

Adenosine and ACh;

prolongs phase 4

142
Q

Adenosine interacts with ……….. receptors on the surface of cardiac cell

A

A1

143
Q

What ion channels and conductance affects adenosine?

A

Activates potassium channels –> increase potassium conductance –> MP remains longer negative

144
Q

What ion channels inhibits adenosine?

A

inhibits L type ca –> prolonged depolarization time

145
Q

Activation of K and inhibition of Ca channels by adenosine results in ………. (effect on HR and AV)

A

Slowing of sinus rate and increase in AV nodal conduction delay

146
Q

What is ACh cardiac pacemaker cells?

A

Increase outward K conductance + decrease inward Ca and Na during phase 4

147
Q

Automaticity is made possible by a ……………………

A

Inward, mixed sodium-potassium current (the funny current)

148
Q

Intracellular calcium regulation plays an important role in ……………..

A

Excitation-contraction coupling

149
Q

in cardiac cell initial calcium influx is sensed by the……………..receptors in the sarcoplasmic reticulum

A

ryanodine receptors

150
Q

calcium-induced calcium release into the cytoplasm increase intracellular calcium concentration ……. fold

A

100

151
Q

In muscle physio, Ca binds ……..

A

Ca binds troponin C

152
Q

What moves tropomyosin away in muscle?

A

Ca-troponin C complex

153
Q

What happens when tropomyosin is pulled away?

A

Exposed myosin binding sites on actin

154
Q

The final stage of excitation-contraction coupling is …………….., which occurs subsequent to ………… from the cytoplasm

A

Myocyte relaxation;

calcium efflux

155
Q

Intracellular calcium is removed primarily via …….. and ……….

A

NCX - Na+/Ca2+ exchange pump

SERCA - sarcoplasmic reticulum Ca2+-ATPase pump

156
Q

NCX ions exchange ratio?

A

1 Ca and 3 Na

157
Q

How works SERCA?

A

Tranfers Ca from cytosol to sarcoplasmic reticulum by using ATP

158
Q

Smooth muscle cells lack of ……………. unlike cardiac and skeletal muscles

A

troponin

159
Q

What is an important substance in smooth muscle cells for contraction?

A

Calmodulin

160
Q

Treatment location of atrial flutter?

A

Cavotricuspid isthmus is a target for radiofrequency ablation

161
Q

Once triggered, atrial fibrillation induces ………… of the atria with the development of ………. refractory periods and …………. conductivity.

A

electrical remodeling
shortened refractory
increased conductivity

162
Q

Why in atrial fibrillation majority of atrial impulses never reach ventricle?

A

Each time the AV node is excited, it enters a refractory period during which additional atrial impulses cannot be transmitted to the ventricles; consequently, the majority of atrial impulses never reach the ventricles

163
Q

What is ventricular rate in atrial fibrillation?

A

90-170/min. but because atrial excitation is chaotic, ventricular rate is irregular with no set intervals between contractions

164
Q

Why type IV antiarrhythmics are used in PSVT?

A

They block calcium channels in slow-response cardiac tissue –> slowing phase 4 –> reduced conduction velocity in SA and AV nodes

165
Q

Why other conduction systems such his, purkinje are normally suppressed? When those systems start to work?

A

Because SA node pacemaker is more rapid.

When they do not get impulse from above, ie SA node

166
Q

Pacemaker rate in SA node?

A

60-100 bpm

167
Q

AV node and His bundle pacemaker rates?

A

40-60 bpm

168
Q

Bundle branches and purkinje system pacemaker rates?

A

25-40 bpm

169
Q

When electrical impulses are initiated below the AV node and His bundle, the heart rate typically slows to ……… bpm

A

25-40 bpm

170
Q

Cavotricuspid isthmus is between ……….. and …………..

A

crista terminalis and tricuspid annulus

171
Q

What is holiday heart syndrome and what heart pathology it causes?

A

Excessive alcohol consumption –> atrial fibrillation

172
Q

What are 3 systemic illnesses that can predispose atrial fibrillation?

A

long-standing hypertension, HF, hyperthyroidism

1 STEP Uworld cardio (7 decks)

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