Conduction system Flashcards
(172 cards)
1
Q
How long lasts paroxysmal AF and persistent AF?
A
Paroxysmal - resolves within 7 days
Persistent - lasts longer than 7 days
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
3
Q
2 factors that induce atrial remodeling.
A
Age-related myocardial changes;
Atrial enlargement from heart disease (HTN, MS)
4
Q
The structural component of atrial remodeling likely involves comorbidities that lead to chronic ……………. and ……………
A
Chronic atrial stretching and dilation
5
Q
How CAD can induce AFib?
A
CAD –> ischemia –> LV dysfunction –> consequent left atrial dilation
6
Q
What are 2 factors that induce AFib by conduction system alterations?
A
Age-related changes and previous AF
7
Q
What (1) facilitates propagation of the arrhythmia?
A
Conduction system changes during AF
8
Q
What is the common location of electrical foci?
A
Pulmonary veins
9
Q
What is the strongest risk factor for AFib?
A
Age-related changes
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
11
Q
AFib 2 main ECG changes
A
Varying R-R intervals = irregularly irregular rhythm
Fibrillary waves present, but no P waves
12
Q
What is a typical cause of AV nodal reentrant tachycardia?
A
An abnormal pathway in the AV node
13
Q
What population is most commonly affected AV nodal reentrant tachycardia?
A
Young patients with normal heart
14
Q
In what 2 diseases can develop cardiac autonomic neuropathy?
A
Parkinson disease;
Poorly controlled DM
15
Q
What is impaired in cardiac autonomic neuropathy?
A
Sympathetic cardiac response
16
Q
Manifestation of cardiac autonomic neuropathy? (2)
A
Exercise intolerance and orthostasis
BUT not contribute to cardiac arrhythmia
17
Q
Conduction system fibrosis often related to ……
A
age
18
Q
Conduction system fibrosis is a primary contributor to …………. including ……… and ……….
A
bradyarrhythmias, including sinus bradycardia (eg sick sinus syndrome) and AV block
19
Q
Enhanced sinoatrial node automaticity causes ……….. (1)
A
sinus tachycardia
20
Q
Sinus tachycardia is caused by ………………
and bradyarrhythmias by ………………..
A
Enhanced sinoatrial node automaticity;
Conduction system fibrosis
21
Q
During AFib, electrical signals in the SA node are suppressed by ……………
A
widespread disorganized electrical activity throughout the atria
22
Q
What drug therapy is recommended in AFib? Why?
A
Long-term anticoagulation;
due to significant risk of systemic thromboembolism
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
24
Q
Approximately 90% of left atrial thrombi are found within the ……………….. in patients with nonvalvular AF
A
left atrial appendage
25
Atrial thrombus can embolize to ....... (3)
brain --> stroke;
acute limb ischemia;
acute mesenteric ischemia
26
LV thrombus develops in .......... (2)
LV aneurysm or severe LV systolic dysfunction
27
Prosthetic valve thrombosis can occur with ........... (2)
bioprosthetic or mechanical mitral valves in patients without adequate anticoagulation.
28
How often occurs thrombosis of pulmonary veins or aortic sinus?
Rare
29
Aortic sinus is called ......
Sinus of Valsalva
30
Is thrombus due to AFib more often occurs in left or right atrial appendage?
In left
31
A right atrial thrombus poses risk of embolization to the .............
Pulmonary circulation
32
Cardiac impulses normally originate in the .............
SA node
33
SA node .................. delivers an electrical impulse to the surrounding .................., which carries the action potential to the ................... at a rate of ..................
Depolarization; atrial myocardium; AV node; 1,1m/sec
34
Speed of conduction in the .......... is the slowest at a rate of ............
AV node; 0,05m/sec
35
The delay in the AV node allows ..............
the ventricles to completely fill with blood during diastole
36
From the AV node, the action potential enters the ................
His-Purkinje system
37
Impulses travel the fastest through the ............ at the rate of ...........
Purkinje fibers (2.2 m/sec)
38
Why s needed fast impulse in Purkinje?
It ensures that the ventricles contract in a bottom-up fashion (necessary for efficient propulsion of blood into the pulmonary artery and aorta).
39
From the Purkinje fibers, the action potential is transmitted to the ..............., where it travels at a rate of ........ m/sec.
ventricular myocardium;
| 0.3 m/sec.
40
Ventricular myocardium gets action potential from .............
From the Purkinje fibers
41
Points 1-2-3-4 are arranged in order of increasing conduction speed (not conduction time), as follows
1 - AV node 0,05 m/sec
2. Ventricular muscle 0,3 m/sec
3. Atrial muscle 1,1 m/sec
4. Purkinje system 2,2 m/sec
42
Conduction speed of the ........... muscle is faster than that of the ........... muscle.
atrial muscle is faster than ventricular muscle.
43
PSVT originates ........... or .......... the ............ node
At or above AV node
44
What is the most common type of PSVT?
AV nodal reentrant tachycardia (AVNRT)
45
AV nodal reentrant tachycardia most commonly occurs in .............. (patients population)
Young patients (eg age <40 y/o)
46
Patients with AVNRT have .................... AV nodal conduction pathways:
2 distinct
47
Description of both pathways participating in AVNRT mechanism.
Fast pathway - long refractory period
| Slow pathway - short refractory period
48
................................ occurs while the fast pathway is still refractory [AVNRT]
Premature atrial contraction (PAC)
49
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
Reentrant circuit
50
How forms reentrant circuit in AVNRT?
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
51
ECG of AVNRT? (4)
No P waves
Narrow QRS
Tachycardia (>15/min)
Regular rythm
52
What is the most common pediatric arrhythmia?
SVT
53
What is heart beat rate in children SVT?
>220/min
54
How persistent tachycardia affect ventricular diastole?
Ventricular diastole shortens --> less time for ventricular relaxation and filling
55
How shortened ventricular diastole affect ventricle? (2) Effect on SV and CO?
Less time for ventricular relaxation and filling --> decreased SV and CO --> hypotension and poor peripheral perfusion
56
How manifest SVT in infants due to persistent tachycardia?
Altered - letargic, poor feeding
| Signs of HF - tachypnea, crackles, hepatomegaly
57
How SVT changes peripheral vascular resistance?
Tachycardia --> short diastole --> low SV and CO --> decreased perfusion --> compensatory increase in peripheral vascular resistance
58
In SVT - hypertention or Hypotension?
hypotension - short diastole leads to low SV and CO
59
Where originate conduction abnormalities in cardiac ischemia? Those abnormalities leads to ----->
In ischemic areas of the LV free wall.
| It leads to ventricular tachycardia
60
What is an arrhythmic abnormality in ischemic myocardium?
Monomorphic ventricular tachycardia
61
Monomorphic VT may occur in what 2 comorbidities?
myocardial ischemia and LV systolic dysfunction
62
ECG of monomorphic VT? (4)
No P waves
Regular (constant R-R intervals)
Tachycardia (>100)
Wide QRS (>0,12 sec)
63
Why in monomorphic VT is regular?
because arrhythmia originates below AV node
64
How is called the most common location of AFib?
Ectopi foci in pulmonary vein ostia
65
ECG of AFib?
No P waves (truly absent)
Iregularly irregular rythm (varying R-R intervals)
narrow QRS
66
What main reason of sick sinu syndrome?
Degeneration of SA node. Therefore it is common in age > 65
67
ECG of sick sinus syndrome? (3)
Sinus bradycardia;
Sinus pauses (delayed P waves)
Sinus arrest
68
Sick sinus syndrome may develop episodes of tachycardia. It is similar to .............. (disorder), but there are normal .............
Similar to PSVT, but normal P waves
69
SA node is responsible for ............
Initiating normal cardiac conduction
70
Impaired signaling from the sinoatrial node can markedly slow the rate of ............, leading to ....................
Ventricular contraction, leading to reduced CO
71
What is the reason of dyspnea, fatigue, lightheadedness, presyncope, and syncope in sick sinus syndrome?
Impaired signaling from SA --> slow rate of ventricular contractions --> reduced CO
72
Sinus pauses refer to ........
Delayed P waves
73
Sinus arrest refers to ......
Dropped P waves
74
What is a type of polymorphic VT?
Torsades de pointes
75
How to describe ECG changes in torsades de pointes?
QRS complexes that oscillate in height and position
76
What is the pathophysiology of torsades de pointes?
Delayed repolarization of ventricular cardiomyocytes
77
Reentrant circuit in atrial flutter involves ..........
Cavotricuspid isthmus
78
What shows ECG in flutter?
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
How is called accessory conduction pathway in WPW?
bundle of Kent/accessory bypass tract
80
Bundle of Kent (accessory conduction pathway connects ..................... and ..........
Atria to the ventricle
81
Bundle of Kent allows electrical impulses to bypass .......................
the AV node
82
Bypass of AV node allows ......................... of the ventricles
Preexcitation (early exctation)
83
3 changes of ECG in WPW?
Short PR interval (<0,12s);
Wide QRS
Delta wave - slurred and broad initial upstroke of the QRS complex
84
Manifestation (combination of ECG and symptoms) in WPW?
WPW pattern on ECG + presence of symptomatic arrhythmia
85
What is the most common arrhythmia that occurs in WPW?
Atrioventricular reentrant tachycardia
86
AVRT symptoms (4)
Intermitent palpitations, sensating of racing heart, lightheadness or syncope
87
2 ways how WPW can manifest. What are both ECG?
WPW pattern on ECG + asymptomatic
| WPW pattern on ECG + symptomatic [symptoms due to AV reentrant tachycardia] = cia jau WPW syndrome
88
In LQTS genetic mutations in ................. lead to ............
Genetic mutations in K channels lead to decreased outward potassium flow --> prolonged action potential
89
Manifestation of torsades de pointes? (4)
Recurrent palpitations, syncope, seizures, SCD
90
Unprovoked syncope in a previously asymptomatic young person may result from a ..............
Congenital QT prolongation syndrome
91
What are 2 important congenital syndromes that cause QT prolongation?
Jervell and Lange-Nielson syndrome;
| Romano-Ward syndrome (more common)
92
What type of arrhythmia is torsades de pointes?
ventricular tachyarrythmia [polymorphic ventricular tachycardia].
93
Long QT + deafness =?
Jervell and Lange-Nielsen syndrome
94
Long QT but no deafness =?
Romano-Ward syndrome
95
QT interval prolongation --> ventricular arrhythmias, which include ........ (2)
Torsades de pointes and ventricular fibrillation
96
Mutation in either .......... on ............... cause brugada syndrome
Cardial sodium or L type calcium channels
97
ECG in Brugada? (2)
Pseudo right bundle branch block
| ST-segment elevation in leads V1-V3
98
Third-degree (complete) AV block involves a total lack of communication between the atria and ventricles due to .....................
AV node dysfunction
99
Third-degree (complete) AV block involves a total lack of communication between the ............. and .......... due to AV node dysfunction
Atria and ventricle
100
Total AV node dysfunction can occur due to ........ (2)
Ischemia
Infiltrative disease
Infection
Age-related fibrosis with cellular degeneration
101
When there is total AV block, where originates impulse?
Intrinsic pacemaker of the His bundle or ventricle is triggered --> junctional or ventricular escape rhythm
102
ECG on total AV block?
Dissociation of P waves and QRS complexes
103
What initiates P waves and QRS complexes in complete AV block? what are the rates?
P waves - SA node (~74/min)
| QRS - His bundle of ventricles (~45/min)
104
How is called rythm that creates QRS in total AV block?
Junctional or ventricular escape rhythm, which originates in His bundle or ventricles
105
Slow ventricular rate in complete AV block leads to ................., which manifest as ............ (4)
Reduced CO --> dyspnea, fatigue, lightheadedness, syncope
106
What is a management of complete AV block?
permanent pacemakers
107
Conduction through the interventricular septum mostly involves the ........................ and .................... branches
Left and right bundle branches
108
QRS complex is widened in bundle branch block due to ...................
Impaired synchronization of ventricular depolarization
109
Resting potential is determined largely by membrane permeability to ............... when in the resting state
K+ ions
110
The resting potential of cardiac myocytes is approximately ................
-90mV
111
Resting potential of skeletal myocytes is approximately ..............
-75mV
112
The highly negative resting potential of cardiac myocytes reduces ....................... as a larger stimulus is needed to excite the cells.
the risk of arrhythmias
113
Phase is called ........... and occurs during ..................
Resting potential;
| diastole
114
Phase 0 is called .............
Rapid depolarization
115
Rapid depolarization is ....... phase
0
116
Resting potential is ............ phase
4
117
Rapid depolarization occurs when ..................
Voltage-gated Na channels open and Na ions rush into the cell
118
Phase 1 is called ...........
initial rapid repolarization
119
Initial rapid repolarization is ........ phase
1
120
In initial rapid repolarization ...................
Occurs rapid closure of Na channels
121
What ions participate in plateu phase? What channels opens and what closes?
Opening of L-type Ca
| Closure of some K
122
Plateu is ............phase
2
123
Phase 2 is called ..........
plateu
124
Phase 3 is called ..........
late rapid repolarization
125
Late rapid repolarization is ......... phase
3
126
What channels open and what close in phase 3?
Closure of Ca
| Opening of K --> efflux
127
Efflux of K+ from the cell .............................. (effect on MP)
Restores the membrane resting potential
128
What are 3 ions in action potential in cardiac cycle?
Incr. permeability to Na and Ca;
| Decr. permeability to K
129
Automaticity of cardiac pacemaker cells is ..............
Slow spontaneous deloparization at regular intervals
130
How is called 0 phase in cardiac pacemaker cells?
Upstroke
131
What is depolarization threshold in cardiac pacemaker cells in upstroke phase?
-40mV
132
What is happens in cardiac pacemaker cells in upstroke phase 0?
opening of voltage gated L type Ca --> influx of Ca into cell
133
How is called phase 3 in cardiac pacemaker cells?
Repolarization
134
What happens in cardiac pacemaker cells in phase 3?
Closure of L type Ca in conjunction with the opening of K --> efflux of K from the cell
135
How is called phase 4 in cardiac pacemaker cells?
Pacemaker potential
136
Pacemaker potential in cardiac pacemaker cells is ...... phase
4
137
Phase 4 in cardiac pacemaker cells begins when ...........
At the end of repolarization starts slow influx of Na+
138
What happens to K when starts phase 4 in cardiac pacemaker cells?
Slow influx of Na and at the same time slow decrease in K+ efflux, because K channels continue to close
139
At what voltage in phase 4 in cardiac pacemaker cells open T type Ca channels?
-50mV
140
At what voltage in phase 4 in cardiac pacemaker cells open L type Ca channels?
-40mV
141
What 2 substances reduce the rate of spontaneous depolarization in cardiac pacemaker cells? What phase?
Adenosine and ACh;
| prolongs phase 4
142
Adenosine interacts with ........... receptors on the surface of cardiac cell
A1
143
What ion channels and conductance affects adenosine?
Activates potassium channels --> increase potassium conductance --> MP remains longer negative
144
What ion channels inhibits adenosine?
inhibits L type ca --> prolonged depolarization time
145
Activation of K and inhibition of Ca channels by adenosine results in .......... (effect on HR and AV)
Slowing of sinus rate and increase in AV nodal conduction delay
146
What is ACh cardiac pacemaker cells?
Increase outward K conductance + decrease inward Ca and Na during phase 4
147
Automaticity is made possible by a ........................
Inward, mixed sodium-potassium current (the funny current)
148
Intracellular calcium regulation plays an important role in .................
Excitation-contraction coupling
149
in cardiac cell initial calcium influx is sensed by the.................receptors in the sarcoplasmic reticulum
ryanodine receptors
150
calcium-induced calcium release into the cytoplasm increase intracellular calcium concentration ....... fold
100
151
In muscle physio, Ca binds ........
Ca binds troponin C
152
What moves tropomyosin away in muscle?
Ca-troponin C complex
153
What happens when tropomyosin is pulled away?
Exposed myosin binding sites on actin
154
The final stage of excitation-contraction coupling is ................., which occurs subsequent to ............ from the cytoplasm
Myocyte relaxation;
| calcium efflux
155
Intracellular calcium is removed primarily via ........ and ..........
NCX - Na+/Ca2+ exchange pump
| SERCA - sarcoplasmic reticulum Ca2+-ATPase pump
156
NCX ions exchange ratio?
1 Ca and 3 Na
157
How works SERCA?
Tranfers Ca from cytosol to sarcoplasmic reticulum by using ATP
158
Smooth muscle cells lack of ................ unlike cardiac and skeletal muscles
troponin
159
What is an important substance in smooth muscle cells for contraction?
Calmodulin
160
Treatment location of atrial flutter?
Cavotricuspid isthmus is a target for radiofrequency ablation
161
Once triggered, atrial fibrillation induces ............ of the atria with the development of .......... refractory periods and ............. conductivity.
electrical remodeling
shortened refractory
increased conductivity
162
Why in atrial fibrillation majority of atrial impulses never reach ventricle?
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
What is ventricular rate in atrial fibrillation?
90-170/min. but because atrial excitation is chaotic, ventricular rate is irregular with no set intervals between contractions
164
Why type IV antiarrhythmics are used in PSVT?
They block calcium channels in slow-response cardiac tissue --> slowing phase 4 --> reduced conduction velocity in SA and AV nodes
165
Why other conduction systems such his, purkinje are normally suppressed? When those systems start to work?
Because SA node pacemaker is more rapid.
| When they do not get impulse from above, ie SA node
166
Pacemaker rate in SA node?
60-100 bpm
167
AV node and His bundle pacemaker rates?
40-60 bpm
168
Bundle branches and purkinje system pacemaker rates?
25-40 bpm
169
When electrical impulses are initiated below the AV node and His bundle, the heart rate typically slows to ......... bpm
25-40 bpm
170
Cavotricuspid isthmus is between ........... and ..............
crista terminalis and tricuspid annulus
171
What is holiday heart syndrome and what heart pathology it causes?
Excessive alcohol consumption --> atrial fibrillation
172
What are 3 systemic illnesses that can predispose atrial fibrillation?
long-standing hypertension, HF, hyperthyroidism
