Conduction system Flashcards
How long lasts paroxysmal AF and persistent AF?
Paroxysmal - resolves within 7 days
Persistent - lasts longer than 7 days
What induces (2 factors) development of AFib? Those factors predisposes to ……..
Both structural and electrical conduction changes.
Predisposes to initiation and maintenance of electrical reentrant circuits and/or ectopic foci
2 factors that induce atrial remodeling.
Age-related myocardial changes;
Atrial enlargement from heart disease (HTN, MS)
The structural component of atrial remodeling likely involves comorbidities that lead to chronic ……………. and ……………
Chronic atrial stretching and dilation
How CAD can induce AFib?
CAD –> ischemia –> LV dysfunction –> consequent left atrial dilation
What are 2 factors that induce AFib by conduction system alterations?
Age-related changes and previous AF
What (1) facilitates propagation of the arrhythmia?
Conduction system changes during AF
What is the common location of electrical foci?
Pulmonary veins
What is the strongest risk factor for AFib?
Age-related changes
Apart from age-related changes, what other changes of what structure strongly increase risk for AFib?
left atrial dilation. Risk increase all comorbidities, that cause left atrial dilation - HTN, HF, MS
AFib 2 main ECG changes
Varying R-R intervals = irregularly irregular rhythm
Fibrillary waves present, but no P waves
What is a typical cause of AV nodal reentrant tachycardia?
An abnormal pathway in the AV node
What population is most commonly affected AV nodal reentrant tachycardia?
Young patients with normal heart
In what 2 diseases can develop cardiac autonomic neuropathy?
Parkinson disease;
Poorly controlled DM
What is impaired in cardiac autonomic neuropathy?
Sympathetic cardiac response
Manifestation of cardiac autonomic neuropathy? (2)
Exercise intolerance and orthostasis
BUT not contribute to cardiac arrhythmia
Conduction system fibrosis often related to ……
age
Conduction system fibrosis is a primary contributor to …………. including ……… and ……….
bradyarrhythmias, including sinus bradycardia (eg sick sinus syndrome) and AV block
Enhanced sinoatrial node automaticity causes ……….. (1)
sinus tachycardia
Sinus tachycardia is caused by ………………
and bradyarrhythmias by ………………..
Enhanced sinoatrial node automaticity;
Conduction system fibrosis
During AFib, electrical signals in the SA node are suppressed by ……………
widespread disorganized electrical activity throughout the atria
What drug therapy is recommended in AFib? Why?
Long-term anticoagulation;
due to significant risk of systemic thromboembolism
What are 3 factors contribute to thrombus development in AF?
Left ventricle enlargement;
Blood stasis - due to ineffective atrial contraction
Atrial inflammation and fibrosis - exerts a procoagulant effect
Approximately 90% of left atrial thrombi are found within the ……………….. in patients with nonvalvular AF
left atrial appendage
Atrial thrombus can embolize to ……. (3)
brain –> stroke;
acute limb ischemia;
acute mesenteric ischemia
LV thrombus develops in ………. (2)
LV aneurysm or severe LV systolic dysfunction
Prosthetic valve thrombosis can occur with ……….. (2)
bioprosthetic or mechanical mitral valves in patients without adequate anticoagulation.
How often occurs thrombosis of pulmonary veins or aortic sinus?
Rare
Aortic sinus is called ……
Sinus of Valsalva
Is thrombus due to AFib more often occurs in left or right atrial appendage?
In left
A right atrial thrombus poses risk of embolization to the ………….
Pulmonary circulation
Cardiac impulses normally originate in the ………….
SA node
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
Speed of conduction in the ………. is the slowest at a rate of …………
AV node; 0,05m/sec
The delay in the AV node allows …………..
the ventricles to completely fill with blood during diastole
From the AV node, the action potential enters the …………….
His-Purkinje system
Impulses travel the fastest through the ………… at the rate of ………..
Purkinje fibers (2.2 m/sec)
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).
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.
Ventricular myocardium gets action potential from ………….
From the Purkinje fibers
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
- Ventricular muscle 0,3 m/sec
- Atrial muscle 1,1 m/sec
- Purkinje system 2,2 m/sec
Conduction speed of the ……….. muscle is faster than that of the ……….. muscle.
atrial muscle is faster than ventricular muscle.
PSVT originates ……….. or ………. the ………… node
At or above AV node
What is the most common type of PSVT?
AV nodal reentrant tachycardia (AVNRT)
AV nodal reentrant tachycardia most commonly occurs in ………….. (patients population)
Young patients (eg age <40 y/o)
Patients with AVNRT have ……………….. AV nodal conduction pathways:
2 distinct
Description of both pathways participating in AVNRT mechanism.
Fast pathway - long refractory period
Slow pathway - short refractory period
………………………….. occurs while the fast pathway is still refractory [AVNRT]
Premature atrial contraction (PAC)
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
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
ECG of AVNRT? (4)
No P waves
Narrow QRS
Tachycardia (>15/min)
Regular rythm
What is the most common pediatric arrhythmia?
SVT
What is heart beat rate in children SVT?
> 220/min
How persistent tachycardia affect ventricular diastole?
Ventricular diastole shortens –> less time for ventricular relaxation and filling
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
How manifest SVT in infants due to persistent tachycardia?
Altered - letargic, poor feeding
Signs of HF - tachypnea, crackles, hepatomegaly
How SVT changes peripheral vascular resistance?
Tachycardia –> short diastole –> low SV and CO –> decreased perfusion –> compensatory increase in peripheral vascular resistance
In SVT - hypertention or Hypotension?
hypotension - short diastole leads to low SV and CO
Where originate conduction abnormalities in cardiac ischemia? Those abnormalities leads to —–>
In ischemic areas of the LV free wall.
It leads to ventricular tachycardia
What is an arrhythmic abnormality in ischemic myocardium?
Monomorphic ventricular tachycardia
Monomorphic VT may occur in what 2 comorbidities?
myocardial ischemia and LV systolic dysfunction
ECG of monomorphic VT? (4)
No P waves
Regular (constant R-R intervals)
Tachycardia (>100)
Wide QRS (>0,12 sec)
Why in monomorphic VT is regular?
because arrhythmia originates below AV node
How is called the most common location of AFib?
Ectopi foci in pulmonary vein ostia
ECG of AFib?
No P waves (truly absent)
Iregularly irregular rythm (varying R-R intervals)
narrow QRS
What main reason of sick sinu syndrome?
Degeneration of SA node. Therefore it is common in age > 65
ECG of sick sinus syndrome? (3)
Sinus bradycardia;
Sinus pauses (delayed P waves)
Sinus arrest
Sick sinus syndrome may develop episodes of tachycardia. It is similar to ………….. (disorder), but there are normal ………….
Similar to PSVT, but normal P waves
SA node is responsible for …………
Initiating normal cardiac conduction
Impaired signaling from the sinoatrial node can markedly slow the rate of …………, leading to ………………..
Ventricular contraction, leading to reduced CO
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
Sinus pauses refer to ……..
Delayed P waves
Sinus arrest refers to ……
Dropped P waves
What is a type of polymorphic VT?
Torsades de pointes
How to describe ECG changes in torsades de pointes?
QRS complexes that oscillate in height and position
What is the pathophysiology of torsades de pointes?
Delayed repolarization of ventricular cardiomyocytes
Reentrant circuit in atrial flutter involves ……….
Cavotricuspid isthmus
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
How is called accessory conduction pathway in WPW?
bundle of Kent/accessory bypass tract
Bundle of Kent (accessory conduction pathway connects ………………… and ……….
Atria to the ventricle
Bundle of Kent allows electrical impulses to bypass …………………..
the AV node
Bypass of AV node allows ……………………. of the ventricles
Preexcitation (early exctation)
3 changes of ECG in WPW?
Short PR interval (<0,12s);
Wide QRS
Delta wave - slurred and broad initial upstroke of the QRS complex
Manifestation (combination of ECG and symptoms) in WPW?
WPW pattern on ECG + presence of symptomatic arrhythmia
What is the most common arrhythmia that occurs in WPW?
Atrioventricular reentrant tachycardia
AVRT symptoms (4)
Intermitent palpitations, sensating of racing heart, lightheadness or syncope
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
In LQTS genetic mutations in …………….. lead to …………
Genetic mutations in K channels lead to decreased outward potassium flow –> prolonged action potential
Manifestation of torsades de pointes? (4)
Recurrent palpitations, syncope, seizures, SCD
Unprovoked syncope in a previously asymptomatic young person may result from a …………..
Congenital QT prolongation syndrome
What are 2 important congenital syndromes that cause QT prolongation?
Jervell and Lange-Nielson syndrome;
Romano-Ward syndrome (more common)
What type of arrhythmia is torsades de pointes?
ventricular tachyarrythmia [polymorphic ventricular tachycardia].
Long QT + deafness =?
Jervell and Lange-Nielsen syndrome
Long QT but no deafness =?
Romano-Ward syndrome
QT interval prolongation –> ventricular arrhythmias, which include …….. (2)
Torsades de pointes and ventricular fibrillation
Mutation in either ………. on …………… cause brugada syndrome
Cardial sodium or L type calcium channels
ECG in Brugada? (2)
Pseudo right bundle branch block
ST-segment elevation in leads V1-V3
Third-degree (complete) AV block involves a total lack of communication between the atria and ventricles due to …………………
AV node dysfunction
Third-degree (complete) AV block involves a total lack of communication between the …………. and ………. due to AV node dysfunction
Atria and ventricle
Total AV node dysfunction can occur due to …….. (2)
Ischemia
Infiltrative disease
Infection
Age-related fibrosis with cellular degeneration
When there is total AV block, where originates impulse?
Intrinsic pacemaker of the His bundle or ventricle is triggered –> junctional or ventricular escape rhythm
ECG on total AV block?
Dissociation of P waves and QRS complexes
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)
How is called rythm that creates QRS in total AV block?
Junctional or ventricular escape rhythm, which originates in His bundle or ventricles
Slow ventricular rate in complete AV block leads to …………….., which manifest as ………… (4)
Reduced CO –> dyspnea, fatigue, lightheadedness, syncope
What is a management of complete AV block?
permanent pacemakers
Conduction through the interventricular septum mostly involves the …………………… and ……………….. branches
Left and right bundle branches
QRS complex is widened in bundle branch block due to ……………….
Impaired synchronization of ventricular depolarization
Resting potential is determined largely by membrane permeability to …………… when in the resting state
K+ ions
The resting potential of cardiac myocytes is approximately …………….
-90mV
Resting potential of skeletal myocytes is approximately …………..
-75mV
The highly negative resting potential of cardiac myocytes reduces ………………….. as a larger stimulus is needed to excite the cells.
the risk of arrhythmias
Phase is called ……….. and occurs during ………………
Resting potential;
diastole
Phase 0 is called ………….
Rapid depolarization
Rapid depolarization is ……. phase
0
Resting potential is ………… phase
4
Rapid depolarization occurs when ………………
Voltage-gated Na channels open and Na ions rush into the cell
Phase 1 is called ………..
initial rapid repolarization
Initial rapid repolarization is …….. phase
1
In initial rapid repolarization ……………….
Occurs rapid closure of Na channels
What ions participate in plateu phase? What channels opens and what closes?
Opening of L-type Ca
Closure of some K
Plateu is …………phase
2
Phase 2 is called ……….
plateu
Phase 3 is called ……….
late rapid repolarization
Late rapid repolarization is ……… phase
3
What channels open and what close in phase 3?
Closure of Ca
Opening of K –> efflux
Efflux of K+ from the cell ………………………… (effect on MP)
Restores the membrane resting potential
What are 3 ions in action potential in cardiac cycle?
Incr. permeability to Na and Ca;
Decr. permeability to K
Automaticity of cardiac pacemaker cells is …………..
Slow spontaneous deloparization at regular intervals
How is called 0 phase in cardiac pacemaker cells?
Upstroke
What is depolarization threshold in cardiac pacemaker cells in upstroke phase?
-40mV
What is happens in cardiac pacemaker cells in upstroke phase 0?
opening of voltage gated L type Ca –> influx of Ca into cell
How is called phase 3 in cardiac pacemaker cells?
Repolarization
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
How is called phase 4 in cardiac pacemaker cells?
Pacemaker potential
Pacemaker potential in cardiac pacemaker cells is …… phase
4
Phase 4 in cardiac pacemaker cells begins when ………..
At the end of repolarization starts slow influx of Na+
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
At what voltage in phase 4 in cardiac pacemaker cells open T type Ca channels?
-50mV
At what voltage in phase 4 in cardiac pacemaker cells open L type Ca channels?
-40mV
What 2 substances reduce the rate of spontaneous depolarization in cardiac pacemaker cells? What phase?
Adenosine and ACh;
prolongs phase 4
Adenosine interacts with ……….. receptors on the surface of cardiac cell
A1
What ion channels and conductance affects adenosine?
Activates potassium channels –> increase potassium conductance –> MP remains longer negative
What ion channels inhibits adenosine?
inhibits L type ca –> prolonged depolarization time
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
What is ACh cardiac pacemaker cells?
Increase outward K conductance + decrease inward Ca and Na during phase 4
Automaticity is made possible by a ……………………
Inward, mixed sodium-potassium current (the funny current)
Intracellular calcium regulation plays an important role in ……………..
Excitation-contraction coupling
in cardiac cell initial calcium influx is sensed by the……………..receptors in the sarcoplasmic reticulum
ryanodine receptors
calcium-induced calcium release into the cytoplasm increase intracellular calcium concentration ……. fold
100
In muscle physio, Ca binds ……..
Ca binds troponin C
What moves tropomyosin away in muscle?
Ca-troponin C complex
What happens when tropomyosin is pulled away?
Exposed myosin binding sites on actin
The final stage of excitation-contraction coupling is …………….., which occurs subsequent to ………… from the cytoplasm
Myocyte relaxation;
calcium efflux
Intracellular calcium is removed primarily via …….. and ……….
NCX - Na+/Ca2+ exchange pump
SERCA - sarcoplasmic reticulum Ca2+-ATPase pump
NCX ions exchange ratio?
1 Ca and 3 Na
How works SERCA?
Tranfers Ca from cytosol to sarcoplasmic reticulum by using ATP
Smooth muscle cells lack of ……………. unlike cardiac and skeletal muscles
troponin
What is an important substance in smooth muscle cells for contraction?
Calmodulin
Treatment location of atrial flutter?
Cavotricuspid isthmus is a target for radiofrequency ablation
Once triggered, atrial fibrillation induces ………… of the atria with the development of ………. refractory periods and …………. conductivity.
electrical remodeling
shortened refractory
increased conductivity
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
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
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
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
Pacemaker rate in SA node?
60-100 bpm
AV node and His bundle pacemaker rates?
40-60 bpm
Bundle branches and purkinje system pacemaker rates?
25-40 bpm
When electrical impulses are initiated below the AV node and His bundle, the heart rate typically slows to ……… bpm
25-40 bpm
Cavotricuspid isthmus is between ……….. and …………..
crista terminalis and tricuspid annulus
What is holiday heart syndrome and what heart pathology it causes?
Excessive alcohol consumption –> atrial fibrillation
What are 3 systemic illnesses that can predispose atrial fibrillation?
long-standing hypertension, HF, hyperthyroidism
