Edited, memorised or added to reading list

on 05-Jan-2020 (Sun)

Do you want BuboFlash to help you learning these things? Click here to log in or create user.

#Cardiologie #Médecine #Physiologie #Rythmologie

Action potential in fast response tissues —

Tissues that depend upon the opening of voltage-sensitive, kinetically rapid (opening in less than a millisecond) sodium channels to initiate depolarization are called fast response tissues [7].

Fast response tissues include the atria, the specialized infranodal conducting system (bundle of His, fascicles and bundle branches, and terminal Purkinje fibers), and the ventricles (figure 2), while the sinoatrial (SA) and atrioventricular (AV) nodes represent slow response tissues.

It is important to recognize that accessory AV pathways (ie, bypass tracts) associated with Wolff-Parkinson-White syndrome are derived from the atria and are thus also fast response tissues dependent upon sodium current for depolarization.

statusnot read reprioritisations
last reprioritisation on reading queue position [%]
started reading on finished reading on

UpToDate
he Na-Ca exchanger uses the power of the Na gradient to pump Ca out of the cell. These and other pumps maintain the ion channel gradient that is important for both excitability and contraction. <span>Action potential in fast response tissues — Tissues that depend upon the opening of voltage-sensitive, kinetically rapid (opening in less than a millisecond) sodium channels to initiate depolarization are called fast response tissues [7]. Fast response tissues include the atria, the specialized infranodal conducting system (bundle of His, fascicles and bundle branches, and terminal Purkinje fibers), and the ventricles (figure 2), while the sinoatrial (SA) and atrioventricular (AV) nodes represent slow response tissues. It is important to recognize that accessory AV pathways (ie, bypass tracts) associated with Wolff-Parkinson-White syndrome are derived from the atria and are thus also fast response tissues dependent upon sodium current for depolarization. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis".) The following is a simplified description of the steps involved in the generation




#Cardiologie #Médecine #Physiologie #Rythmologie
Phase 2 — Following initial repolarization in phase 1, phase 2 represents a plateau that lasts for hundreds of milliseconds and distinguishes the cardiac action potential from nerve and skeletal muscle action potentials, which are significantly shorter. Late inactivating depolarizing calcium and sodium currents are balanced by activating repolarizing potassium currents to maintain the plateau, which is often down-sloping as repolarizing currents begin to dominate.

statusnot read reprioritisations
last reprioritisation on reading queue position [%]
started reading on finished reading on

UpToDate
h a corresponding rapid decay of the sodium current. The degree of repolarization in phase 1 is dependent on the density of Ito and varies between cardiac chambers and regions within chambers. ●<span>Phase 2 — Following initial repolarization in phase 1, phase 2 represents a plateau that lasts for hundreds of milliseconds and distinguishes the cardiac action potential from nerve and skeletal muscle action potentials, which are significantly shorter. Late inactivating depolarizing calcium and sodium currents are balanced by activating repolarizing potassium currents to maintain the plateau, which is often down-sloping as repolarizing currents begin to dominate. ●Phases 3 and 4 — The final rapid repolarizing phase 3 is driven by the decay of the calcium current and progressive activation of repolarizing potassium currents (IKr, IKs). Terminal r




#Cardiologie #Médecine #Physiologie #Rythmologie

Critical components for reentry include both of the following:

● The presence of fast and slow conduction with varying refractory/recovery periods

● A fixed or functional core about which the circuit moves

statusnot read reprioritisations
last reprioritisation on reading queue position [%]
started reading on finished reading on

UpToDate
nced cardiac automaticity".) Reentry — Reentry is the most commonly encountered arrhythmia mechanism and refers to any arrhythmia dependent on an electrical circuit within the heart (figure 5). <span>Critical components for reentry include both of the following: ●The presence of fast and slow conduction with varying refractory/recovery periods ●A fixed or functional core about which the circuit moves Initiation of reentry requires a unidirectional block within the reentrant path, such that one arm of the circuit conducts the approaching electrical wave front and the blocks it in the




#Cardiologie #Médecine #Physiologie #Rythmologie
EADs — EADs are triggered during prolonged action potentials. A prolonged action potential allows a longer window for reopening of L-type Ca2+ channels during phase 2 (or occasionally phase 3) of the action potential. L-type Ca2+ current depolarizes the membrane before repolarization, triggering an afterdepolarization. Due to L-type Ca2+ channel time and voltage dependence, EADs occur at slow stimulation rates or after a ventricular pause when action potential duration (phase 2) is prolonged and they are suppressed with faster heart rates. EADs are thought to initiate the polymorphic ventricular arrhythmias torsades de pointes (TdP) found in inherited and acquired long QT syndrome (LQTS), for example drug-induced LQTS

statusnot read reprioritisations
last reprioritisation on reading queue position [%]
started reading on finished reading on

UpToDate
the previous action potential to trigger them, hence an afterdepolarization is said to be a triggered arrhythmia. However, it is important to understand that DADs and EADs differ in mechanism. ●<span>EADs — EADs are triggered during prolonged action potentials. A prolonged action potential allows a longer window for reopening of L-type Ca2+ channels during phase 2 (or occasionally phase 3) of the action potential. L-type Ca2+ current depolarizes the membrane before repolarization, triggering an afterdepolarization. Due to L-type Ca2+ channel time and voltage dependence, EADs occur at slow stimulation rates or after a ventricular pause when action potential duration (phase 2) is prolonged and they are suppressed with faster heart rates. EADs are thought to initiate the polymorphic ventricular arrhythmias torsades de pointes (TdP) found in inherited and acquired long QT syndrome (LQTS), for example drug-induced LQTS. A point of distinction to be made here is that triggered activity can initiate TdP, but TdP may be a re-entrant mechanism at the organ level with a functional (spiral reentry) rather t




#Cardiologie #Médecine #Physiologie #Rythmologie
Class I — The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting phase 0 depolarization. They are all at least in part positively charged and presumably interact with specific amino acid residues in the internal pore of the sodium channel.

statusnot read reprioritisations
last reprioritisation on reading queue position [%]
started reading on finished reading on

UpToDate
ypokalemia and hyperkalemia. Class 0 — Drugs in the newly proposed Class 0 modulate the pacemaker channel HCN4, affecting the pacemaker current If [11]. The blocker ivabradine slows heart rate. <span>Class I — The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting phase 0 depolarization. They are all at least in part positively charged and presumably interact with specific amino acid residues in the internal pore of the sodium channel. Three different subgroups (table 2 and table 3) have been identified because their mechanism or duration of action is somewhat different due to variable rates of drug binding to and dis




#Cardiologie #Médecine #Physiologie #Rythmologie
Class Ic drugs (flecainide and propafenone) primarily block open sodium channels and slow conduction. They dissociate slowly from the sodium channels during diastole, resulting in increased effect at a more rapid rate (use-dependence). This characteristic is the basis for their antiarrhythmic efficacy, especially against supraventricular arrhythmias. Use-dependence may also contribute to the proarrhythmic activity of these drugs, especially in the diseased myocardium, resulting in incessant ventricular tachycardia

statusnot read reprioritisations
last reprioritisation on reading queue position [%]
started reading on finished reading on

UpToDate
induced by depolarization) and dissociate from the sodium channel more rapidly than other class I drugs. As a result, they are more effective with tachyarrhythmias than with slow arrhythmias. ●<span>Class Ic drugs (flecainide and propafenone) primarily block open sodium channels and slow conduction. They dissociate slowly from the sodium channels during diastole, resulting in increased effect at a more rapid rate (use-dependence). This characteristic is the basis for their antiarrhythmic efficacy, especially against supraventricular arrhythmias. Use-dependence may also contribute to the proarrhythmic activity of these drugs, especially in the diseased myocardium, resulting in incessant ventricular tachycardia. Flecainide and propafenone also have potassium channel blocking activity and can increase the APD in ventricular myocytes. Propafenone has significant beta blocking activity. Another r




#Cardiologie #Médecine #Physiologie #Rythmologie

By blocking catecholamine and sympathetically mediated actions, beta blockers slow the rate of discharge of the sinus and ectopic pacemakers, and increase the effective refractory period of the AV node. They also slow both antegrade and retrograde conduction in anomalous pathways [18].

Carvedilol is a beta-blocker with unique additional properties. In addition to beta- and alpha-adrenergic blockade, carvedilol can also block potassium (KCNH2, formerly HERG), calcium, and sodium currents and modestly prolong APD. However, when administered chronically, carvedilol increases the number of these channels, which is probably a favorable effect in diseased hearts [19].

statusnot read reprioritisations
last reprioritisation on reading queue position [%]
started reading on finished reading on

UpToDate
celeration of phase 0 upstroke velocity or the rate of membrane depolarization. ●An increase in delayed afterpotentials, especially when the cell is calcium loaded, such as in digoxin toxicity. <span>By blocking catecholamine and sympathetically mediated actions, beta blockers slow the rate of discharge of the sinus and ectopic pacemakers, and increase the effective refractory period of the AV node. They also slow both antegrade and retrograde conduction in anomalous pathways [18]. Carvedilol is a beta-blocker with unique additional properties. In addition to beta- and alpha-adrenergic blockade, carvedilol can also block potassium (KCNH2, formerly HERG), calcium, and sodium currents and modestly prolong APD. However, when administered chronically, carvedilol increases the number of these channels, which is probably a favorable effect in diseased hearts [19]. The most recent classification (table 2 and table 3) expands the definition of class II to include "autonomic inhibitors and activators," with subclass IIa as beta adrenergic blockers s




#Cardiologie #Médecine #Physiologie #Rythmologie
Class IV — The class IV drugs are calcium channel blockers. Verapamil has a more pronounced inhibitory effect on the slow response SA and AV nodes than diltiazem.

statusnot read reprioritisations
last reprioritisation on reading queue position [%]
started reading on finished reading on

UpToDate
iarrhythmic activity [11]. Subclass IIIc (transmitter dependent K channel blockers) such as acetylcholine activate potassium channels, with no clinically available drugs yet having this action. <span>Class IV — The class IV drugs are calcium channel blockers. Verapamil has a more pronounced inhibitory effect on the slow response SA and AV nodes than diltiazem. In comparison, the dihydropyridines, such as nifedipine, have little electrophysiologic effect on the heart. Verapamil and diltiazem can slow the sinus rate (usually in the presence of




Flashcard 4761338645772

Tags
#Cardiologie #Médecine #Physiologie #Rythmologie
Question
What are the two components needed for reentry to happen ?
Answer

● The presence of fast and slow conduction with varying refractory/recovery periods

● A fixed or functional core about which the circuit moves


statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

Parent (intermediate) annotation

Open it
Critical components for reentry include both of the following: ● The presence of fast and slow conduction with varying refractory/recovery periods ● A fixed or functional core about which the circuit moves

Original toplevel document

UpToDate
nced cardiac automaticity".) Reentry — Reentry is the most commonly encountered arrhythmia mechanism and refers to any arrhythmia dependent on an electrical circuit within the heart (figure 5). <span>Critical components for reentry include both of the following: ●The presence of fast and slow conduction with varying refractory/recovery periods ●A fixed or functional core about which the circuit moves Initiation of reentry requires a unidirectional block within the reentrant path, such that one arm of the circuit conducts the approaching electrical wave front and the blocks it in the







Flashcard 4761342053644

[unknown IMAGE 4761343626508]
Tags
#Cardiologie #Médecine #Physiologie #Rythmologie #has-images
Question
Early After Depolarizations — EADs are triggered during prolonged action potentials. A prolonged action potential allows a longer window for reopening of [...] channels during phase 2 (or occasionally phase 3) of the action potential.
Answer

L-type Ca2+


statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

Parent (intermediate) annotation

Open it
EADs — EADs are triggered during prolonged action potentials. A prolonged action potential allows a longer window for reopening of L-type Ca2+ channels during phase 2 (or occasionally phase 3) of the action potential. L-type Ca2+ current depolarizes the membrane before repolarization, triggering an afterdepolarization. Due to

Original toplevel document

UpToDate
the previous action potential to trigger them, hence an afterdepolarization is said to be a triggered arrhythmia. However, it is important to understand that DADs and EADs differ in mechanism. ●<span>EADs — EADs are triggered during prolonged action potentials. A prolonged action potential allows a longer window for reopening of L-type Ca2+ channels during phase 2 (or occasionally phase 3) of the action potential. L-type Ca2+ current depolarizes the membrane before repolarization, triggering an afterdepolarization. Due to L-type Ca2+ channel time and voltage dependence, EADs occur at slow stimulation rates or after a ventricular pause when action potential duration (phase 2) is prolonged and they are suppressed with faster heart rates. EADs are thought to initiate the polymorphic ventricular arrhythmias torsades de pointes (TdP) found in inherited and acquired long QT syndrome (LQTS), for example drug-induced LQTS. A point of distinction to be made here is that triggered activity can initiate TdP, but TdP may be a re-entrant mechanism at the organ level with a functional (spiral reentry) rather t







Flashcard 4761348082956

Tags
#Cardiologie #Médecine #Physiologie #Rythmologie
Question
Why do EADs occur at slow heart rates ?
Answer
Due to L-type Ca2+ channel time and voltage dependence, EADs occur at slow stimulation rates or after a ventricular pause when action potential duration (phase 2) is prolonged and they are suppressed with faster heart rates.


statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

Parent (intermediate) annotation

Open it
of L-type Ca2+ channels during phase 2 (or occasionally phase 3) of the action potential. L-type Ca2+ current depolarizes the membrane before repolarization, triggering an afterdepolarization. <span>Due to L-type Ca2+ channel time and voltage dependence, EADs occur at slow stimulation rates or after a ventricular pause when action potential duration (phase 2) is prolonged and they are suppressed with faster heart rates. EADs are thought to initiate the polymorphic ventricular arrhythmias torsades de pointes (TdP) found in inherited and acquired long QT syndrome (LQTS), for example drug-induced LQTS </s

Original toplevel document

UpToDate
the previous action potential to trigger them, hence an afterdepolarization is said to be a triggered arrhythmia. However, it is important to understand that DADs and EADs differ in mechanism. ●<span>EADs — EADs are triggered during prolonged action potentials. A prolonged action potential allows a longer window for reopening of L-type Ca2+ channels during phase 2 (or occasionally phase 3) of the action potential. L-type Ca2+ current depolarizes the membrane before repolarization, triggering an afterdepolarization. Due to L-type Ca2+ channel time and voltage dependence, EADs occur at slow stimulation rates or after a ventricular pause when action potential duration (phase 2) is prolonged and they are suppressed with faster heart rates. EADs are thought to initiate the polymorphic ventricular arrhythmias torsades de pointes (TdP) found in inherited and acquired long QT syndrome (LQTS), for example drug-induced LQTS. A point of distinction to be made here is that triggered activity can initiate TdP, but TdP may be a re-entrant mechanism at the organ level with a functional (spiral reentry) rather t







Flashcard 4761354374412

Tags
#Cardiologie #Médecine #Physiologie #Rythmologie
Question

Class I — The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting phase [...] depolarization.

They are all at least in part positively charged and presumably interact with specific amino acid residues in the internal pore of the sodium channel.

Answer
0


statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

Parent (intermediate) annotation

Open it
Class I — The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting phase 0 depolarization. They are all at least in part positively charged and presumably interact with specific amino acid residues in the internal pore of the sodium channel.

Original toplevel document

UpToDate
ypokalemia and hyperkalemia. Class 0 — Drugs in the newly proposed Class 0 modulate the pacemaker channel HCN4, affecting the pacemaker current If [11]. The blocker ivabradine slows heart rate. <span>Class I — The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting phase 0 depolarization. They are all at least in part positively charged and presumably interact with specific amino acid residues in the internal pore of the sodium channel. Three different subgroups (table 2 and table 3) have been identified because their mechanism or duration of action is somewhat different due to variable rates of drug binding to and dis







Flashcard 4761356733708

[unknown IMAGE 4761358306572]
Tags
#Cardiologie #Médecine #Physiologie #Rythmologie #has-images
Question

Class I

The class I drugs act by modulating or blocking the [...] channels, thereby inhibiting phase 0 depolarization.


They are all at least in part positively charged and presumably interact with specific amino acid residues in the internal pore of the sodium channel.

Answer
sodium


statusnot learnedmeasured difficulty37% [default]last interval [days]               
repetition number in this series0memorised on               scheduled repetition               
scheduled repetition interval               last repetition or drill

Parent (intermediate) annotation

Open it
Class I — The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting phase 0 depolarization. They are all at least in part positively charged and presumably interact with specific amino acid residues in the internal pore of t

Original toplevel document

UpToDate
ypokalemia and hyperkalemia. Class 0 — Drugs in the newly proposed Class 0 modulate the pacemaker channel HCN4, affecting the pacemaker current If [11]. The blocker ivabradine slows heart rate. <span>Class I — The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting phase 0 depolarization. They are all at least in part positively charged and presumably interact with specific amino acid residues in the internal pore of the sodium channel. Three different subgroups (table 2 and table 3) have been identified because their mechanism or duration of action is somewhat different due to variable rates of drug binding to and dis