Antiarryhthmics Dr. Roane Flashcards
Dr. Roane EXAM IV (38 cards)
What determines the duration of cardiac action potentials?
opening of ion channels: (Na, Cl, K)
-> followed by depolarization
Terms describing a fast heart rate
-Tachycardia
-Flutter
-Fibrillation
Which of the ions have high intracellular and extracellular concentrations?
-high extracellular concentration: Na+ and Cl-
-high intracellular concentration: K+
MOA of Lidocaine (Lidoderm)
Sodium channel blocker -> prevents action potential from occurring
-used for local and topic anesthesia by preventing nerve conduction
-also antiarrhythmic
Which channel causes the rapid depolarization phase?
voltage-gated sodium channels
depolarization: the potential becomes positive
What causes the prolonged plateau of depolarization?
slow and prolonged opening of voltage-gated (L-type) Ca2+-channels
+
closing of K+ channels
-> so the potential stays positive
What causes the repolarization phase?
Opening of the K+ channels
-> K+ moves out -> potential becomes negative again
Which phase of the action potential does the P-wave refer to?
depolarization in the atrium
Which phase of the action potential does the QRS complex refer to?
depolarization of ventricles, bc in the ventricles the greatest mass (number of cells is polarized (number of cells)
Which phase of the action potential does the T-wave refer to?
repolarization of Purkinje fibers
What initiates the action potential of the pacemaker?
Funny Na+ channels [1]
-the more Na+ channels are open the steeper the slope
What causes the Ca+ channels [2] to open?
The Ca+ channel opens once the threshold is reached
-once the potential reaches the threshold
-the potential is becoming positive due to the Na+ channel [1] opening
order:
F (Na+)
Transient (Ca2+)
Long-lasting (Ca2+)
K+
How do cardiac cells electrically affect adjacent cells?
-through Connexin channels (pores)
-mechanically through Desmosomes
What causes arrhythmias of the heart to occur?
malfunction of any (or two or three) of the 13 ion channels (Na+, Cl-, K+) -> ions will not flow as they should and when they should
most common due to:
-tissue damage due to ischemia
-pathological remodeling
-Covid-19
-diabetes
-hypertension
-stress/anxiety
Categories of arrhythmias
Tachycardia
Tachycardia
-Atrial fibrillation (Afib): chaotic -> associ. with future stroke
-Atrial flutter: more organized than Afib
-Ventricular fibrillation (Vfib): chaotic ventricles
-Ventricular tachycardia: too fast
-Supraventricular tachycardia: starts above the ventricles
Categories of arrhythmias
Bradycardia
-Sick sinus syndrome: damage around the SA node
-Conduction block at the AV node: the conduction of the depolarization slows down in the AV node (bottleneck), it can be blocked in the AV node - AV block
not Bradycardia:
-premature heartbeat: heart beats too soon before it gets filled up, an extra beat -> palpitation
What does the term functional syncytium mean?
it refers to cells (also muscle cells) being connected to adjacent cells through connexins
Automaticity in cells
if the SA node doesn’t work, some cells can spontaneously depolarize and take the function of the SA node
What is an ectopic cell?
cells with the ability to act as the SA node (pacemaker), when they should not
-impulse-conducting tissues are prone to that, especially when K+ levels are low (hypokalemia)
-damage to ventricular cells can induce automaticity
What induces the automaticity of cells in the heart?
l-ow K+ levels
-damage to ventricular cells
QTc prolongation
QTc prolongation = triggered event due to altered potassium levels
-DAD = delayed afterdepolarization
-EAD = early afterdepolarization
What causes DAD and EAD?
DAD: rapid ventricular beats, and high Ca2+
EAD: high influx of Ca2+ or Na+ or failure to get K+ out
-so too many positive ions
Conduction abnormalities
-Heart block (AV block): impulse doesn’t travel through the AV node as quickly as normal
-Re-entry phenomena: the signal from the SA node travles to the AV node and moves through the outer lining of the heart back to the AV node
atrioventricular re-entry tachycardia
patients with slow (fast refraction) and fast (slow refraction) pathways of conduction
refraction = time where no impulse is possible
the fast pathway goes down and excites cells of the bundle of his but also cells of the slow pathway -> the fast impulse cancels out the slow impulse
-the next impulse will travel along the slow path first bc the refraction is shorter -> it will excite cells of the bundle of his and also cells of the fast pathway retrograde up to the atrium, but also re-enters the slow pathway again -> continuous circuit, causing simultaneous ventricular and atrial contraction
