Tachyarrhythmias Flashcards
Automaticity
Cell’s ability to depolarize itself to a threshold voltage to generate a spontaneous action potential
Normally, the only cells with automaticity are ____.
Normally, the only cells with automaticity are the sinoatrial node, atrioventricular node, and cardiac conduction system (His-Purkinjes).
However, in pathologic situations, some myocardial cells outside the conducting system may also acquire automaticity.
Pacemaker current
Gradual ionic current within phase 4 that results in spontaneous depolarization at a set time (due to a set start point after K+ efflux and a set rate for the current).
These channels are generally sodium channels that allow a small, fixed rate of sodium to re-enter the pacemaker cell
Pacemaker current graph
Ion flow components that make up the pacemaker current
- Slow influx of sodium
- Slow influx of calcium (mostly by L-type channels)
- Slow outflow of potassium
- Additional influx of sodium mediated by the Na-Ca exchanger
The Calcium Clock
This describes the regulation of the Na-Ca exchanger.
It is activated by release of Ca from the sarcoplasmic reticulum.
The number of available (or resting-state) fast sodium channels increases as . . .
The number of available (or resting-state) fast sodium channels increases as the resting membrane potential becomes more negative
So, since sinus and AV nodal cells have their maximum diastolic voltages at -50 to -60 mV compared to the -90 mV in the Purkinjes, more fast sodium channels are inactivated in nodal cells. Thus, their action potential upstroke relies more on the calcium current than does the Purkinjes’.
Variables that determine how fast pacemakers reach their threshold
- Rate of the phase 4 spontaneous depolarization current
- Maxiumum negative diastolic potential
- Threshold potential
Native pacemaker
The SA node
Latent pacemaker
A cell that could act as the dominant pacemaker, but is currently depolarizing under the rhythm of a faster pacemaker.
Sometimes called ‘ectopic’ pacemakers
Rates of different pacemakers at rest
SA node: 60-100 bpm
AV node and His: 50-60 bpm
Purkinjes: 30-40 bpm
Overdrive suppression
Not only does the cell population with the fastest intrinsic rhythm preempt all other automatic cells from spontaneously firing, it also directly suppresses their automaticity. The mechanism is as follows:
As pacemaker cells are forced to depolarize faster than their pacemaker rate, Na/K ATPase becomes more active. This hyperpolarizes pacemaker cells, making their starting voltage following depolarization more negative, and giving the dominant pacemaker cell an even bigger advantage.
In other words, the Na/K ATPase current competes with the If current.
Major contributors in determining which cell is dominant
- Rate
- Overdrive suppression
- Gross anatomic connectivity
- Electrical effects of local anatomic connectivity
Local electric interactions between pacemaker and nonpacemaker cells
Pacemaker cells have a less-negative voltage than myocardium at baseline, and are electrically coupled through low-resistance gap junctions. Thus, there is a tendancy to slightly hyperpolarize pacemaker cells and slightly depolarize non-pacemaker cells.
This hyperpolarizing current in the pacemaker cell also competes with If. Note that by definition, these effects are more pronounced in the more distal aspects of the conduction system. Thus they are felt more by the Purkinjes and His, and to a lesser extent the AV node, and least of all the SA node.
The main abnormalities that lead to arrhythmias
- Altered automaticity of SA node or latent pacemakers
- Abnormal automaticity in atrial or ventricular myocytes
- Triggered activity
Effect of sympathetic stimulation on pacemakers
Acts via β1-adrenergic receptors. Stabilizes open conformation of pacemaker channels, increasing their open probability. Thus, If increases and rate of depolarization increases.
Additionally, the threshold potential is shifted down by similarly stabilizing the open conformation of voltage-sensitive Ca2+ channels. Therefore, diastolic depolarization reaches the threshold potential earlier.
Effects of cholinergic and adrenergic stimulation on pacemaker cells (graph)
Fundamentally, cholinergic and adrenergic innervation of the heart change heart rate via . . .
. . . the same basic mechanism, but just by moving upwards or downwards from a set homeostatic point.
Effects of cholinergic stimulation on the heart that are not controlled by sympathetics
In addition to effects on threshold potential and pacemaker current, cholinergic stimulation stabilizes the open conformation of acetylcholine-sensitive K+ channels. Thus, there is enhanced potassium efflux, resuling in a lower (more negative) resting potential of the pacemaker. This acts via a third mechanism to reduce heart rate.
Escape beats are ___.
Ectopic beats are ___.
Escape beats are late.
Ectopic beats are early.
Things that may induce ectopic beats
- Hypoxemia
- Ischemia
- Electrolyte disturbance
- High local catecholamine concentration
- Digitalis toxicity
Ectopic beats from abnormally acquired automaticity may occur when a myocyte’s membrane potential is reduced to a value less negative than ___.
Ectopic beats from abnormally acquired automaticity may occur when a myocyte’s membrane potential is reduced to a value less negative than -60 mV.
Triggered activity
When action potential ‘triggers’ abnormal depolarizations resulting in extra heart beats or rapid arrhythmias. his process may occur when the first action potential leads to oscillations of the membrane voltage known as afterdepolarizations. Abnormal action potentials are triggered if the afterdepolartization reaches a threshold voltage.
Two types of afterdepolarization
- Early afterdepolarization: Occur during the repolarization phase of the inciting beat
- Delayed afterdepolarization: Occur shortly after repolarization has completed.
Early afterdepolarization graph
Delayed afterdepolarization graph
Causes of early afterdepolarization
Changes in the membrane potential in the positive direction that interrupt normal repolarization. Occur in phase 2 (Ca-dependent upstroke) or 3 (Na-dependent upstroke, early recovery of Na channels). More likely to develop in conditions that prolong the QT interval (action potential duration).
Causes of delayed afterdepolarization
Appear after repolarization is complete, most commonly due to high intracellular calcium (as seen in digitalis toxicity). The intracellular Ca accumulation causes activation of chloride currents or the Na-Ca exchanger, resulting in brief inward currents.
Both early and delayed afterdepolarizations may lead to ___.
Both early and delayed afterdepolarizations may lead to self-perpetuating tachyarrhythmias.
Differentiation of common supraventricular tachyarrhythmias
Atrial premature beats
Occur in healthy and diseased hearts. Originate from automaticity or reentry in an atrial focus outside the SA node and are often exacerbated by sympathetic stimulation and with caffeine, alcohol, emotional stress. Asymptomatic or cause palpitations.
Normal QRS complexes, just an early P wave. May include some blocked P waves which simply fire too soon, before the impulse can be conducted to the ventricles, in which case it is not followed by QRS. This is called a blocked ABP.
Atrial flutter
Rapid, regular atrial activity at 180-350 bpm. Most of these P waves occur during the refractory period and are not conducted to the ventricles, resulting in a much slower ventricular HR, but still tachycardic (~150 bpm). Often described as having a “sawtooth” appearance.
Caused by reentry over a large anatomically fixed circuit, often the atrial tissue along the tricuspid valve annulus. Usually occurs in patients with preexisting heart disease. May be transient. Slow rates often asymptomatic, fast rates cause palpitation, dyspnea, weakness. This condition also predisposes to atrial thrombus formation.
Why may it be dangerous to give a patient with atrial flutter an antiarrhythmic?
Slowing the conduction in a trium down may allow the AV node more time to recover between impulses. In this situation, the node may go from conducting in a 1:2 fashion to a 1:1 fashion, producing even larger ventricular rates.
In patients with limited cardiac reserve, this acceleration may lead to profound decrease in cardiac output and precipitate hypotension.
Treating atrial flutter
- Electrical cardioversion to restore sinus rhythm
- Terminate flutter by rapid atrial stimulation with a temporary or permanent pacemaker
- Patients without immediate need for cardioversion may begin pharmacologic therapy: beta blockers, nondihydropyridine CCBs, or digoxin. Once the atrial rate is slowed, it is safe to give an antiarrhythmic to atrial flutter patients.
- When chronic therapy is required to prevent recurrences, catheter ablation is sometimes a favorable alternative. An electrode catheter is inserted into the femoral vein, passed up to the RA, and used to localize and cauterize part of the reentrant loop, interrupting the flutter circuit.
Atrial fibrillation
Chaotic activity without organized P waves and with irregular QRS rate. The atrial rate may be as high as 600 such that P waves are not discernible on ECG. The regular ventricular rate in unreated afib is 140-160 bpm. Appears as just QRS and T waves on ECG since P waves cannot be seen.
Causes of atrial fibrillation
Likely involves multiple wandering reentrant circuits within atria. In some patients, rhythm repeatedly shifts between atrial fibrillation and atrial flutter.
Afib is often associated with atrial enlargement (right or left)
Paroxysmal
Sudden, unpredictable episodes
Considerations in treating atrial fibrillation
- Ventricular rate control
- Methods to restore sinus rhythm
- Assessment for need of anticoagulation
Catheter ablation of AV node
One extreme possibility for treating atrial fibrillation when sinus rhythm cannot be maintained and HR cannot be pharmacologically controlled. This creates third degree heart block to permanently slow ventricular rate, and is supplemented with implantation of a permanent pacemaker.
Paroxysmal supraventricular tachycardias
Manifest with sudden onset and termination with an atrial rate between 140 and 250. ECGs show normal QRS complexes unless aberrant conduction is present. “Retrograde P waves” occur simultaneously with, and are ‘hidden’ in, the QRS complexes.
Mechanism is often reentry involving the AV node, atrium, or an accessory pathway between the atrium and ventricle.
AV Nodal Reentrant Tachycardia
This is a form of paroxysmal supraventricular tachycardia. Here, the branches off of the AV node conduct at different velocities, producing high-speed and low-speed conducting pathways. Fast pathways, despite conducting faster, have longer refractory periods. Under normal conditions, the fast pathway makes its way to ventricles first and controls rate.
However, if there is a unidirectional block in the fast pathway, the slow pathway may proceed and conduct back up through the fast pathway, which has already repolarized. Here, retrograde atrial depolarization occurs simultaneously with regular ventricular depolarization.
AV Nodal Reentrant Tachycardia on ECG
P waves often hidden within QRS, but may appear as a superimposed terminal reflection in the QRS complex and are inverted in leads II, III, and aVF due to the caudocranial direction of atrial activation.
Termination of reentry by impairing AV node conduction
Transient increases in vagal tone may accomplish this, and may be produced by the Valsalva maneuver or carotid sinus massage.
Pharmacologically, this may be done with intravenous adenosine, or sometimes nondihydropyridine CCBs or beta blockers.
Atrioventricular reentrant tachycardias
Similar to AV nodal reentrant tachycardias, except that one limb of the reentrant loop is via an accessory pathway or bypass tract. These tracts are made up of abnormal bands of myocytes that span the AV groove and connect atrial to ventricular tissue separately from the normal conduction system. Incidence of this anatomical abnormality is ~1/1,500
May result in ventricular pre-excitation syndrome or paroxysmal supraventricular tachycardia.
Ventricular pre-excitation syndrome
Atrial impulses pass in an anterograde direction to ventricles through both the AV nodal pathway and an accessory pathway. Since conduction through accessory is often faster than through the AV node, the ventricles are stimulated earlier than they typically would be, shortening the PR interval (<0.12 sec). The QRS also has a ‘slurred’ rather than sharp upstroke (called a ‘delta wave’) because the initial ventricular activation is slower than that of the Purkinje system. QRS is also often widened due to the two signals.
Orthodromic vs Antidromic
Orthodromic AVRT: Impulse travels anterogradely down the AV node to the ventricles and then retrogradely up the accessory tract back to the atria, with no delta wave.
Antidromic AVRT: Impulses travel anterogradely down the accessory pathway and retrogradely up the AV node. Wide QRS complex due to anterograde accessory conduction activating ventricles. Can be difficult to distinguish by ECG from ventricular tachycardia.
Considerations for treating ventricular pre-excitation syndrome
Recall that digitalis, beta blockers, and nondihydropyridine CCBs block conduction well through the AV node, but not through accessory pathways. In this case such drugs might make things worse by shortening myocyte reftractory period.
Sodium channel blockers (class IA and IC antiarrhythmics) are the preferred drugs for this condition.
Curing ventricular pre-excitation syndrome
Can be done through catheter ablation of the accessory pathway.
Concealed Accessory Pathways
Accessory pathways that do not result in ECG. Often only capable of retrograde conduction.
Because the reentrant circuit travels anterogradely down the AV node, vagal maneuvers and drugs that interrupt conduction over the AV node (e.g., adenosine, verapamil, diltiazem, and β-blockers) can terminate the tachycardia.
Focal atrial tachycardia
Results from gain of automaticity at an ectopic site or re-entry. The ECG has the appearance of sinus tachycardia, but the P-wave morphology is different from that of sinus rhythm, indicating depolarization of the atrium from an abnormal site.
May be paroxysmal and of short duration, or may persist.
Treat with beta blockers, CCBs, class IA, IC, and III antiarrhythmics. Catheter ablation may be possible for certain cases.
Multifocal atrial tachycardia
ECG shows an irregular rhythm with multiple (at least three) P-wave morphologies, and the average atrial rate is >100 bpm. An isoelectric (i.e., “flat”) baseline between P waves distinguishes MAT from the chaotic baseline of AF.
Likely caused by either abnormal automaticity in several foci within the atria or triggered activity and occurs most often in the setting of severe pulmonary disease and hypoxemia. Patients often critically ill from underlying disease, and mortality is high. Treatment aimed at causative disorder.
Verapamil (a nondihydropyridine CCB) is often effective as a temporizing measure.
Ventricular premature beats
Similar to APBs, VPBs are common even among healthy people and are often asymptomatic and benign. A VPB arises when an ectopic ventricular focus fires an action potential.
On the ECG, a VPB appears as a widened QRS complex, because the impulse travels from its ectopic site through the ventricles via slow cell-to-cell connections rather than through the normal rapidly conducting His–Purkinje system. Furthermore, the ectopic beat is not related to a preceding P wave.
When every alternate beat is a VPB, the rhythm is termed bigeminy. When two normal beats precede every VPB, trigeminy is present. Consecutive VPBs are referred to as couplets (two in a row) or triplets (three in a row).
Ventricular tachycardia
VT is a series of three or more VPBs.
Self-terminating episodes are termed nonsustained VT. If it persists for more than 30 sec, produces severe symptoms such as syncope, or requires termination by cardioversion or administration of an antiarrhythmic drug, it is designated as sustained VT
Most commonly in patients with structural heart disease, including myocardial ischemia and infarction, heart failure, ventricular hypertrophy, primary electrical diseases, valvular heart disease, and congenital abnormalities.
Torsades de Pointes
“twisting of the points”. Form of polymorphic VT. Can be produced by early afterdepolarizations (triggered activity), particularly in patients who have a prolonged QT interval. Usually symptomatic, causing light-headedness or syncope, but is frequently self-limited.
In non-drug-related and non-electrolyte related cases, administration of intravenous magnesium often suppresses repeated episodes. QT-shotening by giving beta adrenergic agonists, like dobutamine or isoproterenol, can paradoxically bring down the heart rate by erradicating the arrhythmia.
QT prolongation can result from . . .
Electrolyte disturbances (hypokalemia or hypomagnesemia), persistent bradycardia, and drugs that block cardiac potassium currents, including many antiarrhythmic agents (particularly the class III drugs sotalol, ibutilide, and dofetilide and some class I drugs, including quinidine, procainamide, and disopyramide)
Ventricular Fibrillation
VF is an immediately life-threatening arrhythmia. Disordered, rapid stimulation of the ventricles with no coordinated contractions. The result is essentially cessation of cardiac output and death if not quickly reversed. It is the major cause of mortality in acute myocardial infarction.
The only effective therapy is prompt electrical defibrillation. As soon as the heart has been converted to a safe rhythm, the underlying precipitant of the arrhythmia should be sought and corrected to prevent further episodes.
Often in post-myocardial injury cases of monofocal VT, the precipitating focus is ___.
Often in post-myocardial injury cases of monofocal VT, the precipitating focus is a scar on the myocardium.
Any non-physiologic tachycardia may:
- Compromise diastolic filling and drop preload
- Thus, drop in stroke volume and blood pressure
- Syncopy
- Confusion
- Dizziness
- Decreased coronary artery perfusion with increased cardiac demand
- Ischemia
- Bad ischemia may precipitate VF, and VF may precipitate cardiac arrest
Monomorphic ventricular tachycardia is usually caused by
a scar in the myocardium that generates a single re-entry circuit
Khan Academy AV Re-entry Tachycardia summary
Khan Academy AV Nodal Re-entry Tachycardia Summary
Tachyarrhythmia standard procedure
What does an unstable tachyarrhythmia patient look like?
HR is a guide, but all others indicate need for immediate cardioversion.
- HR > 150 bpm
- Altered mental status
- Ongoing angina
- Hypotension
- Symptoms of shock
Approaching a tachyarrhythmia
- What is the ventricular rate?
- Is the QRS narrow or wide?
- Are the beats regular or irregular?
- Are there P waves?
Vagal maneuvers
- Valsalva
- Blow into a closed system
- Coughing very hard
- Splash very cold water onto face
All of these increase the vagal input into the AV node, slowing its conduction and allowing sinus rhythm to take over again.
If vagal maneuvers don’t work, what do you do?
- Adenosine
- Call a cardiologist
Once symptoms have resolved, what can you give patients to help prevent future arrhythmias?
- Beta blocker
- NDHP CCB
Characteristics of Wolf-Parkinson-White on ECG
- Short PR
- Delta waves
- Wide QRS
- Abnormal ST segments and T waves
Schafer’s tachyarrhythmia algorithm
