4, 7 - Arrhythmias

Positive charge travels to positive electrode =

Positive deflection

Positive charge travels away from positive electrode =

Negative deflection

Negative charge travels towards negative electrode =

Positive deflection

P-wave

• Represents

• Width

• Atrial depolarization

• <0.12sec

PR-segment

• Represents

• AV node holding up the signal

PR-interval

• Represents

• Width

• Start of atrial depolarization to start of ventricular depolarization

• 0.12-0.20 sec

Q wave

• Represents

A negative deflection that represents the left bundle branch depolarizing the interventricular septum

R wave

• Represents

Depolarization of the main ventricular mass

S wave

• Represents

A negative deflection representing depolarization of the bases of the ventricles(moving slightly away from the positive electrode)

ST segment

• Represents

The period where ventricles are depolarized and not repolarizing yet

T-wave

• Represents

• Repolarization of ventricles, a positive deflection because repolarization starts outside to inside, and since it’s a negative charge, the negative charge is moving away from the positive electrode → positive deflection

Sinus P-wave meaning

• Upright in lead II

• Inverse in aVR

• Each one is followed by a QRS

What is altered automaticity?

• Change in how fast pacemaker cells depolarize(in SA node or ectopic locations)

• Increased rate:

  • A physiologic response like to exercise, fever, and thyrotoxicosis. Still controlled by the SA node

  • Ectopic beats like PAC and PVC which fires independently while the SA node is still functional

• Decreased rate

  • Sinus bradycardia: A physiologic phenomenon found in athletes

  • Sick sinus syndrome: SA node disease, such as age-related fibrosis leads to bradycardia

  • SA node failure causes a latent pacemaker to takeover, called an escape beat/rhythm

EKG findings of PAC and PVC

PAC: Sudden early, abnormal P wave on EKG followed by a normal QRS(Because the P-wave is from a abnormal source, it looks weird, but it still goes thru to the AV node like normal)

PVC: Sudden disappearance of P wave followed by a wide, bizzarre QRS(No P-wave because the signal comes from ventricular myocardium)

What is triggered activity?

• An abnormal extra depolarization in atrial/ventricular myocardium/Purkinje fibers, occurring after a normal action potential happens

• Early after depolarization occurs when in phase 2/3, in plateau/repolarization phase, Ca2+ channels suddenly open up again, causing an extra depolarization

• Delayed after depolarization occurs when the cell is in phase 4, the flat resting stage due to increased intracellular Ca2+ is trying to be cleared via the NCX, who trades Ca2+ out for 3 Na+ in, causing a depolarization

Types of abnormal impulse conduction

1. Blocks

2. Reentry

Types of AV blocks and EKG findings

1. First degree: All p-waves are followed by a QRS, but the PR interval is greater than 0.20 sec

2. Second degree(Mobitz1, Wenckebach): Progressive PR prolongation until one beat is skipped(No QRS), then reset

3. Second degree(Mobitz2): Normal PR but with sudden dropped beats

4. Third degree: No atrial impulses reach ventricles, found as independent P waves and QRS complexes, ventricles operating via escape rhythm

PAC and PVC

• EKG findings

• Differentiating PVC types

• Early beat from ectopic atrial focus causes abnormal P-wave followed by normal QRS vs Early beat from ventricular focus leads to no preceding P wave, wide bizarre QRS with opposite direction T-wave and compensatory pause

  • Triggered activity cause: Trigger beat and wide QRS has fixed distance very time(but PVC distance isn’t fixed because not every beat makes a PVC)

  • From automaticity: Each PVC to PVC has the same fixed distance

Reentry

• Requirements

• Mechanism

• Factors that affect it’s sustainability

• Unidirectional block that allows signals to travel retrogradely. Then, one pathway must be fast conducting with a longer refractory period, while the other is slow conducting with a shorter refractory period. A normal beat happens, but the fast pathway wins and reaches the bottom and depolarizes the tissue, but both pathways are in refractory stage now, even if the slower pathway’s signal didn’t trigger anything. Then, a premature beat arrives(like from a PAC), which can now take the path of the slower pathway(which has already recovered). Now, this beat goes through, and by the time it does, if the fast pathway hasn’t recovered yet, then the slow impulse won’t reenter, but if it has recovered, then the slow impulse can enter the pathway retrogradely, and IF the faster pathway that the premature beat took to enter in the first place has already recovered again, it can now reenter and form a loop.

• For more sustainability, it’s best for a reentry circuit to have a large excitable gap, affected by these factors: short refractory period, slow conduction velocity, and a long circuit path

Class 1 Antiarrhythmics

• Group name

• Target cells

• Types/Names and their mechanisms

• ADR

• Sodium channel blockers

• Ordinary heart muscle cells

• IA: Quinidine, procainamide: Blocks Na+ channels to slow conduction and also blocks K+ channels to slow repolarization

  • Prolongs action potential: Widens QRS/Prolongs QT

• IB: Lidocaine: Weak Na+ channel block, used in cases with damaged tissue like MI → faster repolarization via inhibiting Na+ trickle into cells in phase 3

• IC: Flecainide, propafenone: Very strong Na+ channel block, slows conduction without any affect on repolarization(No K+ block)

• Proarrhythmia(a new one)

Why does prolonging action potential and decreasing conduction velocity benefit arrhythmia patients?

It makes it so that arrhythmias are harder to maintain

Class II antiarrhythmics

• Group Name

• Target cells

• Mechanism

• Name

• Beta blockers

• Pacemaker cells

• Blocks beta1 stimulation, slowing down the phase 4 slope(blocks If and Ca2+ channels at SA and AV nodes) → which decreases sinus rate and delays AV node conduction

• Propanolol

Class III antiarrhythmics

• Group Name

• Target cells

• Mechanism

• Name

• Potassium channel blockers

• Ordinary muscle cells

• Blocks K+ channels, prolonging repolarization(prolongs AP)

• Amiodarone(Has a lot of effects, but also side-effects, so it’s broad spectrum only in life-threatening cases)

Class IV arrhythmics

• Group name

• Target cells

• Mechanisms

• Names

• Calcium channel blockers

• Pacemaker cells

• Blocks L type Ca2+ channels which slows down phase 0 Ca2+ depolarization in SA and AV nodes, regardless of sympathetic tone

• Verapamil, Diatilazem

Blocking these phases affect what in arrhythmia, and how? And how do the class I-IV drugs fit in this?

Phase 0

Phase 3

Phase 4

Phase 0: conduction velocity

• Class I: Basically reduces the strength of these impulses and reduces their likelihood of starting re-entry(In phase 0 of myocytes)

• Class IV: Blocks Ca2+ channels, slows down depolarization(In phase 0 of pacemakers)

Phase 3: action potential duration

• Class III: Prolongs action potential duration which increases refractory period, meaning wavefront is more likely to hit the tail of the wave and end the rentry loop

Phase 4(of pacemaker): automaticity/rate

• Class II: If at SA node, reduces amount of abnormal impulses made

Adenosine

• Target cells

• Mechanism

• Use

• Pacemakers

• Binds A1 receptors to trigger K+ efflux, leading to hyper polarization which can slow the AV node or even block it entirely to stop arrhythmias

• PSVT

Digoxin

• Target cells

• Mechanism/Uses

• ADRs(4)

• Ordinary cardiac muscle cells(For inotropy) and pacemakers(For vagal tone)

• Inhibits Na K ATPase pump which boosts inotropy to treat HF, and also boosts vagal tone

• Renal, Skeletal muscle mass, hyperK, digoxin arrhythmias

Magnesium Sulfate

• Type

• Target cells

• Mechanism

• Uses

• Unclassified

• Ordinary cardiac muscle cells

• Blocks L-type Ca2+ channels

• Treats torsade de pointes(caused by excess intracellular Ca2+ boosting early afterdepolarization) and digoxin arrhythmias(from increased Ca2+) by reducing Ca2+

Pacemaker rate of heart cells

1. SA node

2. AV node

3. Bundle of His

4. Bundle branches/Purkinje network

1. SA node: 60-100

2. AV node: 40-55

3. Bundle of His: 40-55

4. Bundle branches/Purkinje network: 25-40

What is an example of what needs to happen for an arrhythmia to be sustained?

An example is reentry

Sinus tachycardia

• What is it

• EKG

• Causes

• Heart rate of over 100 with P-waves followed by QRS every time, and P-waves upright in II, inverse in aVR

• Typically external factors like exercise, anxiety, fever, thyrotoxicosis, etc.

Atrial Fibrillation

• Mechanism

• EKG Finding

• Cause and how it is sustained

• Treatments(4)

• Riskiest part about this condition

• A condition where the the atria don’t depolarize in one sweeping unit, but instead randomly and simultaneously, also called a type of functional reentry

• This shows up as no clear P-wave and an irregular baseline and random QRS intervals that occur whenever an impulse manages to get to the AV node

• Usually when a small patch of tissue near the pulmonary veins starts firing rapidly on it’s own, causing circuits all over. If there are many circuits, they often can create more, but if there are only a few, they often collide and cause each other to terminate. Whether or not it’s sustained is due to the atrial tissue itself(older age, hypertension, fibrosis, etc. can help it be sustained, aka the substrate)

• Rate-controlling drugs to protect ventricles, shocking to simultaneously activate all the atrial tissues at once(but doesn’t rid the risk), pulmonary vein ablation and forming a ring of burnt tissue that can’t conduct signals to the rest of the atria, similar to a Cox-Maze procedure that cuts the atrial tissue itself to stop further conduction

• Clotting because blood in the atria pools(since the atria is quivering, not contracting)

Atrial Flutter

• What is it/mechanism

• Difference from atrial fibrillation

• Adenosine response

• One single, large organized loop of depolarizations passing thru the cavotricuspid isthmus, which leads to a consistent sawtooth pattern

• Flutter is an anatomical reentry, a loop of depolarizations around a fixed structure(the tricuspid annulus) while fibrillation is functional, due to many wavelets with no fixed path

• Sawtooth appearance remains due to the atria not being touched, but the QRS’ disappear due to the AV block

Paroxysmal Supraventricular Tachycardia(PSVT)

• What is it?

• A umbrella for narrow QRS tachycardias with abrupt onset/termination, with 3 types

AVNRT

• Stands for

• What is it?

• AV Nodal Reentrant Tachycardia

• The AV node has 2 routes, fast but slow refractory, slow impulse but fast refractory. A premature beat will exploit the mismatch to take the refracted slow path and form a loop in the AV node

AVRT

• Stands for

• What is it?

• Found in who?

• AV Reentrant Tachycardia

• Similar beat mismatch being exploited, but this time, the AV node itself is one arm, and an accessory pathway called the Bundle of Kent is another. The impulses usually go down via the bundle of Kent, but in the tachycardia, it goes down the AV node and back up the accessory pathway causing the loop

• Patients with WPW syndrome(Short PR, delta wave, wide QRS; these all show up in their normal state)

  • When the pathology occurs, the impulses travel down the AV node(so the delta wave disappears and QRS looks normal) and up the accessory pathway and looping)

AT

• Stands for

• What is it?

• Atrial tachycardia

• Ectopic atrial location firing repeatedly and triggering the AV node, basically causing tachycardia but from an abnormal spot and working faster

AVNRT and AVRT response to adenosine

• AV node blockage = terminates the arrhythmia

When is a PVC now VT?

When there are 3 or more consecutive PVCs without normal beat in between

Types of VT and their EKGs

1. Monomorphic: One source producing a beat(From the ventricles of course), such as abnormal automaticity in one spot, repetitive trigger activity, or anatomical reentry around an MI scar, or RVOT VT(benign) which leads to a bunch of wide, bizarre QRS’

2. Polymorphic: QRS changes each time due to unstable source, like torsades de Pointes, aka from EAD from prolonged QT

What can ventricular tachycardia degenerate into, and what can happen?

Ventricular fibrillation, which leads to ventricles being unable to contract in coordination → 0 cardiac output → cardiac arrest