Pathophysiology part 2 Common clinical arrhythmias & mechanisms

Ventricular tachyarrhythmias

below the bundle of his, (Abnormal, widened qrs)

Based on the following 12-lead ECG, which is the most likely diagnosis? A. Atrial premature contraction B. Multifocal atrial tachycardia C. Junctional tachycardia D. Atrial flutter E. Paroxysmal atrial tachycardia

d

Based on the following 12-lead ECG, which is the most likely diagnosis? A. Normal ECG B. Sinus tachycardia C. Ventricular escape beats D. Sinus bradycardia E. Junctional escape beats

d

Brugada syndrome treatment

Prevent SCD with implantable cardioverter-defibrillator (ICD)

Accelerated Idioventricular Rhythm ekg

Rate: 50 - 100 usually (usually slow) P wave: Obscured by ventricular waves (occur during ventricular contraction) - SA node slower than faster ventricular pacing than should be QRS: Wide QRS Conduction: Ventricular only Rhythm: Regular - benign rhythm that is sometimes seen during acute MI or early after reperfusion. - Rarely sustained, does not progress to vfib, rarely requires treatment

Atrial Flutter

Rate:Atrial 250-350 Ventricular: 100 -175 P: Irregular or absent, often "saw tooth" QRS: Normal Conduction: AV Block (2:1 > 3:1, 4:1) Rhythm: Regular (usually) - Often underlying cardiac disease Carotid massage: increases block

Atrial flutter pathophysiology

Results from circuit re-entry and AV node failing to conduct impulses to the ventricles, which in turn contract slower. AV node usually won't accept more than 180 impulses per min, so every second or third impulse is conducted. Cavotricuspid isthmus: between the IVC and the TV (common area of reentry)

Based on the following 12-lead ECG, which is the most likely diagnosis? A. Sinus tachycardia B. Ventricular tachycardia C. Atrial fibrillation D. Paroxysmal Supraventricular Tachycardia (PSVT) E. Atrial tachycardia

a. Incorrect. There are no sinus P wave. b. Incorrect. Not ventricular tachycardia. c. Incorrect. It is not atrial fibrillation. d. Correct. Regular narrow QRS tachycardia, no visible P waves. AV nodal re-entrant tachycardia (AVNRT) makes up 56% of cases[5] AV reciprocating tachycardia (AVRT) makes up 27% of cases[5]Wolff-Parkinson-White syndrome[3] Paroxysmal atrial tachycardia makes up 17% of cases[5] e. Incorrect. It is not atrial tachycardia.

Based on the following 12-lead ECG, which is the most likely diagnosis? A. Atrial premature contraction B. Atrial flutter C. Ventricular tachycardia D. Atrial fibrillation E. Atrial tachycardia

d. Correct- irregular atrial fibrillation wave (best seen in lead V1 and lead II), irregularly irregular RR intervals.

Brugadna syndrome how and common in who

diminished inward sodium current, particularly in RVOT epicardium, resulting in epicardial dispersion of repolarization Autosomal dominant disorder most common in Asian males. Risk of ventricular tachyarrhythmias and SCD. .

Catecholaminergic polymorphic VT mechanism and main effect

due to leaky cardiac ryanodine receptor (RyR2)-delayed after depolarization genetic disorders of Ca++ release channels (RyR2) and their controlling proteins (ryanodine receptor and calquestrin) Structurally normal heart RyR2 dysfunction is usually worsened by sympathetic excitation like exercise or acute emotion

Supraventricular tachycardia

rate varies btwn 160-250 bpm, regular rhythm, originates from a location above AV node, will start and stop w/o cause. common causes: mitral valve prolapse, cor pulmonale, digitalis toxicity, and rheumatic heart disease

Based on the following 12-lead ECG, which is the most likely diagnosis? A. Normal ECG B. Sinus tachycardia C. Ventricular tachycardia D. Sinus bradycardia E. Junctional tachycardia

b

Atrioventricular Junctional Tachycardia (cause)

enhanced normal automaticity, abnormal automaticity or TA (digitalis toxicity)

Jervell and Lange-Nielsen syndrome

-Congenital/inheritied long QT syndrome -Autosomal recessive, sensorineural deafness

Romano-Ward syndrome

-Congenital;inheritied long QT syndrome -Autosomal dominant, pure cardiac phenotype (no deafness).

Bradyarrhythmias (2 common ways)

1.Failure of impulse generation (decreased automaticity) -sinus bradycardia or arrest SSS 2. Failure of impulse propagation (conduction block) -Sino-atrial block -AV block

monomorphic ventricular tachycardia causes

1.Structural heart disease- predominant reentry ischemic cardiomyopathy non-ischemic cardiomyopathy arrhythmogenic RV dysplasia 2. Structurally normal hearts- Idiopathic VT a. Outflow tract tachycardia-TA b. Fascicular ventricular tachycardia-reentry

A fib common trigger

4. Atrial Fibrillation üThe most common clinically significant arrhythmia üMost often initiated (triggered) by rapid firing from the PV (PV isolation is used to cure AF) -triggers (ectopic foci, abnormal automaticity, TA) and -substrate (remodeled atria for multiple reentries).

AVNRT

AVNRT occurs when a reentrant circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node. ØDual pathway AVN electrophysiology ØSP ablation to cure AVNRT

AIVR Explained

Accelerated idioventricular rhythm is a ventricular rhythm with a rate of between 40 and 120 beats per minute. Idioventricular means "relating to or affecting the cardiac ventricle alone" and refers to any ectopic ventricular arrhythmia.[1] Accelerated idioventricular arrhythmias are distinguished from ventricular rhythms with rates less than 40 (ventricular escape) and those faster than 120 (ventricular tachycardia).[2] Though some other references limit to between 60 and 100 beats per minute.[3] It is also referred to as AIVR and "slow ventricular tachycardia." It can be present at birth.[4] However, it is more commonly associated with reperfusion after myocardial injury.[2] AIVR is generally considered to be a benign abnormal heart rhythm. It is typically temporary and does not require treatment.

Afib vs Aflut

Afib: Ventricular rate is erratic and atrial waves not identical Aflutter: Identical atrial waves AFib In AFib, the two top chambers of your heart (atria) receive disorganized electrical signals. (from other places) The atria beat out of coordination with the bottom two chambers of your heart (ventricles). This leads to a rapid and irregular heart rhythm. A normal heart rate is 60 to 100 beats per minute (bpm). In AFib, the heart rate ranges from 100 to 175 bpm. Atrial flutter In atrial flutter, your atria receive organized electrical signals, but the signals are faster than normal. The atria beat more frequently than the ventricles (up to 300 bpm). Only every second beat gets through to the ventricles. The resulting pulse rate is around 150 bpm. Atrial flutter creates a very specific "sawtooth" pattern on a diagnostic test known as an electrocardiogram (EKG). (reentry)

capvt explained

Alterations to the proteins involved in excitation-contraction coupling can disrupt this carefully regulated process. In those with CPVT, the normally tight regulation of calcium can become deranged, leading to arrhythmias.[9] While calcium is generally released from the sarcoplasmic reticulum in response to an action potential, calcium sparks can also occur spontaneously. In a healthy heart, a spontaneous calcium spark is generally an isolated event and goes no further, but if ryanodine receptors or the proteins that regulate them are abnormal, these sparks can trigger releases from neighbouring ryanodine receptors which spread throughout the cell as a calcium wave.[9] These calcium waves are much more likely to occur when cardiac muscle cells are stimulated by catecholamines such as adrenaline, which increase the concentration of calcium within the sarcoplasmic reticulum and sensitise the ryanodine receptors.[12] The uncontrolled wave of calcium can be forced out through the cell membrane via the sodium-calcium exchanger, causing an electric current known as a delayed afterdepolarisation. Afterdepolarisations, if large enough, can trigger additional action potentials, premature ventricular contractions, or sustained arrhythmias.[13]

avrt

Atrioventricular reentrant tachycardia (AVRT), or atrioventricular reciprocating tachycardia, is a type of abnormal fast heart rhythm and is classified as a type of supraventricular tachycardia (SVT). AVRT is most commonly associated with Wolff-Parkinson-White syndrome, in which an accessory pathway allows electrical signals from the heart's ventricles to enter the atria and cause earlier than normal contraction, which leads to repeated stimulation of the atrioventricular node.[1]

Polymorphic vt causes (syndromes)

Cardiac channelopathies 1. Long-QT syndrome 2. Brugada syndrome 3. Short QT syndrome 4. CPVT

Cardioversion vs Defibrillation

Cardioversion: in sync with QRS, used in AFib, atrial flutter, VT w/ a pulse, SVT Defibrillation: not in sync with QRS, used in VFib and VT without a pulse Defibrillation: VF, Synchronizer off, deliver immediately, require higher energy Cardioversion: Other tachyarrhythmias, such as AF, PSVT or VT. Synchronizer on (with R wave). Avoiding peak of T wave (why?)

Monomorphic VT

In monomorphic ventricular tachycardia, the shape of each heart beat on the ECG looks the same because the impulse is either being generated from increased automaticity of a single point in either the left or the right ventricle, or due to a reentry circuit within the ventricle. The most common cause of monomorphic ventricular tachycardia is scarring of the heart muscle from a previous myocardial infarction (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit around the scar that results in the tachycardia. This is similar to the re-entrant circuits that are the cause of atrial flutter and the re-entrant forms of supraventricular tachycardia. Other rarer congenital causes of monomorphic VT include right ventricular dysplasia, and right and left ventricular outflow tract VT.

Inherited LQT

Inheritied is obvious Outward K+ currents down Inward Na+ or Ca++ currents up LQT1-IKs LQT2-Ikr LQT3-INa LQT4,5.... Acquired is genetic In some apparent healthy people may have some subtle genetic defects

Acquired LQT syndrome ABCDE (names of dieseases or illnesses)

Drug-induced long QT (ABCDE): AntiArrhythmics (class IA, III) AntiBiotics (e.g., macrolides) Anti"C"ychotics (e.g., haloperidol) AntiDepressants (e.g., TCAs) AntiEmetics (e.g., ondansetron)

Brugada syndrome ekg

ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3.

atrial fibrillation ecg

ECG shows "irregularly irregular" baseline;p waves are indistuginshable; irregularly spaced QRS waves (treat with beta blocker, Ca++ blocker, or warfarin for thromboembolism prophylaxis) (irregular r-r intervals)

Acquired LQT syndrome mechanism

Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG; can progress to ventricular fibrillation. Long QT interval predisposes to torsades de pointes. Caused by drugs, ↓K+, ↓ Mg2+, other abnormalities. Treatment includes magnesium sulfate.

Polymorphic VT explained

Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization. The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval. QT prolongation may be congenital or acquired. Congenital problems include long QT syndrome and catecholaminergic polymorphic ventricular tachycardia. Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischemia. Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic. Other relatively common drugs including some antibiotics and antihistamines may also be a danger, in particular in combination with one another. Problems with blood levels of potassium, magnesium and calcium may also contribute. High-dose magnesium is often used as an antidote in cardiac arrest protocols.

Atrial Fibrillation pathophysiology

Stems from the firing of a number of impulses in circuit re-entry. Atrial kick is lost due to atrial quiver instead of contraction, resulting in a significant reduction of cardiac output. Ventricles only respond to impulses that make it through the AV node which prevents the ventricles form the 400-600/min erratic impulses.

Tachyarrhythmias (Automaticity, TA, or reentry) Supraventricular tachyarrhythmias (His & above) (Normal narrow-QRS) (3 common causes)

Supraventricular tachyarrhythmias (His & above) (Normal narrow-QRS) 1. Sinus Tachycardia: -enhanced normal automaticity 2. Atrial premature beat or Atrial tachycardia: -automaticity, TA, or reentry 3. Atrial Flutter: macroreentry

Long QT syndrome explained

The various forms of long QT syndrome, both congenital and acquired, lead to a tendency to abnormal heart rhythms through their effects on the electrical signals used to coordinate individual heart cells. The common theme linking the various causes is a prolongation of the cardiac action potential - the characteristic pattern of voltage changes across the cell membrane that occur with each heart beat.[8] Heart cells when relaxed normally have fewer positively charged ions on the inner side of their cell membrane than on the outer side, referred to as the membrane being polarised. When heart cells contract, positively charged ions such as sodium and calcium enter the cell, equalising or reversing this polarity, at which point the cell is said to be depolarised. After a contraction has taken place, the cell restores its polarity (or repolarises) by allowing positively charged ions such as potassium to leave the cell, restoring the membrane to its relaxed, polarised state. In long QT syndrome it takes longer for this repolarisation to occur, shown in individual cells as a longer action potential while being marked on the surface ECG as a long QT interval.[8] The prolonged action potentials can lead to arrhythmias through several potential mechanisms. The characteristic arrhythmia seen in long QT syndrome, Torsades de Pointes, starts when additional action potentials occur after an initial triggering beat in the form of afterdepolarisations. Early afterdepolarisations, occurring before the cell has fully repolarised, are particularly likely to be seen when action potentials are prolonged, and arise due to reactivation of calcium and sodium channels that would normally switch off until the next heartbeat is due.[27] Under the right conditions, reactivation of these currents, facilitated by the sodium-calcium exchanger, can cause further depolarisation of the cell.[27] The early afterdepolarisations triggering arrhythmias in long QT syndrome tend to arise from the Purkinje fibres of the cardiac conduction system.[28] Early afterdepolarisations may occur as single events, but may occur repeatedly leading to multiple rapid activations of the cell.[27] long aps lead to being depolarized longer and a higher chance of another early depolarization happening like in torsade de ponte EAD is the major issue Inherited disorder of myocardial repolarization, typically due to ion channel defects; risk of sudden cardiac death (SCD) due to torsades de Pointes (TDP).

Short QT syndrome

There is a short QT interval (<330 ms) on a 12-lead ECG. Tall peaked T waves. Sudden death due to ventricular tachycardia or ventricular fibrillation Due to increases IK+ chanels in phase 2 or 3

Based on the following 12-lead ECG, which is the most likely diagnosis? A. Ventricular tachycardia B. Ventricular fibrillation C. Atrial flutter D. Atrial tachycardia E. Sinus tachycardia

a

Ventricular premature beats (causes and ekg)

wide QRS complexes; MC arrhythmia in coronary care unit (have extra premature beat in ventricles) abnormal automaticity, TA or reentry

Catecholaminergic polymorphic VT tx

β-blocker therapy

Wolf-Parkinson-White Syndrome (how and why)

∙Wolff-Parkinson-White syndrome: Most common type of ventricular preexcitation syndrome. Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node → ventricles begin to partially depolarize earlier → characteristic delta wave with widened QRS complex and shortened PR interval. May result in reentry circuit → supraventricular tachycardia. most common type of avrt Type of avrt (acsessory pathway) cured by abalation