Mechanism and Clinical Mechanisms of Cardiac Arrhythmias Flashcards Preview

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Flashcards in Mechanism and Clinical Mechanisms of Cardiac Arrhythmias Deck (39):
1

What is Bradycardia and what does it lead to?

What is Tachycardia and what does it lead to?

 

What do they mean with -arrhythmia

Slow heart rate <60/min potentially leading to a decrease in cardiac
output, hypotension, heart failure and sx (dizziness, syncope,
palpitations)
 

Rapid heart rate >100/min potentially leading to:
• Palpitations (subjective sense of heart beating abnormally)
• Impairment of cardiac output, hypotension, heart failure, ischemia and sx (chest pain, palpitations, dizziness, syncope)

 

 

Bradyarrhthmia and Tachyarrhythmia mean ABNORMAL. Meaning nomral bradycardia found at rest or sleep is not included.

2

  What is supraventricular tachycardia vs. ventricular tachycardia?

What are they called when CHAOTIC?

Abnormal tachycardia which requires participation of either atrial or AV nodal tissue. When chaotic, referred to as atrial fibrillation and NOT svt.

 

Ventricular tachycardia is an abnormal tachycardia originating in the ventricle or his purkinje system. DOES NOT INVOLVE EITHER ATRIUM OR AV NODE. when chaotic called ventricular fibrillation.

3

What is the "Normal gradient of automaticity?"

 

the rate of Sinus Node (60-100/min) > AV Node (50-60/min) >
His-Purkinje System (30-40/min)
 

4

What are "escape" rhythms or pacemakers?

 

Failure of faster structures may allow subsidiary automatic tissues to exhibit automaticity at slower rates
 

remember the normal gradient of automaticity?

Sinus Node (60-100/min) > AV Node (50-60/min) >
His-Purkinje System (30-40/min)

5

What is overdrive suppression?

Quicker pacemaker cells (SPONTANEOUSLY ACTIVE PACEMAKER CELLS) inhibit and suppress slower pacemaker cells (PASSIVELY OVERDRIVEN PACEMAKER CELLS) because by depolarizing the slower pacemaker cells and increasing their intracellular concentration of Na+, you get increased Na+ K+ ATPase transport. This leads to greater hyperpolarization and thus inhibition.

6

What 3 factors regulate the normal automaticity?

1. Rate of diastolic depolarization (mostly If): faster depolarization=faster rate

2. Maximum negative diastolic potential: More negative=slower rate

3. The threshold potential: More negative=Faster rate

7

How does sympathetics affect HR

How does parasympathetics affect HR?

Which dominates at rest?

 

 Sympathetic Effects on Automaticity:
 SN rate is augmented by sympathetic tone
 Beta Stim leads to Increasing the “Open
Probability” of the Pacemaker Current I f. Increases rate of diastolic depolarization.
 Secondarily makes the Threshold Potential More
Negative making it easier to trigger the Ca current.


 Parasympathetic Effects on Automaticity:
 SN rate is depressed by parasympathetic tone
 Decreases the “Open Probability” of the Pacemaker
Current channel I f.
 Secondarily makes Threshold Potential Less
Negative
 Increases probability of acetylcholine sensitive K
channels (IKACh) being open at rest leading to a More
Negative Membrane Diastolic Potential

 

 Parasympathetic tone dominates at rest resulting
in tonic depression of sinus node automaticity.
 

8

What are electrotonic interactions and why is it important?

 

What is the pathologic significance?

due to gap junctions between cells, you get pacemaker cells close to nonpacemaker cells being hyperpolarized (and equivalently the nonpacemaker cells being depolarized). 

 

Why is this important? Automaticity is decreased in pacemaker cells tightly coupled to adjacent working myocardium (at the periphery of the conduction system for example). 

 

In pathologic fibrosis leads to cell decoupling, automacity is enhanced in pacemaker cells normally inhibited by adjacent working myocardium. Thus causing ectopic rhythms by the latent pacemaker tissue

ALSO SA pacemaker cells less coupled to atrial myocytes than AV pacemaker cells. ergo further suppression of the AV pacemaker cells

9

What are

Junctional Escape

Ventricular Escape

Junctional escape: an escape rhythm arising in the AV node. Will have narrow QRS w/o preceding P wave and typically a rate of 40-60/min. Retrograde P may be present (after QRS, inverted inferior leads)

 

Ventricular Escape: an escape rhythm arising in the intranodal tissue. Will have wide QRS. Ventricular escape slower 30-40 bpm, 

10

What are the cellular Tachycardia mechanisms?

Enhanced Automaticity- Increase in rate of tissue normally capable of pacemaker activity (for example sinus tachycardia resulting from administration of catecholamines. eg. AV node)

Abnormal Automaticity- Abnormal impulse formation or automaticity in tissue not normally capable of pacemaker activity. 

Triggered Activity-Single or repetitive cellular activity following a prior action potential. Due to oscillations in membrane potential. Can be EARLY or LATE (afterdepolarizations) EADs or DADs.

11

For EADs and DADs (early afterdepolarizations/late)

What are they?

Promoted by?

Clinical mech?

Early: Membrane oscillations occuring w/in the action potential either in Phase 2 plateau phase or during repolarization phase 3.

Promoted by conditions prolonging the action potential (reflected by QT prolongation on ECG)

Clinical mechanism of Torsades de Pointes Ventricular Tachycardia precipitated by QT prolonging drugs

 

Late: Membrane oscillations occuring after completion of full repolarization phase 4.

Promoted by conditions leading to high intracellular calcium (ie calcium overload). Promoted by catecholamines and inhibited by CA2+ channel blockers

Clinical mech of idiopathic VT. Mech of Digitalis toxicity PVCs and VT

12

What is Long QT syndrome?

Special clinical presentation resulting in early afterdepolarizations.

 

Torsades de pointes.

13

what is reentry?

What are the requirements for reentry?

An abnormal endless loop myocardial propagation and is the primary mech for many pathologic tachycardias.

 

I. 2 distinct paths

II. slowed conduction in at least one path

III. Unidirectional block, tissue capable fo conduction in one but not the opposite direction. such block is often functional and dependent on critical timing creased by an unrelated atrial or ventricular premature beat.

14

What are examples of reentry?

Paroxysmal Supraventricular Tachycardia (SVT)

Figure of Eight Reentry (scar related VT)

Leading Circle Reentry/Rotors (AF and VF)

15

 What is Wolff-Parkinson-White Syndrome (WPW)?

People have additional connection between atrium and ventricle called an accessory pathway or bypass tract. Commonly microscopic fibers spanning the AV groove somewhere along the mitral or triscuspid annuli (bundle of kent).

Accessory pathway tissue conducts impulses faster than the AV node, stimulation of the ventricles during sinus rhythm begins earlier than normal and the PR interval of the ECG shortened also since subsequent spread form accessory pathway tissue is slower, going through ventricular myocardium rather than purkinje system(, you get delta wave a slurred initial upstroke of the QRS complex.

Results in reentrant tachycardia.

16

What is the primary mechanism of ventricular tachycardia in chronic coronary artery disease?

 

How do you cure it?

"Figure of Eight" reentry.

 

Reentry occurs through acquired scar tissue w/ impaired propagation. Upon exiting channel impulses loop around through the normal myocardium like hte loops in a figure 8 to reenter the channel again.

 

Ablate it.

17

Describe a first degree AV block characteristics

Where is the delay?

Causes?

Prognosis?

PR prolonged due to delay between atrial and ventricular depolarization. 

PR> 200ms

1:1 AV relationship

Conduction delay usually w/in AV node

Causes: autonomic, transient AV nodal ischemia, drugs, MI, chronic degenerative disease seen w aging

Prognosis: usually benign and asymptomatic, requiring no specific therapy.

18

Describe a second degree AV block

(Mobitz I Wenkebach)

 

Where is the blockage

Prognosis?

Causes?

 

• PR gradually increases until an
impulse is completely blocked,
after which PR shortens again
to its initial length.
• Conduction is impaired in AV
node.
• Usually benign and
asymptomatic
• Causes include autonomic
tone, acute MI either due to
increased vagal tone or
ischemia AVN.
 

19

Describe a second degree AV block (Mobitz II)

Blockage location?

Prognosis?

Causes?

 

• Sudden intermittent loss of AV
conduction without preceding
gradual PR lengthening.
• Conduction block usually distal
to AVN (His-Purkinje) and QRS
often widened due to His
Purkinje system disease.
• May progress to third degree
AVB without warning, typically
requires pacemaker.

• Results for scar, myocardial
infarct, chronic degenerative
disease of conduction system.
 

20

What is third degree AV block?

What are symptoms?

What is treatment?

Complete failure of conduction between atria and ventricles.

No relationship between P and QRS complexes

 

Symptoms: lightheadedness, syncope, exercise intolerance

Treatment: Permanent pacemaker

21

How are tachyarrhythmias classified?

According to origin

Origin above ventricles including AV NODE!! (supraventricular)

origin within ventricles: (ventricular)

22

What are types of supraventricular arrhthymias?

Describe them.

Sinus tachycardia: Origin SA node. Rate over 100. P and QRS complexes normal in appearance. Results from increased sympathetic or decreased vagal tone. MAy be appropriate or inappropriate.

Atrial Premature Beats/Atrial tachycardia: Automaticity or reentry in an atrial focus outside SA node. Beta blockers often used to treat. usually benign. If automatic focus generates series of consecutive atrial premature beats with resulting HR>100 termed atrial tachycardia

Atrial flutter: Rapid regular atrial activation produced by reentry over a large fixed circuit. (commonly atrial tissue along tricuspid valve annulus. SAW TOOTH PATTERN. Drugs that slow atrial flutter circuit like flecainide may actually promote 1:1 av conduction paradoxically increasing ventricular rate (because the AV node might be able to conduct it now).  May be asymptomatic or assoc w/ palpitations dyspnea weakness or stroke from atrial thrombus.

Atrial Fibrillation: Chaotic rapid rhythm w atrial rates over 400 discharges/min. No distinct P waves. Irregularly irregular rhythm b/c av node refractory. Triggered by rapid firing from atrial foci often localized to atrial muscle extending into pulmonary veins. Sustained by multiple wandering reentrant circuits within the atria. minimum # of circuits required for AF thus enlarged atrium will promote this. 

 

23

Treatment for Atrial flutter?

Rate control: beta blockers, calcium channel blockers, digoxin

Rhythm control: (if greater than 48 hrs need transesophageal echo to rule out left atrial thrombus or 3 wks anticoag prior to conversion. Anticoag continued post cardioversion at least 4 weeks b/c of the delay of recovery of mechanical atrial function)

Electrical cardioverison

Pace termination

Catheter ablation of triscupsid caval isthmus (95% curative)

Antiarrhthmic drug (class I, III agents) for sinus thythm maintenance

24

Clinical consequences and treatment for atrial fibrillation?

Rapid atrial activation results in absence of organized atrial contraction, blood stasis in atrium, thrombus formation especially in left atrial appendage w risk of embolization and stroke. 

 

Treatment: anticoagulation (acute: at time of cardioversion. Chronic: CHADSVasc score)

Rate control OR Restoration Sinus rhythm

Rate control: AV nodal blockade (beta blocker, calcium channel blocker, digoxin)

Restoration Sinus rhythm: Cardioversion (if 48 hrs greater for duration then needs to be preceded by 3 weeks anticoagulation and 4 weeks afterwards or confirm no thrombus by Transesophogeal Echocardiogram). Antiarrhythmic drugs. Catheter ablation.

25

What is AV nodal Reentrant Tachycardia?

In whom does it present?

Acute treatment?

Chronic treatment?

26

CHA2DS2-VASc Score guidelines

 


C Congestive Heart Failure 1 point
H Hypertension 1 point
A2 Age ≥ 75 y 2 points
D Diabetes 1 point
S2 Stroke 2 points
V Vascular disease 1 point
A Age ≥ 65 y 1 point
Sc Sex category, female 1 point


Maximum total score = 9 points.
ESC 2010 Anticoagulation Recommendations: Score = 0 no
therapy or aspirin (no therapy preferred). Score = 1 aspirin or
oral anticoagulation (oral anticoagulation preferred). Score ≥ 2
oral anticoagulation.
 

27

What are the oral anticoags talked about and what is important about them?

Warfarin- Fucks recycling of active form of Vitamin K. Clotting factors II, VII, IX, and X fail to be carboxylated. (S enantiomer more active which is metabolized by CYP 2C9). Polymorphism in the C1 subunit of vitamin K reductase can also affect the susceptibility of the enzyme to warfarin induced inhibition. BLEEDING/BIRTH DEFECTS/ABORTION. Used for prophylaxis and treatment of thromboembolic complications associated with AF and or cardiac valve replacement.

Rivaroxaban/Apixaban(same mech): Selective direct acting factor Xa inhibitor. 1/3 eliminated unchanged by kidneys. 2/3 metabolized by liver and excreted in urine and feces. Dose reduction w decreasing renal fxn. Substrate for Pgp. Hepatotoxicity NOT noted and bleeding lower than other anticoags. Used for prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation.

 

Dabigatran/Bivalirudin(same mech). PRODRUG. Specific reversible direct thrombin inhibitior of free and fibrin bound thrombin. Eliminated from kidney. The prodrug is substrate for Pgp in gut and kidneys (which transports drugs from blood to lumen). BAD FOR RENAIL IMPAIRED PATIENTS. also BAD FOR PT W PROSTHETIC HEART VALVES OR HEMODYNAMICALLY SIGNIFICANT RHEUMATIC VALVULAR HEART DISEASE. Used for preventing stroke and systemic embolism in patients with NONVALVULAR ATRIAL FIBRILLATION.

 

28

What is Atrioventricular Nodal Reentrant Tachycardias?

Acute Treatment?

Chronic Treatment?

EKG?

Most common form of Paroxysmal supraventricular tachycardia

Reentry utilizing 2 AV nodal pathways. Fast(rapid conduction long refractory) and slow (slow conduct and short refractory)

Relies on transient unidirectional block in one pathway and relatively slow conduction in other.Typically anterograde form a to v over slow pathwya and retrograde o reentrant circuit over fast.

Concealed when 

Acute treatment: valsalva maneuvers, adenosine, beta blockers, calcium channel blockers

Chronic treatment: observation, av nodal blockade, catheter ablation targeting slow pathway, Class I and III antiarrhthymic drugs (rarely)

Narrow QRS rapid.

Typical AV Node reentry (Down slow and up fast) show regular tachycardia w nromal width QRS complexes w p waves not apparent b/c retrograde atrial depolarization occuring simultaneously w ventricular depolarization

Atypical AV Node reentry (Down fast and up slow) has inverted p waves in inferior leads.

 

29

What are AV Reentrant Tachycardias and how do they differ from AVNRT?

What is the Wolff-Parkinson-White (WPW) syndrome?

Compared to Nodal, this has reentry utilizing bypass tract or accessory pathway. Which is an abnormal band of muscle cells crossing AV groove. This is in contrast to separate fast and slow pathways within the AV node itself found in AVNRT. AVRT can result in either 1. ventricular pre-excitation syndrome or 2. PSVT resulting from a concealed accessory pathway.

 

WPW (Wolff-Parkinson-White) syndrome is the ventricular pre-excitation with atrial impulses passing in an anterograde direction to the ventricles through both the AV node and the accessory pathway.

Presents w/

1. short PR [lessthan 0.12 sec] (b/c accessory has quick conduction)

2. slurred QRS (because ventricle activation by accessory slow b/c through ventricular activation not HPS.

3. Widened QRS complex b/c represents fusion of 2 excitation wave fronts through ventricles (one from accessory and one from normal HP system).

 

ECG presentations include: Sinus rhythm, Orthodromic AV Reentrant Tachycardia, Antidromic Atrioventricular Reentrant Tachycardia

30

Tratment for WPW?

NOT digoxin, beta blockers, and calcium channel blockers B/C may shorten refractory period of accessory pathways speeding conduction.

USE IV Amiodarone or procainamide, slow accessory pathway conduction

ACUTE: Cardioversion if hemodynamically unstable

Definitive therapy w/ catheter ablation of accessory pathway in symptomatic and high risk patients.

31

What are examples of ventricular arrhythmias?

Premature ventricular beats or contractions (PVC)

Ventricular tachycardia

Ventricular Fibrillation

32

What are PVCs (Premature Ventricular Beats or Contractions)?

EKG?

Complications?

Treatment?

PRoduced by firing of ectopic ventricular focus

Widened QRS b/c impulse originates from ectopic ventricular site and depolarizes ventricles not through the normal rapidly conducting His Purkinje system but via slow cell to cell connection. Either no relationship to P wave or retrograde V-A conduction w/ retrograde P wave inverted in II, III, a VF

If High density PVCs, may produce left ventricular systolic dysfunction, which may be reversible with suppression of PVCs medically or w ablation

Primary therapy is observation and at times beta blockers

33

What is Ventricular Tachycardia?

Series of 3 or more PVCs

 

34

Wide complex tachycardia is going to be...?

Ventricular tachycardia most of the time. Technically can also present in supraventricular tachycardia but we don't need to know about this yet.

35

36

What is Torsades de Pointes?

Specific form polymorphic VT presenting w varying amplitudes of QRS as though complexes twisting about baseline. 

Mechanism is triggered activity, early afterdepolarizations.

Observed in patients w QT prolongation either due to drugs, bradycardia, electrolyte metabolic disturbances or hereditary abnormality of ion channels.

 

• Acute treatment: cardiovert sustained VT to restore sinus rhythm,
IV magnesium, correct underlying abnormalities (stop offending
drugs), elevate heart rate and thus shorten QT either with beta
agonists (isoproterenol) or pacing.
• Chronic treatment: correct underlying triggers. If congenital long QT
consider beta blocker and ICD.

37

What are the potential mutations causing congenital Long QT syndrome?

 

Type Gene Protein Mechanism Prolong APD Inheritance
LQT1 KCNQ1 KvLQT1(I Ks) Decrease outward K+ AD and AR
LQT2 KCNH2 HERG(I Kr) Decrease outward K+ AD
LQT3 SCN5A Nav 1.5 Increase inward Na+ AD
 

38

Management of Ventricular Tachycardia?

Sustained VT is potentially life threatening and may degenerate to ventricular fibrillation or assoc w hemodynamic collapse.

Acute therapy in unstable patient: electrical cardioversion

Acute therapy in stable patient: antiarrhythmic drugs (amiodarone, lidocaine) or sedate/cardiovert

After sinus rhythm restored look for structural heart disease and correct aggravating factor.

Long term consider implantable cardioverter defibrillator (ICD) for secondary prevention and potentailly need for antiarrhythmic drugs or VT ablation

39

Describe Ventricular Fibrillation?

Immediately life threatening

Occurs typically in setting of severe underlying heart disease or acute ischemia

Untreated leads to death

RX: immediate electrical defibrillation and then look for cause. consider IV amiodarone

Survivors usuallyr eceive ICD unless reversible cause identified such as acute myocardial infarctions