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Cardio > Arrhythmias (and some cardiomyopathy/pericarditis) > Flashcards

Arrhythmias (and some cardiomyopathy/pericarditis) Flashcards

1
Q

focal vs reentrant arrhythmias

A

focal: myocytes develop automaticity with rapid rates and override normal sinus rhythm

reentrant: scar from myocardial infarction produces conduction slowing and block that leads to re-entrant arrhythmias

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2
Q

abnormal impulse generation vs abnormal impulse conduction of arrhythmias

A

abnormal impulse generation: increased/decreased normal automaticity, enhanced automaticity of latent pacemakers, triggered activity (early/delayed afterdepolarizations)

abnormal impulse conduction: decremental conduction and block, reentry

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3
Q

how does administration of epinephrine or ACh change the action potential curve of the SA node, respectively?

A

epinephrine increases the slope of phase 4 slow (funny current - Na+) depolarization —> shorter time to AP

ACh decreases the slope of phase 4 funny current depolarization —> longer time to AP

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4
Q

how do myocytes that don’t normally exhibit automaticity develop abnormal automaticity?

A

when cells that don’t normally exhibit automaticity are triggered to depolarizes, they may develop automaticity (abnormal automaticity) - may occur with myocardial ischemia

their AP curve would begin to show phase 4 slow depolarization (funny current - Na+)

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5
Q

how do early or delayed afterdepolarizations occur?

A

triggered activity = impulse initiation dependent on afterdepolarizations, which are oscillations in membrane potential that follow the primary depolarization (phase 0)

early: occur during repolarization
delayed: occur after repolarization

when afterdepolarizations begin to overlap with primary depolarizations, AP curves become wider and arrhythmias can occur

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6
Q

what is Torsade de Pointes caused by and what is the clinical consequence of this condition

A

Torsade de Pointes: prolongation of QT interval (usually by drugs), associated with development of ventricular arrhythmia

early afterdepolarization (triggered activity) is more likely to develop in conditions when AP is prolonged (more calcium influx occurring) —> arrhythmia

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7
Q

what is thought to be responsible for ventricular arrhythmias associated with digitalis toxicity?

A

delayed afterdepolarizations/DADs (triggered activity) are oscillations in membrane potential that follow the primary repolarization

pacing at faster rates increases amplitude of DADs as they being to overlap primary depolarization - when they reach threshold they may begin spontaneous repetitive depolarizations —> arrhythmia

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8
Q

what is “decremental conduction” caused by?

A

decremental conduction: phenomenon in which conduction velocity through AV node decreases as AV node is stimulated at faster rates

this is because AV node is principally dependent on slow inward calcium current (when pace gets too fast, it can’t keep up)

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9
Q

an electrical impulse or wavefront that circulates repeatedly around the same pathway, recurrently depolarizing a region of cardiac tissue

what is?

A

re-entrant excitation: common mechanism of tachyarrhythmias

conduction block (due to refractory tissue) and slow conduction are necessary for reentry to be induced

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10
Q

brady-tachy syndrome

A

resting sinus bradycardia with periods of supraventricular tachycardia often followed by sinus pauses or sinus arrest

because there are periods of both brady- and tachy-cardia, a pacemaker has to be put in before beta blockers are given so bradycardia is not exacerbated

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11
Q

how do atrial premature complexes (APCs) typically appear on ECG?

A

APC/PAC (premature atrial contraction, same thing) are usually followed by normally conducted narrow QRS, but when APC are very premature they may fail to conduct to the ventricles (dropped QRS) or conduct with aberrantly conducted complex due to bundle block

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12
Q

how does acute vs chronic treatment for atrial fibrillation differ?

A

acute: beta blockers and calcium-channel blockers (slow AV conduction), anticoagulation (risk of thrombus dislodgment), cardioversion

chronic: beta blockers and calcium channel blockers, anticoagulation, rhythm control by antiarrhythmic drugs (Class I-C or Class III) or ablation

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13
Q

where is catheter ablation done to treat atrial fibrillation?

A

around the pulmonary veins (want to isolate them)

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14
Q

sudden onset and termination of heart rates between 140 and 250bpm with narrow (normal) QRS complexes

what is

A

paroxysmal supraventricular tachycardia (PSVT)

usually due to AV nodal reentrant tachycardia (60%), AV reentrant tachycardia (30%), or atrial tachycardia (focal or reentrant, 10%)

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15
Q

what usually causes paroxysmal supraventricular tachycardia (PSVT)

A

paroxysmal supraventricular tachycardia (PSVT): sudden onset and termination of heart rates between 140 and 250bpm with narrow (normal) QRS complexes

~60% due to AV nodal reentrant tachycardia (AVNRT)

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16
Q

AVNRT vs AVRT

A

AVNRT = AV nodal reentrant tachycardia (within the node), confined to atria

AVRT: atrioventricular reentrant tachycardia (downstream of the node), includes ventricles - these are faster than AVNRTs generally

treatment for both is ablation of bypass tract

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17
Q

what are the ECG manifestations of ventricular pre-excitation (WPW)? (3)

A
  1. short PR interval
  2. wide QRS
  3. delta wave - slurring of first portion of QRS, due to second pathway of earlier impulse

stimulate ventricle in 2 places, which fuse (fast delta wave, then delayed AV node)

[WPW = Wolff-Parkinson-White]

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18
Q

what cardiac electrical abnormality does this describe?
rate >100bpm, P waves preceding each QRS but with abnormal morphology from sinus rhythm, with sudden termination of conduction

A

atrial tachycardia: does NOT require AV node, can be focal (automatic) or reentrant

(abnormal P waves indicate not sinus rhythm)

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19
Q

how effective will adenosine be for AVNRT, AVRT, and atrial tachycardia, respectively?

A

AVNRT and AVRT: reentry, both require AV node as part of circuit

atrial tachycardia (AT): focal or reentrant, does NOT require AV node

adenosine: slows conduction in AV node - terminates AVNRT/AVRT, but AT will continue (will give you diagnosis of what is causing PSVT/paroxysmal supraventricular tachycardia)

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20
Q

a patient’s ECG shows supraventricular tachycardia at a rate of about 150bpm with a 2:1 block - what should you be thinking?

A

atrial flutter

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21
Q

how can carotid massage break cardiac arrhythmia?

A

pressing on carotid massage will activate high pressure baroreceptors and cause an increase in vagal tone

slowing AV node can break arrhythmias

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22
Q

If a patient is presenting with supraventricular tachyarrhythmia, they will either show a regular or an irregular rhythm. What are the possible causes of SVT with irregular rhythm (2) vs regular rhythm (4)?

A

SVT with irregular rhythm:
1. multifocal atrial tachycardia
2. atrial fibrillation (no P waves)

SVT with regular rhythm:
1. sinus tachycardia
2. reentrant SVTs (AVNRT or ARVT)
3. focal atrial tachycardia (abnormal P waves - not sinus)
4. atrial flutter (saw-tooth)

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23
Q

how do ventricular premature complexes appear on ECG, and why?

A

premature and wide QRS - because impulse travels from ectopic site through the ventricles via slow cell-to-cell connection rather than fast conducting His-Purkinje system

ectopic complex is not related to preceding P wave

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24
Q

how does Torsade de Pointes ventricular tachycardia appear on ECG?

A

polymorphic VT with “twisting of the points”

all Torsade is polymorphic, but not all polymorphic VT is Torsade

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25
Q

what is an ICD device

A

implantable cardioverter defibrillator: can detect fibrillation and intervene automatically

26
Q

what is narrow QRS tachycardia vs wide QRS tachycardia usually attributed to?

A

narrow QRS tachycardia = supraventricular (SVT)

wide QRS tachycardia is either ventricular tachycardia or SVT with aberrancy (such as pre-existing or functional bundle branch block)

[functional BBB = block only induced by high rates]

27
Q

how does congenital long QT syndrome present? what is it caused by?

A

congenital long QT syndrome: ion channel mutation

presents with syncope, sudden cardiac death

precipitated by swimming, auditory stimuli, drugs that interfere with repolarization, hypokalemia

treat with beta-blockers or ICD

28
Q

how does Brugada syndrome appear on ECG?

A

Brugada syndrome: genetic arrhythmogenic disorder, predisposes to ventricular arrhythmias and sudden cardiac death, more common in males

ST elevation with inverted T waves

29
Q

what causes familial catecholaminergic polymorphic ventricular tachycardia?

A

mutation in calcium ryanodine receptor —> causes delayed afterdepolarization (DAD)

presents with stress-induced syncope or sudden cardiac death in patients with normal ECGs and no structural heart disease

treat with beta-blockers or ICD

30
Q

what manifests from arrhythmogenic right ventricular cardiomyopathy?

A

genetic mutation in desmosome proteins leads to progressive replacement of RV myocardium with fatty and fibrous tissue

causes ventricular arrhythmias originating in RV

31
Q

what is the most common arrhythmia and how is it treated?

A

atrial fibrillation - treat with anticoagulation for prevention of strokes (always) and either rate control (AV nodal block) or rhythm control (Class I or III antiarrhymthic drug or ablation)

32
Q

how can adenosine be used both therapeutically and diagnostically?

A

adenosine causes transient AV nodal block

therapeutic for terminating AVNRT or AVRT (both require AV node in their circuit)

diagnostic for atrial tachycardia or atrial flutter (which do not require AV node)

33
Q

how do premature atrial contractions (PAC) appear on ECG?

A

PACs arise from atria, but not in SA node —> ECG shows early P waves that differ in morphology from normal sinus P wave

QRS complex is normal because conduction below the atria is normal

treat with beta blockers if symptomatic

34
Q

how do premature ventricular contractions (PVCs) appear on ECG?

A

PVCs arise from focus in ventricle that spread to other ventricle

appear as wide and bizarre looking QRS, followed by compensatory pause

P waves are not seen because they are buried in the wide QRS

treat with beta blockers if symptomatic

35
Q

what is the preferred drug management for acute atrial fibrillation?

A
  1. rate control with beta blocker (calcium channels as alternative)

if LV systolic dysfunction is present:
2. rhythm control with digoxin or amiodarone

  1. anticoagulants
36
Q

differentiate where automaticity originates in a-fib vs a-flutter

A

atrial fibrillation is due to firing of multiple atrial foci continuously in chaotic pattern (irregularly irregular) - triggered usually at pulmonary veins

atrial flutter is due to one irritable automaticity focus in atria, giving rise to regular atrial contractions - triggered usually between tricuspid valve and IVC

37
Q

which leads are best to look for saw-took ECG pattern of atrial flutter?

A

inferior leads: II, III, aVF

38
Q

what defines multifocal atrial tachycardia? how can it be diagnosed?

A

multifocal atrial tachycardia: variable P wave morphology and variable PR and RR intervals - at least 3 different P wave morphologies are required to make diagnosis

use of vagal maneuvers or adenosine can also be used for diagnosis because they will cause AV block without disrupting the atrial tachycardia (will have no effect on the multiple foci because they are not sinus)

39
Q

multifocal atrial tachycardia vis wandering atrial pacemaker

A

multifocal atrial tachycardia: variable P wave morphology and variable PR and RR intervals - at least 3 different P wave morphologies are required to make diagnosis

wandering atrial pacemaker: same thing, but heart rate is between 60 and 100bpm (not tachycardic)

40
Q

what is the most common arrhythmia associated with digoxin toxicity?

A

paroxysmal atrial tachycardia with 2:1 block

41
Q

what is the treatment for paroxysmal supraventricular tachycardia (AVNRT, AVRT)?

A

maneuvers that stimulate vagus delay AV conduction and block reentry: Valsalva, carotid sinus, head immersion in cold water

pharmacological: adenosine is DOC due to short direction of action (decreases SA/AV nodal activity)

42
Q

how is ventricular tachycardia defined?

A

v-tach: rapid/repetitive firing of 3 or more PVCs (premature ventricular contractions) in a row, at a rate between 100 and 250bpm

AV dissociation is present - sinus P waves continue with their cycle

monomorphic or polymorphic wide/bizarre QRS complexes

43
Q

how does ventricular tachycardia present? (key findings)

A

v-tach: rapid/repetitive firing of 3 or more PVCs (premature ventricular contractions) in a row, at a rate between 100 and 250bpm (appears as wide/bizarre QRS complexes)

cannon A waves in the neck, secondary to AV dissociation - atrial contraction occurring during ventricular contraction

palpitations, dyspnea, angina, syncope

44
Q

what type of arrhythmia is associated with cannon A waves?

A

cannon A waves in the neck due to AV dissociation, resulting in atrial contraction during ventricular contraction

classically seen with ventricular tachycardia

45
Q

dilated cardiomyopathy vs hypertrophic cardiomyopathy vs restrictive cardiomyopathy vs myocarditis

A

dilated: ventricular chambers are big - caused by CAD (post MI), alcohol, Chaga’s disease, hyper/hypothyroidism, peripartum, catecholamines, others

hypertrophic: AD mutation causes hypertrophy, notably in IV septum which causes outflow obstruction - systolic ejection murmur intensity increases with LESS volume in the heart

restrictive: myocardial infiltration decreases ventricular compliance, normal RV/LV size but massive RA/LA - caused by amyloids, chemotherapy/radiation, hemochromatosis, others

myocarditis: myocardial inflammation - caused by virus (Coxsackie), idiopathic, others

46
Q

what kind of cardiomyopathy with Chaga’s disease cause?

A

dilated cardiomyopathy

47
Q

what kind of cardiomyopathy will amyloidosis cause?

A

restrictive cardiomyopathy

48
Q

what kind of cardiomyopathy will excessive alcohol use cause?

A

dilated cardiomyopathy

49
Q

what kind of cardiomyopathy can chemotherapy or radiation cause?

A

restrictive cardiomyopathy

50
Q

when a patient presents with chest pain that is pleuritic, localized to the retrosternal and left precordial regions btu radiating to the trapezius ridge and neck, what are you thinking?

A

acute pericarditis - pain will also be relieved by sitting up and leaning forward, and pericardial friction rub (3 component) will usually be present

[pleuritic means it is associated with breathing - differentiates from MI]

51
Q

how does ECG appear for acute pericarditis?

A

diffuse ST elevation with PR depression

52
Q

what do the following signs collectively indicate: JVD, prominent x and y descents, Kussmaul’s sign, pericardial knock

A

constrictive pericarditis: fibrous scarring of pericardium constricts diastolic filling of the heart

JVD: most prominent physical finding
prominent x and y descents: blood rushing out quickly from atria
Kussmaul’s sign: right atrial pressure does NOT decrease with inspiration (no room for the blood)
pericardial knock: think of heart with constrictive pericarditis as being in a box - it can expand until it hits the walls (knocks on the box!)

53
Q

in which pericardial disease will there be prominent x and y descents, and in which will there be loss of y descent?

A

constrictive pericarditis: fibrous scarring of pericardium constricts diastolic filling of the heart —> prominent x and y descents: blood rushing out quickly from atria

cardiac tamponade: accumulation of pericardial fluid is squeezing heart —> loss of y descent: high atrial pressure

54
Q

what do these signs collectively indicate: JVD, loss of y descent, narrow pulse pressure, pulsus paradoxus, muffled heart sounds

A

cardiac tamponade: accumulation of pericardial fluid is squeezing heart

JVD: most common finding
loss of y descent: pressure is too high in atria for pressure to go down
narrow pulse pressure: due to decreased SV
pulsus paradoxus: exaggerated decrease in arterial pressure during inspiration - pulse gets strong during expiration and weak during inspiration
muffled heart sounds: the heart is under water! (fluid)

55
Q

how can paroxysmal supraventricular tachycardia be differentiated from sinus tachycardia by the way it presents?

A

sinus tachycardia will come on/ fade gradually - response to problem OUTSIDE the heart

paroxysmal supraventricular tachycardia (AVNRT or AVRT) will have SUDDEN onset and termination - most commonly due to reentry

56
Q

what is the DOC for terminating PSVT?

A

adenosine! t1/2 of only a few seconds, effect on AV node is identical to that of Ach (effects K+ channels for fast hyperpolarization!)

PSVT = paroxysmal supraventricular tachycardia

57
Q

what is the most common type of PSVT and what is the mechanism of it? who is usually affected?

A

PSVT (paroxysmal supraventricular tachycardia) is either AVNRT or AVRT (aka WPW)

AVNRT is more common (60%+) and affects F>M

mechanism: dual AV nodal pathways, a fast and slow - the slow pathway conduction blocks when it hits the fast one, allowing it to turn around on the fast side and create reentry (when a premature atrial depolarization occurs)

58
Q

where is atrial flutter vs fibrillation triggered anatomically?

A

atrial flutter: reentrant circuit in RA around perimeter of tricuspid valve

atrial fibrillation: ectopic firing around/within pulmonary veins

59
Q

what is the usual cause of monomorphic vs polymorphic ventricular tachycardia?

A

monomorphic: usually due to reentry (requires unidirectional block + slow conduction)

polymorphic: usually due to long QT

60
Q

prolonged QT intervals and early afterdepolarizations (EADs) put patients at major risk for…

A

Torsades des Pointes

61
Q

what would LOF vs GOF mutation in Phase 0 voltage-dependent Na+ channels cause?

A

LOF: Brugada Syndrome (AD): mutation in only certain regions of heart, causing out of sync firing —> arrhythmias and reentry (cells don’t depolarize properly so they repolarize early) —> increased risk of ventricular arrhythmias and sudden cardiac death

GOF: long QT syndrome

Cardio (39 decks)

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