Arrhythmias (and some cardiomyopathy/pericarditis) Flashcards
focal vs reentrant arrhythmias
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
abnormal impulse generation vs abnormal impulse conduction of arrhythmias
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
how does administration of epinephrine or ACh change the action potential curve of the SA node, respectively?
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
how do myocytes that don’t normally exhibit automaticity develop abnormal automaticity?
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+)
how do early or delayed afterdepolarizations occur?
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
what is Torsade de Pointes caused by and what is the clinical consequence of this condition
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
what is thought to be responsible for ventricular arrhythmias associated with digitalis toxicity?
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
what is “decremental conduction” caused by?
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)
an electrical impulse or wavefront that circulates repeatedly around the same pathway, recurrently depolarizing a region of cardiac tissue
what is?
re-entrant excitation: common mechanism of tachyarrhythmias
conduction block (due to refractory tissue) and slow conduction are necessary for reentry to be induced
brady-tachy syndrome
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
how do atrial premature complexes (APCs) typically appear on ECG?
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
how does acute vs chronic treatment for atrial fibrillation differ?
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
where is catheter ablation done to treat atrial fibrillation?
around the pulmonary veins (want to isolate them)
sudden onset and termination of heart rates between 140 and 250bpm with narrow (normal) QRS complexes
what is
paroxysmal supraventricular tachycardia (PSVT)
usually due to AV nodal reentrant tachycardia (60%), AV reentrant tachycardia (30%), or atrial tachycardia (focal or reentrant, 10%)
what usually causes paroxysmal supraventricular tachycardia (PSVT)
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)
AVNRT vs AVRT
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
what are the ECG manifestations of ventricular pre-excitation (WPW)? (3)
- short PR interval
- wide QRS
- 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]
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
atrial tachycardia: does NOT require AV node, can be focal (automatic) or reentrant
(abnormal P waves indicate not sinus rhythm)
how effective will adenosine be for AVNRT, AVRT, and atrial tachycardia, respectively?
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)
a patient’s ECG shows supraventricular tachycardia at a rate of about 150bpm with a 2:1 block - what should you be thinking?
atrial flutter
how can carotid massage break cardiac arrhythmia?
pressing on carotid massage will activate high pressure baroreceptors and cause an increase in vagal tone
slowing AV node can break arrhythmias
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)?
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)
how do ventricular premature complexes appear on ECG, and why?
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
how does Torsade de Pointes ventricular tachycardia appear on ECG?
polymorphic VT with “twisting of the points”
all Torsade is polymorphic, but not all polymorphic VT is Torsade
what is an ICD device
implantable cardioverter defibrillator: can detect fibrillation and intervene automatically
what is narrow QRS tachycardia vs wide QRS tachycardia usually attributed to?
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]
how does congenital long QT syndrome present? what is it caused by?
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
how does Brugada syndrome appear on ECG?
Brugada syndrome: genetic arrhythmogenic disorder, predisposes to ventricular arrhythmias and sudden cardiac death, more common in males
ST elevation with inverted T waves
what causes familial catecholaminergic polymorphic ventricular tachycardia?
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
what manifests from arrhythmogenic right ventricular cardiomyopathy?
genetic mutation in desmosome proteins leads to progressive replacement of RV myocardium with fatty and fibrous tissue
causes ventricular arrhythmias originating in RV
what is the most common arrhythmia and how is it treated?
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)
how can adenosine be used both therapeutically and diagnostically?
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)
how do premature atrial contractions (PAC) appear on ECG?
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
how do premature ventricular contractions (PVCs) appear on ECG?
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
what is the preferred drug management for acute atrial fibrillation?
- rate control with beta blocker (calcium channels as alternative)
if LV systolic dysfunction is present:
2. rhythm control with digoxin or amiodarone
- anticoagulants
differentiate where automaticity originates in a-fib vs a-flutter
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
which leads are best to look for saw-took ECG pattern of atrial flutter?
inferior leads: II, III, aVF
what defines multifocal atrial tachycardia? how can it be diagnosed?
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)
multifocal atrial tachycardia vis wandering atrial pacemaker
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)
what is the most common arrhythmia associated with digoxin toxicity?
paroxysmal atrial tachycardia with 2:1 block
what is the treatment for paroxysmal supraventricular tachycardia (AVNRT, AVRT)?
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)
how is ventricular tachycardia defined?
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
how does ventricular tachycardia present? (key findings)
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
what type of arrhythmia is associated with cannon A waves?
cannon A waves in the neck due to AV dissociation, resulting in atrial contraction during ventricular contraction
classically seen with ventricular tachycardia
dilated cardiomyopathy vs hypertrophic cardiomyopathy vs restrictive cardiomyopathy vs myocarditis
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
what kind of cardiomyopathy with Chaga’s disease cause?
dilated cardiomyopathy
what kind of cardiomyopathy will amyloidosis cause?
restrictive cardiomyopathy
what kind of cardiomyopathy will excessive alcohol use cause?
dilated cardiomyopathy
what kind of cardiomyopathy can chemotherapy or radiation cause?
restrictive cardiomyopathy
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?
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]
how does ECG appear for acute pericarditis?
diffuse ST elevation with PR depression
what do the following signs collectively indicate: JVD, prominent x and y descents, Kussmaul’s sign, pericardial knock
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!)
in which pericardial disease will there be prominent x and y descents, and in which will there be loss of y descent?
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
what do these signs collectively indicate: JVD, loss of y descent, narrow pulse pressure, pulsus paradoxus, muffled heart sounds
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)
how can paroxysmal supraventricular tachycardia be differentiated from sinus tachycardia by the way it presents?
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
what is the DOC for terminating PSVT?
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
what is the most common type of PSVT and what is the mechanism of it? who is usually affected?
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)
where is atrial flutter vs fibrillation triggered anatomically?
atrial flutter: reentrant circuit in RA around perimeter of tricuspid valve
atrial fibrillation: ectopic firing around/within pulmonary veins
what is the usual cause of monomorphic vs polymorphic ventricular tachycardia?
monomorphic: usually due to reentry (requires unidirectional block + slow conduction)
polymorphic: usually due to long QT
prolonged QT intervals and early afterdepolarizations (EADs) put patients at major risk for…
Torsades des Pointes
what would LOF vs GOF mutation in Phase 0 voltage-dependent Na+ channels cause?
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
