Arrhythmia Flashcards

Question

what are some drug interactions associated with phenytoin?

Answer 1

amiodarone, oral anticoagulants, cimetidine, nifedipine, disopyramide --\> increase toxicity

Answer 2

flecainide, propafenone

Answer 3

SVT, atrial tachycardia, VT

Answer 4

blurred vision, nausea, decrease in contractility, proarrhythmia

Answer 5

amiodarone increases toxicity

Answer 6

SVT, atrial tachycardia, AF, VT

Answer 7

hypotension, decreased contractility, hepatic toxicity, paresthesia, headache, proarrhythmia

Answer 8

increases digoxin levels

Answer 9

propranolol, atenolol, nadolol

Answer 10

SVT, long QT

Answer 11

bradycardia, loss of concentration, school performance problems, bronchospasm, hypoglycaemia, hypotension, heart block, CHF

Answer 12

co-administration with disopyramide, flecainide, or verapamil may decrease ventricular function

Answer 13

bradycardia, loss of concentration, school performance problems

Answer 14

co-admin with disopyramide, flecainide or verapamil may decrease ventricular function

Answer 15

SVT, long QT

Answer 16

bradycardia, loss of concentration, school performance problems, bronchospasm, hypoglycaemia, hypotension, heart block, CHF

Answer 17

co-admin with disopyramide, flecainide, or verapamil may decreased ventricular function

Answer 18

Amiodarone

Answer 19

SVT, JET (junctional ectopic tachycardia), VT

Answer 20

hypothyroidism or hyperthyroidism, elevated triglycerides, hepatic toxicity, pulm fibrosis

Answer 21

digoxin (increases levels), flecainide, procainamide, quinidine, warfarin, phenytoin

Answer 22

digoxin, verapamil, adenosine

Answer 23

SVT (not WPW), atrial flutter, AF

Answer 24

PAC, PVC, bradycardia, AV block, nausea, vomiting, anorexia, prolongs PR interval

Answer 25

quinidine amiodarone, verapamil increase digoxin levels

Answer 26

SVT (not WPW)

Answer 27

bradycardia, asystole, high degree AV block, PR prolongation, hypotension, CHF

Answer 28

use with beta-blocker or disopyramide exacerbates CHF, increases digoxin level and toxicity

Answer 29

chest pain, flushing, dyspnea, bronchospasm, AF, bradycardia, asystole

Answer 30

normal physiologic variation in impulse discharge from sinus node related to respirations. the HR slows during expiration and accelerates during inspiration. Occasionally if sinus rate is slow enough, an escape beat arises from the AV junction region

Answer 31

Drugs that increase vagal tone, such as digoxin, may exaggerate sinus arrhythmia

Answer 32

slow discharge of impulses from the sinus node. A sinu rate \<90 beats/min in neonates and \<60 beats/min in older children is considered sinus bradycardia

Answer 33

hypothyroidism, anorexia nervosa associated with conditions with high vagal tone such as GI obstruction or intracranial processes

Answer 34

intermittent shift in pacemaker from sinus node to another part of the atrium not uncommon in childhood and usually represents a normal variant may be seen in association with sinus bradycardia in which the shift in atrial focus is an escape phenomenon

Answer 35

premature discharge of an ectopic focus that may be situated in the atrium, AV junction, or ventricle. Usually, isolated extrasystoles are of no clinical or prognostic significance. Under certain circumstances, premature beats may be caused by organic heart disease (inflammation, ischaemia, fibrosis) or drug toxicity

Answer 36

Common usually in absence of cardiac disease may result in normal, prolonged, or an absent QRS complex Absent QRS complex - premature impulse cannot conduct to the ventricle due to refractoriness of the AV node or distal conducting system

Answer 37

can arise in any region of the ventricle premature, widenned, bizarre QRS complexes that are not preceded by a premature p wave ventricular extrasystoles are often, but not always followed by a full compensatory pause when frequent, extrasystoles may assume a definite rhythm e.g. bigeminy or trigeminy Most pts are unaware of a single PVC, although some may be aware of a 'skipped beat' over the precordium - sensation caused by increased SV of the normal beat after a compensatory pause

Answer 38

anxiety febrile illness ingestion of drugs or stimulants

Answer 39

* \>2 PVCs in a row * multiform PVCs * increased ventricular ectopic activity with exercise * R-on-T phenomenon (premature ventricular depolarisation occurs on the T wave of the preceding beat) * extreme frequency of beats (e.g. \>20% of total beats on holter monitoring) * presence of underlying heart disease, Hx of heart surgery, or both best tx for benign PVCs is reassurance that the arrhythmia is not life threatening, although very symptommatic individuals may benefit from suppressive therapy

Answer 40

Usually seconday to another medical issue - electrolyte imbalance, hypoxia, drug toxicity, cardiac injury

Answer 41

correct underlying abnormality IV lidocaine bolus and infusion is first line therapy, with more effective drugs such as amiodarone reserved for refractory cases or pts w/ underlying ventricular dysfunction or haemodynamic compromise

Answer 42

reentrant tachycardias using an accessory pathway reentrant tachycardias w/o an accessory pathway ectopic or automatic tachycardias

Answer 43

AVRT involves an accessory pathway and is the most common mechanism of SVT in infants

Answer 44

AVNRT is rare in infancy, but there is an increasing incidence of AVNRT in childhood and into adolescence

Answer 45

rare in children with normal hearts common in pts following cardiac surgery

Answer 46

more often associated with abnormal hearts (cardiomyopathy) and the immediate postoperative period after surgery for CHD

Answer 47

abrupt onset and termination can occur when pt is at rest or exercising and in infants it may be precipitated by an acute infection attacks can last a few seconds or can persist for hours if HR exceptionally rapid or attack is prolonged, precordial discomfort and HF may occur SVT exaverbated by caffeine, nonprescription decongestants, or bronchodilators

Answer 48

occasionally present with HF as tachycardia may go unrecognised for a long time HR may be between 240-300bpm if attack lasts 6-24hr or more, HF may be recognized and infant will have an ashen color and will be restless and irritable, with tachypnea, poor pulses, and hepatomegaly Fetal tachycardia - can cause hydrops fetalis, the in-utero manifestation of HF

Answer 49

Important as sinus tachycardia requires treatment of the underlying problem (e.g. sepsis, hypovolaemia) rather than antiarrhythmic medication If rate \>230bpm with an abrnomal P-wave axis (normal P wave is positive in leads I and aVF), sinus tachycardia is not likely HR in SVT also tends to be relatively unvarying, in sinus tachycardia the HR varies with changes in vagal and sympathetic tone

Answer 50

AVRT uses a bypass tract that may be able to conduct bidirectionally (WPW) or may be retrograde only (concealed accessory pathway) Small but real risk of sudden death if accessory pathway rapidly conducts in antegrade fashion, pt is at risk for AF begetting ventricular fibrillation Risk stratification, including 24hr holter monitoring and exercise study, may help differentiate pts at higher risk for sudden death from WPW Syncope is ominous symptom. Pt with WPW and syncope should have an electrophysiology study (EPS) and likely catheter ablation

Answer 51

short PR interval and slow upstroke of the QRS (delta wave)

Answer 52

May be associated with Ebstein anomaly of the tricuspid valve or hypertrophic cardiomyopathy

Answer 53

Critical anatomic structure is an accessory pathway consisting of a muscular bridge connecting atrium to ventricle on either the R or L side of the AV ring in SR, impulse is carried over both the AV node and the accessory pathway --\> produces a degree of fusion of the 2 depolarisation fronts that results in an abnormal QRS during AVRT, an impulse is carried in antegrade fashion through the AV node (orthodromic tachycardia), results in a normal QRS complex, and in retrograde fashion through the accessory pathway to the atrium, thereby perpetuating the tachycardia In these cases, only after cessation of tachycardia is the typical ECG features of WPW syndrome recognised when rapid antegrade conduction occurs through the accessory pathway during tachycardia, and the retrograde reentery pathway to the atrium is by the AV node (antidromic tachycardia), the QRS complexes are wide, and potential for more serious arrhythmias (VF) is greater, esp if AF occurs

Answer 54

involves 2 functional pathways within the AV node, the slow and fast AV node pathways. More often seen in adolescense. One of few forms of SVT that is occasionally associated with syncope. Arrhythmia is often seen in association with exercise

Answer 55

Vagal stimulation: face in ice water (older kids) or ice bag over face (infants) Vagal maneuvers such as valsalva, straining, breath holding Dont do ocular pressure carotid sinus massage is rarely effective

Answer 56

stable pts - adenosine by rapid IV push (0.1mg/kg, max 6mg) As adenosine can initiate AF, DC cardioversion should be nearby just in case verapamil - can be used as initial treatment in older kids. may reduce CO and produce hypotension and cardiac arrest in infants younger than 1yr and therefore is contraindicated in this age group In urgent situations when sx of HF have already occurred, synchronised DC cardioversion (0.5-2J/kg) is recommended as initial management

Answer 57

Digoxin, CCB

Answer 58

Almost identical

Answer 59

No. They do not have a manifest accessory pathway Episodes are more likely to be brought on by exercise or other forms of stress, and HR can be fast leading to chest pain, dizziness, and occasionally syncope

Answer 60

It is an unconnon tachycardia in childhood

Answer 61

Variable rate (seldom \>200bpm), identifiable P waves with an abnormal axis, and either a sustained or incessant nonsustained tachycardia. This form of atrial tachycardia has a single automatic focus

Answer 62

aided by monitoring ECG while initiating vagal or pharmacologic therapy. Reentry tachycardias "break" suddenly, whereas automatic tachycardias gradually slow down and then gradually speed up again

Answer 63

Atrial ectopic tachycardias are usually more difficult to control pharmacologically than the more common reentrant tachycardias If pharmacological therapy with a single agent is unsuccessful, catheter ablation is suggested and has a success rate \>90%

Answer 64

Atrial tachycardia with \>3 ectopic P waves, frequent blocked P waves, and varying P-R intervals of conducted beats

Answer 65

Infants younger than 1 year, usually w/o cardiac disease, although some evidence suggests an association with viral myocarditis or pulmonary disease

Answer 66

Slowing of ventricular rate, because conversion to sinus may not be possible, and multiple agents are often required. When this arrhythmia occurs in infancy, it usually terminates spontaneously by 3yr of age

Answer 67

automatic (non-reentry) arrhythmia in which the junctional rate exceeds that of the sinus node and AV dissociation results. Most often recognised in the early postoperative period after cardiac surgery and may be extremely difficult to control

Answer 68

Reduction of the infusion rate of catecholamines and control of fever and pain are important

Answer 69

May be seen in absence of surgery Incessant and can lead to dilated cardiomyopathy congenital JET can be cured by catheter ablation, but long-term AV block requiring a pacemaker is a prominent complication

Answer 70

IV amiodarone. Pts who require chronic therapy may respond to amiodarone or sotalol

Answer 71

Atrial activity at a rate of 250-300 bpm in children and adolescents, and 400-600bpm in neonates. Mechanism of common atrial flutter consists of a reentrant rhythm originating in the right atrium circling the tricuspid valve annulus AV node cannot transmit such rapid impulses --\> some degree of AV block is virtually always present, and the ventricles respond to every 2nd to 4th atrial beat Occasionally the reponse is variable, and the rhythm appears irregular

Answer 72

congenital heart disease

Answer 73

acute infectious illnesses, but is most often seen in pts with large stretched atria, such as those associated with long-standing mitral or tricuspid insufficiency, tricuspid atresia, ebstein anomaly, or rheumatic mitral stenosis also can occur after palliative or corrective intraatrial surgery Uncontrolled atrial flutter may precipitate heart failure

Answer 74

Vagal maneuvers or adenosine may produce a temporary slowing of the HR as a result of increased AV block, allowing diagnosis to be made Diagnosis is confirmed by ECG, which demonstrates the rapid and regular atrial saw-toothed flutter waves

Answer 75

DC cardioversion Chronic flutter: increased risk for thromboembolism and stroke and should undergo anticoagulation before elective cardioversion Beta-blockers or CCBs: slow ventricular response by prolonging the AV node refractory period Class I agents: procainamide/propafenone Class III agents: amiodarone and sotalol Catheter ablation, particularly in pts with congenital heart disease with moderate success After cardioversion, neonates w/ normal hearts can be ceased medications, or tx with digoxin/propranolol/sotalol for 6-12 months, after which can be ceased, as neonatal atrial flutter generally does not recur

Answer 76

uncommon in children and is rare in infants irregularly irregular ventricular response and pulse often associated w/ atrial enlargement or disease may be seen in older kids w/ rheumatic mitral valve stenosis

Answer 77

atrial enlargement or disease older kids w/ rheumatic mitral valve stenosis rarely as a complication of atrial surgery L atrial enlargement secondary to L AV valve insufficiency Pts w/ WPW syndrome Thyrotoxicosis, PE, pericarditis, or cardiomyopathy may be suspected in previously well older child or adolescent with AF Rarely AF may be familial

Answer 78

rate control - CCB Digoxin not given if WPW present NSR may be achieved with IV procainamide, ibutilide, or amiodarone DC cardioversion is 1st choice in haemodynamically unstable pts Pts w/ chronic AF are at risk for thromboembolosim and stroke and should under anticoagulation with warfarain Pts have elective cardioversion should undergo anticoagulation

Answer 79

At least 3x PVCs at \>120bpm May be paroxysmal or incessant

Answer 80

myocarditis anomalous origin of a coronary artery arrhythmogenic cardiomyopathy MVP primary cardiac tumors Dilated or hypertrophic cardiomyopathy prolonged WT (either congenital or acquired - proarrhythmic drugs) WPW Drugs (cocaine, amphetamine) can develop years after intraventricular surgery (esp TOF and related defects) or can occur w/o obvious organic heart disease

Answer 81

should be treated promptly as hypotension and degeneration into VF may result Haemodynamically stable: IV amiodarone, lidocaine, or procainamide is the initial drug of choice Correct any underlying abn such as electrolyte imbalance, hypoxia, or drug toxicity Amiodarone is Tx of choice during cardiac arrest Haemodynamically unstable: DC cardioversion Overdrive ventricular pacing, through temporary pacing wires, or permanent pacemaker may be effective, but can cause deterioration to VF

Answer 82

anomalous left coronary artery myocardial tumour

Answer 83

EPS study --\> may need catheter ablation and/or ICD implantation

Answer 84

Occasionally seen in infants defined in same way as VT, but rate is only slightly faster than the coexisting sinus rate (within 10%) generally benign and resolves spontaneously

Answer 85

chaotic rhythm that results in death unless effective ventricular beat is rapidly established

Answer 86

CPR and DC cardioversion usually necessary If defib ineffective or VF recurs --\> amiodarone or lidocaine IV and defib repeated After recovery, need to search for underlying cause EPS indicated unless clear reversible cause is found If WPW noted - catheter ablation should be done If nil correctable abn - ICD is indicated due to high risk of sudden death

Answer 87

genetic abn of ventricular repolarisation estimated incidence of 1 per 10, 000 births

Answer 88

Present as a long QT interval on ECG and associate with malignant ventricular arrhythmias (torsades de pointes and VF) are a cause of syncope and sudden death and may be cause of some cases of SIDS, drowning, and IUFD 80% of cases - identifiable genetic mutation asymptomatic but at-risk pts carrying the gene mutation may not all have a prolonged QT duration. QT interval prolongation may become apparent with exercise or during catecholamine infusions

Answer 89

About 75% of clinically strong LQTS is caused by mutations in 3 genes (35% KCNQ1, 30% KCNH2, 10% SCN5A) encoding for ion channels responsible for cardiac action potential Observed genotype-phenotype correlation include swimming/exertion/emotion with LQT1, auditory triggers/postpartum period with LQT2, and sleep/rest with LQT3

Answer 90

Long QT syndrome Triadin Knockout syndrome Andersen-Tawl Syndrome Timothy Syndrome Short QT syndrome Catecholaminergic polymorphic VT Brugada Syndrome Early Repolarisation Syndrome Idiopathic ventricular fibrillation progressive cardiac conduction disease/defect Sick sinus syndrome (SSS) Ankyrin-B syndrome Familial AF

Answer 91

LQT3 --\> LQT 2 --\> LQT 1

Answer 92

Events induced by stress or exertion

Answer 93

Intermediate pattern, often occurring in the postpartum period or with auditory triggers

Answer 94

Occurs at rest, especially during sleep

Answer 95

most often a syncopal episode brought on by exercise, fright, or a sudden startle; some events occur during sleep (LQT 3) Can initially present with seizures, presyncope, or palpitations 10% are initially in cardiac arrest Dx made on ECG and clinical criteria

Answer 96

HR corrected QT interval of \>0.47s is highly indicative, whereas a QT interval of \>0.44s is suggestive notched T waves in 3 leads, T-wave alternancs, a low HR for age, a hx of syncope (esp with stress), and a FHx of either LQTS or unexplained sudden death

Answer 97

80% Genotyping not useful in ruling out diagnosis in individuals with suspected disease, but when positive is very useful in identifying asymptomatic affected relatives of the index case

Answer 98

Manifest with AF or VF Associated with syncope and sudden death Often caused by gain-of-function mutation in cardiac potassium channels

Answer 99

Beta-blockers at doses that blunt HR response to exercise Propranolol and nadolol may be more effective than atenolol and metoprolol Some pts need a pacemaker due to drug-induced bradycardia. ICD indicated in pts with continued syncope despite tx with beta-blockers, and those who have had a cardiac arrest Genotype-phenotype correlative studies suggest that beta-blockers are not effective in pts with LQT3, and an ICD is usually indicated Recent studies show that mexiletine is helpful in pts with LQT3

Answer 100

Both may cause a sudden pause in the heartbeat Sinus arrest: failure of impulse formation within the sinus node Sinoatrial block results from block between sinus pacemaker complex and surrounding atrium These arrhythmias are rare in childhood except in pts who have had extensive atrial surgery

Answer 101

abnormalities in sinus node or atrial conduction pathways, or both May occur in absence of CHD and has been reported in siblings, but it is most commonly seen after surgical correction of congenital heart defects, esp Fontan procedure and the atrial switch (Mustard or Senning) operation for TGA

Answer 102

depend on HR Most pts remain asymptomatic w/o treatment Dizziness and syncope can occur during periods of marked sinus slowing with failure of junctional escape May have episodes of SVT (tachy-brady syndrome) w/ symptoms of palpitations, exercise intolerance or dizziness

Answer 103

Pacemaker therapy indicated in pts who experience symptoms such as exercise intolerance or syncope Drug therapy to control tachyarrhythmias (propranolol, sotalol, amiodarone) may suppress sinus and AV node function to such a degree that further symptommatic bradycardia may be produced. Pacemaker insertion in conjunction with drug therapy is usually necessay, even in absence of symptoms ascirbable to low HR

Answer 104

PR interval is prolonged but all atrial impulses are conducted to the ventricle

Answer 105

not every atrial impulse is conducted to the ventricle

Answer 106

Variant of second degree HB PR interval increases progressively until a P wave is not conducted In the cycle following the dropped beat, the PR interval normalizes

Answer 107

Type of second degree HB No progressive conduction delay or subsequent shortening of PR interval after a blocked beat. This conduction defect is less common but has more potential to cause syncope and may be progressive Related condition is high-grade second-degree AV block, in which 2 or more P waves in a row fail to conduct - this is more dangerous

Answer 108

no impulses from the atria reach the ventricles. An independent escape rhythm is usually present but may not be reliable, leading to symptoms such as syncope

Answer 109

Presumed to be caused by autoimmune injury of fetal conduction system by maternally derived immunoglobulin G Ab (anti-SSA/Ro, anti-SSB/La) in a mother with overt or, more often, asymptomatic SLE or Sjogren syndrome Autoimmune disease accounts for 60-70% of all cases of congenital complete AV block and 80% of cases in which the heart is structurally normal Mutation in NKX2-5 is described in which congenital AV block is seen most often in association with ASDs

Answer 110

Seen in pts w/ complex CHD and abn embryonic development of the conduction system Associated with myocardial tumours and myocarditis known complication of myocardial abscess secondary to endocarditis also seen in genetic abnormalities, including LQTS and Kearns-Sayre syndrome Post-op AV block can be complication of CHD repair; in particular repairs involving VSD closure

Answer 111

1 per 20, 000 - 25, 000

Answer 112

Often diagnosed in the fetus (secondary to the dissociation between atrial and ventricular contractions seen on fetal echo) and may produce hydrops fetalis Maternal treatment with corticosteroids to halt progression or reverse AV block is cotroversial Infants w/ associated CHD and HF have a high mortality rate In some infants of mother with SLE, complete AV clock is not present at birth but develops within the 1st 3-6 months after birth

Answer 113

often asymptomatic in older children, although syncope and sudden death may occur infants and toddlers may have night terrors, tiredness with frequent naps, and irritability

Answer 114

peripheral pulse is prominent due to compensatory large ventricular stroke volume and peripheral vasodilation; systolic BP is elevated JVP occurs irregularly and may be large when the atrium contracts against a closed tricuspid valve (cannon wave) Exercise and atropine may produce an acceleration of 10-20 bpm or more systolic murmurs are frequently audible along the left sternal border, and apical mid-diastolic murmurs are not unusual first heart sound is variable due to variable ventricular filing with AV dissociation AV block results in enlargement of the heart based on increased diastolic ventricular filling

Answer 115

Dx confirmed by ECG; P waves and QRS complexes have no constant relationship QRS duration may be prolonged, or may be normal if heartbeat is initiated high in the AV node or bundle of His

Answer 116

usually favourable some pts observed to age 30-40 live normal, active lives some pts have episodes of exercise intolerance, dizziness, and syncope (stokes-adams attacks) syncope requires ICD pacemaker should be considered for pts who develop sx such as progressive cardiac dilation, prolonged pauses, or daytime average HR of \<50 bpm prophylactic pacemaker implantation in adolescents is resonable considering the low risk of implant procedure and difficulty in predictitng who will develop sudden severe symptoms

Answer 117

low ventricular rates (\<55bpm) evidence of HF wide complex rhythms CHD (with ventricular rates \<70 bpm)

Answer 118

isoproterenol, atropine, epinephrine

Answer 119

Transthoracic epicardial pacemaker implants have traditionally been used in infants; transvenous placement of pacemaker leads is available for young children

Answer 120

initially managed with temporary pacing wires likelihood of return to sinus rhythm after 10-14 days is low; permanent pacemaker is recommended after that time