Tan$Zeng$Yee$Shalom$

S1745271$

POISONING:$CARDIAC$BEHAVIOURS$IN$DEATH$AND$SELECTED$
CASE$STUDIES$
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ABSTRACT'
The$ingestion$or$uptake$of$certain$substances$above$a$threshold$amount$often,$if$not$always,$leads$to$
adverse$ cardiovascular$ events.$ This$ literature$ review$ examines$ the$ role$ of$ the$ electrocardiogram$
(ECG)$ in$ the$ preliminary$ diagnosis$ of$ patients$ who$ have$ been$ exposed$ to$ poison,$ whether$
intentionally$or$not.$Since$numerous$types$of$poisons$exist,$this$review$will$categorise$various$toxins$
according$to$their$relative$effects.$Selected$cases$will$be$summarised$with$the$purpose$of$illustrating$
ECG$variations$in$poisoning,$and$the$usage$of$ECG$as$a$prognostic$tool$will$be$discussed.$$

1.!INTRODUCTION'
Poisoning$is$the$3rd$leading$cause$of$death$in$Europe,$accounting$for$up$to$14%$of$all$deaths$recorded$
in$the$region$(Sethi,$2006).$Moreover,$it$is$a$common$and$popular$method$used$by$people$intending$
to$take$a$life$$whether$it$is$their$own$or$someone$elses.$Substance$overdose$or$sleeping$with$the$
gas$on,$for$example,$are$relatively$simple$ways$to$depart.$In$poisoning$cases,$cardiovascular]related$
toxicity$is$the$fifth$leading$cause$of$mortality$(Delk$et.$al.,$2007).$
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This$ review$ was$ begun$ with$ the$ intention$ of$ consolidating$ heart$ behaviours$ in$ or$ near$ death$ by$
poisoning.$Without$a$doubt,$retrospective$studies$after$death$in$poisoning$would$not$be$very$useful$
in$ discerning$ erratic$ cardiac$ behaviours.$ However,$ in$ botched$ suicide$ attempts$ or$ accidental$
poisoning,$patients$often$arrive$at$the$hospital$on$the$brink$of$expiration.$The$ECGs$taken$in$these$
circumstances$provide$much$insight$for$the$purposes$of$this$paper.$$
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The$ECG$represents$the$electrical$activity$of$the$heart$as$detected$on$the$bodys$surface$with$the$use$
of$electrodes$at$bipolar,$unipolar,$and$precordial$positions.$A$standard$12]lead$ECG$illustrates$the$
projection$ of$ heart$ vectors$ onto$ each$ lead$ direction$ over$ a$ 10]second$ time$ frame.$ In$ addition$ to$
rhythmic$ issues,$ waveforms,$ amplitudes,$ and$ intervals$ visualised$ can$ be$ used$ to$ recognise$
abnormalities$$if$any$$in$cardiac$behaviour.$ECG$indications$of$cardiotoxicity$can$be$known$through$
the$PR$interval,$QRS$complex,$QT$interval,$ST$segment,$as$well$as$the$T$wave,$all$of$which$will$be$
discussed$in$the$sections$below.$The$ECG$is$non]invasive$and$readily$performed$within$a$matter$of$
minutes,$ which$ makes$ it$ invaluable$ in$ the$ case$ of$ an$ emergency.$ ECG$ evaluation$ also$ helps$ to$
determine$or$exclude$cardiotoxicity$in$poisoning$cases,$as$the$symptoms$of$poisoning$often$overlap$
with$that$of$other$cardiac$complaints$like$chest$pains$and$dyspnea$w(Yates$et.$al.,$2012).$ECGs$in$
poisoned$patients$are$often$abnormal$$approximately$70%$of$poisoned$patients$would$demonstrate$
some$ form$ of$ abnormal$ pattern$ in$ their$ ECG.$ Out$ of$ these,$ 62%$ were$ rhythmic$ and$ 38%$ were$
morphological$(Delk$et.$al.,$2007).$

Notably,$ some$ patients$ may$ be$ severely$ poisoned$ by$ certain$ substances$ that$ do$ not$ have$ direct$
effects$on$cardiac$cells,$but$cardiotoxicity$can$still$be$observed$in$the$context$of$multi]organ$failure$
(Yates$et.$al.,$2012).$Correct$and$timely$ECG$interpretation$is$thus$crucial$for$the$optimised$care$of$
poisoned$or$potentially$poisoned$patients,$including$assessment$of$response$to$ongoing$treatment.$
A$
This$review$will$begin$with$selected$illustrative$cases$to$show$the$wide$ranging$effects$of$poisoning$
on$ the$ myocardium$ and$ the$ corresponding$ ECGs.$ Thereafter,$ the$ main$ categories$ of$ cardiotoxic$
substances$will$be$discussed.$

2.!ILLUSTRATIVE'CASES'
2.1'Tricyclic'antidepressants'overdose'
A$ 33]year]old$ female$ was$ brought$ in$ by$ paramedics$ after$ an$ apparent$ suicide$ attempt$ with$ her$
medications.$ She$ was$ unresponsive,$ without$ a$ pulse,$ and$ in$ cardiopulmonary$ arrest.$ During$
resuscitation$with$intravenous$fluids,$sodium$bicarbonate,$and$magnesium,$cardiac$arrhythmias$were$
noted.$In$spite$of$the$resuscitation$efforts,$the$patient$passed$away;$her$urine$samples$tested$positive$
for$tricyclic$antidepressants$(Tabibiazar$et.$al.,$2014).$
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Her$ ECG$ below$ shows$ wide$ complex$ tachycardia$ without$ clear$ ventricular$ origin$ and$ likely$
superventricular.$QRS$complexes$contain$deep$slurred$S$waves$(especially$in$precordial$leads),$which$
are$indicative$of$a$conduction$disorder,$possibly$right$bundle$branch$block$(Da$Costa$et.$al.,$2002).$

Figure'1:'12+lead'ECG'of'33'y/o'female'with'TCA'overdose'(Tabibiazar'et.'al.,'2014).'

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Tricyclic$antidepressants$(TCAs)$are$used$to$treat$depression$along$with$other$neurological$issues,$
and$intoxication$through$TCA$is$common$because$they$are$accessible$to$patients$with$higher$suicide$
tendencies$ (Gheshlaghi$ et.$ al.,$ 2012).$ TCAs$ function$ by$ inhibiting$ presynaptic$ neurotransmitters$
reuptake,$ as$ well$ as$ competing$ against$ acetylcholine$ receptors.$ This$ mode$ of$ action$ affects$ the$
autonomic,$cardiovascular,$and$central$nervous$systems$(Tabibiazar$et.$al.,$2014).$The$most$relevant$
effect$of$TCAs,$however,$is$their$ability$to$block$cardiac$sodium$channels.'
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2$

Blockage$of$sodium$channels$may$be$partially$resolved$through$raising$the$serum$pH$and$sodium$
levels.$Sodium$bicarbonate$is$commonly$administrated$to$alkalinise$the$blood$and$thus$aid$in$the$
removal$ of$ the$ drug$ from$ the$ sodium$ channels$ through$ increased$ tricyclic$ protein$ binding$ (Tan,$
2006).$ In$ theory,$ treatment$ with$ sodium$ bicarbonate$ also$ helps$ to$ increase$ extracellular$ Na$
concentration,$which$would$in$turn$improve$the$chances$of$overcoming$the$channel$blockade$via$the$
law$of$mass$action$$though$there$have$been$cases$that$prove$otherwise$(Yates$et.$al.,$2012).$It$is$also$
notable$that$signs$of$hypernatremia$like$convulsions$and$consciousness$level$changes$can$overlap$
with$those$of$TCA$intoxication$(Gheshlaghi$et.$al.,$2012).$
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2.2'Aluminium'phosphide'poisoning''
Aluminium$phosphide$(ALP),$is$used$throughout$the$world$as$a$potent$pesticide$against$rats$and$other$
rodents.$Expectedly,$there$are$also$many$cases$of$human$ALP$poisoning.$In$India,$a$majority$of$ALP$
poisoning$cases$are$due$to$intentional$suicide$attempts,$as$ALP$is$both$cheap$and$easily$accessible.$
Upon$ contact$ with$ moisture$ (e.g.$ hydrochloric$ acid$ in$ the$ stomach),$ it$ releases$ PH3,$ the$ active$
pesticidal$ component,$ which$ is$ quickly$ absorbed$ via$ the$ lungs$ and$ causes$ systemic$ poisoning.$
Refractory$myocardial$depression$arising$from$aluminium$phosphate$poisoning$is$not$uncommon$and$
carries$a$mortality$rate$of$up$to$77%$(Shah$et.$al.,$2009).$$
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A$40]year]old$male$patient$was$admitted$with$a$history$of$aluminium$phosphate$ingestion.$Suicidal$
intent$was$suspected,$and$3$hours$had$passed$since$consumption$at$the$time$of$admission.$ECG$taken$
upon$arrival$depicts$greatly$widened$QRS$complexes$and$elevated$ST$segments.$A$CK]MB$(cardiac$
marker)$ test$ for$ presence$ of$ myocardial$ damage$ returned$ an$ extremely$ high$ concentration$ of$
290U/L.$Despite$maximal$resuscitative$action$for$48$hours,$the$patient$expired.$
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Figure'2:'12+lead'ECG'of'40'y/o'male'with'ALP'poisoning'(Shah'et.'al.,'2009).'

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Upon$post]mortem$examination,$there$were$striking$histopathological$changes$observed$in$the$
myocardium.$Severe$myocyte$vacuolation$and$necrosis$was$observed.$
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Figure' 3:' Necrosis' and' myocyte'
lysis.' H' and' E' staining' at' x40'
magnification'(Shah'et.'al.,'2009).'

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The$clinical$spectrum$of$aluminium$phosphide$poisoning$depends$on$the$duration$and$dosage$of$ALP$
consumption.$Cardiotoxicity$due$to$aluminium$phosphide$presents$as$myocardial$injury$and$necrosis$
due$ to$ the$ release$ of$ reactive$ oxygen$ intermediates$ (Zeggwagh$ et.$ al,$ 2012).$ Though$ not$ fully$
observed$in$this$particular$case,$ALP$poisoning$can$also$cause$atrial$fibrillation$(<61%),$right$or$left$
bundle$branch$block$(25%),$as$well$as$T$wave$inversions$(36%),$all$of$which$can$be$identified$through$
the$ECG$(Zeggwagh$et.$al,$2012).$$
$
2.3'Carbon'monoxide'poisoning''
The$irreversible$binding$of$carbon$monoxide$to$haemoglobin$is$well$known.$Deleterious$effects$of$
carbon$monoxide,$i.e.$hypoxia,$the$condition$in$which$regions$of$the$body$are$deprived$of$adequate$
oxygen,$are$almost$always$attributed$to$this$interaction.$As$a$result,$treatments$that$centre$on$the$
administration$of$oxygen$persist$in$the$aftercare$of$such$poisoned$patients.$$
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It$has$been$postulated$that$majority$of$fatal$cases$associated$with$carbon$monoxide$poisoning$are$a$
result$of$cardiac$dysfunction.$Myocardial$injury$in$carbon$monoxide$poisoning$likely$arises$from$tissue$
hypoxia,$ as$ well$ as$ cellular$ damage.$ However,$ the$ dysrhythmias$ caused$ by$ carbon$ monoxide$
poisoning$are$of$an$unusual$nature$that$cannot$be$caused$solely$by$hypoxia$(Roderique$et.$al.,$2015).$$
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The$regulatory$role$and$direct$effect$of$carbon$monoxide$on$different$ionic$channels$has$been$further$
augmented$in$recent$years.$Current$research$indicates$that$cardiac$ion$channels$such$as$potassium$
efflux$ channels,$ voltage]gated$ sodium$ channels,$ and$ L]type$ calcium$ channels$ are$ responsive$ to$
carbon$monoxide$(Roderique$et.$al.,$2015).$$
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4$

Figure'4:'12+lead'ECG'in'acute'carbon'monoxide'poisoning'(Lionte'et.'al.,'2012)'

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In$this$particular$patient$(details$unknown),$ECG$taken$24$hours$after$exposure$to$carbon$monoxide$
exhibited$flattened$T$waves,$ST$segment$elevation,$and$QT$prolongation.$After$4$days,$the$patients$
ECG$was$normalised$and$he$was$discharged.$

3.!CARDIOVASCULAR'TOXICITY'
In$ the$ previous$ section,$ case$ reports$ portraying$ the$ varying$ ways$ a$ single$ poison$ can$ affect$ the$
myocardium$ were$ presented.$ Cardiotoxins$ can$ cause$ loss$ of$ function$ in$ the$ heart$ through$
combinations$of$membrane$potential$disturbances,$autonomic$disturbances$and$metabolic$changes$
(Lionte$et.$al.,$2012).$While$interpreting$ECG$of$the$poisoned$patient,$it$is$important$to$keep$in$mind$
the$known$(side)$effects$of$ingested$or$otherwise$administered$substances.$As$such,$the$causes$for$
the$ genesis$ of$ abnormal$ waveforms$ can$ be$ determined.$ The$ list$ below,$ which$ is$ by$ no$ means$
exhaustive,$summarises$some$of$the$main$classes$of$substances$and$their$impact$on$myocardial$cells.$$
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3.1'Sodium'channel'blockade'
Fast$ sodium$ channels$ on$ the$ cardiac$ cell$ membrane$ are$ responsible$ for$ responsible$ for$
depolarisation.$ The$ prevention$ of$ sodium$ influx$ leads$ to$ delayed$ conduction$ and$ depolarisation$
across$the$myocardium,$as$well$as$inhibition$of$action$potential$generation$$phase$0$of$the$action$
potential$is$prolonged.$Thus,$QRS$complexes,$which$represent$ventricular$contraction$on$the$ECG,$
are$significantly$widened$due$to$slower$Na+$influx.$$
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In$a$toxicological$situation,$QRS$widening$is$likely$a$direct$result$of$sodium$channel$blocking$(Holstege$
et.$al.,$2005).$Additionally,$PR$and$QT$intervals$may$be$prolonged,$as$in$the$case$of$TCA$poisoning$
above.$In$an$overdose,$dire$consequences$on$the$physiological$level$are$to$be$expected.$Na+$channel$
blockers$ can$ also$ cause$ the$ development$ of$ a$ re]entrant$ circuit,$ developed$ through$ slowed$
interventricular$conduction$and$unidirectional$block,$resulting$in$ventricular$tachycardia$as$well$as$
ventricular$defibrillation.$
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Figure'5:'Sodium'channel'blockade'causes'a'
slowing'in'depolarisation'(usually'vertical'
phase'0)'and'a'corresponding'wider'QRS'
complex'(Delk'et.'al.,'2007).''

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Na+$channel$blockade$can$also$induce$the$following$changes$on$the$ECG:$R$wave$elevation$in$aVR,$
bradycardia$with$wide$QRS$$a$sign$of$severe$poisoning,$and$right$bundle$branch$pattern.$Other$than$
TCAs,$Na+$channel$blockers$include$cardiovascular$drugs$like$class$1A$and$IC$antiarrythmics,$narcotic$
pain$relievers,$$and$drugs$of$abuse$like$cocaine$(Lionte$et.$al.$2012;$Delk$et.$al.,$2007).$
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3.2'Potassium'efflux'blockade''
In$phase$2$and$3$of$a$typical$action$potential,$K+$channels$on$the$cardiac$cell$membrane$open$to$allow$
the$efflux$of$potassium$ions$and$repolarisation$of$the$cell$back$to$the$resting$membrane$potential.$
Inhibition$of$K+$efflux$would$result$in$the$lengthening$of$phase$2$repolarisation.$$
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On$the$ECG,$the$primary$manifestation$is$a$prolonged$QT$interval$(>0.45$seconds$in$men$and$>0.47$
seconds$in$women),$which$may$be$accompanied$by$T$wave$abnormalities.$$
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Figure' 6:' Potassium' efflux' blockade' delays' the'
termination' of' phase' 2' and' correspondingly'
prolongs'the'QT'interval'(Delk'et.'al.,'2007).''

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Repolarisation$delay$results$in$less$charge$difference$across$the$membrane$of$the$myocardial$cell$that$
may$initiate$an$inward$depolarisation$current$]$$seen$on$the$ECG$as$prominent$U$waves.$Prolonged$
QT$intervals$thus$predisposes$to$the$development$of$triggered$activity$that$can$degenerate$to$re]
entry$torsade$de$pointes,$a$polymorphic$ventricular$tachycardia$(Holstege$et.$al.,$2005).$K+$channel$
blockers$ also$ include$ TCAs,$ cardiovascular$ drugs$ like$ antiarrhythmics$ and$ vasodilators,$ as$ well$ as$
antihistamines,$antibiotics$like$erythromycin,$and$opium$alkaloids$(Lionte$et.$al.,$2012).$
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3.3'Calcium'channel'blockade'(CCB)'
L]type$ voltage]sensitive$ calcium$ channels$ are$ needed$ for$ the$ conduction$ of$ electrical$ impulses$
through$cardiac$tissues,$particularly$for$pacemaker$cells$in$the$sino]atrial$(SA)$and$atrial]ventricular$
(AV)$nodes.$These$channels$are$found$on$the$surface$of$the$sarcomere$and$allow$for$calcium$ion$influx$
from$ the$ T]tubules.$ In$ turn,$ these$ Ca2+$ ions$ would$ bind$ to$ the$ ryanodine$ receptor$ on$ the$
sarcosplasmic$reticulum$to$trigger$the$release$of$Ca2+$into$the$cytosol.$This$increase$in$intracellular$
calcium$will$then$result$in$an$action$potential$in$pacemaker$cells.$
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Figure'7:'Action'potential'induced'by'Ca2+'ions.'(NataliesCaseBook,'2015).'

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CCB$toxicity$presents$initially$as$sinus$bradycardia$as$a$result$of$slowed$AV$or$SA$node$conduction$
(decreased$chronotropy).$This$is$followed$by$varying$levels$of$AV$blocks$and$junctional$rhythms.$If$
peripheral$hypotensive$effects$persist,$reflex$tachycardia$can$also$occur.$On$the$ECG,$morphological$
changes$include$wide$QRS$complexes$and$ST/T$abnormalities.$Calcium$channel$blockers$include$
phenylalkylamines$and$dihydropyridines$(DHP)$that$are$used$for$the$treatment$of$hypertension$and$
migraines.$
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3.4'Na+/K+SATPase'pump'blockade'
The$Na+/K+]ATPase$pump$moves$3$sodium$ions$out$of$the$cell$for$every$2$potassium$ions$entering.$
It$functions$to$maintain$the$electrochemical$gradient$of$Na+$and$K+$across$the$cell$membrane,$and$
thus$ allow$ for$ cellular$ depolarisation$ at$ the$ resting$ state.$ Sodium$ ions$ are$ concentrated$
extracellularly$while$potassium$ions$are$sequestered$within$cells.$The$action$of$this$pump$is$tied$to$
the$3Na/1Ca$exchanger,$whose$action$is$dependent$on$the$membrane$potential$and$the$chemical$
gradient$of$the$ions.$$
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Cardiac$ glycosides,$ or$ digitalis$ compounds,$ are$ strong$ inhibitors$ of$ the$ Na+/K+]ATPase$ pump.$ Its$
inhibition$causes$an$accumulation$of$intracellular$sodium$that$promotes$the$action$of$the$sodium]
calcium$ exchanger$ to$ remove$ excess$ sodium.$ As$ a$ result,$ intracellular$ calcium$ concentration$
increases,$leading$to$an$upregulation$of$inotropy$and$increased$automaticity$(Delk$et.$al.,$2007).$This$
is$the$intended$therapeutic$function$for$patients$with$congestive$heart$failure.$$
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At$therapeutic$doses,$the$digitalis'effect'$inverted$or$flattened$T$waves,$combined$with$sagging$or$
scooping$ ST$ segments$ ' has$ been$ noted.$ QT$ intervals$ typically$ also$ shorten$ due$ to$ shorter$ time$
intervals$ for$ repolarisation.$ These$ represent$ the$ effect$ when$ cardiac$ tissues$ absorb$ the$ digitalis$
compounds$and$are$not$necessarily$symptoms$of$cardiotoxicity.$Digitalis$compounds$also$act$directly$
on$the$vagal$nerve$to$slow$down$conduction$through$the$SA$and$AV$node$(Holstege$et.$al.,$2005).$
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Cardiac$glycoside$toxicity$occurs$as$a$result$of$increased$automaticity$(increased$Ca2+)$in$combination$
of$slowed$conduction$through$the$AV$node.$In$younger$patients,$bradycardia$and$conduction$defects$
predominate,$ while$ the$ consequences$ for$ older$ patients$ are$ more$ severe,$ typically$ exhibiting$
premature$ventricular$contractions.$$
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Figure'8:'3'ECGs'of'a'56'y/o'man'who'attempted'suicide'with'Digoxin'overdose.'Bradycardia'is'observed'(51+
53bpm),'followed'by'a'brief'period'of'ventricular'tachycardia.'
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3.5'BetaSadrenergic'receptor'blockade'
Beta]blockers$competitively$interfere$with$the$binding$of$endogenous$molecules$of$the$sympathetic$
nervous$system$like$epinephrine$and$norepinephrine$to$the$]adrenergic$receptors.$Of$importance$
are$the$1]adrenergic$receptors$that$are$located$in$the$heart.$Beta$adrenergic$stimulation$causes$a$
cyclic$adenosine$monophosphate$(cAMP)]mediated$increase$in$intracellular$calcium$concentration.$
As$discussed$previously,$this$triggers$the$action$potential$in$pacemaker$cells.$$
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Thus,$ antagonism$ of$ ]adrenergic$ receptors$ decreases$ automaticity$ and$ contractility$ in$ atrial$ and$
ventricular$muscle,$as$well$as$conduction$velocity$in$SA$and$AV$nodes$(Yates$et.$al.,$2007).$By$virtue$
of$their$ability$to$decrease$overall$cardiac$output,$beta$blockers$are$conventionally$prescribed$for$the$
alleviation$ of$ hypertension$ and$ management$ of$ cardiac$ arrhythmias$ as$ a$ means$ of$ preventing$ a$
second$myocardial$infarction.$$
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In$most$cases,$acute$poisoning$from$beta$blockers$manifests$as$sinus$bradycardia$from$decreased$SA$
node$ function.$ Conduction$ inhibition$ often$ also$ causes$ first$ degree$ AV]block.$ In$ higher$ doses$ of$
toxins,$second$to$third$degree$blocks$and$junctional$rhythms$can$occur$as$well.$On$the$ECG,$widened$
QRS$can$be$observed$as$part$of$the$membrane$stabilising$effects$of$the$drugs$(Lionte$et.$al.,$2012).$
Some$ beta$ blockers$ like$ Sotalol$ have$ the$ ability$ to$ block$ K+$ channels$ as$ well$ $ this$ presents$ as$
prolonged$QT$intervals,$which$can$degenerate$into$ventricular$tachycardia$and$torsade$de$pointes.$

4.!CONCLUSION'
As$ demonstrated$ in$ this$ review,$ in$ addition$ to$ the$ myriad$ of$ substances$ that$ can$ be$ classified$ as$
poisonous,$cardiovascular$toxicity$is$also$highly$multifaceted.$The$ECG,$in$this$respect,$is$an$essential$
diagnostic$and$prognostic$tool$when$approaching$the$poisoned$patient.$Systematic$interpretation$of$
the$ECG$components$is$thus$crucial$to$avoid$overlooking$indications$of$poisoning,$especially$when$
symptoms$ can$ overlap$ with$ that$ of$ other$ ailments.$ Additionally,$ even$ in$ cases$ of$ exposure$ to$
substances$without$obvious$cardiovascular$effects,$cardiotoxicity$can$still$occur$in$overdose.$Thus,$
repeated$ ECG$ evaluation$ is$ should$ be$ performed$ in$ patients$ with$ suspected$ cardiotoxicity.$ This$
review$has$focused$mostly$on$drug$related$poisoning,$but$it$is$notable$that$there$are$natural$poisons$
found$in$flora$and$fauna$that$were$not$addressed,$as$the$information$pertaining$to$these$were$beyond$
the$scope$of$this$paper.$$

5.!REFERENCES'
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Delk,$C.,$Holstege,$C.$P.,$&$Brady,$W.$J.$(2007).$Electrocardiographic$abnormalities$associated$with$
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9$

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