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Puls eles s Electrical Ac�vity: [Print] ‐ eMedicine Cardiology

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Pulseless Electrical Activity Pa t rick O'Be irn e , M D, Fellow in Cardiovas cular Medicine, U Mas s Memorial Medical Center Dion ys s ios A R obot is , M D, M PH , FACC, As s is tant Profes s or of Medicine, U nivers ity of Mas s achus etts ; Cons ulting Staff Cardiologis t/Electrophys iologis t, U nivers ity of Mas s achus etts Memorial Medical Center; La wre n ce R os e n t h a l, M D, Ph D, As s ociate Profes s or of Medicine, Director, Section of Cardiac Electrophys iology and Pacing, Fellows hip Director of Clinical Cardiac Electrophys iology, Department of Internal Medicine, Divis ion of Cardiovas cular Medicine, U nivers ity of Mas s achus etts Memorial Medical Center U pdated: May 11, 2009

Int roduct ion Background Puls eles s electrical activity (PEA) is a clinical condition characteriz ed by unres pons ivenes s and lack of palpable puls e in the pres ence of organiz ed cardiac electrical activity. Puls eles s electrical activity has previous ly been referred to as electrom echanical dis s ociation (EM D). While a lack of ventricular electrical activity always im plies a lack of ventricular m echanical activity (as ys tole), the revers e is not always true. In a s ituation of cardiac arres t, the pres ence of organiz ed ventricular electrical activity is not neces s arily accom panied by m eaningful ventricular m echanical activity. The latter clinical s cenario has been called puls eles s electrical activity or electrom echanical dis s ociation. The qualifier “m eaningful” is us ed to des cribe s uch a degree of ventricular m echanical activity that is s ufficient to generate a palpable puls e. In other words , electrical activity is a neces s ary but not s ufficient condition for m echanical activity. Puls eles s electrical activity does not m ean m echanical quies cence. Patients m ay have weak ventricular contractions and recordable aortic pres s ure (ps eudo-PEA). True puls eles s electrical activity is a condition in which cardiac contractions are abs ent in the pres ence of coordinated electrical activity. Puls eles s electrical activity encom pas s es a num ber of organiz ed cardiac rhythm s including s upraventricular rhythm s (s inus vers us nons inus ) or ventricular rhythm s (accelerated idioventricular or es cape). The abs ence of peripheral puls es s hould not be equated with puls eles s electrical activity as it m ay be due to s evere peripheral vas cular dis eas e.

Pat hophysiology Puls eles s electrical activity is the res ult of a m ajor cardiovas cular, res piratory, or m etabolic derangem ent. Situations that caus e s udden changes in preload, afterload, or contractility often res ult in PEA. The initial ins ult weakens cardiac contraction, and this s ituation is exacerbated by wors ening acidos is , hypoxia, and increas ing vagal tone. Further com prom is e of the inotropic s tate of the cardiac m us cle leads to inadequate m echanical activity, even though electrical activity is pres ent. This event creates a vicious cycle, caus ing degeneration of the rhythm and s ubs equent death of the patient. PEA is caus ed by the inability of cardiac m us cle to generate s ufficient force in res pons e to electrical depolariz ation. This form of electrom echanical decoupling m ay be the final res ult of m any factors . PEA is always caus ed by a profound cardiovas cular ins ult (eg, s evere prolonged hypoxia or acidos is or extrem e hypovolem ia or flow-res tricting pulm onary em bolus ). Trans ient coronary occlus ion us ually does not caus e PEA, unles s hypotens ion or other arrhythm ias are involved. H ypoxia s econdary to res piratory failure is

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probably the m os t com m on caus e of PEA with res piratory ins ufficiency accom panying 40-50% of PEA cas es . The com m on m echanis m s involved are as follows : Decreas ed preload: Cardiac s arcom eres require an optim al length (ie, preload) for an efficient contraction. If this length is unattainable becaus e of volum e los s or pulm onary em bolus (caus ing decreas ed venous return to the left atrium ), the left ventricle is unable to generate s ufficient pres s ure to overcom e its afterload. Volum e los s res ulting in PEA is m os t likely to happen in cas es of m ajor traum a. In thes e s ituations , rapid blood los s and s ubs equent hypovolem ia can exhaus t cardiovas cular com pens atory m echanis m s , culm inating in PEA. Cardiac tam ponade m ay als o caus e decreas ed ventricular filling. Decreas ed contractility: Optim al m yocardial contractility depends on optim al filling pres s ure, afterload, and the pres ence and availability of inotropic s ubs tances (eg, epinephrine, norepinephrine, or calcium ). Calcium influx and binding to troponin C is es s ential for cardiac contraction. If calcium is not available (eg, calcium channel blocker overdos e) or if calcium 's affinity to troponin C is decreas ed (as in hypoxia), contractility s uffers . Depletion of intracellular adenos ine triphos phate (ATP) res erves caus es an increas e in adenos ine diphos phate (ADP), which can bind calcium , further reducing energy res erves . Exces s intracellular calcium can res ult in reperfus ion injury by caus ing s evere dam age to the intracellular s tructures , predom inantly the m itochondria. Afterload is invers ely related to cardiac output. Severe increas es in afterload pres s ure caus e a decreas e in cardiac output. H owever, this m echanis m is rarely s olely res pons ible for PEA.

Frequency Unit e d St at e s

The frequency of PEA varies am ong different patient populations . The condition accounts for approxim ately 20% of cardiac arres ts that occur outs ide the hos pital.

R aiz es et al found that PEA was res pons ible for 68% of m onitored in-hos pital deaths and 10% of all 1 in-hos pital deaths . Becaus e of the increas ed dis eas e acuity obs erved in patients who are adm itted, PEA m ay be m ore likely to occur in patients who are hos pitaliz ed. Als o, thes e patients are m ore likely to have pulm onary em boli and s uch conditions as ventilator-induced auto–PEEP (pos itive– end-expiratory pres s ure). N adkarni et al found that PEA was the firs t docum ented rhythm in 32% of adults with in-hos pital 2 cardiac arres t. The us e of beta-blockers and calcium channel blockers m ay increas e the frequency of PEA, pres um ably by interfering with cardiac contractility .

Mort alit y/Morbidit y The overall m ortality rate is high in patients in whom PEA is the initial rhythm during cardiac arres t. In the s tudy by N adkarni et al, only 11.2% of patients who had PEA as their firs t docum ented rhythm s urvived 2 to hos pital dis charge. Given this grim outlook, the rapid initiation of advanced cardiac life s upport (ACLS) and identification of any revers ible caus e are critical. Initiation of ACLS m ay im prove patient outcom e if a revers ible caus e is identified and rapidly corrected.

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Race N o data s ugges t any racial predilection.

Sex Fem ales are m ore likely to develop PEA than m ales . The reas ons for this predilection are unclear but m ay relate to different etiologies of cardiac arres t.

Age The average patient age is 70 years . Older patients are m ore likely to have PEA as an etiology of cardiac arres t. Whether the patient outcom e differs bas ed on age is not known; however, advanced age is likely as s ociated with a wors e outcom e.

Clinical Hist ory Knowledge of prior m edical conditions allows prom pt identification and correction of revers ible caus es . For exam ple, a debilitated patient who develops acute res piratory failure and then m anifes ts PEA m ay have a pulm onary em bolus . If an elderly wom an develops PEA 2-5 days after a m yocardial infarction, a cardiac etiology s hould be cons idered (ie, cardiac rupture, recurrent infarction). H is tory of prior drug intake is crucial, enabling prom pt treatm ent of patients in whom drug overdos e is s us pected. The pres ence of PEA in the s etting of traum a m akes hem orrhage (hypovolem ia), tens ion pneum othorax, and cardiac tam ponade the m ore likely caus es .

Physical By definition, patients with PEA have no puls es in the pres ence of organiz ed electrical activity. The phys ical exam ination s hould focus on identification of revers ible caus es ; for exam ple, tracheal s hift or unilateral abs ence of breath s ounds indicates tens ion pneum othorax, while norm al lung s ounds and dis tended jugular veins point to cardiac tam ponade.

Causes Puls eles s electrical activity can be clas s ified by a num ber of criteria. While an exhaus tive enum eration of caus es has the advantage of com pletenes s , it is not a convenient tool at the beds ide. The Am erican H eart As s ociation (AH A) and European R es us citation Council favor the m nem onic of “H s and Ts ” as follows : H ypovolem ia H ypoxia H ydrogen ion (acidos is ) H ypokalem ia/hyperkalem ia H ypoglycem ia H ypotherm ia

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Toxins Tam ponade, cardiac Tens ion Pneum othorax Throm bos is (coronary or pulm onary) Traum a

The above enum eration of caus es does not offer any cues regarding the frequency or revers ibility of each caus e. As s uch, it m ay be not particularly us eful even for thos e who have com m itted it to m em ory. 3

The "3 and 3 rule" of Des biens is m ore practical as it allows eas y recall of the m os t com m on correctable caus es of PEA. It organiz es PEA caus es into 3 m ajor ones :

Severe hypovolem ia Pum p failure Obs truction to circulation: The 3 m ain caus es of obs truction to circulation are as follows : Tens ion pneum othorax

4

5

Cardiac tam ponade

M as s ive pulm onary em bolus

6

Pum p failure is the res ult of m as s ive m yocardial infarction, with or without cardiac rupture, and s evere heart failure. M ajor traum a can be res pons ible for hypovolem ia, tens ion pneum othorax, or cardiac tam ponade. M etabolic derangem ents (acidos is , hyperkalem ia, hypokalem ia), while rarely the initiators of PEA, are com m on contributing factors . Drug overdos e (tricyclic antidepres s ants , digitalis , calcium channel and beta-blockers ) or toxins are als o rare caus es of PEA. H ypotherm ia s hould be cons idered in the appropriate clinical context of out-of-hos pital PEA. Pos tdefibrillation PEA is characteriz ed by the pres ence of organiz ed electrical activity, occurring im m ediately after electrical cardiovers ion in the abs ence of palpable puls e. Pos tdefibrillation PEA m ay be as s ociated with a better prognos is than continued ventricular fibrillation. A s pontaneous return of puls e is likely, and cardiopulm onary res us citation (CPR ) s hould be continued for as long as 1 m inute to allow for s pontaneous recovery.

Different ial Diagnoses Accelerated Idioventricular R hythm

Workup Laborat ory St udies

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Becaus e of the em ergent nature of the problem , lab tes ts are not likely to be helpful in the im m ediate m anagem ent of the patient. If available rapidly, arterial blood gas es , s erum electrolytes , and glucos e m ay provide inform ation regarding s erum pH , oxygenation, s erum potas s ium and glucos e.

Imaging St udies Beds ide echocardiography m ay rapidly identify revers ible cardiac problem s (eg, cardiac tam ponade, rupture, m as s ive m yocardial infarction). Echocardiography als o identifies patients with weak cardiac contractions who have ps eudo-PEA. This group of patients is m ore likely to benefit from aggres s ive 5 res us citation.

Ot her T est s A 12-lead ECG is diffi cult to obtain during ongoing res us citation but, if available, can provide clues to the pres ence of hyperkalem ia (eg, peaked T waves , com plete heart block, ventricular es cape rhythm ) or acute m yocardial infarction. H ypotherm ia, if not already diagnos ed, m ay be s us pected by the pres ence of Os borne waves . Certain drug overdos es (eg, tricyclic antidepres s ants ) prolong QR S duration.

Procedures Placem ent of an arterial line m ay identify patients with a recordable (but very low) blood pres s ure; thes e patients are likely to have a better outcom e if given aggres s ive res us citation.

T reat ment Medical Care For a patient in whom PEA is s us pected, the Am erican H eart As s ociation - Advanced Cardiac Life 7 Support (AH A-ACLS) guidelines protocol recom m ends the following : Initiate CPR . Place an intravenous line. Intubate the patient. Correct hypoxia by adm inis tering 100% oxygen. Once thes e bas ic m eas ures are in place, revers ible caus es s hould be s ought and corrected, which include the following: H ypovolem ia H ypoxia Acidos is H ypokalem ia/hyperkalem ia H ypoglycem ia H ypotherm ia Toxins (eg, tricyclic antidepres s ants , digoxin, calcium channel blocker, beta-blockers ) Cardiac tam ponade

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Tens ion pneum othorax M as s ive pulm onary em bolus Acute m yocardial infarction The clinical s cenario us ually provides us eful inform ation. Som e exam ples include the following: In a previous ly intubated patient, tens ion pneum othorax and auto-PEEP are m ore likely to occur. In a patient on dialys is , cons ider hyperkalem ia. In a patient with prior m yocardial infarction or CH F, m yocardial dys function is likely. A core tem perature s hould always be obtained if the patient is thought to have hypotherm ia. In patients diagnos ed with hypotherm ia, res us citative efforts s hould be continued at leas t until the patient is rewarm ed becaus e patient s urvival is pos s ible even after prolonged 8 res us citation. Other com ponents of the evaluation include the following: M eas ure QR S duration s ince it has prognos tic s ignificance. Patients with QR S duration of les s than 0.2 s econd are m ore likely to recover, and high-dos e epinephrine m ay be adm inis tered. Acute rightward axis s hifts can s ugges t pos s ible pulm onary em bolus . Invas ive m onitoring (eg, arterial line) m ay be placed if it does not caus e a delay in delivering s tandard ACLS care. Echocardiography, if available, m ay as s is t with identifying the pres ence of cardiac contractions (ps eudo-PEA). Patients with ps eudo-PEA m ay have a rapidly revers ible caus e (eg, auto-PEEP, hypovolem ia). Echocardiography als o is invaluable in identifying cardiac 5 tam ponade, right ventricular enlargem ent, pulm onary hypertens ion s ugges tive of pulm onary em boli, m yocardial dys function, cardiorrhexis , or ventricular s eptal rupture. In refractory cas es , if the patient has s uffered ches t traum a, a thoracotom y m ay be perform ed, provided adequate expertis e is available. Once revers ible caus es are identified, they s hould be corrected im m ediately. This proces s involves needle decom pres s ion of pneum othorax, pericardiocentes is for tam ponade, volum e infus ion, correction of body tem perature, and adm inis tration of throm bolytics or s urgical em bolectom y for pulm onary em bolus . R es us citative pharm acology includes epinephrine, vas opres s in, and atropine. Epinephrine s hould be adm inis tered in 1 m g dos es IV/IO q3-5m in during PEA arres t. H igher dos es of epinephrine have been s tudied and s how no im provem ent in s urvival or neurologic outcom es in m os t patients . Special populations of patients , s uch as thos e who have overdos ed on beta-blockers and calcium channel blockers m ay benefit from higher dos e epinephrine. Vas opres s in 40 U IV/IO m ay replace either the firs t or s econd dos e of epinephrine in patients 9,10 with puls eles s electrical activity. If the underlying rhythm is bradycardia (ie, heart rate <60 bpm ) as s ociated with hypotens ion, then atropine (1 m g IV q3-5m in, up to 3 dos es ) s hould be adm inis tered. This is cons idered the total vagolytic dos e, beyond which no further benefit will occur. N ote that atropine m ay caus e pupillary

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dilation, and this s ign then cannot be us ed to as s es s neurologic function. Sodium bicarbonate m ay be adm inis tered only in patients with s evere s ys tem ic acidos is , hyperkalem ia, or a tricyclic antidepres s ant overdos e. The dos e is 1 m Eq/kg. R outine adm inis tration is dis couraged becaus e it wors ens intracellular and intracerebral acidos is and does not appear to alter the m ortality rate. Prom pt initiation of a cardiopulm onary bypas s m ay have a role in carefully s elected patients . This m aneuver requires availability of expertis e and s upport s ervices . Patient s election is param ount becaus e it s hould be us ed only in patients who have an eas ily revers ible etiology of cardiac dys function. In an anim al m odel, initiation of prom pt cardiopulm onary bypas s res ulted in a higher rate of s ucces s in returning circulation than adm inis tration of high- or s tandard-dos e epinephrine. Cardiac pacing can res ult in electrical capture but does not neces s arily increas e the incidence of m echanical contractions ; hence, this procedure is not recom m ended. N ear puls eles s electrical activity, or a profound low output s tate, m ay als o be addres s ed with different m eans of circulatory as s is t (eg, intra-aortic balloon pum p, extracorporeal m em brane oxygenation, cardiopulm onary bypas s , ventricular as s is t device).

Surgical Care Pericardiocentes is , ches t tube thoracos tom y, and even em ergent cardiac s urgery m ay be lifes aving procedures in appropriate patients .

Consult at ions Once the caus e of PEA is identified and the patient's condition is s tabiliz ed, cons ultation with appropriate s ervices m ay be obtained.

A cardiothoracic s urgery cons ult m ay be appropriate for a pulm onary em bolectom y in patients with large pulm onary em bolus . In patients with drug overdos es , cons ultation with the toxicology departm ent or the local pois on center m ay be us eful after hem odynam ic s tability is res tored.

Medicat ion The goals of pharm acotherapy are to reduce m orbidity and to prevent com plications .

Inot ropic agent s Increas e the central aortic pres s ure and counter m yocardial depres s ion. Their m ain therapeutic effects are cardiac s tim ulation, bronchial s m ooth m us cle relaxation, and dilatation of s keletal m us cle vas culature.

Epine phrine (Adre nalin)

H as alpha-agonis t effects that include increas ed peripheral vas cular res is tance and revers ed peripheral vas odilatation, s ys tem ic hypotens ion, and vas cular perm eability. Beta-agonis t effects of epinephrine include bronchodilatation, chronotropic cardiac activity, and pos itive inotropic effects .

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Dosing Ad ult

1 m g IV q3-5m in P e d iat ric

N ot es tablis hed I nt e ract ions

Increas es toxicity of beta-blocking agents , alpha-blocking agents , and halogenated inhalational anes thetics Cont raindicat ions

Docum ented hypers ens itivity; cardiac arrhythm ias ; angle-clos ure glaucom a; during labor (m ay delay s econd s tage of labor) Pre caut ions P re g nanc y

C - Fetal ris k revealed in s tudies in anim als but not es tablis hed or not s tudied in hum ans ; m ay us e if benefits outweigh ris k to fetus P re c aut io ns

Caution in elderly pers ons and in pros tatic hypertrophy, hypertens ion, cardiovas cular dis eas e, diabetes m ellitus , hyperthyroidis m , and cerebrovas cular ins ufficiency; rapid IV infus ions m ay caus e death from cerebrovas cular hem orrhage or cardiac arrhythm ias ; if ventricular tachycardia or fibrillation (recurrent or pers is tent) develops , m ay be caus ed by effects of epinephrine

Ant icholinergic a gent s Im prove conduction through the atrioventricular (AV) node by reducing vagal tone via m us carinic receptor blockade.

At ropine (At ropair)

U s ed for treatm ent of bradyarrhythm ias . Works to increas e heart rate through vagolytic effects , caus ing increas e in cardiac output. Total vagolytic dos e is 2 m g; dos es <0.5 m g m ay exacerbate bradycardia. Dosing Ad ult

0.5-1 m g IV q 3-5 m in; not to exceed 2 m g P e d iat ric

0.01 m g/kg IV, m ay repeat q5m in; not to exceed 0.4 m g I nt e ract ions

Other anticholinergics have additive effects ; m ay increas e pharm acologic effects of atenolol and digoxin;

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m ay decreas e antips ychotic effects of phenothiaz ines ; TCAs with anticholinergic activity m ay increas e effects Cont raindicat ions

Docum ented hypers ens itivity Pre caut ions P re g nanc y

C - Fetal ris k revealed in s tudies in anim als but not es tablis hed or not s tudied in hum ans ; m ay us e if benefits outweigh ris k to fetus P re c aut io ns

Avoid in patients with Down s yndrom e and/or in children with brain dam age to prevent hyperreactive res pons e; avoid in coronary heart dis eas e, thyrotoxicos is , narrow-angle glaucom a, CH F, cardiac arrhythm ias , and hypertens ion; caution in peritonitis , ulcerative colitis , hepatic dis eas e, and hiatal hernia with reflux es ophagitis ; in pros tatic hypertrophy or pros tatis m , m ay caus e dys uria requiring catheteriz ation

Alkalinizing agent s Are us eful in alkaliniz ation of urine. R outine adm inis tration of s odium bicarbonate is dis couraged becaus e it wors ens intracellular and intracerebral acidos is and is not proven to reduce m ortality rate.

Sodium bicarbonat e (Ne ut )

U s ed only when patient is diagnos ed with bicarbonate-res pons ive acidos is , hyperkalem ia, or TCA or phenobarbital overdos e. R outine us e not recom m ended. Dosing Ad ult

Initial: 1 m Eq/kg IV; depending on res ults of ABGs , additional dos es of 0.5 m Eq/kg m ay be given q10m in (us ual concentration is 7.5%) P e d iat ric

N ot es tablis hed I nt e ract ions

Induces urinary alkaliniz ation, which m ay decreas e levels of lithium , tetracyclines , chlorpropam ide, m ethotrexate, and s alicylates ; increas es levels of am phetam ines , ps eudoephedrine, flecainide, anorexiants , m ecam ylam ine, ephedrine, quinidine, and quinine Cont raindicat ions

Docum ented hypers ens itivity; alkalos is ; hypernatrem ia; hypocalcem ia; s evere pulm onary edem a; abdom inal pain of unknown caus e Pre caut ions

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P re g nanc y

C - Fetal ris k revealed in s tudies in anim als but not es tablis hed or not s tudied in hum ans ; m ay us e if benefits outweigh ris k to fetus P re c aut io ns

Can caus e alkalos is , decreas ed plas m a potas s ium , hypocalcem ia, and hypernatrem ia; caution in electrolyte im balances (eg, CH F, cirrhos is , edem a, corticos teroid us e, renal failure); avoid extravas ation s ince can caus e tis s ue necros is ; m ay caus e precipitation of calcium s alts if adm ixed

Follow-up Furt her Inpat ient Care Once res us citation is s ucces s ful, provide general care bas ed on individual needs . Special care s hould be taken to adequately treat the initial problem that led to puls eles s electrical activity.

T ransf er Som e ins titutions m ay not have the capability to provide s pecializ ed care (eg, cardiac s urgery, pulm onary em bolectom y). Once s tabiliz ed, patients in thes e centers m ay be trans ferred to tertiary care centers for definitive care.

Det errence/Prevent ion The following m eas ures m ay prevent s om e cas es of in-hos pital puls eles s electrical activity: Patients who have been on prolonged bed res t s hould receive deep venous throm bos is (DVT) prophylaxis . Patients who are on ventilators s hould be m onitored carefully for auto-PEEP developm ent. H ypovolem ia s hould be treated aggres s ively, es pecially in patients with active bleeding.

Prognosis The overall prognos is for patients with puls eles s electrical activity is poor, unles s a rapidly revers ible caus e is identified and corrected. Evidence s ugges ts that ECG characteris tics are related to the patient's prognos is . The m ore abnorm al the ECG characteris tics , the les s likely the patient is to recover from puls eles s electrical activity; patients with a wider QR S (>0.2 s ) fare wors e. Interes tingly, patients with out-of-hos pital puls eles s electrical activity are m ore likely to recover than patients who develop this condition in the hos pital. In one s tudy, 98 of 503 (19.5%) patients s urvived out-of-hos pital puls eles s electrical activity. This difference is likely becaus e of different etiologies and s everity of illnes s . Patients who are not in the hos pital are m ore likely to have revers ible etiologies (eg, hypotherm ia). Overall, puls eles s electrical activity rem ains a poorly unders tood entity with a dis m al prognos is . R evers ing this otherwis e lethal condition m ay be pos s ible by aggres s ively s eeking and prom ptly correcting revers ible caus es .

Pat ient Educat ion

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For excellent patient education res ources , vis it eM edicine's Public H ealth Center. Als o, s ee eM edicine's patient education article Cardiopulm onary R es us citation (CPR ).

Miscellaneous Medicolegal Pit f a lls Failure to obtain appropriate docum entation during and after advanced cardiac life s upport procedures .

References 1. R aiz es G, Wagner GS, H ackel DB. Ins tantaneous nonarrhythm ic cardiac death in acute m yocardial infarction. Am J Cardiol. Jan 1977;39(1):1-6. [M edline]. 2. N adkarni VM , Larkin GL, Peberdy M A, Carey SM , Kaye W, M ancini M E. Firs t docum ented rhythm and clinical outcom e from in-hos pital cardiac arres t am ong children and adults . JAMA. Jan 4 2006;295(1):50-7. [M edline]. 3. Des biens N A. Sim plifying the diagnos is and m anagem ent of puls eles s electrical activity in adults : a qualitative review. Crit Care Med. Feb 2008;36(2):391-6. [M edline]. 4. H utchings AC, Darcy KJ, Cum berbatch GL. Tens ion pneum othorax s econdary to autom atic m echanical com pres s ion decom pres s ion device. Emerg Med J. Feb 2009;26(2):145-6. [M edline]. 5. Steiger H V, R im bach K, M üller E, Breitkreutz R . Focus ed em ergency echocardiography: lifes aving tool for a 14-year-old girl s uffering out-of-hos pital puls eles s electrical activity arres t becaus e of cardiac tam ponade. Eur J Emerg Med. Apr 2009;16(2):103-5. [M edline]. 6. Fuz aylov G, Woods B, Dris coll W. Docum entation of res us citation of an infant with puls eles s electrical activity becaus e of venous air em bolis m . Paediatr Anaesth. N ov 2008;18(11):1121-3. [M edline]. 7. H az ins ki M F, N adkarni VM , H ickey R W, O'Connor R , Becker LB, Z arits ky A. M ajor changes in the 2005 AH A Guidelines for CPR and ECC: reaching the tipping point for change. Circulation. Dec 13 2005;112(24 Suppl):IV206-11. [M edline]. 8. N ichols R , Z awada E. A cas e s tudy in therapeutic hypotherm ia treatm ent pos t-cardiac arres t in a 56-year-old m ale. S D Med. Oct 2008;61(10):371-3. [M edline]. 9. Kotak D. Com m ent on Grm ec et al.: A treatm ent protocol including vas opres s in and hydroxyethyl s tarch s olution is as s ociated with increas ed rate of return of s pontaneous circulation in blunt traum a patients with puls eles s electrical activity. Int J Emerg Med. Apr 2009;2(1):57-8. [M edline]. 10. Grm ec S, Strnad M , Cander D, M ally S. A treatm ent protocol including vas opres s in and hydroxyethyl s tarch s olution is as s ociated with increas ed rate of return of s pontaneous circulation in blunt traum a patients with puls eles s electrical activity. Int J Emerg Med. Dec 2008;1(4):311-6. [M edline]. 11. Aufderheide TP, Thakur R K, Stueven H A. El ectrocardiographic characteris tics in EM D. Resuscitation. Apr 1989;17(2):183-93. [M edline]. 12. Berenyi KJ, Wolk M , Killip T. Cerebros pinal fluid acidos is com plicating therapy of experim ental

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cardiopulm onary arres t. Circulation. Aug 1975;52(2):319-24. [M edline]. 13. Chen Q, Scott BH , Bil finger TV, et al. Puls eles s electrical activity after induction of anes thes ia: A witnes s ed cardiac rupture. J Cardiothorac Vasc Anesth. Dec 2004;18(6):767-8. [M edline]. 14. Colwell C, M urphy P, Bryan T. Puls eles s electrical activity. Emerg Med Serv. Sep 2004;33(9):63-6, 68. [M edline]. 15. H erlitz J, R undqvis t S, Bang A, Aune S, Lunds trom G, Eks trom L, et al. Is there a difference between wom en and m en in characteris tics and outcom e after in hos pital cardiac arres t?. Resuscitation. Apr 2001;49(1):15-23. [M edline]. 16. H offm an JR , Stevens on LW. Pos tdefibrillation idioventricular rhythm --a s alvageable condition. West J Med. Feb 1987;146(2):188-91. [M edline]. 17. Kim C, Fahrenbruch CE, Cobb LA, Eis enberg M S. Out-of-hos pital cardiac arres t in m en and wom en. Circulation. N ov 27 2001;104(22):2699-703. [M edline]. 18. Paradis N A, M artin GB, Goetting M G. Aorti c pres s ure during hum an cardiac arres t. Identification of ps eudo- electrom echanical dis s ociation. Chest. Jan 1992;101(1):123-8. [M edline]. 19. Paris h DC, Dines h Chandra KM , Dane FC. Succes s changes the problem : why ventricular fibrillation is declining, why puls eles s electrical activity is em erging, and what to do about it. Resuscitation. Jul 2003;58(1):31-5. [M edline]. 20. Stueven H A, Aufderheide T, Waite EM . Electrom echanical dis s ociation: s ix years prehos pital experience. Resuscitation. Apr 1989;17(2):173-82. [M edline]. 21. Vincent JL, Thijs L, Weil M H . Clinical and experim ental s tudies on electrom echanical dis s ociation. Circulation. Jul 1981;64(1):18-27. [M edline]. 22. Warner LL, H offm an JR , Baraff LJ. Prognos tic s ignificance of field res pons e in out-of-hos pital ventricular fibrillation. Chest. Jan 1985;87(1):22-8. [M edline]. 23. Youngquis t ST, Kaji AH , N iem ann JT. Beta-blocker us e and the changing epidem iology of out-ofhos pital cardiac arres t rhythm s . Resuscitation. M ar 2008;76(3):376-80. [M edline].

Keywords puls eles s electrical activity, electrom echanical dis s ociation, cardiopulm onary res us citation, CPR , advanced cardiac life s upport, ACLS, cardia arres t, treatm ent, s ym ptom s , cardiac arrhythm ia, cardiac contractions , ventricular m echanical activity, ventricular electrical activity, EM D, PEA, ps eudo-PEA

Cont ribut or Informat ion and Disclosures Aut hor

Patrick O'Beirne, MD, Fellow in Cardiovas cular M edicine, U M as s M em orial M edical Center Patrick O'Beirne, M D is a m em ber of the following m edical s ocieties : Am erican College of Cardiology, Am erican M edical As s ociation, M as s achus etts M edical Society, and Phi Beta Kappa Dis clos ure: N othing to dis clos e.

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Coaut hor(s)

Dio nyssio s A Ro b o tis, MD, MPH, FACC, As s is tant Profes s or of M edicine, U nivers ity of M as s achus etts ; Cons ulting Staff Cardiologis t/Electrophys iologis t, U nivers ity of M as s achus etts M em orial M edical Center Dionys s ios A R obotis , M D, M PH , FACC is a m em ber of the following m edical s ocieties : Am erican College of Cardiology, Cardiac Electrophys iology Society, H eart R hythm Society, and M as s achus etts M edical Society Dis clos ure: N othing to dis clos e. Lawrence Ro senthal, MD, PhD, As s ociate Profes s or of M edicine, Director, Section of Cardiac Electrophys iology and Pacing, Fellows hip Director of Clinical Cardiac Electrophys iology, Departm ent of Internal M edicine, Divis ion of Cardiovas cular M edicine, U nivers ity of M as s achus etts M em orial M edical Center Lawrence R os enthal, M D, PhD is a m em ber of the following m edical s ocieties : Am erican College of Cardiology, Am erican H eart As s ociation, H eart R hythm Society, and M as s achus etts M edical Society Dis clos ure: N othing to dis clos e. Me dical Edit or

Eric Vand erb ush, MD, FACC, MD, Chief, Departm ent of Internal M edicine, Divis ion of Cardiology, Clinical As s is tant Profes s or, H arlem H os pital Center and Colum bia U nivers ity Eric Vanderbus h, M D, FACC, M D is a m em ber of the following m edical s ocieties : Am erican College of Cardiology and Am erican H eart As s ociation Dis clos ure: N othing to dis clos e. Pharmacy Edit or

Francisco T alavera, PharmD, PhD, Senior Pharm acy Editor, eM edicine Dis clos ure: N othing to dis clos e. Managing Edit or

Steven J Co mp to n, MD, FACC, FACP, Director of Cardiac Electrophys iology, Alas ka H eart Ins titute, Providence and Alas ka R egional H os pitals Steven J Com pton, M D, FACC, FACP is a m em ber of the following m edical s ocieties : Alas ka State M edical As s ociation, Am erican College of Cardiology, Am erican College of Phys icians , and H eart R hythm Society Dis clos ure: N othing to dis clos e. CME Edit or

Amer Suleman, MD, Cons ultant in Electrophys iology and Cardiovas cular M edicine, Departm ent of Internal M edicine, Divis ion of Cardiology, M edical City Dallas H os pital Am er Sulem an, M D is a m em ber of the following m edical s ocieties : Am erican College of Phys icians , Am erican H eart As s ociation, Am erican Ins titute of Stres s , Am erican Society of H ypertens ion, Federation of Am erican Societies for Experim ental Biology, R oyal Society of M edicine, and Society of Cardiac Angiography and Interventions Dis clos ure: N othing to dis clos e. Chie f Edit or

Jef f rey N Ro ttman, MD, Profes s or of M edicine and Pharm acology, Director, Clinical Cardiac Electrophys iology Fellows hip Program , Vanderbilt U nivers ity School of M edicine; Chief, Departm ent of Cardiology, N as hville Veterans Affairs M edical Center

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Jeffrey N R ottm an, M D is a m em ber of the following m edical s ocieties : Am erican H eart As s ociation and N orth Am erican Society of Pacing and Electrophys iology (N ASPE) Dis clos ure: N othing to dis clos e. Ackn owle dgm e n ts The authors and e ditors of e Me dicine grate fully acknowle dge the contributions of pre vious author Sumit Ve rma, MD, FACC and David S Marks , MD to the de ve lopme nt and writing of this article . Fu r th e r Re adin g Clin ical gu ide lin e s (1) ACC/AH A guide line s for the manage me nt of patie nts with ST-e le vation myocardial infarction. A re port of the Ame rican Colle ge of Cardiology/Ame rican H e art As s ociation Tas k Force on Practice Guide line s (Committe e to re vis e the 1999 guide line s for the Manage me nt of Acute Myocardial Infarction). (2) 2007 focus e d update of the ACC/AH A 2004 guide line s for the manage me nt of patie nts with ST-e le vation myocardial infarction. A re port of the Ame rican Colle ge of Cardiology/Ame rican H e art As s ociation Tas k Force on Practice Guide line s . Ame rican Colle ge of Cardiology Foundation - Me dical Spe cialty Socie ty Ame rican H e art As s ociation - Profe s s ional As s ociation. 1996 Nov 1 (re vis e d 2004 J ul; adde ndum re le as e d 2008 J an). Original guide line : 211 page s ; Focus e d update : 38. NGC:006289 Cardiac arrhythmias in coronary he art dis e as e . A national clinical guide line . Scottis h Inte rcolle giate Guide line s Ne twork - National Gove rnme nt Age ncy [Non-U .S.]. 2007 Fe b. 40 page s . NGC:005528 ACC/AH A/ESC 2006 guide line s for manage me nt of patie nts with ve nt ricular arrhythmias and the pre ve ntion of s udde n cardiac de ath. A re port of the Ame rican Colle ge of Cardiology/Ame rican H e art As s ociation Tas k Force and the Europe an Socie ty of Cardiology Committe e for Practice Guide line s (Writing Committe e to De ve lop Guide line s for Manage me nt of Patie nts With Ve nt ricular Arrhythmias and the Pre ve ntion of Sudde n Cardiac De ath). Ame rican Colle ge of Cardiology Foundation - Me dical Spe cialty Socie ty Ame rican H e art As s ociation - Profe s s ional As s ociation Europe an H e art Rhythm As s ociation - Profe s s ional As s ociation Europe an Socie ty of Cardiology - Me dical Spe cialty Socie ty H e art Rhythm Socie ty - Profe s s ional As s ociation. 2006 Se p 5. 100 page s . NGC:005208 Re s us citation and de fibrillation in the he alth care s e tting — 2004 re vis ion & update . Ame rican As s ociation for Re s piratory Care - Profe s s ional As s ociation. 1993 De c (re vis e d 2004 Se p). 15 page s . NGC:004081 Clin ical tr ials SmartCPR Trial: An Analys is of a Wave form-Bas e d Automate d Exte rnal De fibrillation (AED) Algorithm on Survival From Out-of-H os pital Ve ntricular Fibrillation Pre -Shock Cardiopulmonary Re s us citation to Patie nts With Out-of-H os pital Re s us citation, A Randomis e d Clinical Trial Efficacy of Me thylpre dnis olone for H antavirus Cardiopulmonary Syndrome Re late d e M e dicin e topics As ys tole (Eme rge ncy Me dicine ) Ve ntricular Fibrillation (Cardiology) Ve ntricular Fibrillation (Eme rge ncy Me dicine ) Ve ntricular Fibrillation (Pe diatrics ) Cardiopulmonary Re s us citation (CPR) (Proce dure s ) The rape utic H ypothe rmia (Proce dure s ) © 1994-2009 by Me ds cape . All Rights Re s e rve d (http://www.me ds cape .com/public/copyright)

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