KAMIKAZEKAMIKAZE

CARDIOLOGYCARDIOLOGY

Dr. Sam BendallDr. Sam Bendall

RPAHRPAH

General PrinciplesGeneral Principles

!Think BROADLYThink BROADLY

!Use your sieveUse your sieve

!Big picture stuffBig picture stuff

!Risk stratificationRisk stratification

! Position statements Position statements eg eg MJAMJA

!Know all the available guidelines etcKnow all the available guidelines etc

Approach to VAQ/ SAQApproach to VAQ/ SAQ

! Every word in the question is Every word in the question is imptimpt

! Underline the key wordsUnderline the key words

! Highlight what they want you to do Highlight what they want you to do egeg ““describedescribeand interpretand interpret””/ discuss etc/ discuss etc

! Ask yourself Ask yourself ““what are the key points they wantwhat are the key points they wantherehere””

! Are there any sentinel guidelines/protocols/riskAre there any sentinel guidelines/protocols/riskstratification tools that may applystratification tools that may apply

! Motherhood statement so they get that you get itMotherhood statement so they get that you get it

! Clear headings Clear headings –– do this so you don do this so you don’’t forgett forget

Thinking broadlyThinking broadly……

! SAQ 1SAQ 1 February/May 2008February/May 2008

A 68 year old woman has collapsed with a brief loss of consciousnessA 68 year old woman has collapsed with a brief loss of consciousnessin church this morning. She has been transported by ambulance toin church this morning. She has been transported by ambulance toyour emergency department and is currently asymptomatic.your emergency department and is currently asymptomatic.

DescribeDescribe your your assessment (assessment (hxhx/exam/Ix) /exam/Ix) and and risk stratificationrisk stratificationof this patient. (100%)of this patient. (100%)

The overall pass rate for this question was 48/62 (77.4%).The overall pass rate for this question was 48/62 (77.4%).

The examiners described this as a straight forward question on aThe examiners described this as a straight forward question on acommon presentation. Good answers directed their assessment to thecommon presentation. Good answers directed their assessment to thecommon potential causes in the given scenario. Poor answers eithercommon potential causes in the given scenario. Poor answers eitherfailed to answer the question by listing causes only or produced afailed to answer the question by listing causes only or produced atextbook answer in isolation to the scenario.textbook answer in isolation to the scenario.

So what are they really askingSo what are they really asking

about?about?

!Key points:Key points:

!! Older patient Older patient –– 68 68

!! Syncope Syncope –– causes IN HER POPULATION causes IN HER POPULATION

!! How are you going to risk stratify her forHow are you going to risk stratify her for

causes of syncope (and therefore how will thiscauses of syncope (and therefore how will this

affect your Ix/disposition)affect your Ix/disposition)

!! DESCRIBE question: DESCRIBE question: HxHx/exam/Ix/exam/Ix

Subarachnoid hemorrhageSubarachnoid hemorrhage

Saddle embolus resulting in outflow tract obstruction or severe hypoxiaSaddle embolus resulting in outflow tract obstruction or severe hypoxia

Pulmonary embolismPulmonary embolism

! Tissue rupture: aortic aneurysm, spleen, ovarian cyst, ectopic pregnancy, retroperitoneal hemorrhage Tissue rupture: aortic aneurysm, spleen, ovarian cyst, ectopic pregnancy, retroperitoneal hemorrhage

! Gastrointestinal bleeding Gastrointestinal bleeding

! Trauma with significant blood loss ** Less likely in THIS pt** Trauma with significant blood loss ** Less likely in THIS pt**

Significant hemorrhageSignificant hemorrhage

! Aortic dissection Aortic dissection

! Cardiac Cardiac tamponadetamponade

! AtrialAtrial myxomamyxoma

! CardiomyopathyCardiomyopathy (ischemic, dilated, hypertrophic) (ischemic, dilated, hypertrophic)

! ValvularValvular heart disease: aortic heart disease: aortic stenosisstenosis, mitral , mitral stenosisstenosis

Structural AbnormalitiesStructural Abnormalities

! Acute coronary syndrome, myocardial infarctionAcute coronary syndrome, myocardial infarction

IschaemiaIschaemia

! SignificantSignificant sinus pause >3 seconds sinus pause >3 seconds

! BradycardiaBradycardia: : MobitzMobitz type II or 3rd degree heart block type II or 3rd degree heart block

! BrugadaBrugada syndrome syndrome

! Long QT syndrome Long QT syndrome

! Ventricular tachycardia Ventricular tachycardia

ArrhythmiaArrhythmia

Cardiovascular syncope Cardiovascular syncope (from Up to Date 2008: major life threatening causes of syncope)(from Up to Date 2008: major life threatening causes of syncope)

Other Common Causes of Syncope Other Common Causes of Syncope (from Up to Date 2008:(from Up to Date 2008:

major life threatening causes of syncope)major life threatening causes of syncope)

! Diuretics Diuretics

AntiarrhythmicsAntiarrhythmics, , antiemeticsantiemetics, antipsychotics/depressants, antipsychotics/depressants

! Medications affecting the QT interval Medications affecting the QT interval

Alpha and beta blockers, calcium channel blockers, nitrates, antihypertensiveAlpha and beta blockers, calcium channel blockers, nitrates, antihypertensive

medications, diuretics, erectile dysfunction medicationsmedications, diuretics, erectile dysfunction medications

! VasoactiveVasoactive medications medications

Medication related syncopeMedication related syncope

! DeconditioningDeconditioning, prolonged bed rest, prolonged bed rest

! Autonomic Dysfunction Autonomic Dysfunction

! Volume Loss Volume Loss

Orthostatic HypotensionOrthostatic Hypotension

! Shaving Shaving

! Circumferential neck compression ( Circumferential neck compression (egeg neck tie) neck tie)

! Head turning Head turning

Carotid Sinus HypersensitivityCarotid Sinus Hypersensitivity

! Situational Situational

! GlossopharyngealGlossopharyngeal nercenerce

! Deglutination Deglutination

! Cough Mediated Cough Mediated

! Defecation Defecation

! MicturitionMicturition

NeurocardiogenicNeurocardiogenic Syncope Syncope

Stratification ToolsStratification Tools

! San Francisco Syncope RuleSan Francisco Syncope Rule

!Risk stratification Risk stratification –– ACS ACS –– high/med/low high/med/low

risk pt. Discussion of Ix with 2 CE risk pt. Discussion of Ix with 2 CE vsvs

admission for stress test etcadmission for stress test etc

!Risk stratification PE Risk stratification PE –– Wells /PERC/Revised Wells /PERC/Revised

Geneva ScoreGeneva Score

! The The San Francisco Syncope RuleSan Francisco Syncope Rule (SFSR) is a simple rule for evaluating the risk of adverse (SFSR) is a simple rule for evaluating the risk of adverseoutcomes in patient who present with outcomes in patient who present with faintingfainting or or syncopesyncope..

! The mnemonic for features of the rule is CHESS:The mnemonic for features of the rule is CHESS:! •• CC - History of congestive heart failure - History of congestive heart failure! •• HH - - HematocritHematocrit < 30% < 30%! •• EE - Abnormal - Abnormal EKGEKG! •• SS - Shortness of breath - Shortness of breath! •• SS - Triage systolic - Triage systolic blood pressureblood pressure < 90 < 90

! A patient with any of the above measures is considered at high risk for a serious outcomeA patient with any of the above measures is considered at high risk for a serious outcome(death, MI, (death, MI, arrhythmiaarrhythmia, PE, , PE, strokestroke, SAH, need for transfusion, return emergency department, SAH, need for transfusion, return emergency departmentvisits within 30 days).visits within 30 days).

! SFSR has a sensitivity of 74-98% and specificity of 56%.SFSR has a sensitivity of 74-98% and specificity of 56%.[1][1] [2][2] This means that 74-98% of This means that 74-98% ofpatients who had a serious outcome had a positive test. This makes the test good for rulingpatients who had a serious outcome had a positive test. This makes the test good for rulingout hospital admissions for patients with syncope.out hospital admissions for patients with syncope.

! Syncope accounts for 1-2% Syncope accounts for 1-2% emergency departmentemergency department visits. Half are hospitalized and of these, visits. Half are hospitalized and of these,50% have unclear diagnosis and 85% will be simply monitored. Given these statistics, the50% have unclear diagnosis and 85% will be simply monitored. Given these statistics, theSFSR will help reduce inefficient admissions.SFSR will help reduce inefficient admissions.

! ReferencesReferences! ^̂ Quinn J, McDermott D, Quinn J, McDermott D, StiellStiell I, Kohn M, Wells G (May 2006). "Prospective validation of the I, Kohn M, Wells G (May 2006). "Prospective validation of the

San Francisco Syncope Rule to predict patients with serious outcomes". San Francisco Syncope Rule to predict patients with serious outcomes". Ann Ann EmergEmerg Med Med 4747(5): 448(5): 448––54. 54. doidoi::10.1016/j.annemergmed.2005.11.01910.1016/j.annemergmed.2005.11.019. . PMID 16631985PMID 16631985..

! ^̂ BirnbaumBirnbaum A, A, EssesEsses D, D, BijurBijur P, P, WollowitzWollowitz A, Gallagher EJ (February 2008). "Failure to Validate A, Gallagher EJ (February 2008). "Failure to Validatethe San Francisco Syncope Rule in an Independent Emergency Department Population". the San Francisco Syncope Rule in an Independent Emergency Department Population". AnnAnnEmergEmerg Med Med. . doidoi::10.1016/j.annemergmed.2007.12.00710.1016/j.annemergmed.2007.12.007. . PMID 18282636PMID 18282636..

! FROM WIKIPEDIAFROM WIKIPEDIA

MD CALCMD CALC

! San Francisco Syncope Rule to Predict Serious OutcomesSan Francisco Syncope Rule to Predict Serious Outcomes! CCongestive Heart Failure history?ongestive Heart Failure history? Yes +1Yes +1

! HHematocritematocrit < 30%? < 30%? Yes +1Yes +1! EECG Abnormal ?CG Abnormal ? Yes +1Yes +1

! SShortness of Breath History?hortness of Breath History? Yes +1Yes +1! SSystolic BP < 90 mmHg at ystolic BP < 90 mmHg at Triage?YesTriage?Yes +1 +1

! Score points Note: This rule has a 96% sensitivity and 62% specificityScore points Note: This rule has a 96% sensitivity and 62% specificityfor serious outcome. Negative predictive value: 99.2%; positivefor serious outcome. Negative predictive value: 99.2%; positivepredictive value 24.8%.predictive value 24.8%.

! Serious Outcome in this study is defined as "death, myocardialSerious Outcome in this study is defined as "death, myocardialinfarction, arrhythmia, pulmonary embolism, stroke, subarachnoidinfarction, arrhythmia, pulmonary embolism, stroke, subarachnoidhemorrhage, significant hemorrhage, or any condition causing ahemorrhage, significant hemorrhage, or any condition causing areturn ED visit and hospitalization for a related event."return ED visit and hospitalization for a related event."

Validation of the San Francisco Syncope Rule

The rule looks promising for identifying patients at risk for serious outcomes.

The causes of syncope range from potentially fatal to inconsequential. As a result, many patients are hospitalized forobservation and work-up who might safely have been discharged home with follow-up. Admitted patients rarely have anywork-up beyond 24 hours of cardiac monitoring and simple blood testing.

These authors previously derived a syncope risk-stratification tool, dubbed the San Francisco Syncope Rule, and in thisstudy they sought to prospectively validate it.

The rule categorizes patients as at high risk for serious outcomes if they have a history of congestive heart failure,hematocrit <30%, electrocardiogram abnormality, shortness of breath, or systolic blood pressure <90 mm Hg (the criteriacan be remembered by the mnemonic, CHESS).

Serious outcomes were defined broadly as death, myocardial infarction, arrhythmia, pulmonary embolism, stroke,subarachnoid hemorrhage, significant hemorrhage or anemia requiring transfusion, a procedural intervention to treat arelated cause of syncope or any condition causing or likely to cause a return emergency department visit, andhospitalization for a related event.

The authors applied the rule to 791 ED patients who presented with syncope, defined as any transient loss of consciousnessnot due to trauma, intoxication, or seizure. Patients were followed up at 30 days. Overall, 411 patients (52%) werecategorized as high risk. At follow-up, 53 patients (6.7%) had serious outcomes that were not clinically apparent at EDpresentation. The rule was 98% sensitive and 56% specific for predicting these events.

Comment: Syncope often presents a conundrum, as patients often look remarkably well after the syncopal episode, yetdischarging a patient who has a significant cause of syncope may have dire consequences. The San Francisco SyncopeRule might make discharge decisions easier, but before we can adopt it, larger, multicenter studies are needed.

— Richard D. Zane, MD, FAAEM

Published in Journal Watch Emergency Medicine July 21, 2006

Citation(s):Quinn J et al. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann

Emerg Med 2006 May; 47:448-54.Medline abstract (Free)

Miller CD and Hoekstra JW. Prospective validation of the San Francisco Syncope Rule: Will it change practice? Ann Emerg

Med 2006 May; 47:455-6.

The San Francisco Syncope Rule in the Land Down UnderThe rule was no better than physician judgment for predicting serious adverse outcomes in this Australian study.

The San Francisco Syncope Rule was developed to identify syncope patients who could safely be discharged home withoutrisk for serious short-term adverse outcomes. To evaluate the utility and performance of the rule in an Australian setting,researchers studied 89 adult patients with syncope or presyncope who were identified either prospectively when theypresented to the emergency department (87%) or retrospectively by chart review (13%).

The rule classifies patients as high risk if they have any one of five features: abnormal electrocardiogram, hematocrit lessthan 30%, shortness of breath, history of congestive heart failure, or systolic blood pressure less than 90 mm Hg. In thisstudy, serious adverse outcomes were defined as occurrence of any of the following within 7 days after presentation:myocardial infarction, arrhythmia, pulmonary embolism, stroke, subarachnoid hemorrhage, significant hemorrhage, orunscheduled admission or acute intervention in a hospitalized patient.

Patients had a median age of 74 (range, 20–93); 42% were men and 39% were admitted. Ten patients (11%) had a total of 12serious adverse events, including one death after MI. Application of the rule predicted 43 patients as high risk for a seriousadverse event; 9 suffered a serious event. The remaining patient with a serious adverse event was classified by the rule aslow risk. Of the admitted patients, 66% were classified as high risk. The rule had an overall sensitivity of 90%, specificity of57%, positive predictive value of 21%, and negative predictive value of 98% for identifying patients at risk for serious adverseoutcomes. Physicians’ clinical judgment performed similarly well, with a sensitivity of 90% and a specificity of 60%.

In an editorial, one of the originators of the rule reminds us that syncope patients cost the U.S. healthcare system anestimated $2 billion, and that low-risk patients account for a large proportion of that amount.

Comment: This small study of nonconsecutive patients with only 80% follow-up does not permit us to either embrace or

discard the San Francisco Syncope Rule. What the study illustrates, as the editorialist suggests, is that physicians in other

countries may already be discharging a much higher percentage of syncope patients than their medical-legal risk-averse

U.S. colleagues. Until we have better prospective validation of syncope rules, clinical judgment will remain the gold

standard.

— Kristi L. Koenig, MD, FACEP

Published in Journal Watch Emergency Medicine June 8, 2007

Citation(s):Cosgriff TM et al. External validation of the San Francisco Syncope Rule in the Australian context. CJEM 2007 May; 9:157-61.

Medline abstract (Free)

Quinn J. Risk stratification of patients with syncope. CJEM 2007 May; 9:174-5.Medline abstract (Free)

San Francisco Syncope Rule: Less Sensitive Than Previously ReportedAn independent validation study demonstrated a sensitivity of only 74% for predicting serious outcomes.

Most patients who present with syncope have benign etiologies, but, for some, syncope is caused by a potentially

life-threatening condition. Differentiating between the two etiologies is often difficult in an emergency department,

and, as a result, many patients are admitted who might not require inpatient work-up. The San Francisco

Syncope Rule was developed to identify low-risk syncope, and the original study reported 96% sensitivity for

detection of short-term (7-day) serious outcomes, defined as death, myocardial infarction, arrhythmia, pulmonary

embolism, stroke, subarachnoid hemorrhage, significant hemorrhage, or any condition causing or likely to cause

a return ED visit and hospitalization for a related event. Although sensitivity was 98% in a subsequent validation

study (JW Emerg Med Jul 21 2006, more recent studies have not reproduced those results (Ann Emerg Med

2007; 49:420).

The rule categorizes patients as high risk for serious outcomes if they have any of the following features(remembered by the mnemonic CHESS): history of congestive heart failure, hematocrit <30%, abnormalelectrocardiogram, shortness of breath, or systolic blood pressure <90 mm Hg.

In a prospective, observational cohort validation study, researchers applied the rule to 713 adult patientswho presented to a university hospital ED with acute syncope or near syncope and followed the patientsat 7 days to detect serious outcomes. Of 61 patients (9%) with serious outcomes, 16 (26%) had not been

identified as high risk by the rule. Sensitivity of the rule to predict serious outcomes was 74%, specificitywas 57%, negative likelihood ratio was 0.5, and positive likelihood ratio was 1.7.

Comment: Although the San Francisco Syncope Rule initially seemed promising, further study has

shown that it might not be sufficiently sensitive or specific to differentiate benign from potentially

dangerous causes of syncope. The rule should not be used.

— Richard D. Zane, MD, FAAEM

Published in Journal Watch Emergency Medicine September 19, 2008

Citation(s):Birnbaum A et al. Failure to validate the San Francisco Syncope Rule in an independent emergency

department population. Ann Emerg Med 2008 Aug; 52:151.Medline abstract (Free)

ACS risk stratificationACS risk stratification

PE risk stratificationPE risk stratification

!WELLSWELLS

! PERCPERC

!Revised Geneva ScoreRevised Geneva Score

!Wells' Criteria for Assessment ofWells' Criteria for Assessment of

PretestPretest Probability for Pulmonary Probability for Pulmonary

•Hemoptysis

•Malignancy (on treatment, treated in the past six months or

palliative)

•Previous DVT or PE

•Immobilization or surgery in the previous four weeks

•Heart rate >100 beats per minute

•An alternative diagnosis is less likely than PE

•Suspected DVT

Criteria

1.0

1.0

1.5

1.5

1.5

3.0

3.0

PointsPoints

>6 points

2 to 6

points

<2 points

Scorerange

66.7

20.5

3.6

Meanprobabilityof PE, %

High

Moderate

Low

Interpretationof risk

•Stop pathway if no risk PE

•Further PE investigation:•CTPA – unless C/I

•Can have V/Q if :•On site

•Normal CXR

•No CAL / CCF

•Can be done in

timely fashion

•Book CTPA

•Contact either:•Respiratory registrar

•Medical registrar

•Respiratory consultant

on call

•discuss anticoagulation

If D/C home

•U/S legs ( outpt .)

•GP follow up

•If DVT – return to ED

•If no DVT – repeat U/S

14 days

Is the PERC rule ready for general use based upon availableevidence? As recently stated, "larger prospective validation

with interrater reliability testing is needed beforewidespread implementation of the PERC rule is made" (1).

The Pulmonary Embolism Rule-out Criteria (PERC Rule)1. Age <502. Pulse oximetry > 94% (breathing room air)3. Heart rate <100 beats/min4. No prior VTE5. No recent surgery or trauma (requiring hospitalization or

intubation within prior 4 weeks)6. No Haemoptysis7. No estrogen use8. No unilateral leg swelling

References: (1) Wolf SJ, et al. Assessment of the pulmonaryembolism rule-out criteria rule for evaluation of suspectedpulmonary embolism in the emergency department Am JEmerg Med 2008; 26 181-185

(2) Kline JA, Mitchell AM, Kabrhel C, et al.. Clinical criteria toprevent unnecessary diagnostic testing in emergencydepartment patients with suspected pulmonary embolism. JThromb Haemost. 2004;2:1247–1255.

Acute Coronary SyndromeAcute Coronary Syndrome

ACS - other pointsACS - other points

!Risk stratification (mentioned earlier)Risk stratification (mentioned earlier)

!Know patterns and what is special aboutKnow patterns and what is special about

each oneeach one

!! EgEg Inferior infarct Inferior infarct –– RV involvement, prone to RV involvement, prone to

hypotension so need to keep pt well preloaded.hypotension so need to keep pt well preloaded.

Avoid nitrates. Consider dissection as Avoid nitrates. Consider dissection as aetiologyaetiology

if consistent with if consistent with HxHx

!! WellensWellens syndrome syndrome

VAQ 1 February/May 2007VAQ 1 February/May 2007

! A 54 year old man presents with one hour of severe central chest pain.A 54 year old man presents with one hour of severe central chest pain.! His initial observations are:His initial observations are:! BP 80/60 mmHg supineBP 80/60 mmHg supine! O2 saturation 97% room airO2 saturation 97% room air! His 12 lead ECG is shown, with three additional right-sided His 12 lead ECG is shown, with three additional right-sided praecordialpraecordial leads. leads.! a. Describe and interpret the a. Describe and interpret the ECGsECGs. (50%). (50%)! b. Outline your treatment of his hypotension. (50%)b. Outline your treatment of his hypotension. (50%)

! ECG showed changes consistent with a right ventricular and inferior wall leftECG showed changes consistent with a right ventricular and inferior wall leftventricular infarct.ventricular infarct.

! The overall pass rate for this question was 38/55 (69.1%).The overall pass rate for this question was 38/55 (69.1%).! This question was regarded as highly discriminative by the examiners. GoodThis question was regarded as highly discriminative by the examiners. Good

answers provided a systematic approach to the ECG and a good discussion ofanswers provided a systematic approach to the ECG and a good discussion offluid loading and reperfusion strategies. Failed responses failed to adequatelyfluid loading and reperfusion strategies. Failed responses failed to adequatelyinterpret the ECG and/or mention reperfusion.interpret the ECG and/or mention reperfusion.

ArrhythmiasArrhythmias

!AF AF –– new 2008 guidelines new 2008 guidelines –– rate rate vsvs rhythm rhythm

controlcontrol

The Bottom LineThe Bottom Line

AFAF

! AnticoagulationAnticoagulation

! Stroke incidence Stroke incidence vsvs Risk of Risk of haemorrhagehaemorrhage –– (Dunn (Dunn

pg 119)pg 119)

! Medication options for rate and rhythm controlMedication options for rate and rhythm control

! CardioversionCardioversion

! InvestigationsInvestigations

! *** Excellent overview of AF Dunn pgs 118 *** Excellent overview of AF Dunn pgs 118 –– 122) 122)

ECGsECGs –– espesp for for VAQsVAQs

- General Principles- General Principles

!Do the basics well.Do the basics well.

!Rate, rhythm, axis, P wave, PR intervalRate, rhythm, axis, P wave, PR interval

(any depression??), QRS complex, ST(any depression??), QRS complex, ST

segment, T waves, U waves. Any extras?segment, T waves, U waves. Any extras?

! Interpret Interpret –– BROAD differential BROAD differential

!! Implications for RxImplications for Rx

!! PrognosisPrognosis

!! DispositionDisposition

ECGsECGs –– pop pop quizzquizz

Pop Pop quizzquizz 2. The patient 2. The patient’’s ECGs ECG

without pain. (normal initial ECGwithout pain. (normal initial ECG

with pain)with pain)

Pop Pop quizzquizz 3 3

Pop Pop quizzquizz 4 4

My My DDxDDx for last slide for last slide

! Electrolyte abnormalities Electrolyte abnormalities –– likely likely HyperkalaemiaHyperkalaemia

! IschaemiaIschaemia

! Toxins : TCA + any other Na channel blocking agents (31Toxins : TCA + any other Na channel blocking agents (31drugs drugs –– see pg 275 Chan), potentially ABCD drugs see pg 275 Chan), potentially ABCD drugs ––amiodaroneamiodarone, B blockers (, B blockers (espesp mixed such as mixed such as sotalolsotalol)**, Ca)**, Cachannel blockers, channel blockers, DigoxinDigoxin ( (hyperkalaemiahyperkalaemia))

! ** Certain B blockers have membrane ** Certain B blockers have membrane stabilisingstabilising activity activitywhich has been attributed to the blockade of fast sodiumwhich has been attributed to the blockade of fast sodiumchannels in myocardial cells by these agents. Na channelchannels in myocardial cells by these agents. Na channelblockade prolongs the action potential and causesblockade prolongs the action potential and causeswidening of the QRS complex > 0.12s.widening of the QRS complex > 0.12s.

Implications for managementImplications for management! Rx of Rx of hyperKhyperK ( (salbutamolsalbutamol/Ca/insulin and dextrose/resonium/HCO3/dialysis)/Ca/insulin and dextrose/resonium/HCO3/dialysis)

! BUT if BUT if HxHx suggestive of suggestive of DigoxinDigoxin toxicity toxicity –– do NOT give calcium for do NOT give calcium for hyperkalaemiahyperkalaemia

!! (Dig inactivates the Na/K (Dig inactivates the Na/K ATPaseATPase pump which usually maintains the electrochemical membrane pump which usually maintains the electrochemical membranepotential by conducting Na potential by conducting Na extracellularlyextracellularly and K and K intracellularlyintracellularly..

!! When inhibited the Na/Ca exchanger removes accumulated Na in exchange for Ca. This exchangeWhen inhibited the Na/Ca exchanger removes accumulated Na in exchange for Ca. This exchangeincreases increases sarcoplasmicsarcoplasmic Ca thereby causing the positive Ca thereby causing the positive inotropyinotropy. Dig toxicity results from an. Dig toxicity results from anexaggeration of its therapeutic action.)exaggeration of its therapeutic action.)

!! Pathological in OD Pathological in OD –– intracellular Ca overload in dig toxic patients causes delayed intracellular Ca overload in dig toxic patients causes delayedafterdepolarizationsafterdepolarizations and gives rise to triggered and gives rise to triggered dysrhythmiasdysrhythmias. So Do NOT give Ca for. So Do NOT give Ca forhyperkalaemiahyperkalaemia in Dig toxicity in Dig toxicity..

! Ca channel blocker OD Ca channel blocker OD –– calcium, insulin & dextrose calcium, insulin & dextrose euglycaemiceuglycaemic Rx, Catecholamine infusion, Rx, Catecholamine infusion,HCO3 for metabolic acidosis, cardiac (ventricular) pacing, Cardiopulmonary bypass/IABP.HCO3 for metabolic acidosis, cardiac (ventricular) pacing, Cardiopulmonary bypass/IABP.

! B blocker B blocker –– Atropine, adrenaline / Atropine, adrenaline / isoprenalineisoprenaline/glucagon, insulin dextrose /glucagon, insulin dextrose euglycaemiceuglycaemicinotropyinotropy. Wide QRS = HCO3. . Wide QRS = HCO3. TorsadesTorsades des pointes des pointes –– isoprenaline/MgSO4/ Overdrive pacing (** isoprenaline/MgSO4/ Overdrive pacing (**propranololpropranolol acts as an Na channel blocker) acts as an Na channel blocker)

! TCA (and other Na channel blockers = HCO3 ++/ fluids/ TCA (and other Na channel blockers = HCO3 ++/ fluids/ inotropes/lignocaineinotropes/lignocaine as second line Rx as second line Rxwhen pH> 7.5)when pH> 7.5)

! DigoxinDigoxin –– Dig Dig fabfab fragments (HCO3/Insulin & dextrose for hyper K, Atropine for AV block/ fragments (HCO3/Insulin & dextrose for hyper K, Atropine for AV block/LignocaineLignocaine for ventricular for ventricular dysrhythmiasdysrhythmias) AVOID CALCIUM) AVOID CALCIUM

! IschaemiaIschaemia –– as per ACS- aspirin/ as per ACS- aspirin/ clopidogrelclopidogrel /heparin/ reperfusion /heparin/ reperfusion

! Seek and treat other causes Seek and treat other causes egeg SAH SAH –– CT head/ LP CT head/ LP

Prognosis/DispositionPrognosis/Disposition

!HyperkalaemiaHyperkalaemia –– prognosis depends on prognosis depends onunderlying cause and ability to reverseunderlying cause and ability to reverseunderlying causes. Diastolic arrest likely ifunderlying causes. Diastolic arrest likely ifnot treated emergentlynot treated emergently

!Dig/Ca Channel blocker/B blocker/TCA Dig/Ca Channel blocker/B blocker/TCA ––Need definitive Rx/ supportive care andNeed definitive Rx/ supportive care andmaintenance of cardiac output maintenance of cardiac output –– ICU ICU

! IschaemiaIschaemia –– reperfusion. Risk of reperfusion. Risk ofarrhythmias.arrhythmias.

VAQ 6 February/May 2005VAQ 6 February/May 2005

! A 65 year old woman is brought to the emergency department following a collapse at home. She isA 65 year old woman is brought to the emergency department following a collapse at home. She ispale with a BP of 75 mmHg (systolic), respiratory rate of 25/minute, a GCS of 13/15 and an SaO2 ofpale with a BP of 75 mmHg (systolic), respiratory rate of 25/minute, a GCS of 13/15 and an SaO2 of92% on 6 92% on 6 litreslitres/minute of oxygen. An ECG is performed. /minute of oxygen. An ECG is performed. The ECG shows a bizarre broadThe ECG shows a bizarre broad

! complex rhythm at about 70 complex rhythm at about 70 bpmbpm with non capturing dual pacemaker spikes. with non capturing dual pacemaker spikes.

! a. Describe and interpret her ECG. (50%)a. Describe and interpret her ECG. (50%)! b. Outline your initial management priorities for this woman. (50%)b. Outline your initial management priorities for this woman. (50%)

! Overall pass rate for this question was 37 / 44 (84.1%).Overall pass rate for this question was 37 / 44 (84.1%).

! Examiners felt this VAQ tested fundamental emergency medicine knowledge and skills. It wasExaminers felt this VAQ tested fundamental emergency medicine knowledge and skills. It was

! essential that the description include essential that the description include hyperkalemiahyperkalemia as a possible explanation for the broad as a possible explanation for the broadcomplex rhythm. Stronger answers noted the presence of the pacing spikes though this was notcomplex rhythm. Stronger answers noted the presence of the pacing spikes though this was notconsidered essential to pass.considered essential to pass.

! It was expected that other possible explanations such as It was expected that other possible explanations such as ischaemiaischaemia and drug toxicity and drug toxicity would wouldbe considered.be considered.

! Management needed to include full resuscitation area supportiveManagement needed to include full resuscitation area supportivecare but had to focus on urgent management of the presumedcare but had to focus on urgent management of the presumedhyperkalaemiahyperkalaemia as well as volume loading, maintenance of as well as volume loading, maintenance ofoxygenation and probable need for oxygenation and probable need for chronotropes/inotropeschronotropes/inotropes..

Have a Broad DifferentialHave a Broad Differential

! IschaemiaIschaemia

!Toxicological causesToxicological causes

! Electrolyte abnormalitiesElectrolyte abnormalities

!Metabolic abnormalities (eg hypothermia)Metabolic abnormalities (eg hypothermia)

!Other cardiac eg Other cardiac eg tamponnadetamponnade, pericarditis, pericarditis

!Congenital Congenital AbormalitiesAbormalities eg WPW eg WPW

! Extracardiac eg neurological (SAH)/Extracardiac eg neurological (SAH)/Respiratory (PE)Respiratory (PE)

ECGsECGs you NEED to know - you NEED to know - these arethese are

pathognomonicpathognomonic for certain conditions for certain conditions

1.1. PE PE –– S1 Q3 T3 S1 Q3 T3

2.2. Broad Complex Tachycardia Broad Complex Tachycardia –– both VT and SVT with aberrancy both VT and SVT with aberrancy

3.3. WPW WPW –– orthodromicorthodromic and and antidromicantidromic

4.4. BrugardaBrugarda Syndrome Syndrome

5.5. 33rdrd Degree heart blocks Degree heart blocks inclincl B blocker, Ca channel blockers, B blocker, Ca channel blockers, DigoxinDigoxin (BCD) (BCD)

6.6. 22ndnd degree blocks degree blocks –– WenkebachWenkebach/ / MobitzMobitz type II type II

7.7. Posterior infarctPosterior infarct

8.8. RV infarctRV infarct

9.9. Electrolyte abnormalities Electrolyte abnormalities –– hyper and hypo K/ Ca/ Mg hyper and hypo K/ Ca/ Mg

10.10. Na channel blockade Na channel blockade –– TCA, Class TCA, Class IaIa, , IcIc and III and III antiarrhythmicsantiarrhythmics

11.11. Prolonged Prolonged QTcQTc and CAUSES and CAUSES

12.12. Pericarditis/myocarditisPericarditis/myocarditis

13.13. ACSACS

14.14. WellensWellens syndrome syndrome

15.15. Hypothermia Hypothermia –– Osborn J waves Osborn J waves

16.16. TorsadesTorsades des pointes des pointes

17.17. PaediatricPaediatric ECG ECG –– RV dominant RV dominant –– know what is normal! know what is normal!

Electrolyte effects on ECGElectrolyte effects on ECG

! HyponatraemiaHyponatraemia: low voltage ECG complexes: low voltage ECG complexes

! HyperkalaemiaHyperkalaemia

!! Altered Altered repolarisationrepolarisation causes tall peaked T waves causes tall peaked T waves

!! AtrialAtrial paralysis paralysis

!! Prolongation of the QRS complexesProlongation of the QRS complexes

!! Ventricular arrhythmiasVentricular arrhythmias

!! Decreased resting membrane potential Decreased resting membrane potential –– fibresfibres eventually become unexcitable and the heart stops eventually become unexcitable and the heart stopsin diastolein diastole

! HypokalaemiaHypokalaemia

!! Prolongation of the PR intervalProlongation of the PR interval

!! Prominent U wavesProminent U waves

!! Occasional late T wave inversion in Occasional late T wave inversion in praecordialpraecordial leads leads

!! QT interval appears prolonged if T and U waves merge (the real QT interval is not prolongedQT interval appears prolonged if T and U waves merge (the real QT interval is not prolonged

!! Widened QRS if severeWidened QRS if severe

! HypercalcaemiaHypercalcaemia

!! Rarely high enough to affect the heartRarely high enough to affect the heart

!! Enhances myocardial contractilityEnhances myocardial contractility

!! Less diastolic relaxationLess diastolic relaxation

!! Heart eventually stops in systoleHeart eventually stops in systole

! HypocalcaemiaHypocalcaemia

!! Prolongs the ST segment and QT intervalProlongs the ST segment and QT interval

Pop Pop quizzquizz 5 5

! During ORT the ventricle is depolarised via the normal conduction system, and is aDuring ORT the ventricle is depolarised via the normal conduction system, and is a

narrow complex tachycardia with a short RPnarrow complex tachycardia with a short RP’’ interval (short RP interval (short RP’’ tachycardia) tachycardia)

So whatSo what’’s this?s this?

And this?And this?

• AF: AF is encountered in 10% to 35% of patients with WPW syndrome. AF with rapid conduction via

the AP is recognised by an irregular WCT with a varying degree of ventricular pre-excitation. Patientswith a rapidly conducting AP or multiple APs are at a risk for VF due to rapid ventricular stimulation.

And thisAnd this……

• Atrial flutter and atrial tachycardia: Atrial flutter and atrial tachycardia can result in a regular pre-

excited WCT. Atrial flutter is encountered in 5% to 10% of patients with WPW syndrome. If theconduction is rapid, especially during atrial flutter with 1:1 AV conduction, then rapid stimulation ofventricle can also result in VF. AV nodal Wenckebach pattern over the AV node or the AP in atrial

flutter and AF can result in an irregular WCT.

So what do you DO about WPW?So what do you DO about WPW?

! OrthodromicOrthodromic conducted - treat like any other SVT conducted - treat like any other SVT

! AntidromicAntidromic (SVT) (SVT)–– do NOT give Ca channel blockers or anything that do NOT give Ca channel blockers or anything thatwill block the AV node and therefore increase conduction in thewill block the AV node and therefore increase conduction in theABNORMAL accessory pathway ABNORMAL accessory pathway –– may precipitate VT. may precipitate VT.!! ProcainamideProcainamide or or flecainideflecainide are usually effective alternatives are usually effective alternatives

!! Electricity!Electricity!

! AF/ Flutter + WPW AF/ Flutter + WPW –– verapamilverapamil and and digoxindigoxin enhance conduction enhance conductionthrough accessory pathway.through accessory pathway.

! Adenosine unlikely to be of benefit and may increase ventricularAdenosine unlikely to be of benefit and may increase ventricularresponse.response.

! FlecainideFlecainide = drug of choice for AF + WPW in the structurally normal = drug of choice for AF + WPW in the structurally normalheart without coronary disease. Slows heart without coronary disease. Slows conducionconducion in accessory in accessorypathways.pathways.!! Dose = 150mg IV over 30 mins (2mg/kg)Dose = 150mg IV over 30 mins (2mg/kg)

Prolonged Prolonged QTcQTc! Causes of prolonged QT interval:Causes of prolonged QT interval:

! At normal sinus rates greater than 0.44 At normal sinus rates greater than 0.44 secssecs..

! General rule of thumb is that General rule of thumb is that qtcqtc should be less than half the preceding RR interval. should be less than half the preceding RR interval.

! Congenital Long QT syndromesCongenital Long QT syndromes::

! familial QT prolongation assoc with syncope, sudden death and congenital deafness = familial QT prolongation assoc with syncope, sudden death and congenital deafness = JervellJervell and Lange- and Lange- NeilsenNeilsensyndrome.syndrome.

! Similar = Romano ward but no hearing loss.Similar = Romano ward but no hearing loss.

! MV MV prolapseprolapse –– may occur and may be marker of ventricular may occur and may be marker of ventricular dysrhythmiadysrhythmia..

! CNSCNS: SAH, ICH, : SAH, ICH, thromboembolicthromboembolic CVA. CVA.

! Also get a marked increase in T wave amplitude often with deep symmetric T wave inversion (roller coaster TAlso get a marked increase in T wave amplitude often with deep symmetric T wave inversion (roller coaster Twaves) is another characteristic.waves) is another characteristic.

! Metabolic syndromesMetabolic syndromes::

!! HypokalaemiaHypokalaemia and hypocalcaemia and hypocalcaemia –– cause QT prolongation. cause QT prolongation.

!! HypomagnasaemiaHypomagnasaemia doe NOT directly prolong the QT interval BUT effects in presence of low Mg may be due doe NOT directly prolong the QT interval BUT effects in presence of low Mg may be dueto low K and Ca existing concurrently.to low K and Ca existing concurrently.

!! HypokalaemiaHypokalaemia also causes ST depression, T wave flattening and U waves. also causes ST depression, T wave flattening and U waves.

!! Hypocalcaemia does not cause these.Hypocalcaemia does not cause these.

! HypothyroidismHypothyroidism: may cause QT : may cause QT prologationprologation + + bradycardiabradycardia + low voltage + T wave changes. + low voltage + T wave changes.

! HypothermiaHypothermia: can cause prolongation of all intervals in cardiac cycle. Seek characteristic J waves ( Osborn waves): can cause prolongation of all intervals in cardiac cycle. Seek characteristic J waves ( Osborn waves)after the QRS complex as well as after the QRS complex as well as bradyarrhythmiasbradyarrhythmias (sinus brady/ AF with slow ventricular response). (sinus brady/ AF with slow ventricular response).

! Drug EffectsDrug Effects::

!! -K channel blockers-K channel blockers

!! Some Some antiarrythmicsantiarrythmics: : espesp Vaughan Williams class 1a 1c and III agents. May prolong the QT interval with or Vaughan Williams class 1a 1c and III agents. May prolong the QT interval with orwithout widening the QRS complex depending on the drug.without widening the QRS complex depending on the drug.

!! Psychotropic meds Psychotropic meds inclincl haloperidol and haloperidol and DroperidolDroperidol. . OlanzapineOlanzapine less less

!! Antibiotics: Antibiotics: sparfloxacinsparfloxacin, erythromycin, , erythromycin, clarithromycinclarithromycin, , pentamidinepentamidine. *** LOOK IN TOX BOOK FOR DRUG. *** LOOK IN TOX BOOK FOR DRUGLIST!!LIST!!

Broad complex TachycardiaBroad complex Tachycardia

- - DDxDDx

VT : ECG criteriaVT : ECG criteria! Main aim is to differentiate VT from SVT + aberrant conduction (rare)Main aim is to differentiate VT from SVT + aberrant conduction (rare)! Absent RS complex in ANY Absent RS complex in ANY praecordialpraecordial lead lead = nearly 100% specific for = nearly 100% specific for

VTVT! RS intervalRS interval –– between onset of the R wave and the deepest part of the S between onset of the R wave and the deepest part of the S

wave. If >100ms < 95% specific for VTwave. If >100ms < 95% specific for VT! QRS widthQRS width =usually > 140ms (only needs to be > 100ms in children) =usually > 140ms (only needs to be > 100ms in children)! AV dissociationAV dissociation –– can be seen as notching of the ARS complex at different can be seen as notching of the ARS complex at different

positions positions –– this is present in 40% of cases and less commonly seen in this is present in 40% of cases and less commonly seen inpaediatricpaediatric VT. Indicates VT in 75% of cases VT. Indicates VT in 75% of cases

! Fusion beatsFusion beats = a QRS complex may be seen with morphological features = a QRS complex may be seen with morphological featuresintermediate between a beat of ventricular origin and one of intermediate between a beat of ventricular origin and one of supraventricularsupraventricularorigin but with a constant RR interval.origin but with a constant RR interval.

! Capture beatsCapture beats: a narrow QRS complex with a slightly shorter RR interval in: a narrow QRS complex with a slightly shorter RR interval inamongst broad complexes. Indicates AV dissociation.amongst broad complexes. Indicates AV dissociation.

! Concordance of QRS vectors in PRAECORDIAL LEADSConcordance of QRS vectors in PRAECORDIAL LEADS (all + (all +veve or all or all––veve). 20% sensitivity 90% specificity). 20% sensitivity 90% specificity

! RSR1 with delayed VAT or QS or RS in V1 (85% of cases of SVT + aberrancyRSR1 with delayed VAT or QS or RS in V1 (85% of cases of SVT + aberrancyvsvs 10% cases of VT 10% cases of VT

! RS, QRS in V1 (50% of cases of VT RS, QRS in V1 (50% of cases of VT vsvs 2% of cases of SVT) 2% of cases of SVT)! LAD or RAD make VT more likelyLAD or RAD make VT more likely. VT axis is usually +90 - +180.. VT axis is usually +90 - +180.! Comparison with sinus rhythm Comparison with sinus rhythm –– axis change > 40 degrees axis change > 40 degrees suggests suggests

VT. Change in QRS morphology suggests VTVT. Change in QRS morphology suggests VT

VT VT –– Historical Criteria Historical Criteria

!As reliable for differentiation as otherAs reliable for differentiation as other

methodsmethods

! 2 or more of the following factors indicate a2 or more of the following factors indicate a

95% probability of VT95% probability of VT

!! Age > 35Age > 35

!! Active AnginaActive Angina

!! Previous AMIPrevious AMI

Shown are the six precordial ECG leads (V1-V6). The QRS complex is

wide and bizarre and the rhythm is ventricular tachycardia (VT). Thesixth (+) and seventh (*) QRS complexes show a change inmorphology, resembling a normal QRS complex; these

represent fusion beats, with partial (+) or complete (*)

normalization of the QRS complex. The seventh QRS complex (*) ispreceded by a distinct P wave, which is probably conducted,capturing the ventricle for one beat, but not terminating the VT; this

is also known as a Dresseler beat. Reproduced with permission bySamuel Levy, MD.

SgarbossaSgarbossa Criteria Criteria

! Acute MIAcute MI — — The sequence of The sequence of repolarizationrepolarization is altered in LBBB, with the ST segment and is altered in LBBB, with the ST segment andT wave vectors being directed opposite to the QRS complex. These changes may maskT wave vectors being directed opposite to the QRS complex. These changes may maskthe ST segment depression and T wave inversion induced by ischemia.the ST segment depression and T wave inversion induced by ischemia.

! On the other hand, the diagnosis of an acute MI or ischemia can occasionally be madeOn the other hand, the diagnosis of an acute MI or ischemia can occasionally be madein a patient with underlying LBBB if certain ST-T changes are seen, particularly if the ST-in a patient with underlying LBBB if certain ST-T changes are seen, particularly if the ST-T vectors are in the same direction as the QRS complex as in the T vectors are in the same direction as the QRS complex as in the SgarbossaSgarbossa criteria criteriadescribed belowdescribed below..

!! ST segment elevation (STE) greater than or equal to 1mm CONCORDANT with the QRSST segment elevation (STE) greater than or equal to 1mm CONCORDANT with the QRScomplex = score of 5complex = score of 5

!! ST segment DEPRESSION greater than or equal to 1mm in leads V1, V2 or V3 = score of 3ST segment DEPRESSION greater than or equal to 1mm in leads V1, V2 or V3 = score of 3

!! STE greater than or equal to 5mm DISCORDANT with the QRS complex = score of 2STE greater than or equal to 5mm DISCORDANT with the QRS complex = score of 2

!! Total score of 3 or more suggests that the pt is likely having an AMI based on the ECG criteria.Total score of 3 or more suggests that the pt is likely having an AMI based on the ECG criteria.

!! ** subsequent studies have suggested that this clinical prediction rule is less useful than initially** subsequent studies have suggested that this clinical prediction rule is less useful than initiallyreported with decreased sensitivity and inter-rater reliability BUT at least it is a toolreported with decreased sensitivity and inter-rater reliability BUT at least it is a tool

!! Remember also: Remember also: PseudonormalizationPseudonormalization of previously inverted T waves is of previously inverted T waves issuggestive but suggestive but not diagnostic of ischemia.not diagnostic of ischemia.

SgarbossaSgarbossa Criteria (Up to Date) Criteria (Up to Date)

! SgarbossaSgarbossa criteria criteria — — A large trial of thrombolytic therapy for acute MI (GUSTO-1) provided an opportunity toA large trial of thrombolytic therapy for acute MI (GUSTO-1) provided an opportunity torevisit the issue of the electrocardiographic diagnosis of evolving acute MI in the presence of LBBB [3] . Amongrevisit the issue of the electrocardiographic diagnosis of evolving acute MI in the presence of LBBB [3] . Among26,003 North American patients who had a myocardial infarction confirmed by enzyme studies, 131 (0.5 percent)26,003 North American patients who had a myocardial infarction confirmed by enzyme studies, 131 (0.5 percent)had LBBB. A scoring system, often called the had LBBB. A scoring system, often called the SgarbossaSgarbossa criteria, was developed from the coefficients assigned by criteria, was developed from the coefficients assigned bya logistic model for each independent criterion, on a scale of 0 to 5.a logistic model for each independent criterion, on a scale of 0 to 5.

! The three ECG criteria with an independent value in the diagnosis of acute infarction and the score for eachThe three ECG criteria with an independent value in the diagnosis of acute infarction and the score for eachwere:were:

1 .1 . ST segment elevation of 1 mm or more that was in the same direction (CONCORDANT) as the QRS complex inST segment elevation of 1 mm or more that was in the same direction (CONCORDANT) as the QRS complex inany lead any lead —— score 5. score 5.

2 .2 . ST segment depression of 1 mm or more in any lead from V1 to V3 ST segment depression of 1 mm or more in any lead from V1 to V3 —— score 3. score 3.

3 .3 . ST segment elevation of 5 mm or more that was DISCORDANT with the QRS complex (ST segment elevation of 5 mm or more that was DISCORDANT with the QRS complex (ieie, associated with a QS, associated with a QSor or rSrS complex) complex) —— score 2. score 2.

! A minimal score of 3 was required for a specificity of 90 percent.A minimal score of 3 was required for a specificity of 90 percent.

! The first two criteria are similar to those described previously since the ST segment is concordant rather thanThe first two criteria are similar to those described previously since the ST segment is concordant rather thandiscordant with the QRS complex. However, the third finding requires further validation, since a high take-off ofdiscordant with the QRS complex. However, the third finding requires further validation, since a high take-off ofthe ST segment in leads V1 to V3 has been described with uncomplicated LBBB, particularly if there is underlyingthe ST segment in leads V1 to V3 has been described with uncomplicated LBBB, particularly if there is underlyingleft ventricular hypertrophy.left ventricular hypertrophy.

! In a In a substudysubstudy from the ASSENT 2 and 3 trials, the third criteria added litt le diagnostic or prognostic value [15] . from the ASSENT 2 and 3 trials, the third criteria added litt le diagnostic or prognostic value [15] .

! A A SgarbossaSgarbossa score of score of !! 3 was highly specific ( 3 was highly specific (ieie, few false positives) but much less sensitive (36 percent) in the, few false positives) but much less sensitive (36 percent) in thevalidation sample in the original report [3] . Similar findings were noted in a subsequent meta-analysis of 10 studiesvalidation sample in the original report [3] . Similar findings were noted in a subsequent meta-analysis of 10 studiesof 1614 patients in which a of 1614 patients in which a SgarbossaSgarbossa score of score of !! 3 had a sensitivity of 20 percent and a specificity of 98 percent 3 had a sensitivity of 20 percent and a specificity of 98 percent[16] . The sensitivity may increase if serial or previous [16] . The sensitivity may increase if serial or previous ECGsECGs are available [13] . are available [13] .

! In addition to their utility in diagnosis, the In addition to their utility in diagnosis, the SgarbossaSgarbossa criteria may also predict prognosis in patients with acute MI. criteria may also predict prognosis in patients with acute MI.Among the 300 patients in the HERO 2 trial (which compared outcomes among 300 patients with presumed newAmong the 300 patients in the HERO 2 trial (which compared outcomes among 300 patients with presumed newLBBB at presentation to those of 15,340 patients with normal LBBB at presentation to those of 15,340 patients with normal intraventricularintraventricular conduction; all patients received conduction; all patients receivedthrombolytic therapy [41]) with LBBB, 92 (31 percent) had concordant ST elevation thrombolytic therapy [41]) with LBBB, 92 (31 percent) had concordant ST elevation !! 1 mm in any lead or ST 1 mm in any lead or STdepression depression !! 1 mm in any lead V1 to V3. These two abnormalities are the major 1 mm in any lead V1 to V3. These two abnormalities are the major SgarbossaSgarbossa criteria that are used criteria that are usedto assist in the diagnosis of acute MI in patients with LBBB.to assist in the diagnosis of acute MI in patients with LBBB.

Other attempts to improveOther attempts to improve

ECG ECG DxDx in LBBB in LBBB! Attempts to improve ECG diagnosisAttempts to improve ECG diagnosis — — Several studies have systematically evaluated the valueSeveral studies have systematically evaluated the value

of different ECG findings of acute MI in LBBB. An analysis by of different ECG findings of acute MI in LBBB. An analysis by WackersWackers correlated ECG changes correlated ECG changesin LBBB with localization of the infarct by thallium in LBBB with localization of the infarct by thallium scintigraphyscintigraphy [2] . The most useful ECG [2] . The most useful ECGcriteria were:criteria were:

!! Serial ECG changes Serial ECG changes —— 67 percent sensitivity 67 percent sensitivity

!! ST segment elevation ST segment elevation —— 54 percent sensitivity 54 percent sensitivity

!! Abnormal Q waves Abnormal Q waves —— 31 percent sensitivity 31 percent sensitivity

!! Initial positivity in V1 with a Q wave in V6 Initial positivity in V1 with a Q wave in V6 —— 20 percent sensitivity but 100 percent 20 percent sensitivity but 100 percentspecificity for specificity for anteroseptalanteroseptal MI MI

!! Cabrera's sign Cabrera's sign —— 27 percent sensitivity overall, 47 percent for 27 percent sensitivity overall, 47 percent for anteroseptalanteroseptal MI MI

! Cabrera's sign refers to prominent (0.05 sec) notching in the ascending limb of the S wave inCabrera's sign refers to prominent (0.05 sec) notching in the ascending limb of the S wave inleads V3 and V4; a similar finding is prominent notching of the ascending limb of the R waveleads V3 and V4; a similar finding is prominent notching of the ascending limb of the R wavein lead V5 or V6 (Chapman's sign) [2] . These signs have a specificity that approaches 90in lead V5 or V6 (Chapman's sign) [2] . These signs have a specificity that approaches 90percent. However, there may be a high degree of percent. However, there may be a high degree of interobserverinterobserver variability in accurate variability in accurateidentification and their sensitivity is quite low.identification and their sensitivity is quite low.

! A number of the other criteria, including those of A number of the other criteria, including those of WackersWackers mentioned above [2] , were not mentioned above [2] , were notfound to be useful. A difference may be that the GUSTO criteria were applied within hours offound to be useful. A difference may be that the GUSTO criteria were applied within hours ofthe MI as part of the GUSTO-1 trial, while those of the MI as part of the GUSTO-1 trial, while those of WackersWackers were often applied much longer were often applied much longerafter the acute event. Furthermore, only the after the acute event. Furthermore, only the WackersWackers study attempted to localize the infarct. study attempted to localize the infarct.

! From Up to Date 2008From Up to Date 2008

IschaemiaIschaemia and Paced Rhythms and Paced Rhythms

(Up to Date 2008)(Up to Date 2008)

! Ventricular pacingVentricular pacing — — A similar problem is theA similar problem is thediagnosis of an acute MI in the presence of a ventriculardiagnosis of an acute MI in the presence of a ventricularpaced rhythm, which is usually associated with a leftpaced rhythm, which is usually associated with a leftbundle branch block pattern.bundle branch block pattern.

! Thirty-two patients in the GUSTO-1 trial (0.1 percent ofThirty-two patients in the GUSTO-1 trial (0.1 percent ofenrolled patients) had a ventricular paced rhythm.enrolled patients) had a ventricular paced rhythm.

! The only ECG criterion with a high specificity andThe only ECG criterion with a high specificity andstatistical significance for the diagnosis of anstatistical significance for the diagnosis of anacute MI was ST segment elevation acute MI was ST segment elevation !! 5 mm in 5 mm inleads with a negative QRS complex [5] .leads with a negative QRS complex [5] .

! Two other criteria with acceptable specificity were: STTwo other criteria with acceptable specificity were: STelevation elevation !! 1 mm in leads with concordant QRS polarity 1 mm in leads with concordant QRS polarityST depression ST depression !! 1 mm in leads V1, V2, or, V3 1 mm in leads V1, V2, or, V3

VAQ 7 2007VAQ 7 2007

! A 64 year old woman presents with acute chest pain, A 64 year old woman presents with acute chest pain, dyspnoeadyspnoea at atrest and palpitations.rest and palpitations.

! Her observations are:Her observations are:! BP 90/65 mmHg (supine)BP 90/65 mmHg (supine)! HR 96 /minHR 96 /min! SaO2 89% O2 via Hudson mask at 6 L/minSaO2 89% O2 via Hudson mask at 6 L/min! Temperature 37 Temperature 37 oCoC

! a. Describe and interpret her ECG. (50%)a. Describe and interpret her ECG. (50%)! b. List your treatment priorities. (50%)b. List your treatment priorities. (50%)

! ECG showing paced rhythm.ECG showing paced rhythm.

! Overall pass rate for this question was 40/57 (70.2%).Overall pass rate for this question was 40/57 (70.2%).! The examiners felt this was a challenging question and was an excellentThe examiners felt this was a challenging question and was an excellent

discriminator. Pass/fail criteria were a reassured description of paced rhythmdiscriminator. Pass/fail criteria were a reassured description of paced rhythmand comprehensive approach to hypotension in the setting of paced rhythm.and comprehensive approach to hypotension in the setting of paced rhythm.

Heart FailureHeart Failure

! NHYA (New York Heart Association Classification)NHYA (New York Heart Association Classification)

! Class I = Class I = SxSx on abnormal exertion on abnormal exertion

! Class II Class II –– SxSx on ordinary activity, comfortable at on ordinary activity, comfortable at

restrest

! Class III Class III –– SxSx on less than usual activity, on less than usual activity,

comfortable at restcomfortable at rest

! Class IV Class IV –– SxSx at rest, any activity increases at rest, any activity increases SxSx

! ACEP ACEP –– BNP in heart failure BNP in heart failure

ACEP Heart FailureACEP Heart Failure

! CRITICAL QUESTIONSCRITICAL QUESTIONS

! 1. Does a B-type 1. Does a B-type natriureticnatriuretic polypeptide (BNP) or polypeptide (BNP) or NTProBNPNTProBNP measurement improve the measurement improve thediagnostic accuracy over standard clinical judgment in the assessment of possible acutediagnostic accuracy over standard clinical judgment in the assessment of possible acuteheart failure syndromes in the ED?heart failure syndromes in the ED?Patient Management RecommendationsPatient Management RecommendationsLevel A recommendations. Level A recommendations. None specified.None specified.LeveILeveI B recommendations. B recommendations. The addition of a single BNP or The addition of a single BNP or NT-NT-proBNPproBNP measurement can measurement canimprove the diagnostic accuracy improve the diagnostic accuracy compared to standard clinical judgment alone in the diagnosiscompared to standard clinical judgment alone in the diagnosisof acute heart failure syndrome among patients presenting to the ED with acute of acute heart failure syndrome among patients presenting to the ED with acute dyspneadyspnea..Use the following guidelines:Use the following guidelines:•• BNP <100 pg/ BNP <100 pg/dLdL or NT- or NT-proBNPproBNP <300 pg/ <300 pg/dLdL acute heart failure syndrome unlikely* (Approximate acute heart failure syndrome unlikely* (ApproximateLR- 01)LR- 01)•• BNP >500 pg/ BNP >500 pg/dLdL or NT- or NT-proBNPproBNP >1,000 pg/ >1,000 pg/dLdL acute heart failure syndrome likely (Approximate LR acute heart failure syndrome likely (Approximate LR6)6)

! Level C recommendations. Level C recommendations. Non Non pdfidpdfid..

! BNP is produced by cardiac BNP is produced by cardiac myocytesmyocytes in response to increased end-diastolic pressure and volume, as in response to increased end-diastolic pressure and volume, asoccurs in the setting of heart failure. Pre-occurs in the setting of heart failure. Pre-proBNPproBNP is synthesized within is synthesized within myocytesmyocytes and cleaved to and cleaved toproBNPproBNP. The latter is released into the circulation and then cleaved to the active BNP and an inactive. The latter is released into the circulation and then cleaved to the active BNP and an inactiveN-terminal fragment, called N-terminal fragment, called NTproBNPNTproBNP..

! During the past decade, both BNP and NT-During the past decade, both BNP and NT-proBNPproBNP have been studied as markers for aiding in the have been studied as markers for aiding in thediagnosis of acute heart failure syndrome in patients presenting with diagnosis of acute heart failure syndrome in patients presenting with dyspnoeadyspnoea in the acute setting. in the acute setting.

! Although BNP is a rapidly transcribed protein in theAlthough BNP is a rapidly transcribed protein in the body, animal data suggest that BNP levels may lag body, animal data suggest that BNP levels may lagan hour or more behind the clinical picture. 2an hour or more behind the clinical picture. 2

IlcorIlcor/ARC Question/ARC Question

! SAQ 4 February/May 2007SAQ 4 February/May 2007

! ““Compare and contrast the cardiac arrest algorithmCompare and contrast the cardiac arrest algorithmfor for asystoleasystole between adults and children older than between adults and children older thanone year. (100%)one year. (100%)””

! The overall pass rate for this question was 22/55 (40.0%).The overall pass rate for this question was 22/55 (40.0%).

! The examiners felt that this was an excellent core knowledge questionThe examiners felt that this was an excellent core knowledge questionon a topic recently overviewed in widely discussed on a topic recently overviewed in widely discussed concensusconcensusstatements (ILCOR/AHA/ARC). It was thought to have been overallstatements (ILCOR/AHA/ARC). It was thought to have been overallanswered very poorly by most candidates. Good responses identifiedanswered very poorly by most candidates. Good responses identifiedthe differences in the differences in pathophysiologypathophysiology (and hence, priorities) in children, (and hence, priorities) in children,highlighted the potential reversible causes and exhibited knowledge ofhighlighted the potential reversible causes and exhibited knowledge ofthe recently published algorithms in this area. Common errors inthe recently published algorithms in this area. Common errors inanswering this question were incorrect drug doses, incorrect CPRanswering this question were incorrect drug doses, incorrect CPRratios/rates, failure to mention ratios/rates, failure to mention intraosseousintraosseous vascular access vascular accesstechniques and disregard of the differing techniques and disregard of the differing pathophysiologypathophysiology..

IlcorIlcor vsvs ARC ARC

Paediatric ALSPaediatric ALS

Neonatal ResuscitationNeonatal Resuscitation

Aortic DissectionAortic Dissection! Stanford and De Stanford and De BakeyBakey Classifications Classifications

! DebakeyDebakey –– I, II, III I, II, III

! Stanford Type A (= Stanford Type A (= DebakeyDebakey I & II) I & II)! Stanford Type B = Stanford Type B = DebakeyDebakey’’ss III III

! HxHx features, Exam features features, Exam features

! ECG ECG egeg inferior ST elevation due to RCA involvement inferior ST elevation due to RCA involvement

! Other investigations Other investigations –– sens and spec. CXR (features/ECG/Serum sens and spec. CXR (features/ECG/Serummarkers markers inclincl D D dimerdimer/ Echo/ TOE/Angiography/ CT/ Echo/ TOE/Angiography/ CTangiography/ MRI ) Discuss pros and cons of eachangiography/ MRI ) Discuss pros and cons of each

! Rx, supportive care, dispositionRx, supportive care, disposition

Infective Infective EndocarditisEndocarditis

! Prophylaxis Prophylaxis –– antibiotic guidelines antibiotic guidelines

! Likely organisms for different populationsLikely organisms for different populations

! IVDU / prosthetic valvesIVDU / prosthetic valves

! HxHx and examination findings and examination findings

! Investigations Investigations inclincl ECG findings ( ECG findings (egeg RBBB, heart RBBB, heart

block or PR depression if valve ring block or PR depression if valve ring abcessabcess is is

present)present)

! ManagementManagement

! ComplicationsComplications

VAQ 2007VAQ 2007

! A 49 year old woman presents to your emergency department with centralA 49 year old woman presents to your emergency department with centralchest pain.chest pain.

! Her observations are:Her observations are:! BP 110/70 mmHg supineBP 110/70 mmHg supine! O2 saturation 97% room airO2 saturation 97% room air! a. Describe and interpret her ECG. (50%)a. Describe and interpret her ECG. (50%)! b. How might echocardiography aid in clarifying her diagnosis? (50%)b. How might echocardiography aid in clarifying her diagnosis? (50%)! ECG showed widespread T wave inversion, concave up ST elevation and PRECG showed widespread T wave inversion, concave up ST elevation and PR

depression inviting in this clinical context a discussion re a number ofdepression inviting in this clinical context a discussion re a number ofdifferentials.differentials.

! Overall pass rate for this question was 32/55 (58.2%).Overall pass rate for this question was 32/55 (58.2%).! This was viewed as a difficult but relevant ECG which was satisfactorilyThis was viewed as a difficult but relevant ECG which was satisfactorily

interpreted by most candidates. The discussion re echocardiography wasinterpreted by most candidates. The discussion re echocardiography wasgenerally superficial and was the major reason for poor scores.generally superficial and was the major reason for poor scores.

! ** ** PericarditisPericarditis and causes but ALSO infective and causes but ALSO infective endocarditisendocarditis!!! -!!! -ECHO/TOEECHO/TOE

Congenital Heart diseaseCongenital Heart disease

!Children Children vsvs corrected adults corrected adults

!Know PDA Know PDA –– avoid avoid NSAIDsNSAIDs

!Cyanotic Cyanotic vsvs acyanoticacyanotic

!Complications and at risk periodsComplications and at risk periods

Cardiac TransplantCardiac Transplant

! ImmunosuppressionImmunosuppression/ rejection/ rejection! Infections Infections espesp CMV CMV! Malignancy Malignancy –– occurs in 20% - skin/lymphoma occurs in 20% - skin/lymphoma! Painless Painless ischaemiaischaemia! DenervatedDenervated heart does not respond to indirectly acting heart does not respond to indirectly acting

substances such as atropine/dig/substances such as atropine/dig/quinidinequinidine/carotid sinus/carotid sinusmassagemassage

! VERY sensitive to adenosine VERY sensitive to adenosine –– BRADYASYSTOLIC BRADYASYSTOLICRHYTHMS POST ADENOSINE. If pt is severely RHYTHMS POST ADENOSINE. If pt is severely bradycardicbradycardicand unresponsive to conventional Rx use and unresponsive to conventional Rx use aminophyllineaminophylline = =adenosine antagonist (250mg IV bolus)adenosine antagonist (250mg IV bolus)

! DenervatedDenervated heart responds to humeral but not neural heart responds to humeral but not neuralmechanisms.mechanisms.

Respiratory MedicineRespiratory Medicine

! PE PE –– Wells/PERC/Revised Geneva scores Wells/PERC/Revised Geneva scores! Have a look at Liverpool guidelinesHave a look at Liverpool guidelines

! D- D- dimerdimer –– aware of spec and aware of spec and senssens

! Pneumonia Pneumonia –– PSI / CURB 65 PSI / CURB 65

! AsthmaAsthma

! PneumothoraxPneumothorax

! OSAOSA

! NIV ****NIV ****

! ABG and ABG and spirometryspirometry

And just remember there ISAnd just remember there IS…………