chest pain cardiology in the ed ballarat emergency medicine training hub contributors – dr jaycen...

Chest PainCardiology in the ED

Ballarat Emergency Medicine Training Hub

Contributors – Dr Jaycen Cruickshank

Mark Hartnell & Ballarat ED physicians

Material from DR.MUHAMMAD FAROOQUE MB BS DTCD

Chest pain & syncopeLearning objectivesNote syncope covered in another presentation

This session will examine contrasting clinical cases of chest pain that may be due to potentially lethal causes such as myocardial infarction or more benign causes such as costochondritis. Important features in the history that help discriminate different causes of chest pain and syncope will be discussed along with appropriate initial investigations.

Learning objectives

To name the common and important medical conditions that cause chest pain and their characteristic features on history.

To rapidly diagnose and manage acute myocardial infarction To interpret ECGs in myocardial ischaemia and arrhythmias. To name the common and important medical conditions that cause syncope

and their characteristic features on history and exam.

Refer to ED lecture series and self directed workbooks

Pre reading

Hughes T & Cruickshank J. Adult Emergency Medicine at a Glance. Chichester, West Sussex, UK : John Wiley & Sons, 2011. 

Chapter 21 Slow heart rate. Chapter 32 Fast heart rate. Chapter 34 Chest pain: cardiovascular. Chapter 35 Chest pain: non cardiovasular

Other learning resources BHS guidelines

Follow this link to the presentation on BHS intranet (http://dev-intranet/node/370)

MJA consensus guidelines https://www.mja.com.au/sites/default/files/issues/184_08_170406/suppl_170406_fm.pdf https://www.mja.com.au/sites/default/files/issues/191_06_210909/bri10275_fm.pdf

  Cruickshank J. Initial management of cardiac arrhythmias. Vol 37, (7) 516-

520 2008 Australian Family Physician. http://www.racgp.org.au/afp/200807/200807cruickshank.pdf

Learning objectivesFocus on cardiac ischaemia

To rapidly diagnose and manage acute myocardial infarction – BHS and national guidelines and systems.

To interpret ECGs in myocardial ischaemia and arrhythmias

Investigation and treatments in myocardial ischaemia - what and when

Pitfalls and red flags Including what to do with atypical presentations

Causes of Chest Pain Oesophageal

Oesophagitis Oesophageal spasm

Musculoskeletal Muscle injury, spasm Costochondral joint

inflammation Skin

Herpes Zoster (Shingles)

Emergency Medicine6 deadly causes of chest pain

Acute coronary syndromes Aortic dissection Pulmonary Embolus ** most commonly presents with dyspnea

Pericardial Tamponade / Myo- & Pericarditis Oesophageal Rupture Tension Pneumothorax

(6 things on a list is too many, but…)

….but luckily some diagnoses predictable for clinicians…

Myo/pericarditis – a diagnostic ECG Oesophageal rupture – a classic historyHx Tension pneumothorax – a classic

examination Pleuritic pain has a differential diagnosis that

generally does not include cardiac ischaemia Leaving three ‘problems’:

Acute Coronary Syndromes, Aortic dissection Pulmonary Embolus

Assessment

Pre- and post test probability Pre test probability influenced by factors such as: History of previous coronary disease Angina, AMI, coronary angiogram or angioplasty,

coronary surgery History of cardiac risk factors Smoking, Hypertension, High Cholesterol, Diabetes

Mellitus Diagnostic approach to Acute Coronary Syndromes is

often a ‘risk assessment’ rather than a ‘diagnosis’

History of the complaint

By far the most predictive assessment Do it well, saves time!

Know the classic story for the complaints but beware of the pitfalls

If you can make a confident diagnosis DON’T do tests “JUST IN CASE”

History – typical descriptions Pleuritic Pain = Pain

worse on inspiration Sharp, stabbing Localised Worse on inspiration,

coughing May be worse on sitting

up or leaning forward Not related to exertion

Oesophageal pain• Usually “Burning” but

may be dull ache• Worse after meals• Worse on lying down• Relieved by antacid• Oesophageal spasm

may be relieved by GTN

History & ECG: pericarditis

• Due to pericardial inflammation: pericarditis• Central or Left side• Sharp, stabbing• Worse on movement, on breathing, lying flat• Relief sitting forward

History typical of Myocardial ischaemia

• “Angina Pectoris” = Pain in the chest• Central chest pressure, tightness,

squeezing• Intensity increases over a few

minutes• Radiation to shoulders, arms, neck,

jaw• Worse with exertion• May be relieved by rest• May be relieved by Glyceryl Tri

Nitrate (GTN)• Associated sweating, nausea,

dyspnoea

Often not described as a “pain” but as Pressure Discomfort Ache Tightness

May be mistaken by patient (and doctor) for indigestion

History pitfalls

Response to analgesia type does not make a diagnosis cardiac pain can get

better with antacid Oesophageal pain

improves with GTN

“Atypical” pain Is common Does not exclude

ischaemia May be more common in

women, renal failure Some patients have no pain

“Silent” ischaemia or infarction

More common in diabetics due to neuropathy

ACS – history pitfalls

Painless AMI common with age, women and diabetics Prev stroke or heart failure also risks

By age 85 MAJORITY of AMI painless Anginal ‘equivalents’ include:

Dyspnoea (commonest) With age: syncope, weakness, confusion Elderly women also: cold sweats & dizziness

Which features of pain make myocardial ischaemia more or less likely?

More likely Radiates to shoulders Worse on exercise Associated dyspnoea

Less likely Stabbing, sharp Pleuritic Worse on changing position Very localised Reproduced by palpation or

movement Very brief (seconds) Very prolonged (constant for

days) Radiates to the legs No past history of AMI or angina

Response to analgesia

The “GI cocktail” has only been studied poorly, mostly other drugs get given around the same time

Not safe to make a discharge decision based on the response

Chest wall tender & AMI

7% of AMI or unstable angina have partially or fully reproducible pain

Important to note if the pain produced is the same one

Be suspicious if there is no proceeding history of injury

Acute coronary syndromes

https://www.mja.com.au/sites/default/files/issues/191_06_210909/bri10275_fm.pdf

ECG interpret in <5mins.

ECG – your opinion?

Basic investigations

ECG, CXR and bloods In Emergency Department an ECG in most if not

all patients. More useful as ‘rule in’ than ‘rule out’

ECG in AMI 50% sensitivity, 90% specificity ECG not useful in PE or aortic dissection

Acute Coronary Syndrome

Difference between risk Ax & diagnosis Blood tests are not diagnostic tests (unless

positive) Ruling out AMI in a stable patient with a non-

diagnostic ECG is the difficulty

prognosis v diagnosis #1

The same coronary lesion in one patient might be tolerated or a disaster

Increased rate of complications with: LV dysfunction DM HTN / LVH Probably renal failure

prognosis v diagnosis #2

Diagnostic probability determines approach to diagnosis… ?EST / ?angiography / ?inpatient or outpt. Dif tests different risks & level of sensitivity

Risk profile defines Rx decisions… Risk v benefit of dif antiplatelet Rx Admit to CCU or ward

Assessing risk

Risk factors don’t help in the ED ECG and biomarkers do Many systems, none perfect, and following

the guideline of your hospital including getting expert help is sensible and medico-legally correct

ED role: determine disposition immed RX Risk Ax of complications = discharge

TIMI 7 rule (for an example)

5 on Hx: Age>65, >2 IHD RF’s, known stenosis, >2

episodes angina in 24H, aspirin use 2 tests: ECG changes / positive troponin

HIGH risk = ECG / trop +ve / TIMI > 2 LOW risk = normal ECG & trop, TIMI <3

30 day mortality 1.7%

ECG as rule out AMI test

Not known how useful a normal ECG is: AMI rate ?<1%, up to 7%

It is known that an abnormal non-diagnostic ECG = risk for missed AMI

Probably with passing time a normal ECG begins to decrease likelihood of at risk ACS but this has not been shown

Blood markers - troponin

Troponin I or T rise within 3-6H and then remain elevated for about one week

Serial testing, at least 6H after symptom onset improves sensitivity

In ACS an increased troponin is a marker for increased risk of AMI and death

Does NOT diagnose cardiac ischaemia

myoglobin

One study showed excellent rule out figures for 90 minute testing of troponin and myoglobin levels

Rx in ACS

Aspirin should be given immediately alternative clopidogrel if truly contraindicated

Rapid decisions on reperfusion Based on ECG only

All other decisions less time dependent Can involve further consultation Need risk / benefit analysis

Adjunctive Rx in ACS

Further antiplatelet options: Heparin (LMW v unfractionated) clopidogrel Glycoprotein IIb/IIIa inhibitors

Symptomatic / pain control GTN / morphine

Secondary prevention BBlockade / statins

Thrombolysis (fibrinolysis)

50% flow return rate where indicated But 15% re-occlude (and do badly) 1% patients have a major bleed

Usually intra-cranial haemorrhage Using LMW heparin as opposed to UFH:

Some evidence more benefit

PCI v thrombolysis

Guideline varies with: time from symptom onset Time to get to catheter lab (balloon inflation) Lesser factors inc localisation of AMI and relative

risk / benefit thrombolysis All other things being equal esp in anterior

AMI PCI better option

Guideline for PCI v ‘lysis

CABG’s

Routine after STEMI Considered if poor LVF ‘appropriate’ anatomy

Means LAD or severe vessel disease Emergency

Considered in cardiogenic shock Failed reperfusion and persistent pain

All above is level B recommendation

Role of PCI high risk ACS

Still being defined: ‘current problem versus the next one’

Different approaches tried: Risk stratify & PCI high risk Maximise non-invasive Rx

Then PCI ‘breakthrough’ PCI all patients

PCI high risk ACS

PCI all approach reduces hospitalisations But low risk patients potentially do worse

Peri-procedural AMI

Current Cochrane recommendation is that ‘may be a benefit in early PCI if risk stratification in high category’

AORTIC DISSECTION

Challenging diagnosis, lethal if missed (75% in 2/52), prob.s if Rx as ACS

Classic Hx: Sudden onset ripping /

tearing PIC, radiates to back (interscapular, migratory) & Hx HTN

Not sensitive enough Best approach is risk factor

assessment Be aware of atypical

presentations

Risk factors for Aortic Dissection

HTN Aortic valve

Bicuspid, previous surgery Abnormal Aorta – mainly congenital

Coarctation / Marfan’s / Ehlers-Danlos Arteritis (Giant cell)

Aortic ‘stresses’ PREGNANCY, COCAINE, TRAUMA

Atypical presentations AD

Atypical history Non-classical pain, chest or back only, severe &

sharp pain, abdo pain Syncope Acute stroke (& peripheral neuro)

Others just get too weird & make you paranoid Eg. Pulsatile stenoclavicular joint!!

AD - imaging

Widened mediastinum (62%) and abnormal aortic contour (50%) most sensitive CXR findings

Normal CXR may decrease the likelihood but if examination, Hx and RF’s raise suspicion needs further imaging

Oesophageal rupture

Ruptures due to developing a tear due to raised intra-luminal pressure

Classical triad is forceful emesis, chest pain and subcutaneous emphysema

Prefer to sit up and may have chest signs CXR usually abnormal on left side

Oesophageal rupture - problems

Definitive diagnosis usu on CT, can do oesophagogram (can be false negatives)

Vomiting can be absent in 21% Can occur in kids, can be right

sided Patients are UNWELL, only

needs pursuing in atypical case if SICK

Myo and pericarditis

Pulmonary Embolism

Classic triad about 20%: Pleuritic PIC, dyspnoea & haemoptysis

Typically some combination of: SOB, PIC, tachypnoea, tachycardia

Dypnoea commonest (about 80%) Pleuritic pain not sensitive or specific

44% with, 30% without in one study

Needs infarction more likely in existing lung disease, implies smaller clot?

PE investigations

No test is ideal Can have normal tests & be very unlucky

Classic diagnosis for combining pre- and post-test clinical probability

PE – more worrying facts

Mortality hasn’t changed Rate of asymptomatic PE not known Not known what the actual incidence is Most diagnosed at autopsy in US 10% deaths after diagnosis, 90% before Up to a third of PE’s asymptomatic?

PE - ECG

ECG has many reported associations All from study of pt. s AFTER diagnosis

S1Q3T3 about 12% of PE & normal pt.s Sinus tachy not that common

Range is 8-69% in 6 studies Commonest is anterior T wave inversion

68% pt.s with confirmed PE ECG doesn’t ‘rule in’ or ‘rule out’

PE - ABG

Tells you nothing about the cause of hypoxia only the magnitude

If you know there is hypoxia already you don’t need to do it

If you really need to you can calculate an A-a gradient WITHOUT removing O2

PE – pre test probabilty

Multiple systems for doing this Most widespread and validated is Well’s

score Note dif. Well’s score for PE & DVT

PE – Well’s criteria

3 points for: PE ‘most likely diagnosis’ Signs and symptoms suggesting DVT

1.5 points for: PR>100, past Hx (PE/DVT), immobilisation

1 point for: Haemoptysis or malignancy

<2 low (10%), 2-6 i/med (25%), >6 high (50%)

Well’s – use in practice

Need to not automatically apply Eg. some pt.s will be moderate risk almost

everty time they come to ED (& DON’T need a scan everytime)

D-dimer

Only use is in a low risk patient A negative test makes PE very unlikely A slightly positive test IS a positive test

Imaging – CTPA and VQ

CTPA has high negative predictive value Alternative diagnosis up to 40% Better if abnormal CXR (VQ less useful) Inconclusive rates up to 10%

VQ scanning if normal perfusion scan effectively excludes (but only in 14%)

PE – more on VQ scanning

Normal perfusion excludes (14% of pt.s) ‘non-diagnostic’ (73%) covers:

Low probability, 15-30% have PE Intermediate, >30% have PE

High probability, >85% have PE

VQ – combining pre & post test assessment

Low clinical and low scan, <5% have PE Low clinical and i/med scan, same % PE

Also negative LL ultrasound, <3% PE High probability clinical & scan, >95% PE

Main problem is high clinical and low/intermediate scans, rate is 15-75% (often cardiopulmonary disease, past PE)

Imaging pregnant patients

Most advice is to investigate as normal D-dimer will be positive in pregnancy No consistant agreement re VQ v CTPA

VQ isotopes renal excreted, bladder near uterus CTPA has contrast as well as radiation

Tempting to try leg ultrasound But only 80% PE have LL DVT

The ‘Gold Standard’

There isn’t one! Pulmonary angiography was once but

mortality almost 1%, morbidity 2-5%

Compared to warfarin: 1-2% mortality 5-25% morbidity

Food for thought

What is the mortality rate of a d-dimer?

I didn’t think it was a PE, just thought I better do one anyway….

The result is ‘not negative’… Better order a CTPA…

Anaphylactic contrast reaction? Cancer? False positive, warfarin, car accident?

PERC rule – test free!

A rule which is applied after ‘gestalt’ Defined as <15% by physician after Ax This was the case in 2/3 of patients These patients had VTE rate of 3.3%

Rule aimed for false negative rate of <2% Approx rate PE/death after –ve imaging Further tests inc. false +ve (not less miss)

PERC rule…

The rule is: Age<50, PR<100, no haemoptysis, no E2 Rx, no

surgery 4/52 (=ETT), no past VTE, no unilateral leg swelling (from looking!)

“PERC negative” AND gestalt = <1% Study centres inc NZ (more like us??)

Thought to reduce tests by 20% Idea is not to do ANY tests

PE – less worrying facts

A spectrum of disease ranging from a normal physiological process to death?

Process of using a pre-test and post-test probability seems to work

“PERC positive” and –ve gestalt = PE 5% Ie less than the suspected 15%

The PERC rule also determined that immobilisation was 6H knees bent

Spot diagnoses

Spot diagnoses

Some final points

Examine patients properly Expose and look at the chest (eg. Zoster)

Beware chest wall tenderness in AMI but back tenderness reproducing chest pain is

very useful How you get rid of the patients pain does not

diagnose but HELPS THE PATIENT!! Give them everything ASAP