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Chest Pain Cardiology in the ED PowerPoint Presentation

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Description : Check out this medical presentation on Angina, which is titled "Chest Pain Cardiology in the ED", to know about the 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.

Tags : Angina, Chest Pain, Cardiology, ED

Published on : May 25, 2021 | Views : 678 | Downloads : 9

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Slide 1-

Chest Pain Cardiology 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
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Chest pain & syncope Learning objectives Note 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
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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
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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
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Learning objectives Focus 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
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Causes of Chest Pain Oesophageal Oesophagitis Oesophageal spasm Musculoskeletal Muscle injury, spasm Costochondral joint inflammation Skin Herpes Zoster (Shingles)
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Emergency Medicine 6 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…)
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….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
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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’
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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”
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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
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History & ECG: pericarditis Due to pericardial inflammation: pericarditis Central or Left side Sharp, stabbing Worse on movement, on breathing, lying flat Relief sitting forward
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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
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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
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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
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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
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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
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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
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Acute coronary syndromes https://www.mja.com.au/sites/default/files/issues/191_06_210909/bri10275_fm.pdf
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ECG interpret in <5mins.
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ECG – your opinion?
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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
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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
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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
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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
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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
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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%
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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
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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
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myoglobin One study showed excellent rule out figures for 90 minute testing of troponin and myoglobin levels
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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
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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
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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
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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
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Guideline for PCI v ‘lysis
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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
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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
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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’
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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
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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
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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!!
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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
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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
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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
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Myo and pericarditis
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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?
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PE investigations No test is ideal Can have normal tests & be very unlucky Classic diagnosis for combining pre- and post-test clinical probability
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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?
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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’
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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
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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
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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%)
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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)
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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
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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%)
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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
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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)
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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
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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
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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?
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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)
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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
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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
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Spot diagnoses
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Spot diagnoses
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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