Microsoft PowerPoint - CHEST PAIN

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                                                To identify causes of chest pain in
                                                patients presenting to the ED.
                                                To identify and risk stratify patients
                                                presenting with acute coronary
          Dr Susan Hertzberg                    syndromes.
          Emergency Department                  To initiate management of patients with
          Prince of Wales Hospital              acute coronary syndromes in the ED

Causes of chest pain:                          Causes of chest pain

Pulmonary causes:usually involve the pleura;   Cardiac causes:
 pleurisy                                       Acute coronary syndromes
  PE                                            pericarditis
                                                thoracic aortic dissection
Causes of chest pain:                       Causes of chest pain:

GIT causes:                                 Chest wall causes:
 gastroesophageal reflux disease (GORD)      trauma
 Peptic ulcer disease                        musculoskeletal pain
 esophageal spasm                            rib fractures
 biliary tract disease                       thoracic nerve root pain
                                             herpes zoster

Pathology of ACS                            Acute coronary syndromes

 Imbalance between supply and demand         Angina-stable/ unstable
 for myocardial oxygen                       Non-stemi
 Atherosclerotic plaques cause narrowing     Stemi
 Plaques thicken                             Variant angina (Prinzmetal angina)
 Plaques rupture exposing thrombogenic
 surface, platelets aggregate and thrombi
Unstable angina                             Stable angina

 New-onset exertional angina                 Similar nature and pattern of previous
 Angina at rest
                                             episodic pain lasting 5-15 minutes
 Angina of increasing frequency or
 duration or refractory to nitroglycerin     provoked by exertion

                                             relieved by rest or nitroglycerin

STEMI                                       NON-STEMI

 Chest pain with acute ST elevation on       Ischaemic chest pain
                                             ST-T wave changes consistent with
 ST elevation of 1mm or more in 2 or more    ischaemia ( ST depression, T wave
 contiguous limb leads                       inversion)
 ST elevation of 2mm or more in 2
 continuous chest leads                      plus biochemical marker elevation
Variant angina              History: nature of the pain

 Coronary artery spasm       Pain described as pressure or heaviness
                             Pain may be in neck, jaw or arms
 occurs primarily at rest    Pain may be absent in elderly, diabetic or
 transient ST elevation      Associated with SOB, nausea, vomiting,
                             diaphoresis, dizzy

History                     Risk Factors for ACS

 Past cardiac history        5 primary risk factors
 past vascular history         family history
                               cigarette smoking
 risk factor profile
Other risk factors                                   Gender

 Male gender                                          Incidence of ACS is higher in males if
 Advanced age                                         younger than 70 years
 Prior cerebrovascular accident   7.5% of pts with
                                                      At 15 years post-menopause, incidence of
 Methamphetamine use                                  angina equal frequency in both sexes

Age                                                  Likelihood of CAD
                                                          There are 5 major factors on history (ranked
 Incidence of angina increases with age                   in order of importance) :
 40-70 years of age angina more common                    1. Typical angina pain
 in men.                                                  2. Prior MI
 Over age 70 incidence is the same in both                3. Male gender
 sexes.                                                   4. Age
                                                          5. Number of risk factors
Likelihood (cont)                           Physical examination

 Other features relating to likelihood:      Usually normal
   Examination revealing hypotension,
   cardiac failure, sweating
                                             look for CCF, new murmurs, hypotension
   New ECG changes- ST deviation or T
    wave inversion
   Elevated troponins

ECG                                         ECG (2)

 Most important diagnostic tool in the ED    Abnormalities:
 Moment in time-repeat liberally.               transient ST elevation
 Normal ECG does not exclude ischaemic          ST depression (0.5 mm significant)
 cause of chest pain                            dynamic T wave changes: inversion,
                                               flattening, hyperacute changes
                                                Deep symmetrical T wave inversion (consider
                                               CNS events)
Bloods                                       Troponins                     1

 Troponin                                     Troponin is a contractile protein not
 CKMB                                         normally found in serum.
 FBC                                          TnI and TnT are immunologically distinct
 Renal function                               in both skeletal and cardiac muscle
                                              TnI and TnT are both used to detect
                                              myocardial damage

Troponins                          2         Troponins                     3

 Most bound to myofilaments                   Very sensitive
 some cytosolic pool cf CK                    minor elevations identify patients at risk
 sensitivity at 12 hours is approx 98%        for subsequent cardiac events
 Both are detectable in the serum 3-6         elevation proportional to mortality
 hours after infarction with increased        remain elevated for 7-10 days (TnI) and
 sensitivity up to 12 hours after onset of    10-14 days ( TnT)
 pain                                         may be elevated in other conditions
CKMB                                         CXR

 Begins to rise within 4 hours of injury      Looking for other causes of chest pain
 peak 18-24 hours
 subside over 3-4 days                        Looking for signs of LVF
 ULN is 3-6% of total CK
 at 6-9 hours sensitivity increases to
 approx 90% and by 24 hours near 100%

Goals of ED care                             Risk stratification

 Identify patients with acute coronary        Risk stratification in the ED is aimed at
 syndromes                                    determining the likelihood of symptoms
 Exclude alternative causes of chest pain     representing ACS and then the short-term
 Risk stratify patients with ACS into low,    risk of death or nonfatal MI in those
 intermediate or high risk groups,            patients with ACS.
High risk                                  Intermediate risk

  CP at rest >10mins needing IV             CP at rest >10 mins now resolved
  ST deviation (>0.5mm)                     Diabetes
  T wave inversion (>2mm) in ≥ 3 leads,     Age >65 yrs
    new BBB                                 Nocturnal pain
  Elevated serum markers                    History of MI or revascularisation
  A/w syncope, hypotension, new LVF or      Pathological Q waves or T wave inversion
 new murmur                                 <3 leads

Low risk                                   ED CARE

 New onset angina more than 2 weeks         Obtain IV access, administer O2 if
 before presentation                        saturation <95%, apply BP and heart
 No high or intermediate risk features.     monitoring
 Normal ECG and serum markers.              Obtain ECG within 5 minutes of arrival
 Normal ECG during period of discomfort.    Complete focused history, including
                                            relevant risk factors, physical examination
                                            Identify complication of ACS
                                        Goals of care in ACS
ED CARE                                 patients

 Serial ECGs may be required             To preserve or improve patency of
                                         coronary artery and improve blood flow
 Frequent reassessment of vital signs    through stenotic lesions thus reducing
                                         myocardial damage.

 Bloods for biochemical markers

 Early appropriate consultation

Medications                             Analgesia

 Analgesics                              Reduce pain and decrease sympathetic
 Nitrates                                stress
 Antiplatelet agents                     morphine reduces preload
 Anti-coagulants                         morphine 2.5-5mg bolus titrate to effect
 beta-blockers                           caution in hypotension
Nitrates                                      Anti-platelet agents

 Oppose coronary artery spasm, causes          Aspirin
 relaxation of vascular smooth muscle thus     clopidogrel
 reducing preload and after load               Glycoprotein llb/llla antagonists ( tirofigan,
 nitroglycerin-sublingual tablet or spray,     abciximab, eptifibatide)
 topical, of intravenous infusion
 titrate to MAP and effect

Aspirin                                       Anticoagulants

 Inhibits cylcooxygenase which produces        To prevent recurrence of clot after
 thromboxane A2 a potent platelet              spontaneous fibrinolysis
 activator                                     does not actively lyse the clot but inhibits
 Early administration of aspirin may reduce    further thrombogenesis
 mortality in patients with AMI by up to       Fractionated (LMWH) or unfractionated
 23%                                           (UFH) heparin
 150-300mg po
                                               Low molecular weight
Heparins                                       heparins

 Augments activity of antithrombin lll and      Enoxaparin reduces cardiac ischaemic
 prevents conversion of fibrinogen to fibrin    events and death by up to 15% in
 continuous intravenous infusion                patients with unstable angina
 monitored by APTT testing                      Main effect via inactivation of factor Xa,
                                                higher anti Xa to anti factor lla ratio
                                                1mg/kg bd sc
                                                convenient- no need for APTT monitoring


 Have anti-ischaemic, anti-hypertensive
 and anti-arrhythmic properties
 Reduce myocardial oxygen demand,
 reduce wall stress and afterload
 decrease infarct size in AMI
 reduce short and long term mortality after

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