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Case 1
Chest Pain
Dina Hazwani binti Azlang
Izyan Izzaidah binti Zali
History
C/C - a 54 years-old malay man with crushing chest
pain
HOPI- CS , 54-year-old man with hypertension who presents to the ED
at 5.00a.m with crushing chest pain and difficulty breathing. He
awoke at 4.00a.m with substernal pressure that he describes as
feeling “as if someone were standing on my chest”. He felt
shortness of breath and began to sweat. On the way to the hospital,
he received sublingual nitroglycerin 0.4mg with some relief. He
vomited once in the ambulance. On arrival to the ED, he still
complains of chest pressure that radiates to his neck and jaw. He
denies back or abdominal pain. His breathing has improved with
oxygen and he has mild nausea. He has never had similar pain and
has no history of cardiac disease.
• PMHx: HTN, hypercholesterolemia
• Meds: Amlodipine(Norvasc)5mg PO QD,
atorvastatin(Lipitor) 40mg QD
• Ahx: NKDA
• SHx:occasional alcohol use, no cocaine use, smoked
1ppd for 20 years, quit 10 years ago.
• FHx:Father died of cardiac problem at 58 yrs of age
• V/S:Temp.37.2 C, HR 110, BP 95/58, RR 26, SaO2 97%̊
on 15 liters O2.
Provisional ∆:Myocardial infarction
∆∆: Unstable angina
Pulmonary embolism
Tension pneumothorax
What would be the initial
management?
Management
CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
What investigations would you request to confirm a
diagnosis?
• STEMI diagnosed by :
 Clinical history of ischaemic type chest pain
 12 lead ECG changes
 confirmed later with a rise in cardiac enzymes .
ECG
-classic ECG changes of full-thickness MI are:
- ST elevation
- T waves begin to invert over 24h and ST elevation resolves
- Q waves dev. w/in 24-72h of MI.
Blood test
Indicators of myocardial damage-Troponin T and troponin I
-Creatine kinase
U&E-may be deranged or worsen d/t poor fenal perfusion in cardiogenic shock
Blood glucose-DM must be control aggresively after MI
FBC-anemic may precipitate acute MI in pts who have angina.
There is often a leucocytosis after acute MI
Serum cholesterol-measured w/in 24h of MI
-hypercholesterolemia is RF(must be treated)
-chol level fall artificially low level 24h after MI,true reading-obtained 2 mth after MI
chest radiograph -determine cardiac size and look for pulmonary oedema.
ECG of 54 years-old man with crushing chest pain
Acute anterior wall myocardial infarction (MI) ST-elevation
(STEMI), consistent with proximal left anterior descending (LAD)
occlusion, with Q waves (V1-V3) and ST elevations (V1-V5).
Page interventional cardiology, stat!
Cardiac troponins& CKMB – most specific cardiac enzyme
- takes about 4-8 hrs after an AMI
for them to rise
CKMB – is sensitive to AMI at 6 hrs after the onset of chest pain
Troponin – is highly specific and sensitive after 12 hrs and
remains up to 14 days after an infarct.
*For most pts, blood should be obtained for testing on hospital
admission, and again at 12-24hrs.
CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
Final Diagnosis
Acute anterior wall myocardial infarction (MI) ST-
elevation (STEMI)
CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
Fibrinolytic therapy
• Has been shown to reduce mortality when given within
appropriate time frame.
• given within 1 hr from time of onsets of symptoms-
• most beneficial and able to abort the infarction and
reduce mortality by up to 50%.
• should made be available in all hospital and
emergency department.
CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH
Malaysia.
• Symptom consistent with AMI
• Presentation within 12 hr of chest pain with:
• ST elevation >2mm in 2 or more chest leads or
• ST elevation > 1 mm in 2 or more limb leads or
• New or presumably new left bundle branch block.
• Time from onset of symptoms
- Less than 6 hrs : most beneficial
- 6-12 hrs : lesser but still important benefits
-more than 12hrs: no significant benefit except in
pts with ongoing ischemic
CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
Indication for thrombolytic
therapy
Fibrinolytic
contraindication
CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
Choice of fibrinolytic
agent
1) Streptokinase- most widely used agent
2) tPA – the used of should be considered for pts who:
- been given streptokinase within the last 2 yrs
- allergic to streptokinase
- have systolic bp < 90 mmHg
* t-PA unlike streptokinase does not coz hypotension
• Complication??
- Bleeding
- Hypotension
- Allergic reaction
CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
1̊ PTCA
CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
• > effective
• Limited availability
• Indication:
– As an alternative
reperfusion strategy.
– In pts who have definite c/I
for thombolytic therapy.
– In pts presenting with
cardiogenic shock.

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case scenario 1-chest pain

  • 1. Case 1 Chest Pain Dina Hazwani binti Azlang Izyan Izzaidah binti Zali
  • 2. History C/C - a 54 years-old malay man with crushing chest pain HOPI- CS , 54-year-old man with hypertension who presents to the ED at 5.00a.m with crushing chest pain and difficulty breathing. He awoke at 4.00a.m with substernal pressure that he describes as feeling “as if someone were standing on my chest”. He felt shortness of breath and began to sweat. On the way to the hospital, he received sublingual nitroglycerin 0.4mg with some relief. He vomited once in the ambulance. On arrival to the ED, he still complains of chest pressure that radiates to his neck and jaw. He denies back or abdominal pain. His breathing has improved with oxygen and he has mild nausea. He has never had similar pain and has no history of cardiac disease.
  • 3. • PMHx: HTN, hypercholesterolemia • Meds: Amlodipine(Norvasc)5mg PO QD, atorvastatin(Lipitor) 40mg QD • Ahx: NKDA • SHx:occasional alcohol use, no cocaine use, smoked 1ppd for 20 years, quit 10 years ago. • FHx:Father died of cardiac problem at 58 yrs of age • V/S:Temp.37.2 C, HR 110, BP 95/58, RR 26, SaO2 97%̊ on 15 liters O2. Provisional ∆:Myocardial infarction ∆∆: Unstable angina Pulmonary embolism Tension pneumothorax
  • 4. What would be the initial management? Management CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
  • 5. CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
  • 6. What investigations would you request to confirm a diagnosis? • STEMI diagnosed by :  Clinical history of ischaemic type chest pain  12 lead ECG changes  confirmed later with a rise in cardiac enzymes . ECG -classic ECG changes of full-thickness MI are: - ST elevation - T waves begin to invert over 24h and ST elevation resolves - Q waves dev. w/in 24-72h of MI. Blood test Indicators of myocardial damage-Troponin T and troponin I -Creatine kinase U&E-may be deranged or worsen d/t poor fenal perfusion in cardiogenic shock Blood glucose-DM must be control aggresively after MI FBC-anemic may precipitate acute MI in pts who have angina. There is often a leucocytosis after acute MI Serum cholesterol-measured w/in 24h of MI -hypercholesterolemia is RF(must be treated) -chol level fall artificially low level 24h after MI,true reading-obtained 2 mth after MI chest radiograph -determine cardiac size and look for pulmonary oedema.
  • 7. ECG of 54 years-old man with crushing chest pain Acute anterior wall myocardial infarction (MI) ST-elevation (STEMI), consistent with proximal left anterior descending (LAD) occlusion, with Q waves (V1-V3) and ST elevations (V1-V5). Page interventional cardiology, stat!
  • 8. Cardiac troponins& CKMB – most specific cardiac enzyme - takes about 4-8 hrs after an AMI for them to rise CKMB – is sensitive to AMI at 6 hrs after the onset of chest pain Troponin – is highly specific and sensitive after 12 hrs and remains up to 14 days after an infarct. *For most pts, blood should be obtained for testing on hospital admission, and again at 12-24hrs. CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
  • 9. Final Diagnosis Acute anterior wall myocardial infarction (MI) ST- elevation (STEMI)
  • 10. CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
  • 11. Fibrinolytic therapy • Has been shown to reduce mortality when given within appropriate time frame. • given within 1 hr from time of onsets of symptoms- • most beneficial and able to abort the infarction and reduce mortality by up to 50%. • should made be available in all hospital and emergency department. CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
  • 12. • Symptom consistent with AMI • Presentation within 12 hr of chest pain with: • ST elevation >2mm in 2 or more chest leads or • ST elevation > 1 mm in 2 or more limb leads or • New or presumably new left bundle branch block. • Time from onset of symptoms - Less than 6 hrs : most beneficial - 6-12 hrs : lesser but still important benefits -more than 12hrs: no significant benefit except in pts with ongoing ischemic CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia. Indication for thrombolytic therapy
  • 13. Fibrinolytic contraindication CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
  • 14. CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
  • 15. Choice of fibrinolytic agent 1) Streptokinase- most widely used agent 2) tPA – the used of should be considered for pts who: - been given streptokinase within the last 2 yrs - allergic to streptokinase - have systolic bp < 90 mmHg * t-PA unlike streptokinase does not coz hypotension • Complication?? - Bleeding - Hypotension - Allergic reaction CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia.
  • 16. 1̊ PTCA CPGs, Management of Acute STEMI, 2007, 2nd Edition, MOH Malaysia. • > effective • Limited availability • Indication: – As an alternative reperfusion strategy. – In pts who have definite c/I for thombolytic therapy. – In pts presenting with cardiogenic shock.

Editor's Notes

  1. Blood test Indicators of myocardial damage-Troponin T and troponin I -Creatine kinase U&amp;E-may be deranged or worsen d/t poor fenal perfusion in cardiogenic shock Blood glucose-DM must be control aggresively after MI FBC-anemic may precipitate acute MI in pts who have angina. There is often a leucocytosis after acute MI Serum cholesterol-measured w/in 24h of MI -hypercholesterolemia is RF(must be treated) -chol level fall artificially low level 24h after MI,true reading-obtained 2 mth after MI chest radiograph -determine cardiac size and look for pulmonary oedema (shawdowing, small effusion at costophrenic angle, Kerley B line (linear opacities) must be performed.