2. Acute Coronary Syndromes
Michelle Welsford, MD, FRCPC
Fall Recertification 2004

3. ACS Overview Definition Pathophysiology Risk Factors Clinical Features
Assessment
Management

4. ACS Definition
Myocardial ischemia: insufficient blood supply to the heart muscle that results from coronary artery disease
ACS: Any group of symptoms compatible with myocardial ischemia.
Represent a continuum of the same disease process:
Angina
Unstable angina
Non-ST elevation MI
STEAMI
The title “Acute Coronary Syndromes” refers to events producing acute ischemic pain or its equivalents. As such, a common component of ALL ACS is sudden myocardial ischemia.
While the phrase acute coronary syndromes represents a spectrum of one disease, there are at least three conditions identified within this continuum.
The Acute Coronary Syndromes consist of acute myocardial infarction, which is subdivided into Q wave and non-Q infarctions, and a related condition referred to as Unstable Angina.
As their name implies, Q wave MI (QMI) and non-Q wave MI (NQMI) are differentiated by the presence or absence of a pathological Q wave on the 12-lead ECG. Both produce tissue necrosis, QWMI tends to produce more necrosis and, therefore, may be a larger infarct.
Unstable Angina (USA) does not produce infarction, that is does not show evidence of tissue necrosis, but is included in ACS because of its common pathophysiology.

5. ACS Pathophysiology
All ACS - sudden ischemia that cannot be differentiated initially
Three common events:
Plaque rupture
Thrombus formation
Vasoconstriction
Realize that the plaque generally accumulates in the walls of the coronary artery and does not come into contact with the circulating blood. In fact, if plaque contents are exposed to the blood, the clotting mechanism will be initiated. Therefore, plaque rupture is usually the initiating event for all of the ACS.
Lumen
Lipid Core
Fibrous Cap

6. ACS Pathophysiology Plaque rupture
Thrombus formation - Platelet aggregation
Platelets not only stick to the tissue exposed by the plaque rupture, they begin to attract additional platelets and then stick to each other. As these platelets aggregate they can produce significant occlusions.
Remember that this process is merely the body’s normal clotting mechanism. This process includes the the ability to remove or spontaneously lyse a clot. In some patients, that is just what happens: the clot formation is halted and reversed and the plaque rupture ultimately heals. The patient may have never known anything happened.
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In addition to platelet aggregation the body can create a “frame” to further solidify the clot. This framework is produced from fibrin.
Fibrin creates a “mesh” or “net” to catch red blood cells; ultimately the fibrin shrinks down and solidifies the clot.
At this point the clot is harder to lyse.
RECAP: thrombus formation includes platelet adherence, aggregation and fibrin formation.
The third event contributing to coronary artery occlusion in the ACS is vasoconstriction.
Thrombus formation - Fibrin cross-linking

7. Risk Factors Hypertension Hyperlipidemia Diabetes mellitus Smoking
Family history
Males and post-menopausal women
Advancing age

8. Clinical Features Typical Atypical – 25% of all AMIs
Pleuritic or sharp/stabbing CP
Palpable CP (10-33% AMI)
Arm pain only
Indigestion
SOB only (40% in elderly)
“Dizziness” (5% AMI)
Nausea
Syncope

9. Assessment – Examination
Exam usually normal (85%)
May have:
Diaphoresis
Extra heart sounds (S3, S4 or rubs)
Dysrhythmias
Evidence of new or worsening heart failure
Hypotension

10. Assessment – EKG 12-lead EKG May be normal in ACS
May be nonspecific: ST or T wave ischemic changes
May be suspicious for injury: ST elevation
STEAMI
Fibrinolytic checklist
While it is not always possible to identify which of the ACS a patient is experiencing, it is possible to determine if a patient can benefit from acute reperfusion therapy.
The indication for acute reperfusion therapy is ST segment on the 12-lead ECG. For EMS to identify this subset of patients, a diagnostic 12-lead must be obtained .
“The 12-lead ECG stands at the center of the decision making pathway in the management of patients with ischemic chest pain, and delays in obtaining the 12-lead ECG must be eliminated.”
AHA, ACLS Textbook, 1997, 9-13
When you suspect a patient’s symptoms are due to ACS, take a 12-lead ECG with the first set of vital signs. And, like you do with other vital signs, repeat the 12-lead frequently.

11. EKG - AMI Diagnosis AMI Diagnosis: At least 2 of 3 criteria
Clinical history suggestive of AMI
EKG criteria
Laboratory diagnosis
ST elevation 1 mm or more in 2 anatomically contiguous leads
OR BBB

12. EKG - Contiguous Leads I aVR V1 V4 II aVL V2 V5 III aVF V3 V6
Limb Leads
Chest Leads

13. EKG - AMI Imitators Causes of ST elevation AMI LVH BBB
Ventricular beats – PVCs
Pericarditis
Early repolarization
Others

14. EKG Practice 1
Anterior AMI

15. EKG Practice 2
Inferior AMi

16. EKG Practice 3
High lateral AMI

17. EKG Practice 4
Inferolateral AMI

18. Management – Prehospital
Oxygen
ASA
Nitro
Morphine
Dysrhythmia treatment
Medication
Defibrillation
12-lead EKG with notification of receiving hospital
Prehospital thrombolysis
Triage to PCI facility

19. Management – Hospital Hospital Oxygen, ASA, Nitro, Morphine
Dysrhythmia management
Anticoagulation - heparin
Reperfusion
Fibrinolysis
PCI - percutaneous coronary intervention
Thrombolytics or fibrinolytics (eg: tPA, rPA, SK) are pharmacological agents administered IV that break up e a coronary thrombus.
PCI is an intervention that utilizes a balloon or other device, inserted through a large artery, to create a larger lumen in the offending coronary artery. A stent is often placed afterwards to keep the artery open.
Atherectomy procedures remove the occlusion by laser or cutting mechanisims.

20. ACS Management Summary
History/Assessment
Risk factors
EKG
Medical Management

21. Questions ?