This highly energetic lecture presents the pathophysiology of S-T elevation myocardial infarction in an easy to understand style to help you best identify, triage and treat patients presenting with acute coronary syndromes. Using the latest research behind the AHA Guidelines changes, AHA National Faculty Rom Duckworth will help you better coordinate with you partners along the continuum of cardiac care. Emphasis is placed on risk factors, recognizing truly sick patients and coordinating care with hospital personnel. Learning Objectives: Students will learn: -The pathophysiology of S-T elevation myocardial infarction. -The difference between STEMI, NSTEMI and unstable angina. -Differing treatment methods and priorities for different cardiac syndromes. -The function and importance of 12 lead ECG and prehospital diagnostic testing. -The roles and responsibilities of EMS providers as the key element in “door-to-balloon” and “door-to-needle” time for STEMI patients. www.romduck.com www.RescueDigest.com

1. Tuesday, January 22, 2013

18. From the AHA/ACC STEMI guidelines
NSTEMI STEMI

19. Stenotic Lesion
Fibrotic
Thick Cap
Stable
Less Enlargement
+ Sx
BAD!
Non-Stenotic
Lipid Rich
Thin Cap
Unstable
Enlargement
Catastrophic
WORSE!!!
Detectible?

22. vs
FMC TO DEV: 90 MIN.

28. Early Recognition of ACS (red flags)
Dispatch Resources & Pre-Arrival ASA
EMS Recognition & Stabilization
Initial Care & Comfort

29. 12 Lead – STEMI identification.
MONA+ Medications
Triage & Pre-notify ED
Education & Prevention

31. Central Anterior Chest Pain
Pressure, Tightness, Dull, Crush
Radiating to Arms, Neck, Back
Approx. 50% ACS Patients

32. Musculoskeletal or Positional
Sharp or Stabbing
Epigastric Discomfort
Many Elderly, Female, Diabetic

33. Dyspnea
Palpitations
Syncope
Diaphoresis
Nausea / Vomiting
General Weakness

34. Over 65 y/o
Known CHD
HTN
DM
High Cholesterol
Sedentary Lifestyle

35. Over 45 y/o
Obese
Black
Cocaine Abuse
Smoking
Being a character in “Pulp Fiction”

37. 1. Ischemia (Angina or NSTEMI)
a) lack of oxygenation
b) ST depression or T inversion
2. Injury (STEMI)
a) prolonged ischemia
b) ST elevation
3. Infarct (DEAD)
a) dead tissue
b) may or may not show in Q wave

39. ST segment elevation (STEMI)
• Limb leads [I, II, III, AVL, AVF] >one mm (1 small box)
• Precordial leads [V1-V6] >two mm (2 small boxes)
New or presumed new LBBB = ST elevation (STEMI)
ST segment depression (Angina or NSTEMI)
• One mm or more (one small box)
T Wave Inversion (Angina or NSTEMI)
Q Wave (MI)?
• One mm or more (1 small box)

48. A “normal” ECG does NOT rule out ACS. “Non-Diagnostic”
ST segment depression or T wave inversion represents ischemia (Angina, NSTEMI).
ST segment elevation is evidence of injury (STEMI).
Q wave indicative of MI. Not all MI=Q wave
Indicators can come in any combination.
Process may go forwards or backwards.
There are always exceptions to the rules.
Look for reciprocal changes
Evaluate Rate and Rhythm (DEFIB)
Evaluate for Axis Deviation
Evaluate QRS Duration and more…

50. • Morphine (class I, level C)
• Analgesia
• Reduce pain/anxiety—decrease sympathetic tone,
peripheral vascular resistance and oxygen demand.
• Careful with hypotension, hypovolemia, respiratory
depression, RVI
• Oxygen (> 94% sPO2) (class I, level C)
• Up to 70% of ACS patient demonstrate hypoxemia
• May limit ischemic myocardial damage by increasing
oxygen delivery/reduce ST elevation
• Shown to have limited benefit, possible harm if >100%

51. • Nitroglycerin (class I, level B)
• Analgesia—titrate infusion to keep patient pain free
• Dilates coronary vessels—increase blood flow
• Reduces systemic vascular resistance and preload
• Careful with recent ED meds, hypotension, bradycardia, tachycardia,
RVI
• Aspirin (160-325mg chewed &
swallowed) (class IIa, level B)
• Irreversible inhibition of platelet aggregation
• Stabilize plaque and arrest thrombus
• Reduce mortality in patients with STEMI
• Careful with active ulcers, hypersensitivity, bleeding disorders
 In AMI, ASA reduced the risk of death by 20-25%
 In UA, ASA reduced the risk of fatal or nonfatal MI by 71% during the
acute phase.

52. • Thienopyridines (Prasugrel, Plavix)
(class I, level A)
• Irreversible inhibition of platelet aggregation
• Used in support of cath / PCI intervention or if
unable to take aspirin
• 3 to 12 month duration depending on scenario
• Glycoprotein IIb/IIIa inhibitors (Integrilin)
(class IIa, level B)
• Inhibition of platelet aggregation at final common
pathway
• In support of PCI intervention as early as possible
prior to PCI.

53. • Proton Pump Inhibitors (Prilosec, Pepcid)
• Given to reduce ulcers and increase compliance
• May reduce blood thinning mechanisms of Plavix.
• Hyperglycemia control in STEMI (Insulin)
(class IIa, level B)
• Control of hyperglycenia (180 mg/dl) recommended.
• May reduce inflammation and increase LV Ejection
Fraction.

54. • Beta-Blockers (class I, level A)
• 14% reduction in mortality risk at 7 days at 23% long
term mortality reduction in STEMI
• Approximate 13% reduction in risk of progression to MI
in patients with threatening or evolving MI symptoms
• Be aware of contraindications (CHF, Heart block,
Hypotension)
• Reassess for therapy as contraindications resolve.
• ACE-Inhibitors (class I, level A)
• Start in patients with anterior MI, pulmonary
congestion, LVEF < 40% in absence of
contraindication/hypotension
• Start in first 24 hours

55. • Unfractionated Heparin (class I, level A)
– Concurrent with reperfusion therapies of all types.
• Reduces clotting during acute in-hospital treatment.
• Aldosterone blockers (class I, level A)
– Post-STEMI patients
• no significant renal failure (cr < 2.5 men or 2.0 for women)
• No hyperkalemis > 5.0
• LVEF < 40%
• Symptomatic CHF or DM

61. Education/
Thrombolytics Prevention
/ Angioplasty
Pre Arrival
Instructions / ASA
Triage
Hospital Focused
Assessment
Patient
MONA+ Comfort
Pre-Hospital
12 Lead

62. Education/
Thrombolytics Prevention
/ Angioplasty
Pre Arrival
Instructions / ASA
Triage
Hospital Focused
Assessment
Patient
MONA+ Comfort
Pre-Hospital
12 Lead