PowerPoint Presentation

STEMI / ACSWhat youve been missing

Rommie L. Duckworth, EMT-PTuesday, January 22, 13

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Our Goals

Our Challenges

Our Path

RECOGNIZE

Who has to recognize? Us. Them. Dispatchers.5

STEMINSTEMIAngina PectorisUnstable AnginaCoronary Heart DiseaseAtherosclerosisChest PainCardiacCompromiseAcute Coronary SyndromesMyocardial Infarction

Chest Pain

What causes CP?7

Cardiac Compromise

Angina Pectoris

Coronary Heart DiseaseAtherosclerosis

Coronary Heart DiseaseKILLER

Acute Coronary Syndromes

Acute Coronary SyndromesAcuteAcute

Acute

Acute Coronary Syndromes

Acute Coronary Syndromes

AHA Heart Disease & Stroke Statistics 2009 Update

Acute Coronary Syndromes

17Proximal occlusion usually = STEMI, Distal occlusion usually = NSTEMI, Angina, but not always

From the AHA/ACC STEMI guidelines NSTEMISTEMIAcute Coronary Syndromes

18Figure 2. Acute coronary syndromes. The top half of the figure illustrates the chronology of the interface between the patient and the clinician through the progression of plaque formation, onset and complications of STEMI along with relevant management considerations at each stage. The longitudinal section of an artery depicts the "timeline" of atherogenesis from a normal artery (1) to (2) lesion initiation and accumulation of extracellular lipid in the intima, to (3) the evolution to the fibrofatty stage, to (4) lesion progression with procoagulant expression and weakening of the fibrous cap. An acute coronary syndrome develops when the vulnerable or high risk plaque undergoes disruption of the fibrous cap (5); disruption of the plaque is the stimulus for thrombogenesis. Thrombus resorption may be followed by collagen accumulation and smooth muscle cell growth (6). Following disruption of a vulnerable or high-risk plaque, patients experience ischemic discomfort resulting from a reduction of flow through the affected epicardial coronary artery. The flow reduction may be caused by a completely occlusive thrombus (bottom half, right side) or subtotally occlusive thrombus (bottom half, left side). Patients with ischemic discomfort may present with or without STsegment elevation on the ECG. Of patients with ST-segment elevation, most (large red arrow in bottom panel) ultimately develop a Q-wave MI (QwMI), while a few (small red arrow) develop a nonQ-wave MI (NQMI). Patients who present without ST-segment elevation are suffering from either unstable angina or a nonSTsegment elevation MI (NSTEMI) (large open arrows), a distinction that is ultimately made on the presence or absence of a serum cardiac marker such as CK-MB or a cardiac troponin detected in the blood. Most patients presenting with NSTEMI ultimately develop a NQMI on the ECG; a few may develop a QwMI. The spectrumof clinical presentations ranging from unstable angina through NSTEMI and STEMI are referred to as the acute coronary syndromes.

Stenotic LesionFibroticThick CapStableLess Enlargement+ SxBAD!

Non-StenoticLipid RichThin CapUnstableEnlargementCatastrophicWORSE!!!Detectible?Acute Coronary Syndromes

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O2, ASA, ECG, IV, Nitro, MorphineDrive Fast!

AngioplastyThrombolysisvsReperfusionSooner is BetterDoor to N: 30 min.FMC to Dev: 90 min.

2222the appropriate and timely use of some form of reperfusion therapy is likely more important than the choice of therapy Guidelines for the performance of primary PCI were formulated in collaboration with the 2011 PCI Guideline writing group.2 Primary PCI is indicated (class I) in patients with ischemic symptoms 94% sPO2) (class I, level C)Up to 70% of ACS patient demonstrate hypoxemiaMay limit ischemic myocardial damage by increasing oxygen delivery/reduce ST elevationShown to have limited benefit, possible harm if >100%

MONA & More

Nitroglycerin (class I, level B)Analgesiatitrate infusion to keep patient pain freeDilates coronary vesselsincrease blood flowReduces systemic vascular resistance and preloadCareful with recent ED meds, hypotension, bradycardia, tachycardia, RVI

Aspirin (160-325mg chewed & swallowed) (class IIa, level B)Irreversible inhibition of platelet aggregationStabilize plaque and arrest thrombusReduce mortality in patients with STEMICareful with active ulcers, hypersensitivity, bleeding disordersIn 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.

MONA & More

Thienopyridines (Prasugrel, Plavix) (class I, level A)Irreversible inhibition of platelet aggregationUsed in support of cath / PCI intervention or if unable to take aspirin3 to 12 month duration depending on scenario

Glycoprotein IIb/IIIa inhibitors (Integrilin) (class IIa, level B)Inhibition of platelet aggregation at final common pathwayIn support of PCI intervention as early as possible prior to PCI.

MONA & More

Proton Pump Inhibitors (Prilosec, Pepcid) Given to reduce ulcers and increase complianceMay 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.

MONA & More

Beta-Blockers (class I, level A)14% reduction in mortality risk at 7 days at 23% long term mortality reduction in STEMIApproximate 13% reduction in risk of progression to MI in patients with threatening or evolving MI symptomsBe 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/hypotensionStart in first 24 hours

MONA & More

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 > 5.0LVEF < 40%Symptomatic CHF or DM

MONA & More

5656Antman EM, et al. J Am Coll Cardiol. 2008; 51:210-47.

Our Goals

Our Path

bit.ly/ACSSTEMIRESOURCESACS / STEMI DefinitionsACS / STEMI Assessment & Tx12 Lead ECG Acquisition and Interp.This Presentation

TriageHospitalPre-Hospital12 LeadEducation/PreventionFocusedAssessmentPatientComfortMONA+Pre ArrivalInstructions / ASA

Thrombolytics/ Angioplasty

EMS Does Matter

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TriageHospitalEducation/PreventionFocusedAssessmentPatientComfortPre ArrivalInstructions / ASA

Thrombolytics/ Angioplasty

EMS Does MatterPre-Hospital12 LeadMONA+

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www.RescueDigest.comwww.RomDuck.com

FOR MORE INFO

bit.ly/ACSSTEMI

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