chapter 9 - acs i & ii

BASE HOSPITAL GROUPONTARIO

Chapter 9 for 12 Lead Training

- Acute Coronary Syndromes – I & II-

Ontario Base Hospital GroupEducation Subcommittee

2008

TIME IS MUSCLE

OBHG Education Subcommittee

Acute Coronary Syndromes – I & II

REVIEWERS/CONTRIBUTORS

Neil Freckleton, AEMCA, ACPHamilton Base Hospital

Jim Scott, AEMCA, PCPSault Area Hospital

Ed Ouston, AEMCA, ACPOttawa Base Hospital

Laura McCleary, AEMCA, ACPSOCPC

Tim Dodd, AEMCA, ACPHamilton Base Hospital

Dr. Rick Verbeek, Medical DirectorSOCPC2008 Ontario Base Hospital Group

AUTHOR

Greg Soto, BEd, BA, ACPNiagara Base Hospital


Chapter 9 Objectives

Define ACSDescribe the timeline for atherosclerosis

and thrombus formation in ACSList the 3 initiating events in an ACSDifferentiate stable and vulnerable

plagues.


Chapter 9 Objectives

Describe the process of thrombus formation

List and differentiate the 3 I’s of ACSDescribe the myocardial coronary blood

supplyName the major coronary arteries and

locations they serve


Acute Coronary Syndromes I

Pathophysiology and Anatomy


Acute Coronary Syndromes

Definition:Sudden ischemic disorders of the

heartInclude unstable angina and acute

myocardial infarctionRepresent a continuum of a similar

disease process


Thrombus Formation and ACS

UA NQMI STEMI

Plaque Rupture

Thrombus Formation

Non-ST-Segment Elevation Acute Coronary Syndrome

(ACS)

ST-Segment Elevation

Acute Coronary Syndrome

Old Terminology:

NewTerminology:


Acute Coronary Syndromes

All have sudden ischemia

Often can not be differentiated in the first hours

All have the same initiating events


Initiating Events

Plaque rupture

Thrombus formation

Vasoconstriction


Lumen

Plaque Rupture

Lipid Core

Fibrous Cap

Stable Vulnerable

LumenLipid Core

Fibrous Cap


Plaque Rupture

Lipid Core

Fibrous Cap

Lumen


Thrombus Formation

Lipid Core

Fibrous Cap

Platelets Adhere


Thrombus Formation

Platelet Aggregation

Lipid Core


Thrombus Formation

Platelet Aggregation

Lipid Core

Fibrin


Vasoconstriction


Epicardial Coronary Artery

Lateral Wall of LV

Positive Electrode

Septum

Left Ventricular

Cavity

Inferior Wall of LV

Well Perfused Myocardium


Normal ECG


Will Infarct Occur?

Tissue Death?

Plaque Rupture

Thrombus Formation

CoronaryVasoconstriction

CollateralCirculation

MyocardialOxygen Demand


The Three I’s of ACS

Ischemia - permanent damage avoidable lack of oxygenationST depression or T wave inversion

Injury - permanent damage avoidableprolonged ischemiaST elevation

Infarctdeath of myocardial tissuemay have Q wave


Evolution of AMI

A - pre-infarct

B - Tall T wave

C - Tall T wave & ST elevation

D - Elevated ST, inverted T wave, Q wave

E - Inverted T wave, Q wave

F - Q wave


Epicardial Coronary Artery

Lateral Wall of LV

Positive Electrode

Septum

Left Ventricular

Cavity

Inferior Wall of LV

Ischemia


Ischemia

Inadequate oxygen to tissue

Subendocardial

Represented by ST depression or T inversion

May or may not result in infarct


ST depression


Thrombus

Ischemia

Injury


Injury

Prolonged ischemia

Transmural

Represented by ST elevation

Usually results in infarct


ST elevation


Infarct

Death of tissue

Represented by Q wave

Not all infarcts develop Q waves


Infarcted AreaElectrically Silent

Depolarization Many infarcts do not develop Q waves

Infarction

Thrombus


Q Waves


Infarcted Area Electrically Silent

Thrombus

Depolarization

Ischemia

A bit of everything


Summary

A normal ECG does NOT rule out ACSST segment depression represents

ischemia Possible infarct

ST segment elevation is evidence of AMI

Q wave MI may follow ST elevation or depression


Coronary Arteries

Branch off of the aorta, just above the leaflets of the aortic valve

Three major arteries

Each supplies a specific area


Right Coronary Artery

Inferior wall of LV Right ventricle Posterior LV Posterior fascicle of

LBB SA and AV node


Left Anterior Descending

Anterior wall of LV Septum Bundle Branches Major pumping

mass of LV Sudden occlusion of

the Left Main coronary artery leads to sudden death (from massive infarction).


Left Circumflex ArteryUpper lateral wall

of LV (Leads I and aVL)

SA node in 45%AV node in 10%Posterior fascicle

of LBB


QUESTIONS?


Acute Coronary Syndromes II

Rapid Recognition and

Treatment of ACS


Goal for ACS II

Rapidly recognize and treat patients with sudden myocardial ischemia


Small Group Task

List and rank risk factors

Describe symptoms of the last AMI patient attended

Describe the symptoms of a friend or relative when they suffered an AMI


Immediate Evaluation

O2, Cardiac monitor, SPO2

Incident history

Risk factors

Treatment?

12 Lead ECG


Clinical Presentations of ACS

Classic ischemic chest pain

Atypical chest pain

Ischemic equivalents


Classic Anginal Chest Pain

Central anterior chest

Dull, fullness, pressure, tightness, crushing

Radiates to arms, neck, back


Atypical Pain

Musculoskeletal, positional or pleuritic features

Often unilateral

May be described as sharp or stabbing

Includes epigastric discomfort

Females often express atypical pain


Ischemic Equivalents

Dyspnea

Palpitations

Generalized weakness

Dizziness

Syncope or pre-syncope


Who do you wanna be? A case in point about syncope and AMI60 yr old ♂; CC= syncope alone at home

am; awoke feeling well1000: bilateral shoulder pain; pt thought it

due to new exercise programWent to mall, returned home, had 4 drinks

and laid on couch.Had syncopal episode at 1530 while rising

from couch; hit forehead on floor → laceration.

Pt activated EMS at 15:40 hours


EMS encounter1550: Found by crew sitting on couch,

CAOx3 O/E: skin = pink, warm, dry; P = 80 NSR,

BP=110/68, spo2=96% on room air, PEARL; airway patent, denied headache, minor ½” lac + hematoma to forehead, denied chest pain or SOB

Pmhx: smoker, ↑BP, ↑cholesterolCurrently ASYMPTOMATICResistant to 12 LECG but agreed if crew

would then leave him at home…


EMS 12 Lead – uh oh!


Still don’t want to go? Patient stated he felt fine and was reluctant of

further assessment/care; refused treatment or transport.

Crew encouraged patient to go to hospital and explained 12 Lead ECG findings and risks associated with STEMI.

BHP Patch for advice – pt still refused. ACP told patient the story of her parents who each

had an AMI Dad: no treatment for ischemic chest pain, late

ED presentation, no reperfusion therapy; despite quad bypass he experienced CHF & poor quality of life until he died prematurely.


So who do you wanna be?Mom: had sudden onset of chest pain in the

presence of daughter (the ACP)Received early ED thrombolysisSuccessful reperfusion and is now living active

and fulfilling life (travelling, exercise, boyfriends)Medic asked the patient: “So who do you

wanna be…my dad or my mom?”The patient enthusiastically sided with the Mom.Patient reperfused (PCI) with an excellent

outcome and good left ventricle ejection fraction (>60%)


Atypical Presentations

Often seen in:

FemaleDiabeticsElderly


Reasons EMS were missing ACS treatment

Protocols get in the way 50% of AMI patients have classic

chest pain presentation 20% of AMI patients have atypical

pain presentation 30% don’t have any pain at all

If we focus assessment on classic ischemic presentation we miss half of AMI patients!


Important Notation

Note EXACT time symptoms began

Duration of symptoms may effect therapeutic options and destination decisions


Review Group Activity

How many had presentations with classic anginal pain?

How many had atypical pain?

How many were anginal equivalents?

How many risk factors did you list?


Risk Factors of ACS

DiabetesSmokingHypertensionAge Cholesterol

Family history of CAD

ObesityStressSedentary


Consider Risk FactorsPatients with severe or multiple risk

factors should be evaluated with a high index of suspicion for acute coronary syndrome

Don’t let the patient get burnedGet the 12 Lead!


Age

Infarct can occur at any age

Increasing age = increasing risk


Remember!!

Unstable angina and acute myocardial infarction are indistinguishable in the first few hours

“Atypical” presentations are common

Risk factor evaluation helps identify ACS patients


Chronic Stable Angina vs. ACS

Not chronic stable angina if… New onsetLower exertion threshold Change in pattern of reliefNew or different associated

symptoms


PCP General Therapy for ACS

AssessmentMonitor Lead II ECG & SP02

Vital signsStory and risksExpose & listen to the chest

12 Lead Acquisition*

TreatmentOxygenNTGAspirinIV if certified


ACP General Therapy for ACS

AssessmentMonitor Lead II ECG & SP02

Vital signsStory and risksExpose & listen to the chest

12 Lead Acquisition*

TreatmentOxygenNTGAspirinIVMorphine


Note from previous two slides

BLS and ALS Standards currently do not include 12 Lead as a standard of care.

12 Lead is an Auxiliary Medical Directive for ACP and PCPDecision to proceed is based upon the

cooperative effort and decisions by the Base Hospital and Service Operator


General Therapy for ACS

Assessment and therapy occur simultaneously

Findings may alter therapeutic path


Oxygen

High flow mask is indicated if ischemia is suspected

Advanced airway care for continued or severe hypoxia where indicated


Vital Signs

Respiratory rate and effortPulse rate, rhythm, volumeBlood pressure in both arms,

manual then automaticCardiac monitor SP02 monitor

12 Lead ECG


12 Lead ECG

Obtain after the first set of vital signs

Repeat as often as necessary (enroute to hospital)


IV Access

Adequate line in a suitable vein

Follow approved Medical Directives


Aspirin

ASA - chew & swallowAdhere to Medical Directive for

contraindications to ASAIssues:

Asthma patients may have been told to avoid ASA

Patients on anti-coagulantsTaken ASA already today


Nitroglycerin

Dilates conduit arteries

Antagonizes vasospasm

Improves collateral circulation

Inhibits venous return

Reduces intra-myocardial wall tension


Nitroglycerin

NTG sublingual Repeat every five minutes as per

Medical Directive

Contraindications include; Hypotension ED Rx within 48 hours

Known hypersensitivity

Check MD


NTG Precautions

Avoid hypotension

Limit systolic drop

Don’t use NTG as an analgesic

Watch for right ventricular infarction (RVI)


Morphine

Morphine as per protocol May require several doses for adequate

relief of pain

Decreases myocardial oxygen requirements

Watch for respiratory depression and hypotension


Case 1

48 year old male Sudden onset of dull central chest pain 2/10,

began at rest

Pale and wet

Overweight, smoker

Vital signs: RR 18, P 80, BP 180/110, Sa02 94% on room air


Case 1

Incident Hx/Exam

Risk factors

Treatment

ECG


Case 1 - ECG


Case 268 year old female

Sudden onset of anxiety and restlessness,States she “can’t catch her breath”Denies chest pain or other discomfort

History of IDDM and hypertension

RR 22, P 110, BP 190/90, Sa02 88% on NRBM at 10 lpm.


Case 2

Incident Hx/Exam

Risk factors

Treatment

ECG


Case 2 - ECG


Case 2

Now what is the order?StoryRisk factorsECGTreatment?

What is the pharmacological treatment plan for this patient?

Can you treat this patient under your medical directives?


12 Lead ECG Documentation

Time Proced.Code

TreatmentDescription

Result

2234 313 12 Lead ECG Non-diagnostic or NO STEMI

2250 313 12 Lead ECG STEMI : Inferior reciprocal changes.

SAMPLE


Sample Thrombolytic

Checklist


QUESTIONS?


Well Done!

Education Subcommittee

START QUIT

chapter 9 - acs i & ii

Healthcare

q wavee inverted t wave

t inversionmay

artery wall

intermediate lesion

type of advanced lesion

plaque dynamics

foam cells

st elevationusually