12 Lead-ACS

Fleming CollegeParamedic Program

Focus of ACS

Common reason for transport Much can be done during transfer Reduce risk of morbidity and mortality

The first step = recognizing the ACSSigns and symptomsECG changesBiochemical changes

Summary

Strategies for reducing morbidity and mortality

Reduce cardiac workload Improve perfusion to cardiac tissue Reduce risk of fatal arrhythmias Reduce extension of clot formation Reperfuse the ischemic myocardium

Myocardial Infarction

ASA (2 x 80 mg) P.O. O2 therapy IV access NTG via SL, transdermal, and/or IV Morphine Heparin and/or Beta blockers 12 Lead ECG as soon as possible

Pre-hospital Thrombolysis

Air Ambulance-Ornge Oshawa Land ALS Positive empirical trends

Pre-hospital Thrombolysis

prolonged transport time

no thrombolysis at the sending facility

Long delays

Indications - Thrombolysis

Ischemic C.P.

Less than 12 hours duration

Ischemic Chest Pain?

O - at rest or with exertion P – better or worseQ - heaviness, tightening, sharp,

weakness etcR - neck, jaw and/or left armS - variesT - consistent, does NOT come & go

12 Lead ECG Criteria

ST segment elevation

New onset Left Bundle Branch Block with S&S?

Some acute coronary syndromes (A.C.S.) do not benefit from thrombolysis

LBBB-FYI ONLY!

Cannot reliably diagnose AMI in the setting of a LBBB

Collaborative data (history, enzymes etc.) in the setting of a new LBBB is an indication for thrombolysis

What are the Benefits?

Varies between sub-groups of patients

Time to thrombolysis “Infarct to Drug Time” shorter the better the

outcome

Its all about Timing

Thrombolytics within one hour of onset of CP - 50% reduction in infarct size

Thrombolytics within two hour of onset of CP - 30% reduction in infarct size

Thrombolytics within 3-4 hour of onset of CP - 13% reduction in infarct size

TIME IS MUSCLE - after 6-12 hours less helpful

Examples of Thrombolytics

Retaplase Tenectoplase (TNK) Streptokinase Tissue plasmingen activator (TPA)

Absolute Contraindications for Thrombolytics

Aortic dissection

Active (significant) bleeding

Pericarditis

Relative Contraindications

CPR >10 minutes Pregnancy Uncompressible puncture site (from IV

etc) Age (>75) Recent surgery or trauma or stroke

(>2 wks) Current use of warfarin or other

anticoagulant

Aortic Dissection

How to not get fooled

CP radiating into back Tearing vs pressure Unequal pulses or blood pressures in limbs Neurological symptoms Hypertension ++ (or low if they are

leaking) CXR

Things to do BEFORE Thrombolysis

Venipunctures

CXR

Blood analysis INR, aPTT, CBC etc.

Explain risk/benefits to patient

Pericarditis

How not to get fooled?

Non-specific CP - sometimes severe

ST segment elevation (ah..ha! But where?)

Pericarditis

How to not get fooled

Atypical ischemic CP Sitting forward can decrease discomfort Fever or systemic illness Younger without cardiac risk factors ST elevation is diffuse, no anatomical

pattern Serial ECG’s

Active Bleeding

Non-compressible site(s)

most common are GI and GU

More Relative Contraindications

The grey area

intracranial/intraspinal surgery

intracranial neoplasm, A-V malformation, aneurysm

bleeding diathesis

severe hypertension

What is the Risk?

Intracranial hemorrhage

Overall rate - 0.9%

Varies considerably between patients

What is the Risk?

Baseline risk w/o RF - 0.75%

2-3% up to 5% in anterior

As low as 1% in inferior

What is the Risk?

Age > 65 add 0.5%

Add another 0.5% > 75 y.o. >80 y.o. >85 y.o.

What is the Risk?

SBP > 160 add 0.5% SBP > 180 add another 0.5% Weight < 70 kg add 0.5% Any previous stroke add 2-4%

In the right patient the risk is significant

All stroke risks!!

Other Treatment Options

ASA Heparin Beta Blockers IIB/IIIA inhibitors

Primary PTCA

Best option in patients with increased risk or in patients with limited benefit

Potential for ambulances close to these centers (tertiary care centres) e.g Peterborough, Kingston, toronto, Ottawa

Percutaneous Transcoronary Angiography (PTCA)

Success

Approx. 70% of patients regain patency of the vessel

Pain relief Reduction in ST segment deviation Arrhythmia's

Access

Specialty procedure

Rescue angioplasty (fast transfers!!) high risk for thrombolytics Rx thrombolytics failed to correct the problem

Watch for reperfusion arrhythmias Usually benign Usually transient Watch for signs of bleeding

Watch for signs of bleeding!

Post Thrombolytic Care

Now to the 12 lead bit….

Introduction to 12 Lead ECG

Diagnostic 12 lead is performed to rule in/out various pathologies

Standard limb leads (I,II,III)

Augmented vector leads (aVL,aVR, aVF)

Precordial or chest leads

The Importance of a 12 lead EKG

Many calls involve the CVS

12 lead ECG is a useful tool in the cardiac assessment.

What Can be Assessed on the 12 lead EKG?

Axis Bundle branch conduction Hypertrophy Fascicular conduction Ischemia/Injury/Infarction patterns Pericarditis Electrolyte disturbances Drug intoxication AND MUCH MUCH MORE!!!!!

Required Skills to Interpret the 12 lead EKG

Comprehension of electrophysiology electrolyte and cellular functions during

normal and abnormal de/repolarization

Advanced knowledge of cardiac pathophysiology

Recognizing normal versus abnormal

Ability to follow an organized and sequential approach

LOTS AND LOTS OF PRACTICE!!!!!

Fundamentals of 12 Lead Interpretation

Review of cardiac conduction Refresh the understanding of the anatomy and physiology applicable to EKGinterpretation

Cardiac Conduction

Sinoatrial nodeRight atriumNear superior

vena cava Depolarizing

the atria through intranodal tracts

Atrioventricular nodeRight atrium Near the

septum Mediates

conduction to the ventricles

Cardiac Conduction

Bundle of HisOriginates in

the AVN Left and right

branches Spreads action

potential throughout ventricles

Cardiac Conduction

12 Lead EKG - Limb Leads Lead I

Right arm to left arm

Left positive Lead II

Right arm to Left leg Left leg positive

Lead III Left arm to Left leg Left leg positive

Bipolar leads form Einthoven’s triangle

Reference points are the lead origins

This is important !

12 Lead EKG - Limb Leads

12 Lead EKG - Augmented Leads Augmented lead

right (aVR) Origin point to the right

Augmented lead left (aVL) Origin point to the left

Augmented lead foot (aVF) Origin point downward

Unipolar leads form Goldberger’s triangle

Origin point is the heart

This is an important reference!

A tip: imagine this triangle within the Einthoven’s triangle!

12 Lead EKG - Augmented Leads

I 0°

II +60 °

III +120 °

aVL -30 °

aVR -150 °

aVF +90 °

The 6 Limb Leads

What Part of the Heart? Frontal plane leads look at different

segments of the heart

Know what area the leads focus on

Relationship Leads II, III and aVF view the inferior

wall Leads I and aVL view the lateral wall Lead aVR is not helpful here

Purpose of the 12 Lead

Identify ST elevation/depression

T wave inversion

Identify VT in wide complex rhythms

Electrical axis and hypertrophy

Bundle branch blocks

Indications?

Ischemic chest pain (unstable angina)

Chest pain – NYD

Change in chest pain presentation

To rule out cardiac involvement

Rule of Thumb

Perform a 12-lead when considering differential diagnoses It could be angina It could be an MI It could be an aneurysm It could be pericarditis

Don’t do it unless you are prepared (or someone else is) to act on the result!

Precordial Leads - 12 Lead

Precordial Leads - How are they placed?

V1 - 4th intercostal space, R sternal border V2 - 4th intercostal space, L sternal border V4 - 5th intercostal space, midclavicular line V3 - between V2 and V4 V6 - 5th intercostal space, midaxillary line V5 – anterior axillary line between V4 and V6

The 6 Chest Leads

12 Lead ECG - LP 12 Attach limb leads as per normal

Attach precordial leads to multi-lead adapter

Attach to patient as per prior diagram

Press ’12 lead’ button DON’T TOUCH PATIENT

DURING NEXT 20-30 SECS. ASK PATIENT NOT TO MOVE

Receive 12 lead from Printer

12 Lead ECG

Each of the 12 leads views the left ventricle from the positive electrode

In the precordial leads, it is assumed this is in the center of the heart

Review 12 lead information in Bledsoe

Myocardial Infarction

The BIG ONE!

Lead Perspective

Lead I and aVL = lateral wall

Lead II, III and aVF = inferior wall

aVR is not helpful here

V1 and V2 = anterior-septal wall

V3 and V4 = anterior wall

V5 and V6 = lateral wall

ST Segment Deviation ST segment is typically isoelectric ST segment represents total ventricular depolarization ST segment changes are caused by cellular changes Causes of ST segment changes

During ischemia the resting membrane potential is lowered relative ST segment elevationrelative ST segment elevation

Asynchronous depolarization of multiple cardiac cells true ST segment elevationtrue ST segment elevation

Criteria for Cardiac Injury on the EKG Transmural cardiac injury

Limb ST segment elevation of 1mm and extending at least 2mm out from the J point

Precordial ST segment elevation of 2mm

Other findings may include Inverted or flipped T wavesPathological Q waves

Phases of an Acute MI

Hyper acute phase - ST segment elevation begins in the first hours and

may last 1-6 weeks Evolved phase

- deep T waves and onset of pathological Q waves

Resolution phase - T waves return to normal morphology and position

Chronic phase - pathological Q waves

How can we determine the affected vessels?

The left coronary artery

bifurcates into two primary branches

circumflex artery left anterior

descending

Determining the Affected Vessels?

The right coronary artery

right atria & ventricle

inferior wall of the left ventricle

2/3 of the posterior wall

part of the left lateral wall

How can we determine the affected vessels?

Observe the vessel mapping!

Knowledge Application!

Is there any ST segment

deviation? What leads

are affected? What area

do these leads look at?

Reciprocal Changes

ST changes opposite from the anatomical location of the injured region

‘mirror-like’ image ST segment depression is

reciprocal to ST elevation Investigate further to rule out/in

injury pattern

Practice!

Differential Diagnosis - ST Segment Elevation

Acute myocarditis Hyperkalemia Hypothermia Acute cor pulmonale Cerebrovascular hemorrhage Cardiac tumor Even occasionally in healthy

individuals!!!

Ischemia

Electrophysiology - Ischemia

Cells quickly lose O2 and nutrient supply

CO2 removal is impeded Unable to completely repolarize ECG

depressed ST segment and/or inverted T waves

T waves = ventricular repolarization ST depression of 2mm or greater =

pathology

Other Multi-lead ECG Other Multi-lead ECG ConfigurationsConfigurations

15 lead ECG15 lead ECG

andand

18 lead ECG18 lead ECG

Right Side EKG To provide a more specific look at the right

ventricle

Leave V1 in place - this becomes V2R Leave V2 in place - this becomes V1R Move V4 to the 5th ICS on the right midclavicular

line = V4R Move V3 halfway between V2R and V4R = V3R Move V5 to the right anterior axillary line in the

5th ICS = V5R Move V6 to the right midaxillary line = V6R

Posterior EKG

To provide a closer look at the posterior wall of the heart

Move 3 precordial leads to the same horizontal plane as

V5 & V6Be sure to note which leads you have

repositioned Position them at the bottom of the left

shoulder blade left of the vertebral column

Utility of a 12 Lead ECG

It is only as good as the interpretation

Treat the patient first!

Start with the basics - O2, NTG, MS, IV etc.

Closely monitoring patients with suspected ACS

Practice Practice

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Try it on everyone in EMERG with chest pain!

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