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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
prolonged transport time
no thrombolysis at the sending facility
Long delays
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
More Relative Contraindications
The grey area
intracranial/intraspinal surgery
intracranial neoplasm, A-V malformation, aneurysm
bleeding diathesis
severe hypertension
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!!
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
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
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
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 - 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
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
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
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
Differential Diagnosis - ST Segment Elevation
Acute myocarditis Hyperkalemia Hypothermia Acute cor pulmonale Cerebrovascular hemorrhage Cardiac tumor Even occasionally in healthy
individuals!!!
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