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Chapter 9 - ACS I & II
1. ONTARIO
BASE HOSPITAL GROUP
Chapter 9
for 12 Lead Training
- Acute Coronary Syndromes – I & II-Ontario
Base Hospital Group
Education Subcommittee
2008
TIME IS
MUSCLE
2. Acute Coronary Syndromes – I & II
REVIEWERS/CONTRIBUTORS
Neil Freckleton, AEMCA, ACP
Hamilton Base Hospital
Jim Scott, AEMCA, PCP
Sault Area Hospital
Ed Ouston, AEMCA, ACP
Ottawa Base Hospital
Laura McCleary, AEMCA, ACP
SOCPC
Tim Dodd, AEMCA, ACP
Hamilton Base Hospital
Dr. Rick Verbeek, Medical Director
OBHG Education Subcommittee
AUTHOR
Greg Soto, BEd, BA, ACP
Niagara Base Hospital
2008 Ontario Base Hospital Group SOCPC
3. Chapter 9 Objectives
Define ACS
Describe the timeline for atherosclerosis
and thrombus formation in ACS
List the 3 initiating events in an ACS
Differentiate stable and vulnerable
plagues.
OBHG Education Subcommittee
4. Chapter 9 Objectives
Describe the process of thrombus
formation
List and differentiate the 3 I’s of ACS
Describe the myocardial coronary blood
supply
Name the major coronary arteries and
locations they serve
OBHG Education Subcommittee
6. Acute Coronary Syndromes
Definition:
Sudden ischemic disorders of the
heart
Include unstable angina and acute
myocardial infarction
Represent a continuum of a similar
disease process
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7. Thrombus Formation and ACS
UA NQMI STEMI
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Plaque Rupture
Thrombus Formation
Non-ST-Segment Elevation
Acute Coronary Syndrome
(ACS)
ST-Segment
Elevation
Acute
Coronary
Syndrome
Old
Terminology:
New
Terminology:
9. Acute Coronary Syndromes
All have sudden ischemia
Often can not be differentiated
in the first hours
All have the same initiating
events
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21. The Three I’s of ACS
Ischemia - permanent damage avoidable
lack of oxygenation
ST depression or T wave inversion
Injury - permanent damage avoidable
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prolonged ischemia
ST elevation
Infarct
death of myocardial tissue
may have Q wave
22. Evolution of AMI
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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
23. Ischemia
Epicardial Coronary Artery
Lateral Wall of
LV
Positive Electrode
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Septum
Left
Ventricular
Cavity
Inferior Wall of LV
24. OBHG Education Subcommittee
Ischemia
Inadequate oxygen to tissue
Subendocardial
Represented by ST depression
or T inversion
May or may not result in infarct
32. A bit of everything
Thrombus
Infarcted Area
Electrically Silent
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Depolarization
Ischemia
33. OBHG Education Subcommittee
Summary
A normal ECG does NOT rule out ACS
ST segment depression represents
ischemia
Possible infarct
ST segment elevation is evidence of
AMI
Q wave MI may follow ST elevation or
depression
34. OBHG Education Subcommittee
Coronary Arteries
Branch off of the
aorta, just above
the leaflets of the
aortic valve
Three major
arteries
Each supplies a
specific area
35. Right Coronary Artery
Inferior wall of LV
Right ventricle
Posterior LV
Posterior fascicle of
LBB
SA and AV node
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36. 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).
OBHG Education Subcommittee
37. Left Circumflex Artery
Upper lateral wall
of LV (Leads I and
aVL)
SA node in 45%
AV node in 10%
Posterior fascicle
of LBB
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39. ONTARIO
BASE HOSPITAL GROUP
Acute Coronary Syndromes II
Rapid Recognition and
Treatment of ACS
40. OBHG Education Subcommittee
Goal for ACS II
Rapidly recognize and treat
patients with sudden myocardial
ischemia
41. OBHG Education Subcommittee
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
42. Immediate Evaluation
O2, Cardiac monitor, SPO2
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Incident history
Risk factors
Treatment?
12 Lead ECG
45. OBHG Education Subcommittee
Atypical Pain
Musculoskeletal, positional or pleuritic
features
Often unilateral
May be described as sharp or
stabbing
Includes epigastric discomfort
Females often express atypical pain
47. Who do you wanna be? A case
in point about syncope and AMI
60 yr old ♂; CC= syncope alone at home
am; awoke feeling well
1000: bilateral shoulder pain; pt thought it
due to new exercise program
Went 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
OBHG Education Subcommittee
48. OBHG Education Subcommittee
EMS encounter
1550: 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, ↑cholesterol
Currently ASYMPTOMATIC
Resistant to 12 LECG but agreed if crew
would then leave him at home…
49. EMS 12 Lead – uh oh!
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50. 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.
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51. So who do you wanna be?
Mom: had sudden onset of chest pain in the
presence of daughter (the ACP)
Received early ED thrombolysis
Successful 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%)
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53. Reasons EMS were missing ACS
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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!
54. Important Notation
Note EXACT time symptoms
began
Duration of symptoms may
effect therapeutic options and
destination decisions
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55. 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?
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56. Risk Factors of ACS
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Diabetes
Smoking
Hypertension
Age
Cholesterol
Family history of
CAD
Obesity
Stress
Sedentary
57. Consider Risk Factors
Patients 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 burned
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Get the 12 Lead!
59. OBHG Education Subcommittee
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
60. Chronic Stable Angina vs. ACS
Not chronic stable angina if…
New onset
Lower exertion threshold
Change in pattern of relief
New or different associated
symptoms
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61. PCP General Therapy for ACS
Assessment
Monitor Lead II ECG & SP02
Vital signs
Story and risks
Expose & listen to the chest
12 Lead Acquisition*
Treatment
Oxygen
NTG
Aspirin
IV if certified
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62. ACP General Therapy for ACS
Assessment
Treatment
Monitor Lead II ECG & SP02
Oxygen
Vital signs
NTG
Story and risks
Aspirin
Expose & listen to the chest
IV
12 Lead Acquisition*
Morphine
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63. 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 PCP
Decision to proceed is based upon the
cooperative effort and decisions by the
Base Hospital and Service Operator
OBHG Education Subcommittee
64. General Therapy for ACS
Assessment and therapy occur
simultaneously
Findings may alter therapeutic
path
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65. OBHG Education Subcommittee
Oxygen
High flow mask is indicated if ischemia
is suspected
Advanced airway care for continued or
severe hypoxia where indicated
66. OBHG Education Subcommittee
Vital Signs
Respiratory rate and effort
Pulse rate, rhythm, volume
Blood pressure in both arms,
manual then automatic
Cardiac monitor
SP02 monitor
12 Lead ECG
67. OBHG Education Subcommittee
12 Lead ECG
Obtain after the first set of
vital signs
Repeat as often as necessary
(enroute to hospital)
69. OBHG Education Subcommittee
Aspirin
ASA - chew & swallow
Adhere to Medical Directive for
contraindications to ASA
Issues:
Asthma patients may have been told to
avoid ASA
Patients on anti-coagulants
Taken ASA already today
71. OBHG Education Subcommittee
Nitroglycerin
NTG sublingual
Repeat every five minutes as per
Medical Directive
Contraindications include;
Hypotension
ED Rx within 48 hours
Known hypersensitivity
Check MD
72. OBHG Education Subcommittee
NTG Precautions
Avoid hypotension
Limit systolic drop
Don’t use NTG as an
analgesic
Watch for right ventricular
infarction (RVI)
73. OBHG Education Subcommittee
Morphine
Morphine as per protocol
May require several doses for adequate
relief of pain
Decreases myocardial oxygen
requirements
Watch for respiratory depression
and hypotension
74. OBHG Education Subcommittee
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
77. OBHG Education Subcommittee
Case 2
68 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.
80. OBHG Education Subcommittee
Case 2
Now what is the order?
Story
Risk factors
ECG
Treatment?
What is the pharmacological treatment plan for
this patient?
Can you treat this patient under your medical
directives?
81. 12 Lead ECG Documentation
OBHG Education Subcommittee
Time Proced.
Code
Treatment
Description
Result
2234 313 12 Lead ECG Non-diagnostic or
NO STEMI
2250 313 12 Lead ECG STEMI : Inferior
reciprocal
changes.
SAMPLE
With the background of material presented thus far, we are now ready to examine the central issue: recognition and treatment of the acute coronary syndromes.
A good understanding of ACS and its management changes how we look at “cardiac” patients. Even some of the assumptions we have held for years may be challenged.
To illustrate how some of our assumptions may need re-evaluation, let’s do a simple exercise....
<number>
We previously stressed the recognition of acute myocardial infarction (AMI). The next two components of this chapter broaden the scope by placing emphasis on the Acute Coronary Syndromes (ACS), of which AMI is one component.
The title “Acute Coronary Syndromes” refers to events producing acute ischemic pain or its equivalents. As such, a common component of ALL ACS is sudden myocardial ischemia.
While the phrase acute coronary syndromes represents a spectrum of one disease, there are at least three conditions identified within this continuum.
<number>
This slide discusses old and new terminology as they relate to ACS:
OLD: unstable angina (UA), non-Q-wave myocardial infarction (NQMI), and ST-segment elevation myocardial infarction (STEMI) are all parts of the spectrum of clinical manifestations of acute coronary syndrome (ACS).
NEW: The older terminology has now been replaced with terminology that divides ACS into non-ST-elevation ACS (NSTE-ACS) and ST-segment-elevation.
It has now been demonstrated that atherosclerosis begins in the first decade of life - much early than previously thought.
Go step by step through timeline developments listed at the top of this slide in terms of Foam cells, fatty streaks, etc particularly focussing on Fibrous plague development and lesion/plague rupture.
<number>
While each of the acute coronary syndromes have their own particular distinctions, it is their commonalities that cause them to be grouped together.
First, as previously mentioned, all the acute coronary syndromes are a result of acute myocardial ischemia.
Second, their clinical presentation may be indistinguishable in the first hours, making early differentiation difficult or impossible. One may SUSPECT the presence of an ACS based upon a targeted history, however is often not possible to determine which syndrome is present.
The third reason is that they all have the same initiating events.
<number>
These three events are present, to one degree or another, in all of the acute coronary syndromes.
Understanding these events not only explains why the three syndromes are grouped together, but it also provides a framework for understanding exactly how the treatments you provide will benefit the ACS patient.
So let’s look at each of these in more detail.
<number>
Both of these illustrations represent a cross section of a coronary artery. Notice the diameter of the lumen in each of them. Which artery has the greater lumen diameter?
Answer: the vulnerable artery
Most heart attacks are not caused by the GRADUAL narrowing of a coronary artery until it ultimately becomes occluded. Rather, something happens inside the artery to induce the occlusion.
The event most likely to induce an occlusion is a rupture in the arterial wall covering the plaque exposing its contents to circulating blood.
The second illustration is considered “vulnerable” because the fibrous cap is very thin.
This sets up a situation in which plaque rupture is more likely to occur. Often the vulnerable sites have less stenosis than more stable sites.
<number>
Realize that the plaque generally accumulates in the walls of the coronary artery and does not come into contact with the circulating blood. In fact, if plaque contents are exposed to the blood, the clotting mechanism will be initiated. Therefore, plaque rupture is usually the initiating event for all of the ACS.
<number>
When the cap ruptures, the cascade of clotting begins.
The first event is that platelets begin to adhere to the tissues exposed by the rupture.
At this point, any occlusion present is the result of the rupture. While extensive and deep plaque ruptures can cause occlusion, it is often the next step in the process that produces significant occlusions.
<number>
Platelets not only stick to the tissue exposed by the plaque rupture, they begin to attract additional platelets and then stick to each other. As these platelets aggregate they can produce significant occlusions.
Remember that this process is merely the body’s normal clotting mechanism. This process includes the the ability to remove or spontaneously lyse a clot. In some patients, that is just what happens: the clot formation is halted and reversed and the plaque rupture ultimately heals. The patient may have never known anything happened.
However, many patients are not that lucky.
NOTE: The balance between clot formation and clot lysing is referred to as the “Systemic Thrombotic Tendency”.
<number>
If the aggregation continues, a more significant occlusion is produced. This is still not the end of the story. The clot may be extensive but it has not yet completely matured.
<number>
In addition to platelet aggregation the body can create a “frame” to further solidify the clot. This framework is produced from fibrin.
Fibrin creates a “mesh” or “net” to catch red blood cells; ultimately the fibrin shrinks down and solidifies the clot.
At this point the clot is harder to lyse.
RECAP: thrombus formation includes platelet adherence, aggregation and fibrin formation.
The third event contributing to coronary artery occlusion in the ACS is vasoconstriction.
<number>
The processes described to this point will often induce coronary artery vasoconstriction. Such constriction at the site of rupture can cause a partial occlusion to completely occlude the artery.
These events, plaque rupture, thrombus formation and vasoconstriction are usually present to some degree in all of the acute coronary syndromes. This begs the question: “If they all have the same events, why do some result in tissue necrosis (Q-wave MI and Non-Q-wave MI) while others do not?”
<number>
Point out the epicardial artery and it’s branches reaching toward the endocardium.
The endocardium is less well perfused and has higher oxygen demand than epicardial tissue. Illustrate higher demand with glass of water.
When the myocardium is well perfused, the ST segments are isoelectric (equal to the T-P segment).
<number>
ST segments are isoelectric – meaning they are consist with the TP segments that follow and proceed.
<number>
Whether tissue necrosis occurs as in AMI or does not occur resulting in unstable angina is determined by the interplay of several factors.
This underscores why it is usually impossible to determine which syndrome is present and why we should instead concentrate on identifying the the presence of any ACS.
The issue of suspecting ACS will be addressed after a brief explanation of the terms ischemia, injury and infarction.
<number>
The vessel lumen is now narrowed by a clot. If the clot is incomplete or collateral circulation is good, only the hardworking, poorly perfused sub-endocardial tissue will become ischemic.
This is represented on the ECG by ST depression or T wave inversion.
<number>
Define ischemia.
Inadequate oxygen to tissue.
SUBENDOCARDIAL DEFINED
Represented by ST depression or T inversion.
May or may not result in infarct (duration of clot and demand).
If infarct develops, may or may not display Q wave.
The direction of ST deviation is a poor predictor of Q wave development.
<number>
Note widespread ST depression and T waves inverted in several leads.
Recent evidence suggests that broad patterns of ST-depression and T-wave inversion may present a pattern of subendocardial injury or preinfarct if you will. The patients should have repeat 12 Lead ECGs performed by paramedics while enroute to the ED or while in the ED on delay as they may change to ST-elevation.
<number>
If the clot is complete or the collateral circulation is poor, the ischemia will be transmural (through to wall). This is seen on the ECG as ST segment elevation.
Most often this occurs due to a complete and persistent clot. Spontaneous lysis at this point is rare and the tissue is expected to infarct unless acute reperfusion therapy can be rapidly initiated.
ST segment elevation is presumptive evidence of ACUTE MI.
<number>
Define injury. Ischemia affecting the epicardium represented by ST elevation.
Lack of oxygenation to tissue
TRANSMURAL = injury pattern extends through the full wall of the affected myocardium
Represented by ST elevation. Refereed to as the “injury pattern”.
Usually results in infarct (presumptive evidence of MI)
If infarct develops, may or may not develop Q wave
The direction of ST deviation is a poor predictor of Q wave development.
<number>
Ask group to look for ST elevation.
The ST elevation implied epicardia ischemia (injury pattern).
<number>
Death of tissue.
Traditionally represented by wide (equal to or greater than 40ms) Q wave.
Not all infarcts develop Q waves.
The direction of ST deviation (elevation or depression) is a poor predictor of Q wave development.
<number>
Death of myocardial tissue may result in the development of a pathologic Q wave.
Q wave development can not be predicted by the direction of ST segment deviation.
It does not occur with all infarcts.
<number>
Pathologic Q waves present in II, III and aVF suggest necrosis has occurred in the inferior region of the left ventricle.
<number>
During the evolution of an infarct, Q waves, ST elevation, and T inversion may occur together.
ST elevation is the most important finding to the emergency care provider. It is presumptive evidence of acute myocardial infarction.
<number>
A normal ECG does NOT rule out any Acute Coronary Syndrome.
ST segment depression represents ischemia, infarction is possible.
ST segment elevation represents epicardial ischemia, and is presumptive evidence of AMI.
Since necrosis may occur under all the these situations, a Q wave MI may follow ST elevation, ST depression or even a normal ECG.
This is a good time to discuss how knowing which artery feeds different areas can make your reading the 12-lead much easier and help to anticipate trouble.
Take this time to discuss and refer back to which coronary artery blockages lead to STE in which parts.
Review a few ECG samples here and discuss the coronary artery involved.
With the background of material presented thus far, we are now ready to examine the central issue: recognition and treatment of the acute coronary syndromes.
A good understanding of ACS and its management changes how we look at “cardiac” patients. Even some of the assumptions we have held for years may be challenged.
To illustrate how some of our assumptions may need re-evaluation, let’s do a simple exercise....
<number>
The FIRST goal is to RAPIDLY identify patients with sudden myocardial ischemia (sudden myocardial ischemia is the same as ACS).
Information collected by Acute Coronary Syndrome Consultants, Inc. shows that many EMS systems commonly fail to identify up to 50% of the patients with a diagnosis of AMI. Furthermore, in some systems that number has approached 70%. These numbers may be surprising and even sound inconceivable, but they are accurate results of data evaluation.
Part of the problem is that traditional training failed to adequately address atypical presentations of sudden myocardial ischemia.
<number>
Small group exercise:
Break into small groups of three to six.
Each group should select a spokesman/recorder
Have each group produce a list of risk factors for coronary artery disease, ranking them from highest to lowest
Have each group discuss the last AMI cases they encountered. List the presenting symptoms
Have each group discuss the symptoms of a family member or friend that has suffered an AMI
Upon completion, return to the lecture and advise the students that this material will be used later in this module.
<number>
The patient’s incident history and risk factors are the principle factors used to determine the likelihood of ACS.
Providers should be able to recognize the typical and atypical presentations of the Acute Coronary Syndromes. When the "story" is weak, the risk factors weigh heavily into the equation.
<number>
The clinical presentations associated with ACS may be placed into one of these three general categories.
"Classic angina" or "classic ischemic chest pain" refers to the traditional description of ischemic chest pain (dull, crushing, substernal, etc). Remind paramedics that they are likely very familiar with the description of classic ischemic chest pain.
The phrase “atypical” presentation encompasses the remaining categories.
Ischemic equivalents refers to non-pain symptoms that may be consistent with ACS.
<number>
EMS typically recognizes patients with classic anginal chest pain as potentially suffering an acute coronary syndrome. However, approximately one-half of all patients with acute coronary syndrome will NOT present with this classic pain pattern.
<number>
Approximately 20% of ACS patients will present with atypical pain.
Females often present with atypical pain. Most EMS personnel have been taught that sharp or unilateral pain is almost never related to cardiac disease. We should have a high index of suspicion for all chest pain, especially in patients with a history of coronary artery disease or a number of risk factors.
Of course, not everyone with chest pain is suffering from an ACS.
<number>
Ischemia can cause dysrhythmias and varying degrees of ventricular failure. Symptoms of these complications may the only presenting complaints when chest pain is absent.
The elderly may present more often with dyspnea secondary to sudden decompensated ventricular failure.
Diabetics frequently present with weakness, dizziness and syncope. Up to 30% of ACS patients will present with an anginal equivalent.
PHECG Interpretation: Inferior AMI
The thoughtful investigation by the paramedics in this case are likely the reason this patient had a good outcome and remains alive today.
The lesson in this case is to assess atypical symptoms along with risk factors in order to acquire 12 Leads that may impact STEMI reperfusion time and results.
<number>
Female, diabetic and/or elderly patients are most likely to present with atypical presentations which include atypical pain and anginal equivalents.
“Protocols get in the way”: Most paramedic medical directives related to ACS events limit the provider from treating non-chest pain patients as ischemic, even if only 50% of AMI patients present with classic chest pain. This slide sums up the previous slides on symptoms related to ACS with a mind to encouraging participant paramedics to use the 12 Lead ECG as a diagnostic tool for patients based on symptoms that fit atypical pain and anginal equivalents.
<number>
It is important to note exactly when the patient’s symptoms began. Have the patient describe the time and onset as specifically as possible.
Treatment decisions are often based on duration of symptoms. Acute reperfusion therapies have risks that outweigh the benefits after several hours of symptoms. Usually there is a 12-hour cutoff point for thrombolytics.
Explore when their symptoms became constant as that is often the time used in making decisions about therapy. For example, if a patient has had episodic chest pain for two days and the pain became constant two hours ago, the window for therapy is now at two hours. If the patient has difficulty estimating time, ask what they were doing at the time. One paramedic reported he carries a TV guide and asks the patients what show was on at the time their pain started or changed.
te exactly when
<number>
Regroup into the small groups.
Have them review the AMI patients they discussed.
Categorize each as classic, atypical or anginal equivalent.
How many of their patients were typical presentations and how many were atypical (atypical CP or anginal equivalents)?
How many in the friends and family catagory had classic ALS?
Often there will be more typical presentations in the "patient”category and more atypical presentations in the friend or family category. Could this be because we fail to recognize atypical presentations in our patients?
<number>
A review of risk factors.
Discuss how you determine these risks.
The definition of a “Family history of CAD – family history of <55 year old men, <65 year old women – first degree relative.
Note that recent evidence suggests that elderly male patients with no major risk factor of coronary artery disease may be at higher risk of AMI as a result of anxiety. Anxiety and other mental health problems may be something to watch for in future research related to CVS risk factors.
Source:
Shen BJ, Avivi YE, Todaro JF, et al. Anxiety characteristics independently and prospectively predict myocardial infarction in men. The unique contribution of anxiety among psychologic factors. J Am Coll Cardiol 2008; DOI:10.1016/j.jacc.2007.09.033. Available at: http://content.onlinejacc.org.
<number>
Risk factors help in the overall evaluation and decision pathways with potential ACS patients.
<number>
Although myocardial ischemia and infarction has been known to occur at any age, patients in these categories are the most suspect. In general, the older the patient is, the more risk is present.
<number>
Since AMI and unstable angina are indistinguishable in the first few hours we use the term Acute Coronary Syndrome to identify the group.
Remember that emergency personnel should think about ACS when evaluating patients with atypical chest pain or anginal equivalents.
Risk factors are especially useful when the story is atypical.
<number>
"Classic ischemia" is the term used to describe ischemic chest pain, not the disease chronic stable angina pectoris.
"Classic ischemic chest pain" may occur with NSTEMI or STEMI.
Patients with previously diagnosed stable angina should be evaluated for ACS if there is any change in pattern of onset such as lower exertions threshold, relief, i.e., requiring more nitro or recovery time, or new associated symptoms.
New onset chest pain not previously diagnosed with stable angina is assumed to be an acute coronary syndrome until proven otherwise.
Lower exertional threshold refers to angina pain brought on a lower exertion. For instance, the patient walks her dog for 30 minutes and sometimes feels some mild chest tightness that rarely needs NTG and usually resolves with rest. Today it did not resolve with either rest or NTG – she called EMS.
Change in pattern of relief: normally resolves with one to two NTG but today the patient has taken 7 with no change in pain.
New/different symptoms: usually angina presents as mild chest tightness that resolves – today it is associated with Left arm pain which is a new symptom for this patient.
<number>
Although there is general therapy for ACS, local protocols and medical direction supersede this reference.
All patients suspected of ACS should receive the indicated components of this list. Those from the ST elevation/acute reperfusion subset should be efficiently triaged for reperfusion treatment.
Point of Emphasis: Save for the 12 Lead acquisition and interpretation there is NOTHING above that is different or should be different than what PCPs are already doing. The interplay of assessment and treatment continues as it always has except after a complete review of presentation, history, risk factors and initial treatment – then a 12 Lead ECG is acquired and interpreted.
<number>
Although there is general therapy for ACS, local protocols and medical direction supersede this reference.
All patients suspected of ACS should receive the indicated components of this list. Those from the ST elevation/acute reperfusion subset should be efficiently triaged for reperfusion treatment.
*Same Point of Emphasis: Save for the 12 Lead acquisition and interpretation there is NOTHING above that is different or should be different than what ACPs are already doing. The interplay of assessment and treatment continues as it always has except after a complete review of presentation, history, risk factors and initial treatment – a 12 Lead ECG is acquired and interpreted.
Scene management to reduce on scene time:
In Niagara, we have not scene increases in scene time with the introduction and proliferation of Prehospital 12 Lead ECG. One reason is that we have a high number of ACPs and ALS capture. Most ACP-PCP partners have evolved to efficiently acquire a 12 Lead ECG:
ACP starts IV while PCP acquires the 12 Lead ECG. The benefit of this approach is that there is simultaneous action that wastes no time.
An important point for consideration of the template of care for ACPs is that if they have progressed in MAC protocol for ischemia to the point of administration of Morphine without having acquired a 12 Lead ECG they should seriously rethink this approach. While pain management is important for patient comfort, it is reperfusion therapy for STEMI that will ultimately determine clinical outcome for the ACS patient.
<number>
Patient evaluation and treatment occur simultaneously. Exact sequence will vary due to a variety of factors including number and certification level of personnel on the scene, available equipment and resources, local protocol etc.
Efficient, rapid assessment and transport of ACS patient is of utmost importance.
<number>
High flow 02 via non-rebreather mask is generally not necessary for uncomplicated ACS patients. Watch the respiratory rate and Sa02. Remember that a good Sa02 sat (>95) in the presence of tachypnea is a sign of compensation and may indicate severe impending decompensation and hypoxia.
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The 12-lead ECG is obtained with the first set of vital signs.
This establishes an early baseline.
Some practitioners prefer to obtain a 12-lead ECG before administering oxygen. This is acceptable in uncomplicated cases (no hypoxia, shock, etc.) as long as the 12-lead ECG is obtained rapidly (within two to four minutes) and without delay.
Blood pressure should be obtained in both arms. This is usually required on thrombolytic checkoff lists as it helps identify patients with dissecting thoracic aneurysm.
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Rules of prehospital acquisition:
ECG after the first set of vitals
Repeat as needed – perhaps enroute to hospital in cases where STEMI has been found
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Initial venous access may be via a lock or line.
A stable free flowing vein (forearm or ACF) cannulated with a reasonable size line (18-20 gauge) is suitable for the initial access line.
Draw initial blood for point of care cardiac markers and glucometer checks where indicated.
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The only absolute contraindication to ASA is known hypersensitivity.
Many patients have been told by their physicians to avoid ASA products for a variety of reasons including gastric irritation and prolongation of clotting time with anticoagulant therapy. The small single dose given for ACS is generally not harmful to these patients. If a patient is apprehensive about taking ASA the decision can be deferred to the emergency department.
Asthmatics may have been instructed not to take aspirin; however they may receive ASA if they have not had an allergic reaction to it.
Many services administer ASA even when the patient states he takes ASA daily. Patient compliance is not always reliable and this is probably a harmless practice.
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Some of the many benefits of NTG therapy.
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Systolic BP should be at least 100mmHg for NTG administration.
Ask about Viagra or similar erectile dysfunction drug use in private if possible.
Right ventricular infarct will be discussed in a later module, and is associated with hypotension.
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Do not allow the systolic BP to drop below 100. Do not lower the BP more than 30% in hypertensive patients or 10% in normotensive patients.
NTG is not an analgesic.
Right ventricular infarct will be discussed in Module 5.
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Pain relief is an important factor in managing ACS, a fact that is often not fully appreciated in the prehospital community.
Patients in severe pain may require a significantly high dosing and multiple administrations of morphine to attain pain relief. Up to to 30mg may be needed to control the pain.
Of course, all of the standard contraindications and cautions are still valid.
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Finding suggests some ST changes possibly consistent with an ACS: ST-depressions in V1-V3 but not STEMI AT THIS TIME.
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Note risk factors are significant for this patient but ischemia protocol can not be started as patient does not have chest pain.
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Inferolateral STEMI with RCs. This patient is likely experiencing an STEMI with atypical symptoms. She is at great risk. Other than initiating STEMI triage to ED, what treatment if any can be applied at this time?
Ask the group:
What is the pharmacological treatment plan for this patient?
Can you treat this patient under your medical directives?
Some paramedics may want to treat with NTG & ASA and do so despite specific wording in protocols related to chest pain.
Some don’t treat based on strict interpretation of protocols
Other recognize the best answer: patch to BHP (where permitted) for order for ASA & NTG.
Documentation:
The first 3 columns are universal for all paramedics and Base Hospitals. However, what is documented in the RESULTS section may vary according to local Base Hospital preferences.
TWO choices seem to used in prehospital programs for result where no ST-elevation is present:
NO STEMI
Non-diagnostic
The choice about which term is better is subject to debate. In one program, “non-diagnostic” was used to avoid confusion with STEMI (i.e.: trouble differentiating positive and negative 12 Lead with poor writing.). However paramedics found this wordy and most use “no STEMI” or “NON-STEMI”.
An important documentation result consideration is to feedback to paramedics that NSR (or any other rhythm interpretation documentation under Result is not acceptable. 12 Lead ECG and Rhythm Interpretation should never be confused.
Thrombolytic checklists can be obtained from local hospitals or drug companies. Get with the hospital you transport to and adopt their checklist. It will speed up the door-to-drug time in most cases.
