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As soon as the crew arrives on the scene, the lead medic immediately calls for a
thorough scene survey and an interview with the grandson. Our patient says that
his symptoms began while he was watching television. He says he has no chest
pain, no shortness of breath, no recent trauma, no numbness, and no history of
similar symptoms in the past.
He has not been ill recently. Simultaneously, our lead medic initiates the ABCs and
calls for a full set of vital signs and the patient to be placed on a monitor. This is
extremely important in any situation when acute coronary syndrome is possible.
Once you identify a STEMI (ST-elevation MI) on the EKG, it’s time to think “load
and go.” On-scene time is the largest fraction of “pre-hospital time.”
As mortality can be reduced with rapid coronary reperfusion, STEMI patients should
be identified rapidly, with minimum scene times, and rapid transport to the
appropriate receiving facility.
Armed with an EKG showing an acute STEMI, the crew accurately decides to “load
and go”. The remainder of the SAMPLE history and head-to-toe performed as the
patient is moving towards the back of the ambulance and eventually the treating
hospital. The grandson is briefed about his grandfather’s condition and rides along
to the hospital.
Our Case
You are presented with a 75-year-old man. His grandson calls 911 because he was
having left arm pain, sweating, and nausea for the past 15 minutes. His
vital signs and physical exam are relatively unremarkable, except that he is anxious
and sweating. His symptoms started while he was watching TV. Our patient has no
known medical history. The EKG reveals the most compelling evidence with ST
elevation in leads V3, V4, and V5 with reciprocal T wave inversions inferiorly. We
have now diagnosed an acute anterior wall STEMI (ST-elevation MI).
Summary Of History
Left arm pain, sweating, and nausea. No chest, arm or back pain. No nausea or
vomiting. No shortness of breath. No significant past medical history, except for
smoking 1 pack of cigarettes per day for the past 50 years.
Age
Smoking
High cholesterol
Diabetes
Hypertension
Family history
Unstable angina
Quit smoking
In the United States, more than 600,000 die each year from coronary artery
disease (CAD)
Electrical conduction system of the heart. Impulses that originate in the SA node spread through
the atria and along the internodal pathways to the AV node. From the AV node, they travel down
the bundle of His and right and left bundle branches and into the Purkinje network of
the ventricles.
Cocaine abusers
Sweating
Lightheadedness
Palpitations
Syncope
EKG changes
Signs of shock
Atypical Presentations Of MI
Women
Elderly
Diabetics
Pearls Of Wisdom
More men have heart disease than women, but more women die of heart disease.
Why? Women often present with atypical presentations (i.e., nausea, sweating,
lightheaded, etc.) making diagnosis more difficult. Be aggressive in considering
acute coronary syndrome in the female patient population with atypical symptoms.
Sudden cardiac death is always a possibility within the spectrum of the various
acute coronary syndromes. Half of the deaths from acute coronary syndrome occur
before patients reach a hospital. This makes efficient diagnosis and treatment of
acute coronary syndrome so imperative in the prehospital environment.
Identification of patients with STEMI and triage for early reperfusion therapy
Myocardial infarction (MI) is typically the result of a blockage in one of the coronary
arteries due to an atheroscleroticplaque. The partial or complete blockage of this
coronary blood vessel causes the lack of oxygenated blood to be delivered to a
portion of the heart causing an infarction (death of heart muscle). As time is
muscle, the quicker these patients are treated with either fibrinolytics (clot busters)
or angioplasty, the better. The goal in both treatment modalities is to open the
blocked coronary artery as soon as possible.
Caution
Be aware of abnormal heart rhythms. In an ICU setting, between 72% and 100% of
heart attack patients will have an abnormal heart rhythm. Be prepared for
bradycardia, heart blocks, and ventricular fibrillation. MI patients are extremely
vulnerable to lethal heart rhythms and it is always a good idea to have the AED or
defibrillator ready in case it is needed.
"MI" is another term for "heart attack" and is used to describe irreversible necrosis
(or death) of the heart muscle due to ischemia (lack of oxygen). This is the reason
for the adage that "time is muscle." MI is the result of an occlusion of a coronary
artery by a clot (thrombus), spasm of a coronary artery (cocaine is common cause),
or any reduction in overall blood flow (shock, arrhythmias, pulmonary embolism).
Coronary artery obstruction from clot (thrombus) is the most common reason for
an acute MI.
O - Onset - How did chest pain or symptoms begin? Ever had this before?
P- Provoked - What brought symptoms on? Exertional? Non-exertional? What were
you doing when symptoms started? What makes symptoms better? Worse?
Q - Quality - What does discomfort feel like? Dull? Pressure? Sharp? Squeezing?
Tightness?
R- Radiate - Does pain radiate? Arm? Neck? Back? Abdomen?
S - Severity - How bad is discomfort/pain on a scale from 1-10?
T - Timing - When did symptoms start? How long did symptoms last? When did it get
worse or better? Constant? Wax and waning?
ABC's
The EKG reveals the most compelling evidence with ST elevation in leads V 3 , V 4 ,
and V 5 with reciprocal T wave inversions inferiorly. Our crew has quickly diagnosed
an acute anterior wall STEMI (ST-elevation MI).This is a classic EKG presentation of
an acute anterior wall infarction, which typically involves the left anterior
descending artery.
From the information we have been given in this scenario, this patient's diagnosis is
acute anterior wall STEMI.
Our patient does not have any chest pain, yet his EKG suggests that he is having an
acute MI. The teaching point here is that chest pain is not always present with an
acute myocardial infarction. Not all patients will have the classic symptoms of a
heart attack. In fact, 30% of MI patients will have a silent MI, or atypical symptoms
of MI.
"I have seen patients in the ER present with nothing more than sweating while they
were in the midst of having an acute MI. I have seen many patients die from an MI
without ever having chest pain. Although you should be aware of the classic
symptoms of an MI, equally important is to keep in mind that there are many
exceptions to the rule, and many different clinical presentations of the acute MI
patient."
Continuous monitoring
Oxygen
Aspirin
Nitroglycerin
Cialis (Tadalafil)
Viagra (Sildenafil)
Levitra (Vardenafil)
Morphine
ST-Elevation
Posterior Wall MI: Don’t forget to always consider and look for a
posterior wall MI. It does not present with ST elevation when
looking at the EKG conventionally! Typical pattern includes tall
and fat R wave, ST depression, and upright T wave in leads
V 1 and V 2 .
o Good trick: If you turn the EKG upside down, and look at the EKG
through the back of the paper, you will see ST elevations in V 1 and
V 2 with an acute posterior wall MI.
In our patient’s scenario, the EKG shows ST elevation in leads V1, V2, and V3 with
reciprocal ST depresion inferiorly (II, III, aVF). This is a classic EKG presentation of
an acute anterior wall infarction, which typically involves the left anterior
descending artery.
Our patient felt better with the oxygen, aspirin, and nitroglycerin administered by
our crew. He was taken to a hospital where he had emergency angioplasty. Once
the cardiologist injected the dye to visualize the coronary arteries, the patient was
found to have a 99% blockage in the left anterior descending artery. The patient
had the vessel opened and a stent placed. His door-to-balloon time was 30
minutes, and the patient was discharged from the hospital 3 days later, very
appreciative of all of the life-saving professionals that cared for him.
Documentation
Diagnosing and treating a STEMI is serious business, and a task that the public
expects from its ALS providers. Your documentation should reflect the seriousness
of that task. What are the patient’s symptoms, when did they start? What are your
patient’s signs? Are they diaphoretic, pale, hypotensive? Does your charting
accurately reflect the picture you were presented? Does your charting have
accurate times, i.e., time on scene, time the initial and subsequent EKGs were
obtained, time the hospital was called notifying them of a suspected STEMI? How
about scene time? Were any delays on scene adequately documented? How did the
patient’s clinical situation change while they were in your care? Did the pain or
symptoms get better or worse? Is this clearly documented? Was more than one
EKG obtained? Are these EKG interpretations properly documented? Was a right-
sided EKG obtained? Adequately and systematically documenting your patient’s
symptoms, vitals, scene times, and actions is always important, but especially
important in the STEMI patient.
Glossary
References