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Cardiac Case Study: 50-Year-Old Male with Chest Pressure by Stephen J.

NREMT-P On Sep 1, 2005

Use this case study as an educational tool by answering the questions posed by the
author, then reviewing the answers further down.

At 6:45 a.m., your unit is dispatched for a 50-year-old male with chest pain. You and
your partner proceed to the scene, with a response time of approximately eight
minutes. The closest hospital from the scene is 40 miles away.

You arrive at the scene, don appropriate BSI precautions and ensure that the area is
safe, then knock on the door of the patient's residence. A middle-aged male
answers the door and identifies himself as the patient. You note that he is
diaphoretic and anxious, and is clenching his fist against the center of his chest.

1. What is the significance of the patients clenched fist in the center of his chest?

You sit the patient down and perform an initial assessment (Table I). Your partner
attaches a pulse oximeter and prepares to administer oxygen to the patient.

Your partner administers 100% oxygen to the patient with a nonrebreathing mask
while you perform a focused history and physical examination (Table II). The patient
tells you that his doctor prescribed nitroglycerin for him; however, because he
recently moved into the house, he thinks it's still packed in one of the boxes.

Table I: Initial Assessment

Level of consciousness: Conscious and alert to person, place and time; restless and
Chief complaint: "My chest feels tight and I feel really weak."
Airway and breathing: Airway is patent; respirations are slightly increased and
Oxygen saturation: 97% (on room air).
Circulation: Radial pulse is rapid, strong and regular; skin is cool, clammy and pale.

Table II: Focused History and Physical Examination

Onset: "This began suddenly. It woke me from my sleep."

Provocation/Palliation: "This pressure in my chest is constant. Nothing that I do
makes it better or worse."
Quality: "My chest feels very tight."
Radiation/Referred: "The pressure stays in my chest. I don't hurt anywhere else."
Severity: Seven on a 0--10 scale.
Time of onset: "This began about an hour ago."
Interventions prior to EMS arrival: None.
Chest exam: No sign of trauma, chest wall is symmetrical and nontender.
Breath sounds: Clear and equal bilaterally to auscultation.
Jugular veins: Normal, not distended.

2. What are the physiologic effects of nitroglycerin?

After confirming no history of bleeding disorders or allergies, you administer 324 mg

of aspirin to the patient. Your partner obtains baseline vital signs and a SAMPLE
history (Table III). The patient remains conscious and alert, but is becoming
increasingly restless. You attach the patient to a cardiac monitor and interpret his
cardiac rhythm as sinus tachycardia at 110 beats per minute.

After administering 0.4 mg of nitroglycerin sublingually to the patient, you and your
partner attach the remaining ECG leads and obtain a 12-lead tracing of the patient's
cardiac rhythm. As your partner stands up to retrieve the stretcher from the
ambulance, you tell him that it looks as though the patient may be having an
anterior wall MI.

Table III: Baseline Vital Signs and SAMPLE History

Blood pressure: 160/92 mmHg.

Pulse: 112 beats/min, strong and regular.

Respirations: 22 breaths/min and unlabored.
Oxygen saturation: 99% (on 100% oxygen).
Signs and symptoms: Chest pressure, restlessness, diaphoresis, tachycardia,
Allergies: None. He is not allergic to aspirin.
Medications: Nitroglycerin (as needed) and Vasotec. He has not taken any Viagra.
Pertinent past history: "I have high blood pressure and the doctor told me I may
have a heart attack if I don't start exercising. He gave me the nitro to take when I
have chest pain."
Last oral intake: "I ate supper last night, but can't remember the exact time."
Events leading to the present illness: "I was asleep when the pressure in my chest
woke me up."

3. How could this patient's current blood pressure and heart rate affect his

The patient's chest pressure is unrelieved following two more doses of sublingual
nitroglycerin. You place him on the stretcher and load him into the ambulance. En
route to the hospital, you continue oxygen therapy and successfully establish an IV
of normal saline with an 18-gauge catheter. Reassessment of his blood pressure
reveals a reading of 140/88 mmHg. Because three doses of nitroglycerin failed to
relieve his pain, you administer 2 mg of morphine sulfate via IV push. Within 10
minutes, the patient tells you that the pressure in his chest has improved and is
now a "3" on a 0--10 scale. With an estimated time of arrival at the ED of 20
minutes, you begin an IV infusion of nitroglycerin at 10 g/min and perform an
ongoing assessment (Table IV).

The patient's condition continues to improve en route to the hospital. You ask him if
he has a history of ulcers, bleeding disorders, recent surgeries or stroke. He tells
you that other than his high blood pressure and occasional chest pain, he has no
other medical problems. You call your radio report to the receiving facility and
continue to monitor the patient.

Table IV: Ongoing Assessment

Level of consciousness: Conscious and alert to person, place and time; less restless.
Airway and breathing: Airway remains patent; respirations are 20 breaths/min and
Oxygen saturation: 99% (on 100% oxygen).
Blood pressure: 130/84 mmHg.
Pulse: 88 beats/min, strong and regular.
ECG: Normal sinus rhythm at 90 beats/min.
Chest pain severity: 3 on a 0--10 scale.

4. Why are you asking the patient these specific questions?

The patient tells you that he is still experiencing chest pressure; however, it is less
severe. Since his blood pressure remains stable (130/84 mmHg), you administer
another 2 mg dose of morphine via IV push. You continue to monitor the patient's
vital signs and cardiac rhythm. Your estimated time of arrival at the hospital is 5--10

5. Are there any special considerations for this patient?


Upon arriving at the emergency department, the patient states that he is pain-free.
You give your verbal report and field-obtained 12-lead ECG to the attending
physician. Following additional assessment in the emergency department, the
patient is diagnosed with an acute anterior wall myocardial infarction. Following
successful treatment with fibrinolytic therapy, he is admitted to the cardiac care
unit and transferred to a cardiac rehabilitation facility 10 days later.

Cardiac Case Study: Answers and Summary

1. What is the clinical significance of the patients clenched fist in the center of his

Ischemic cardiac chest pain is typically described as being crushing, tight,

oppressive, pressuring or constricting in nature. Patients may describe their pain as
though a vise were placed around their chest or the sensation that an elephant is

sitting on their chest, while others may only report a vague or "strange" sensation
in their chest. The pain associated with cardiac ischemia is usually substernal;
however, it may be localized to the epigastrium and is commonly mistaken for

A clenched fist in the center of the chest (the precordium) conveys the feeling of
pressure or squeezing and is called Levine's sign (see the photo on page 50). The
presence of Levine's sign is suggestive, but not conclusive, of cardiac-related chest
pain and should increase your index of suspicion.

Chest pain or discomfort is the most common presenting symptom of an acute

coronary syndrome (ACS), occurring in 70%--80% of patients. However, 20% or
more of patients with acute myocardial infarction present with no pain or discomfort
at all. Elderly patients and patients with diabetes may present without classic
symptoms or with only vague, nonspecific symptoms, such as malaise,
lightheadedness, syncope, changes in mentation or sudden diaphoresis.

Patients with cardiac ischemia may also present with referred pain to other areas of
their body, such as the jaw, arm, shoulder or back. Less commonly, patients may
present with atypical chest pain, which may be described as sharp or stabbing in

During your general impression of the patient with chest pain or pressure, look for
clues suggestive of cardiac compromise, such as diaphoresis, restlessness or
apprehension. The absence of chest pain or the presence of atypical chest pain,
however, does not rule out an ACS--especially if the patient has other signs and
symptoms and a history of cardiac disease (e.g., prescribed nitroglycerin).

Acute coronary syndrome is a term used to describe many types of compromised

circulation to the heart muscle, including unstable angina pectoris or acute
myocardial infarction. Because the clinical presentations of the two are extremely
similar, if not identical (i.e., unrelieved chest pain, ECG changes, diaphoresis),
treatment should focus on the assumption that acute myocardial infarction is

2. What are the physiologic effects of nitroglycerin?

Before discussing the physiologic effects of nitroglycerin, a brief review of coronary

atherosclerosis, myocardial ischemia and angina pectoris is in order.

Coronary atherosclerosis is a progressive disease characterized by the buildup of

lipid-laden plaque within the lumen (channel) of the coronary artery. Atherosclerosis
causes narrowing of the artery (decreasing coronary blood flow) and hardening of
the artery (limiting the ability of the artery to dilate). These negative consequences
of atherosclerosis reduce the ability of the heart to accommodate increases in
myocardial oxygen demand, such as that caused by stress or exertion.

When the scale of myocardial oxygen supply and demand is unbalanced, the patient
develops ischemic chest pain or pressure (angina pectoris). Ischemia, which is
defined as a relative deprivation of oxygen, occurs when oxygen demand exceeds
supply, and is a reversible condition with prompt treatment.

Angina is described as being stable or unstable. Stable angina is characterized by a

relatively predictable sequence of events. Patients are often aware of the extent of
exertion that precipitates their chest pain (e.g., walking one block); therefore, they
limit their activities in order to avoid symptoms. Additionally, patients are also
aware of what they need to do to resolve their symptoms (e.g., a specific period of
rest, nitroglycerin). Following resolution of their chest discomfort, many patients
with stable angina never call EMS.

Unstable angina occurs when the patient experiences a change in his typical
anginal pattern, indicating advanced coronary atherosclerosis and an oxygen
supply-demand mismatch that is not so easily balanced with rest and nitroglycerin.
Relative to stable angina, the patient with unstable angina experiences "off-pattern"
chest pain, such as when exertion is minimal or when myocardial oxygen demand is
otherwise low (e.g., during sleep). Additionally, the usual treatment modalities of
rest and/or nitroglycerin afford them minimal or no relief from their symptoms. This
change may prompt a call to EMS.

Nitroglycerin (NTG) causes relaxation of vascular smooth muscle (vasodilation),

promoting systemic pooling of venous blood. This decreases the volume of blood
that is returned to the heart (preload), as well as the amount of resistance that the
heart must pump against (afterload). The combined effects of decreased preload
and afterload cause an overall decrease in myocardial oxygen demand and

Additionally, nitroglycerin may dilate the coronary arteries and promote collateral
circulation, thus improving oxygen supply to the ischemic myocardium. Collateral
circulation, also referred to as "arteriogenesis," is a process in which smaller arteries
that are normally closed become patent (open up) and connect two larger arteries
or different parts of the same artery. Over time, myocardial ischemia can promote
collateral vessels to grow, forming a "detour" for blood flow around the blocked
coronary artery.

Because nitroglycerin dilates the systemic blood vessels, it can result in

hypotension. Therefore, its use is generally contraindicated in patients with a
systolic BP of less than 90 mmHg, as well as in patients who have taken Viagra
(sildenafil), Levitra (vardenafil) or Cialis (tadalafil) within the past 24--36 hours.
These drugs, which are used to treat sexual dysfunction, also cause vasodilation
and, when used concomitantly with nitroglycerin, can result in potentially lifethreatening hypotension. EMS providers should follow local protocol or contact
medical control as needed regarding the use of nitroglycerin.

3. How could this patient's current blood pressure and heart rate affect his

This patient's history, physical examination and 12--lead ECG findings suggest acute
myocardial infarction (AMI) involving the anterior (front) wall. The patient's
hyperdynamic vital signs--hypertension and tachycardia--indicate a discharge of
epinephrine and norepinephrine from the sympathetic nervous system, most likely
caused by a combination of pain, anxiety/fear and myocardial ischemia and injury.
Epinephrine increases the rate (chronotropy) and strength (inotropy) of cardiac
contractions and norepinephrine increases systemic blood pressure by constricting
the blood vessels.

This patient's vital signs represent a classic case of "more is not better!" In order for
the heart to beat stronger and faster, it requires and uses more oxygen.
Additionally, an elevated blood pressure increases afterload (ventricular resistance),
further increasing myocardial oxygen demand.

Unfortunately, in this patient, an occluded coronary artery is blocking the flow of

oxygenated blood to the area of the myocardium that needs it most--the injured
area. This increase in myocardial oxygen demand and consumption and decrease in
myocardial oxygen supply can enlarge the area of injury, resulting in greater
myocardial damage.

The anterior wall is the largest part of the heart and tends to sustain significant
damage as the result of an MI. As the area of injury increases, lethal cardiac
dysrhythmias, such as ventricular fibrillation (v--fib) or ventricular tachycardia (v-tach), can occur. Additionally, if an extensive area of the anterior wall is damaged,
the patient can develop acute CHF and, in more severe cases, cardiogenic shock.
Cardiogenic shock, which has a very high mortality rate, occurs when the heart is
severely damaged and is no longer able to adequately perfuse the body.

4. Why are you asking the patient these specific questions?

This patient is a potential candidate for fibrinolytic (clot-buster) therapy; therefore,

you should conduct a field screening to determine if he is eligible for this treatment.
Although fibrinolytic therapy is not commonly initiated in the prehospital setting,
the information you obtain regarding the patient's eligibility or ineligibility, in
addition to the 12-lead ECG obtained in the field, will be valuable to the physician
and can decrease the "door-to-drug" time when the patient arrives in the
emergency department.

Fibrinolytic agents (Table V) work by a chemical process that converts plasminogen

to plasmin, the central enzyme of the physiologic plasminogen system. Plasmin in
turn digests fibrin, the active component of the clot matrix, through a process called
fibrinolysis. Fibrinolysis dissolves the clot that is occluding the coronary artery, thus
reestablishing distal perfusion. The goal of fibrinolytic therapy is to halt the
infarction process and salvage areas of ischemic and injured myocardium.

The indications or inclusion criteria for fibrinolytic therapy are summarized in Table
VI. Although EMT-Basics and EMT-Intermediates are not usually trained to interpret
ECG rhythms, they can, through index of suspicion based on the patient's signs and
symptoms, suspect AMI and conduct a field screening, especially if the time of onset
is less than 12 hours.

Because of the interaction of fibrinolytics with the body's hematologic system, strict
criteria must be met before the patient can be eligible for fibrinolytic therapy. If
given to the wrong patient, fibrinolytics can cause life-threatening hemorrhage.
Table VII summarizes the absolute and relative contraindications or exclusion
criteria for fibrinolytic therapy. Some patients with certain relative contraindications
may still be eligible for fibrinolytic therapy, based on a careful evaluation by the

Table V: Common Fibrinolytic Agents

Alteplase, recombinant (tPA)

Anistreplase (Eminase, APSAC)
Reteplase (Retavase)
Streptokinase (Streptase)
Tenecteplase (TNKase)

Table VI: Inclusion Criteria for Fibrinolytic Therapy

Signs and symptoms of acute myocardial infarction:

> 1 mm ST-segment elevation in >2 contiguous leads

New, or presumably new, left bundle-branch block (Only a 12-lead ECG can
qualify these findings)
Onset of symptoms is 12 hours or less


Table VII: Exclusion Criteria for Fibrinolytic Therapy

Absolute contraindications:

History of hemorrhagic stroke

Ischemic stroke or transient ischemic attack (TIA) within the past year
Suspected aortic dissection
Active internal bleeding (excluding menses)

Relative contraindications:

Severe, uncontrolled hypertension (Initial BP >180/110 mmHg)

Known bleeding disorders (e.g., hemophilia)
Current use of anticoagulants (e.g., Coumadin)
Trauma within the past 2--4 weeks
Major surgery in the past 3 weeks
Internal bleeding in the past 2--4 weeks
Active peptic ulcer disease
Known allergy to streptokinase
Administration of streptokinase or anistreplase within the past year.

5. Are there any special considerations for this patient?

There are several issues to consider when treating and monitoring this patient. As
previously discussed, nitroglycerin (being administered to this patient via
continuous IV infusion) can cause hypotension. Therefore, careful monitoring of the
patient's blood pressure is essential. Hypotension in a patient with a sick heart can
have disastrous consequences.

You have also administered a total of 4 mg of morphine to the patient. Morphine, a

narcotic analgesic, can depress the central nervous system, resulting in a decreased
level of consciousness, hypoventilation, bradycardia and hypotension. While most
people will not experience significant CNS depression with low doses of morphine,
you should have a BVM handy to assist ventilations, as well as naloxone (Narcan) to
reverse the effects of the morphine. Narcan competitively binds with opiate receptor
sites in the body and reverses the CNS depression associated with narcotic

Continuous cardiac monitoring is an essential part of cardiac patient management,

especially in this patient, whose 12-lead ECG indicates that an MI is in progress. You
must be alert for the development of warning signs of a potentially lethal
dysrhythmia, such as premature ventricular complexes (PVCs). You should also
observe the patient for any sudden changes in his heart rate. Anterior wall MIs can

result in significant tachycardia or bradycardia, both of which can further complicate

the clinical picture.

When caring for a potentially unstable cardiac patient, especially when your
transport time is lengthy, you must remain cognizant of the fact that because you
are alone in the back with the patient, your capabilities are limited to defibrillation
and one-person CPR if the patient develops cardiac arrest. Therefore, it would be
prudent to request additional assistance or arrange to rendezvous with another EMT
or paramedic while en route to the hospital.


This case study represented a patient with a relatively uncomplicated myocardial

infarction that, after prompt prehospital care and transport, was successfully halted
in the emergency department with fibrinolytic therapy.

This patient was provided excellent care in the prehospital setting because the
paramedic and his EMT-B partner worked together effectively as a team. Although
ECG monitoring, IV therapy and medication administration are beyond the usual
scope of practice of an EMT-B, many EMS systems are training their EMT-Bs to assist
with these important procedures and interventions. This involves preparing IV
equipment and supplies, applying the cardiac monitor, and recognizing and
handling the various paramedic medications. This enhanced role of the EMT-B allows
the paramedic to perform a more focused and careful patient assessment.

A cohesive working relationship between BLS and ALS personnel is absolutely

crucial to the outcome of the patient. Although each level of prehospital provider
possesses a different knowledge of pathophysiology and patient management, it is
the combined contributions and efforts of each provider that will afford patients the
high quality of care they deserve.


ACLS for EMT-Basics. Jones and Bartlett, Publishers/AAOS, 2003.

Advanced Cardiac Life Support: Principles and Practice. American Heart
Association, 2003.
Emergency Care and Transportation of the Sick and Injured, 8th Edition. Jones and
Bartlett, Publishers/AAOS, 2002.

Prehospital Advanced Cardiac Life Support, 2nd Edition. Brady Publishing, 2004.