452
U N I T 5
Circulatory Function
pain and vagal stimulation. The epigastric distress may be
mistaken for indigestion, and the person may seek relief
with antacids or other home remedies; this behavior may
delay medical interventions.
Sudden death from acute MI is death that occurs within
1 hour of symptom onset.
12
It usually is attributed to fatal
arrhythmias, which may occur without evidence of infarc-
tion. Early hospitalization after onset of symptoms greatly
improves the chances of averting sudden death because
appropriate resuscitation equipment and personnel are
immediately available should a ventricular arrhythmia
occur. The recent distribution of automatic external defibril-
lators in multiple public arenas highlights the importance of
early defibrillation in the survival of patients with STEMI.
Diagnosis and Treatment.
Because STEMI diagnosis
can be challenging before biomarkers and ECG data
are available, the immediate management of unstable
angina/NSTEMI and STEMI is similar.
12,14
Acute coro-
nary syndrome prognosis is associated with the risk of
two general complications—arrhythmias and mechani-
cal (pump) failure. The majority of deaths from ACS are
due to sudden cardiac death related to the development
of ventricular fibrillation. Therefore, seeking prompt
medical care is a critical element in the effective manage-
ment of persons with ACS. The immediate deployment
of an emergency medical team capable of resuscitation
procedures—specifically defibrillation and expeditious
transport to a hospital equipped to initiate reperfusion
therapy, manage arrhythmias, and provide advanced
cardiac life support—is crucial.
12
The emergency department goals for management of
ACS include rapid identification of persons who are can-
didates for reperfusion therapy. Evaluation of the person’s
chief complaint, typically chest pain, along with other
associated symptoms is essential in differentiating ACS
from other diagnoses. For any person presenting with
symptoms of ACS, providers should perform a 12-lead
ECG and continuous ECG monitoring. Treatment regi-
mens also include administration of oxygen, aspirin,
nitrates, morphine, antiplatelet and anticoagulant ther-
apy,
β
-adrenergic blocking agents (beta blockers), and an
angiotensin-converting enzyme (ACE) inhibitor.
12,14
The administration of oxygen augments the oxygen
content of inspired air and increases the oxygen satu-
ration of hemoglobin. Arterial oxygen levels may fall
precipitously after acute MI, and oxygen administra-
tion maintains oxygen content of the blood perfusing
the myocardial tissue. Platelets play a major role in the
thrombotic response to atherosclerotic plaque disruption;
therefore, inhibition of platelet aggregation is an impor-
tant aspect in the early treatment of both unstable angina/
NSTEMI and STEMI. Aspirin (i.e., acetylsalicylic acid)
is the preferred antiplatelet agent for preventing platelet
aggregation in persons with ACS. Aspirin, which acts by
inhibiting synthesis of the prostaglandin thromboxane
A
2
, is thought to promote reperfusion and reduce the
likelihood of re-thrombosis. For patients who are aspirin-
intolerant, another antiplatelet drug such as clopidogrel
may be prescribed. Clopidogrel exerts its effects by inhib-
iting the ADP pathway in platelets
18
(see Chapter 12).
The severe pain of acute MI gives rise to anxiety and
recruitment of autonomic nervous system responses,
both of which increase the work demands on the heart.
Control of pain in acute MI is accomplished through a
combination of nitrates, analgesics (e.g., morphine), and
beta-blocking agents.
12
Nitroglycerin is administered
because of its vasodilating effect and ability to relieve
coronary pain. The vasodilating effects of the drug
decrease venous return (i.e., reduce preload) and arterial
blood pressure (i.e., reduce afterload), thereby reducing
oxygen consumption. Although a number of analgesic
agents have been used to treat the pain of acute MI,
morphine is usually the drug of choice to be given intra-
venously for rapid onset of action.
11
Beta antagonists
block
β
-receptor–mediated functions of the sympathetic
nervous system and thus decrease myocardial oxygen
demand by reducing heart rate, cardiac contractility
(i.e., inotropy), and systemic arterial blood pressure.
Immediate reperfusion therapy through use of phar-
macologic agents (fibrinolytic therapy), percutaneous
coronary intervention, or coronary artery bypass graft-
ing is usually indicated for persons with ECG evidence
of STEMI.
Fibrinolytic drugs
degrade blood and plate-
let clots, and their use is associated with positive out-
comes such as reduced mortality and incidence of lethal
Ischemia
Injury
Necrosis
Healthy
tissue
FIGURE 19-6.
Zone of myocardial infarction
with associated ECG changes. (Adapted
from Anatomical Chart Company. Atlas of
Pathophysiology. 3rd ed. Philadelphia, PA:
Wolters Kluwer Health | Lippincott Williams &
Wilkins; 2010:63.)
