You are in the middle of your shift in the coronary care unit (CCU) of a large urban medical center. Your new admission, C.B., a 47-year-old woman, was just flown to your institution from a small rural community more than 100 miles away

Question

She had a STEMI (ST segment elevation myocardial infarction) last evening. Her current vital signs (VS) are 100/60, 86, 14. After you make C.B. comfortable, you receive
this report from the flight nurse: "C.B. is a full-time homemaker with four children. She has had episodes
of 'chest tightness' with exertion for the past year, but this is her first known MI. She has a history of
hyperlipidemia and has smoked one pack of cigarettes daily for 30 years. Surgical history consists of total
abdominal hysterectomy 10 years ago after the birth of her last child. She has no other known medical
problems. Yesterday at 8 pm, she began to have severe substernal chest pain that referred into her neck
and down both arms. She rated the pain as 9 or 10 on a 0-to-10 scale. She thought it was severe indigestion
and began taking Maalox with no relief. Her husband then took her to the local emergency department,
where a 12-lead electrocardiogram (ECG) showed hyperacute ST elevation in the inferior leads II,
III, aVF and V5 to V6. Before tissue plasminogen activator could be given, she went into ventricular fibrillation
(V-fib). CPR was started and when the code team arrived, she was successfully defibrillated after
two shocks. She then was started on nitroglycerin (NTG), heparin, and amiodarone drips. She was given
IV metoprolol and aspirin 325 mg to chew and swallow. This morning her systolic pressure dropped into
the 80s, and she was placed on a low-dose norepinephrine drip and urgently flown to your institution for
coronary angiography and possible percutaneous transluminal coronary angioplasty. Currently, she has
amiodarone infusing at 1 mg/min, heparin at 1200 units/hr, and norepinephrine at 0.5 mcg/kg/min. The
NTG has been stopped because of low blood pressure. Laboratory work that was done yesterday showed
Na 145 mEq/L, K 3.6 mEq/L, HCO3 19 mEq/L, BUN 9 mg/dL, creatinine 0.8 mg/dL, WBC 14,500/mm3, Hct
44.3%, and Hgb 14.5 g/dL."

Because the 12-lead ECG can tell you the location of the infarction, evaluate the leads that
showed ST elevation. What areas of C.B.'s heart have been damaged?

Given the diagnosis of acute myocardial infarction (MI), what other laboratory results are
you going to look at?

Indicate the expected outcome for C.B. associated with each medication she is receiving. For
each of the drugs listed, state the purpose.
a. Intravenous (IV) nitroglycerin (NTG)
b. IV heparin
c. IV amiodarone
d. IV metoprolol
e. Aspirin, chewed and swallowed
f. IV norepinephrine

Laboratory Test Results
Creatine Phosphokinase (CK) Levels
On ED admission 95 units/L
4 hours 1931 units/L
8 hours 4175 units/L
CK-MB Isoenzymes
On ED admission 5%
4 hours 79%
8 hours 216%
LDL 160 mg/dL
PT 11.9 sec
INR 1.02
aPTT (before heparin) 26.9 sec
Mg 2.2 mg/dL
K 3.3 mEq/L

You review the lab work on her chart. For each laboratory value listed previously, interpret the result, and evaluate the meaning for C.B.

List at least two complications C.B. is at risk for at this time and the assessments that are
needed to identify these risks.

You note that C.B.'s Spo2 on oxygen (O2) at 6 L/min by nasal cannula is 92%. How do you interpret this result?

What can be done to promote her oxygenation at this time?

Answer 1

Leads II, III, and aVF "look at" the heart from below. ST elevation in these leads indicates inferior wall
damage. Leads V5 and V6 view the heart from the left side. ST elevation in these leads indicates lateral
wall damage.

• Creatinine kinase (CK) and its isoenzymes; troponins T and I
• Cholesterol and triglyceride levels: high-density lipoprotein (HDL), low-density lipoprotein (LDL),
very-low-density lipoprotein (VLDL) (drawn fasting)
• Arterial blood gases
• PT/INR (prothrombin time and international normalized ratio) and PTT (partial thromboplastin
time)
• Magnesium (Mg)
• CMP (complete metabolic panel)

a. IV NTG (a coronary vasodilator) is given to dilate coronary arteries and improve collateral blood
flow to ischemic areas of the heart muscle. In addition, it causes peripheral vasodilation.
b. IV heparin (an anticoagulant) is given to prevent extension of existing thrombi or new clot
formation.
c. IV amiodarone is given to prevent lethal dysrhythmias, which are common after MI.
d. IV metoprolol (a beta-blocker) is given to reduce mortality after MI; it protects the damaged heart
from stimulation by circulating catecholamines.
e. The aspirin, when chewed and swallowed, is a rapid platelet aggregation inhibitor that helps to
prevent clots from forming.
f. IV norepinephrine (a vasopressor) is used to correct severe hypotension.

• The normal CK level for a female patient should be 30 to 135 units/L; the CK-MB isoenzymes should
be 0%. CK is released from several tissues after damage. The MB isoenzyme is specific for damaged
cardiac muscle. Because the CK level is proportional to the amount of myocardial injury, CK levels
give a good indication of the severity of the MI. C.B. has had a massive MI.
• LDL: 160 mg/dL with a known coronary disease. The latest National Cholesterol Education Program
guidelines recommend an LDL level below 100 mg/dL. C.B.'s LDL level is elevated.
• The PT/INR and aPTT are within normal limits for someone who is not receiving anticoagulant
therapy.
• Hypomagnesemia can cause cardiac dysrhythmias. The usual goal is to keep serum Mg at 2 mg/dL
or greater. C.B.'s Mg level is within normal limits.
• A common normal reference level for serum potassium is 3.5 to 5 mEq/L. Hypokalemia might lead
to increased electrical instability and ventricular dysrhythmias. In light of C.B.'s history of V-fib, it is
important to monitor her potassium level and supplement as needed.

• Dysrhythmias, such as tachycardia or bradycardia, or complete heart block, or life-threatening
dysrhythmias such as ventricular tachycardia or fibrillation. Monitor the patient's ECG continuously
for any rhythm changes. An increase in premature ventricular contractions (PVCs) may precede
ventricular tachycardia and fibrillation.
• Heart failure (HF) occurs when the ability of the heart to pump has been reduced. The signs and
symptoms (S/S) of HF depend on the severity of the damage done to the heart after the MI. Watch
for mild dyspnea, agitation, restlessness, or a slight increase in heart rate. As HF progresses, other
signs may include crackles on auscultation of the lungs, S3 or S4 heart sounds, and jugular vein
distention. A chest x-ray examination would reveal pulmonary congestion.
• Papillary muscle dysfunction occurs if the infarction damages the papillary muscle that attaches
to the mitral valve. Assess for a new systolic murmur at the apex. An echocardiogram should be
ordered to confirm the diagnosis.
• Ventricular aneurysm occurs after damage to the left ventricle leaves the ventricle thin; during
contractions, the wall bulges out. Monitor the patient for S/S of HF, dysrhythmias, and angina.
Ventricular aneurysms may develop thrombi that can lead to emboli and strokes, and rupture of
the aneurysm results in death.

Ideal Spo2 values are 95% to 100%, depending on altitude. Her oxygen saturation on 6 L/min is not
adequate!

Convert the oxygen delivery system to a non-rebreather mask, which will provide a higher
percentage (60% to 100%) of oxygen. Elevate the head of her bed, and promote rest. Monitor Spo2
values with a goal of 95% to 100%.