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Chapter 28 CONGESTIVE HEART FAILURE AND ACUTE PULMONARY EDEMA198
16. What is the treatment of acute pulmonary edema?
First, follow the ABCs (airway, breathing, and circulation). In severe hypoxia, airway and
breathing may be compromised and the patient needs to be intubated. The use of noninvasive
mask continuous or bilevel positive airway pressure (BiAP) has decreased the need for
intubation of patients with pulmonary edema; however, this has not significantly affected
in-hospital mortality. Intubation may also be avoided with aggressive medical treatment. It is
important to continuously re-evaluate the patient with an eye on intervening with more
aggressive measures. For example, you might decide, “I will intubate if the patient is not better
in 15 minutes or worsens during that time.” Administer oxygen to maintain sufficient oxygen
saturation (.90%), either by nasal cannula or nonrebreather mask, continuous positive airway
pressure, or BiPAP. Continuously monitor oxygen saturation with pulse oximetry.
17. What about drug therapy?
Drug therapy is aimed at decreasing preload. Nitrates are first-line drugs and are useful in the
form of sublingual nitroglycerin (NTG), topical NTG paste, or intravenous NTG drip. NTG is
predominantly a venodilator, reducing preload, but also dilates coronary arteries, so it may be
especially helpful in the setting of coronary artery disease. Diuretics should only be administered
in patients with signs of obvious fluid overload (i.e., peripheral edema, elevated jugular venous
distension). In most cases of acute CHF, patients are actually euvolemic and the administration
of diuretics is associated with worse outcomes. When indicated, furosemide is given as a 40-mg
intravenous bolus (larger amounts if the patient is already on diuretics although high-dose
diuretics are associated with worse outcomes). Initially, within 5 to 15 minutes of the injection,
venodilation occurs, although this is of limited clinical benefit in the setting of nitrates. This
action is followed within 30 minutes by diuresis. In addition to furosemide, morphine may be
given, 5 to 10 mg, intravenously, to decrease anxiety and the work of breathing. It also is a mild
venodilator, further decreasing preload. With decreased anxiety, there is decreased sympathetic
response and decreased afterload.
KEY POINTS: ED MANAGEMENT OF CHF
1. Noninvasive mask ventilation may prevent the need for intubation
2. Frequent re-evaluation of the patient with an eye toward increasingly aggressive measures is
important
3. Nitrates are first-line pharmacotherapy
4. Diuretics should be reserved for patients with fluid overload
18. Are there other drugs that are useful in the treatment of acute pulmonary
edema?
Yes. For the patient who is hypertensive, it is often helpful to lower the blood pressure
(afterload). Hypertension and tachycardia generally result from reflex mechanisms because
of the acute decompensation and often correct themselves with the initial treatment
outlined previously. With severe hypertension, nitroprusside is the treatment of choice. It
is a venodilator and arterial dilator, reducing preload and afterload. Start the infusion at
10 mcg/min and titrate upward every 5 minutes. It is important to monitor the blood
pressure closely. If the patient becomes hypotensive, stopping the infusion causes a
prompt increase in blood pressure because nitroprusside has such a short half-life.
Generally, doses of 0.5 to 2 mcg/kg/min are sufficient.
19. What about giving positive inotropic drugs?
Digoxin, which is used in the treatment of chronic CHF, has little role in the treatment of acute
pulmonary edema. Inotropic agents that are helpful include dobutamine, dopamine, and
Chapter 28 CONGESTIVE HEART FAILURE AND ACUTE PULMONARY EDEMA 199
milrinone. Dobutamine and dopamine are positive inotropic agents. Dopamine has more alpha
effect, especially at higher doses, and should be reserved for hypotensive patients. In
cardiogenic shock that is refractory to these agents, milrinone infusion may be given. The
ideal situation for administering these agents is in an intensive care unit (ICU) with pulmonary
artery monitoring to measure filling pressures, CO, and other hemodynamic parameters.
20. When the initial treatment has begun, what else needs to be done?
After the patient is stabilized, routine tests are done, the most important being chest
radiograph and electrocardiogram (ECG). Cardiac monitoring is begun; pulse oximetry is
monitored continuously, and vital signs are recorded frequently. It is generally necessary to
insert a Foley catheter for close monitoring of urine output. The search is on to try to discover
the underlying reason for acute decompensation (almost always ischemic in nature, although
occasionally related to arrhythmias).
21. Do all patients with CHF need to be admitted to the hospital?
Patients with a new diagnosis of CHF need an inpatient work-up that includes serial cardiac
enzymes and an assessment of the global function of the heart. Patients with known CHF who
have mild symptoms or signs may be managed on an outpatient basis, assuming that they are
compliant with medications, have an appropriate social network, and follow up with their
primary care physician. All patients with acute CHF require admission.
22. What are the usual precipitating causes of CHF exacerbations?
The most common cause of the subacute CHF exacerbation is undermedication, either as a
result of patient noncompliance with medication orders, dietary salt restrictions, or as a result
of a change in medication under a physician’s supervision. The patient gradually retains more
and more fluid, resulting in eventual overload and presentation to the ED. Causes of acute CHF
exacerbations are principally cardiac and include acute myocardial infarction, arrhythmias, and
rarely severe hypertension (as previously noted, hypertension is usually the result and not the
cause of the acute exacerbation). Noncardiac causes include infection and anemia. When
precipitating factors are identified, specific therapy should be initiated.
23. What is the outpatient treatment of CHF?
Angiotensin-converting enzyme (ACE) inhibitors are the mainstay of long-term treatment of
CHF, leading to a decrease in mortality and an increase in functional capacity. Other drugs that
act on the renin-angiotensin system (angiotensin receptor antagonists and spironolactone)
also are effective. b-blockers are useful in that they block the cardiac effects of long-term
adrenergic stimulation. Diuretics also are beneficial, especially in patients with volume
overload. Digoxin causes an improvement in symptoms but no overall decrease in mortality.
Combined therapy with hydralazine and isosorbide dinitrate has shown a decrease in mortality
and is particularly useful in patients who have contraindications to other classes of drugs.
24. How do ACE inhibitors work in CHF?
In response to cardiac decompensation, the renin angiotensin system is activated. Angiotensin
is a potent vasoconstrictor, leading to increased afterload. Stimulation of aldosterone leads to
sodium retention and extracellular fluid volume expansion and increased preload. ACE
inhibitors help to decrease afterload by decreasing angiotensin II-mediated vasoconstriction
and decrease preload by blocking sodium retention and volume expansion.
25. What is the long-term prognosis for patients with CHF?
Prognosis depends on the cause and severity of the heart failure. The prognosis is good when
the underlying cause can be corrected, as in valvular heart disease. Patients with mild disease
that can be controlled with ACE inhibitors with or without low doses of diuretics generally do
well. Overall, however, patients with CHF have a 10% to 20% yearly death rate, and fewer than
half survive 5 years.
Chapter 28 CONGESTIVE HEART FAILURE AND ACUTE PULMONARY EDEMA200
ACKNOWLEDGMENT
The editors gratefully acknowledge the contributions of Rodney W. Smith, MD, author of this
chapter in the previous edition.
BIBLIOGRAPHY
1. Carson P: Beta-blocker therapy in heart failure. Cardiol Clin 19:267–278, 2001.
2. Dao Q, Krishnaswamy P, Kazanegra R, et al: Utility of B-type natriuretic peptide in the diagnosis of congestive
heart failure in an urgent-care setting. J Am Coll Cardiol 37:379–385, 2001.
3. DeNofrio D: Natriuretic peptides for the treatment of congestive heart failure. Am Heart J 138:597–598, 1999.
4. Digitalis Investigation Group: The effect of digoxin on mortality and morbidity in patients with heart failure.
N Engl J Med 336:525–533, 1997.
5. Gomberg-Maitland M, Baran DA, Fuster V: Treatment of congestive heart failure: guidelines for the primary
care physician and the heart failure specialist. Arch Intern Med 161:342–352, 2001.
6. Graff L, Orledge J, Radford MJ, et al: Correlation of the Agency for Health Care Policy and Research
congestive heart failure admission guideline with mortality: Peer Review Organisation Voluntary Hospital
Association Initiative to Decrease Events (PROVIDE) for congestive heart failure. Ann Emerg Med 34:429–437,
1999.
7. Masip J, Roque M, Sánchez B, et al: Noninvasive ventilation in acute cardiogenic pulmonary edema:
systematic review and meta-analysis. JAMA 294(24):3124, 2005.
8. McCullough PA, Nowak RM, McCord J, et al: B-type natriuretic peptide and clinical judgment in emergency
diagnosis of heart failure: analysis from the Breathing Not Properly (BNP) Multinational Study. Circulation
106:416–422, 2002.
9. Miller AB, Srivastava P: Angiotensin receptor blockers and aldosterone antagonists in chronic heart failure.
Cardiol Clin 19:195–202, 2001.
10. Pang D, Keenan SP, Cook DJ, et al: The effect of positive pressure airway support on mortality and the need
for intubation in cardiogenic pulmonary edema. Chest 114:1185–1192, 1998.
11. Wigder HN, Hoffmann P, Mazzolini D, et al: Pressure support noninvasive positive pressure ventilation
treatment of acute cardiogenic pulmonary edema. Am J Emerg Med 19:179–181, 2001.
12. Yealy DM, Hsieh M: BNP is not a value-added routine test in the emergency department. Ann Emerg Med
53(3):387, 2009.
201
CHAPTER 29
ISCHEMIC HEART DISEASE
Edward P. Havranek, MD
1. How is ischemic heart disease classified?
a. Chronic stable ischemic heart disease
n
Asymptomatic
n
With angina
n
Postmyocardial infarction (MI), with or without angina
b. Acute coronary syndromes
n
Unstable angina
n
Acute non-ST segment elevation myocardial infarction (NSTEMI)
n
Acute ST segment elevation MI (STEMI)
2. How do patients with acute ischemic heart disease present?
The most common presenting symptom is central chest discomfort. The discomfort also may
be felt (in descending order of frequency) in the right or left chest, the right or left shoulder or
arm, the throat or jaw, the epigastrium, and rarely, the ear. Less commonly, patients may
present with episodic dyspnea. Some patients may have ischemia and even acute MI with no
symptoms.
3. To define the discomfort better, what information should be obtained?
n
Chronology
n
Frequency
n
Location
n
Precipitating factors
n
Radiation
n
Alleviating factors
n
Duration
n
Quality
n
Intensity
n
Associated symptoms
4. Describe the typical features of chest discomfort in ischemic heart disease.
Typically, patients with stable angina have discomfort during exertion relieved within
minutes by rest. The degree of exertion bringing on the discomfort can vary from day to
day. The discomfort is often vague, is described most often as a tightness, pressure, or
heaviness, and is substernal in location, with radiation to the jaw, shoulder, or upper
extremity common.
Patients with unstable angina usually have similar pain, but it occurs with progressively
less exertion (crescendo angina) or at rest. Patients with unstable angina who have pain at
rest also should have pain with exertion. Prinzmetal’s angina, which is caused by coronary
artery spasm, is an exception to this rule. Patients with Prinzmetal’s angina typically have pain
at rest, usually in the early morning hours, and often do not have exertional discomfort. True
vasospastic angina is uncommon.
Patients with acute MI typically have pain that is more severe than any preceding angina.
It may be described as crushing but usually not ripping or tearing.
Chapter 29 ISCHEMIC HEART DISEASE202
5. What other symptoms are associated with the chest discomfort of ischemic
heart disease?
Shortness of breath commonly accompanies angina. Many conditions other than angina that
cause chest discomfort, such as pulmonary disease and anxiety disorder, also are
accompanied by shortness of breath. Diaphoresis occurs less frequently with angina but
should raise one’s level of suspicion of angina because it does not occur often with other
disorders that cause chest pain. Nausea and vomiting can occur with acute MI—the larger the
infarction, the more common are nausea and vomiting. Thus, patients with anterior MI are
more likely to have nausea and vomiting than are patients with inferior MI.
KEY POINTS: TYPICAL FEATURES OF ANGINA
1. Substernal location
2. Radiation to the arm, neck, or jaw
3. Precipitation by exertion, relief with rest
4. Sensation of tightness, pressure or heaviness
5. Accompanied by shortness of breath
6. Is there anything different about evaluating elderly patients?
The symptoms associated with ischemic heart disease in patients older than 75 years are
more likely to be atypical. The older the patient, the more atypical the symptoms become.
7. What about diabetics?
Although it is often taught that patients with diabetes are more likely to present with atypical
symptoms or no symptoms at all, the literature suggests that diabetic patients present just
like everyone else except perhaps for being a little more likely to have shortness of breath.
8. Should demographic features and the presence or absence of coronary risk
factors change your mind about the diagnosis?
They are not particularly useful for making a diagnosis except in patients who have objective
evidence of prior ischemic heart disease in whom the likelihood of another ischemic event
occurring is rather high. A young woman with no risk factors but with typical symptoms and
electrocardiogram (ECG) changes should be suspected of having ischemic disease.
Conversely, a middle-aged man with diabetes and hypertension whose chest pain has no
typical features should still be treated as if he may have the disease but may be less likely to
have the disease.
9. List the key elements of the initial evaluation of a patient with a suspected
acute coronary syndrome.
n
The patient should be placed on O
2
and a cardiac monitor and have intravenous (IV) access
established.
n
The patient should have an ECG within 5 minutes of arrival.
n
Vital signs are vital. The presence of hypertension, hypotension, or tachycardia must be
dealt with early.
n
A history directed at the key elements described previously and a cardiovascular
examination come next; the examination is useful for ruling out other diagnoses, such as
pericarditis and aortic dissection.
n
Administer aspirin (325 mg).
Chapter 29 ISCHEMIC HEART DISEASE 203
10. What is the significance of abnormal ST segment changes on an ECG?
Abnormal ST segment changes may or may not represent ischemic cardiac injury. The current
of injury that accompanies ST segment elevation MI is typically a convex-downward elevation of
the ST segment. It may be confused with pericarditis or early repolarization. Other causes of ST
elevation are as follows:
n
Left ventricular hypertrophy
n
Acute pericarditis
n
Acute cor pulmonale
n
Hyperkalemia
n
Hypercalcemia
n
Hypothermia
n
Left ventricular aneurysm
ST depression may be caused not only by cardiac ischemia but also by such things as
ventricular hypertrophy, drugs (e.g., digoxin), atrioventricular junctional rhythm with a
retrograde P wave, and electrolyte abnormalities.
11. What is the typical time course of ECG changes in ischemic cardiac injury?
The initial changes are T-wave prolongation and increased T-wave magnitude, either upright or
inverted. Next, the ST segment displays elevation or depression. A Q wave may be seen in the
initial ECG or may not develop for hours to days. As the ST segment returns to baseline,
symmetrically inverted T waves evolve. This classic evolution is documented in approximately
65% of patients with acute MI.
12. Can the ECG be normal while a patient is having cardiac ischemia or an
acute MI?
Although serial ECGs showing evolving changes are diagnostic for acute MI in greater than
90% of patients, 20% to 50% of initial ECGs are normal or show only nonspecific
abnormalities. The initial ECG may be diagnostic for acute MI in only half of patients.
Therefore, an early repeat ECG may be helpful.
13. Are cardiac markers useful in the ED?
Maybe. Troponin I, the most commonly used cardiac marker, doesn’t rise definitively until 4 to
6 hours after the onset of ischemia, but borderline elevations in high-sensitivity assays may
begin to rise before then. Single determinations are generally not sufficiently specific to make
a diagnosis. One should not wait to see an elevated troponin before making a decision to treat
for acute coronary syndrome.
14. How can echocardiography be useful in ED patients with suspected acute
coronary syndrome?
It may be useful when the ECG is nondiagnostic, such as when there is a left bundle-branch
block or minimal ST elevation. The presence of a wall motion abnormality is evidence that
supports the diagnosis of ischemia, although it may be the result of an old rather than acute
infarction. Echocardiography also may provide information about complications, such as
mitral regurgitation and pericardial effusion.
The sensitivity of echocardiography is limited. A negative echocardiogram in the setting of
a typical history and ECG does not rule out the diagnosis of an acute coronary syndrome.
Waiting for the results of an echocardiogram may unnecessarily delay treatment.
15. What other diagnoses should be considered in a patient with chest pain?
The patient’s history is paramount:
n
A life-threatening condition, dissecting aortic aneurysm, also may cause sustained chest
pain or typical angina.
n
Pleuritic chest pain may be caused by pleuritis, pericarditis, pneumothorax, or pulmonary
embolism.
Chapter 29 ISCHEMIC HEART DISEASE204
n
Nonanginal pain may be found with the onset of herpes zoster or with cervical or thoracic
nerve root compression.
n
Esophagitis, esophageal spasm, and esophageal rupture may mimic pain of cardiac origin.
n
Patients with anxiety or depression syndromes often complain of chest pain.
16. What are the indications for reperfusion therapy in acute MI?
n
ST elevation greater than 1 mm in two leads
n
Pain and ST elevation not immediately responsive to nitroglycerin
n
Pain lasting less than 6 hours (In many patients, reperfusion therapy still may be of benefit
12 hours after the onset of pain.)
17. What if persistent ST elevation is not present?
There is no proven benefit to thrombolytics or immediate angiography and coronary
intervention.
18. What is the preferred method of reperfusion therapy in acute MI with ST
elevation (STEMI), thrombolytic therapy, or primary coronary intervention?
Angioplasty (usually with coronary stenting) in the setting of acute MI if done within
approximately 90 minutes of arrival reduces mortality to a greater degree than does
thrombolytic therapy. Primary coronary intervention has the added advantages of lower rates
of reocclusion in the subsequent few days and lower risks of intracranial bleeding. The
problem is that studies that include data from nontertiary hospitals show that optimally
delivered angioplasty is not often accomplished. Unless a skilled catheterization laboratory
team can intervene within 90 minutes after presentation, thrombolytic therapy is preferable.
19. What if cardiac intervention is not available on site?
Transfer to an intervention-capable facility is beneficial if the time to reperfusion will be less
than 90 minutes. Although some studies have suggested that transfer is beneficial, even if
time-to-reperfusion might be longer, current guidelines favor thrombolytic therapy under these
circumstances.
20. How do you choose which thrombolytic agent to use?
Streptokinase (and its modified form, anistreplase) is currently the least popular agent in
acute MI because it is thought to be slightly less effective than the other available agents.
Reteplase and tenecteplase have become more popular than alteplase because they can be
administered in bolus form rather than an infusion with a varying dose schedule. No matter
which agent is chosen, it should be given within 30 minutes of arrival.
21. What is the preferred therapy for cardiogenic shock?
The only therapy shown to decrease the historically high mortality associated with this
syndrome is primary coronary intervention (angioplasty, generally with stent implantation).
This should be performed without delay. The added benefit of immediate transfer to a
catheterization laboratory is that this facilitates insertion of an intra-aortic balloon pump
(IABP). An IABP is thought to be superior to pharmacologic therapy for decreasing afterload
and augmenting cardiac output.
An exception to this is cardiogenic shock caused by right ventricular infarction. This
problem should be suspected whenever shock accompanies an acute inferior MI. The
presence of jugular venous distention is an important clue to the diagnosis of this syndrome,
and volume expansion usually reverses the hypotension.
22. List the contraindications to thrombolytic therapy.
Absolute contraindications
n
Active bleeding
n
Major surgery or trauma in the past 3 weeks
n
Neurosurgery or stroke in the past 3 months
Chapter 29 ISCHEMIC HEART DISEASE 205
n
Prolonged (.10 minutes) or traumatic cardiopulmonary resuscitation (CPR)
n
Hypertension (systolic .180 mm Hg, diastolic .110 mm Hg)
Relative contraindications
n
Major trauma or surgery more than 3 weeks ago
n
Neurosurgery or stroke more than 3 months ago
n
Active peptic ulcer
n
Hemorrhagic ophthalmic condition, especially diabetic retinopathy
Patients with a known allergy to streptokinase or anistreplase (also known as APSAC
[anisoylated plasminogen-streptokinase activator complex]) should be treated with another
agent. Exposure to streptokinase or anistreplase in the previous 6 months or streptococcal
infection in the previous 6 months are reasons to use another agent.
23. What other diagnoses should be considered before giving thrombolytic
therapy?
Aortic dissection and acute pericarditis can mimic acute MI. Both have had fatal outcomes
when thrombolytics were given. Dissection can be excluded with a careful history, examination
of peripheral pulses, and chest radiograph or chest CT scan. Pericarditis can be excluded by
carefully listening for a rub and examining the ECG for widespread, concave-upward ST
elevation.
24. What is the risk for fatal complications of thrombolytic therapy for acute MI?
Mortality, which almost invariably results from intracranial hemorrhage, occurs in about 0.5%
of treated patients.
25. What other medications are useful adjuvants to reperfusion therapy?
n
Morphine. MI can cause excruciating pain and severe fear and anxiety. IV morphine sulfate
should be administered in increments of 2 to 4 mg to alleviate these symptoms.
n
Aspirin and other anti-platelet agents. Unless the patient has had an aspirin, it should be
given immediately because it reduces mortality independent of other therapy. In patients
who will undergo immediate intervention, it may be beneficial to start abciximab and a
thienopyridine, such as clopidogrel, but this decision should be a collaborative one
involving the emergency physician and the cardiologist.
n
b-blockers. Metoprolol, atenolol, or esmolol given intravenously reduce mortality and
infarct size. They are better tolerated than one may think and are underused.
Contraindications include heart failure, bradycardia (heart rate ,55 beats per minute), and
bronchospasm.
n
Heparin and other anticoagulants. With tissue plasminogen activator (tPA), initiation of
heparin is imperative at least 1 hour before the completion of the thrombolytic infusion.
With streptokinase or APSAC, administration of heparin should be delayed 4 to 6 hours.
Anticoagulants should be continued for at least 48 hours. In addition to unfractionated
heparin, fondaparinux and the low-molecular-weight heparin, enoxaparin, have been shown
to be acceptable alternatives.
n
Nitroglycerin. If control of blood pressure is an issue, nitroglycerin is the preferred agent.
KEY POINTS: MOST IMPORTANT MEDICATIONS
FOR ALL PATIENTS WITH AN MI IN THE ED
1. Aspirin
2. IV b-blockers
Chapter 29 ISCHEMIC HEART DISEASE206
26. What other arrhythmias occur with acute MI?
Ventricular irritability, with frequent premature ventricular contractions (PVCs), nonsustained
ventricular tachycardia, and ventricular fibrillation, may occur. Secondary causes such as
drugs and electrolyte imbalance should be looked for and treated. Isolated PVCs usually
respond to b-blockade. Higher grades of ventricular arrhythmias should be treated with
lidocaine or amiodarone. Sustained ventricular tachycardia (lasting .30 seconds) is
uncommon in acute MI. Accelerated idioventricular rhythm (heart rate, 60–100 beats per
minute) should not be treated.
Bradyarrhythmias also may occur. Second-degree or third-degree heart block that
accompanies inferior MI is usually transient, and a temporary pacemaker generally is not
required. When heart block accompanies an anterior MI, a temporary pacer is required. A
prophylactic temporary pacer should be considered when severe conductive system disease
(bifascicular block or left bundle-branch block plus first-degree block) accompanies an
anterior acute MI.
27. Which patients with unstable angina are at highest risk for MI and benefit
from more aggressive treatment?
n
ECG changes: Transient or fixed ST segment depression or T-wave inversion, especially
when these changes are in leads V
1
through V
3
n
Elevated troponin levels
n
Age greater than 65
n
Known coronary artery disease
n
Presence of three or more coronary risk factors (i.e., smoking, hypertension, diabetes,
elevated cholesterol, family history)
n
Severe angina within the prior 24 hours
These patients are thought to benefit more from more aggressive medical treatment (see
question 24) and early catheterization.
28. What medications are useful in the acute coronary syndromes: unstable
angina and acute MI without ST elevation (NSTEMI)?
n
Always administer aspirin. If the patient is intolerant of aspirin or if management without
angiography is planned, a thienopyridine, such as clopidogrel, should be added. If
angiography is planned, a thienopyridine, such as clopidogrel (including a loading dose),
tirofiban, eptifibatide, or abciximab should be added to aspirin. The emergency physician
and the cardiologist should coordinate management closely here. For instance, abciximab
may be the best choice if there will not be a delay before angiography and if it is highly
likely angioplasty and stenting will occur. Otherwise, one of the other agents may be a
better choice.
n
Heparin should be started. Current thinking is that unfractionated heparin and the low-
molecular-weight heparin preparation, enoxaparin, are equally effective. Less evidence is
available for bivalirudin and fondaparinux, but both appear to be effective. Fondaparinux is
thought to be preferable when the patient is at high risk for a bleeding complication. Here
again, plans for an invasive strategy may make one agent preferable over another, and
collaboration between emergency physician and cardiologist is important.
n
Virtually all patients with unstable angina should be treated with b-blockers. It may be
desirable to start this therapy in the ED.
n
For patients with ongoing pain, always treat with nitroglycerin. Start with the sublingual
route of administration, and move to IV nitroglycerin if that does not work. Nitroglycerin is
the preferred agent when the patient has concurrent hypertension.
n
Add calcium channel blockers when symptoms recur despite aspirin, nitrates, and
b-blockers. Never use short-acting dihydropyridines, such as nifedipine, without
b-blockers. In the setting of unstable angina, use of calcium channel blockers without
concurrent b-blockade increases the risk of MI.
Chapter 29 ISCHEMIC HEART DISEASE 207
29. Which is better, low-molecular-weight heparin or unfractionated heparin?
There is no consensus about which type of heparin is clinically more effective, so practical
considerations are important. The advantage of low-molecular-weight heparin is that it can be
given in the ED as a single bolus and doesn’t require an infusion pump. The major
disadvantage of low-molecular-weight heparin is that it may be difficult to communicate to
other providers that the patient has received it (as a result some patients have gotten double
doses) and that the effects last longer, making invasive procedures more problematic.
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Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction):
developed in collaboration with the American College of Emergency Physicians, American College of
Physicians, Society for Academic Emergency Medicine, Society for Cardiovascular Angiography and
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method for prognostication and therapeutic decision making. JAMA 284:835–842, 2000.
3. Antman EM, Hand M, Armstrong PW, et al: 2007 focused update of the ACC/AHA 2004 Guidelines for the
Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Group to Review New
Evidence and Update the ACC/AHA 2004. Guidelines for the Management of Patients with ST-Elevation
Myocardial Infarction). J Am Coll Cardiol 51:210–247, 2008.
4. Fraker TD Jr, Fihn SD, writing on behalf of the 2002 Chronic Stable Angina Writing Committee: 2007 chronic
angina focused update of the ACC/AHA 2002 Guidelines for the Management of Patients with Chronic Stable
Angina: a report of the American College of Cardiology/ American Heart Association Task Force on Practice
Guidelines Writing Group to Develop the Focused Update of the 2002 Guidelines for the Management of
Patients With Chronic Stable Angina. J Am Coll Cardiol 50:2264–2274, 2007.
5. Funk M, Naum JB, Milner KA, et al: Presentation and symptom predictors of coronary heart disease in patients
with and without diabetes. Am J Emerg Med 19:482–487, 2001.
6. Kentsch M, Rodemerk U, Gitt AK, et al: Angina intensity is not different in diabetic and non-diabetic patients
with acute myocardial infarction. Z Kardiol 92:817–824, 2003.