458 CHAPTER 33 Cardiovascular Emergencies
patient response to fluids. Expansion of circulating volume
is needed when there has been unexpected loss of blood vol-
ume (e.g., ruptured abdominal aortic aneurysm, trauma).
Volume expansion is accomplished with crystalloids (e.g.,
normal saline, lactated Ringer’s solution) or colloids (e.g.,
albumin). Fluid therapy is also beneficial in circumstances
in which the patient has decreased cardiac output (e.g., sec-
ondary to acute myocardial infarction).
Because of adverse effects on cerebral tissue, dextrose
solutions are not recommended during CPR. Recommended
fluids in cardiac arrest are normal saline or lactated Ringer’s
solution. Dextrose solutions are reserved for patients with
actual or suspected hypoglycemia. All emergency drugs rou-
tinely administered for cardiac arrest are stable in 0.9% nor-
mal saline solution.10
Drug Therapy
Emergency drug therapy is dependent on ECG rhythm and
hemodynamic stability. Table 33-4 provides an overview of
commonly used emergency medications. Epinephrine is the
first-line drug in management of cardiac arrest, specifically
asystole, pulseless electrical activity (PEA), VF, and pulse-
less VT. Vasopressin can be used for VF and pulseless VT
followed by epinephrine if the rhythm does not convert. It is
important to remember that management of VF and pulse-
less VT is immediate defibrillation before any medications
are administered.
Patients with ventricular dysrhythmias associated with
cardiac-cardiopulmonary arrest benefit from amiodarone
(cordarone) administration. Other antidysrhythmic agents
considered for management of patients with VF or pulseless
VT include lidocaine (xylocaine), magnesium, and pro-
cainamide (pronestyl). After the ventricular dysrhythmia is
controlled, an infusion of the medication is necessary to sus-
tain therapeutic drug levels. These pharmacologic agents
should not be given to patients with third-degree AV block
and with an escape rhythm or patients with bradycardia and
premature ventricular contractions (PVCs). Ectopic beats
may contribute to the patient’s cardiac output; therefore, li-
docaine could effectively reduce output and cause further
decompensation or asystole.
Bradycardia dysrhythmias are initially managed with at-
ropine, which blocks stimulation of the vagus nerve. Atropine
may not be effective for high-degree AV block dysrhythmias.
Atropine can also be used for asystole and PEA. Isoproterenol
(Isuprel) is a -adrenergic agonist and may be used to in-
crease cardiac output in bradydysrhythmias in some cases.
Routine use of isoproterenol is not recommended because of
effects on ventricular irritability; however, it is considered a
first-line drug for the heart transplant patient with sympto-
matic bradycardia. Bradycardic rhythms that affect hemody-
namic stability may ultimately require cardiac pacing.
Supraventricular rhythms can impair effective cardiac
output (because of decreased filling time) and hemodynamic
stability. Adenosine (Adenocard) is an extremely fast-acting
agent (half-life 10 seconds) for reentry dysrhythmias. The
drug must be given rapidly and followed with a 20-ml saline
bolus to maximize effects. Side effects include transient
Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
bradycardia, transient asystole, ventricular ectopy, flushing,
dyspnea, hypotension, and chest pain. Symptoms usually
terminate spontaneously without further intervention. Other
pharmacologic agents such as Ibutilide,  -adrenergic block-
ing drugs (e.g., metoprolol [Lopressor]) and calcium chan-
nel blocking agents (e.g., verapamil [Calan] and diltiazem
[Cardizem]) can be used for controlling ventricular response
rate in patients with supraventricular tachycardias (e.g.,
atrial fibrillation, atrial flutter, paroxysmal supraventricular
tachychardia, atrial tachycardia). Monitor for bradycardia
and hypotension when administering these drugs. Drugs
should be used only for narrow complex supraventricular
tachycardia (SVT), because of the potential to induce or
worsen reentry ventricular dysrhythmias.10
Other miscellaneous drugs that may be used during
cardiac arrest include sodium bicarbonate, calcium, and
magnesium sulfate. Sodium bicarbonate is reserved for spe-
cific clinical situations, including hyperkalemia, preexisting
bicarbonate-responsive acidosis, and tricyclic antidepressant
overdose. Magnesium is considered useful in treatment of
torsades de pointe, suspected hypomagnesemia, and refrac-
tory VF. Calcium, an ion essential to myocardial contraction
and impulse formation, is recommended for hyperkalemia,
hypocalcemia, and calcium channel–blocker toxicity.
During cardiopulmonary arrest, hemodynamic status is
unstable and requires intervention to stabilize not only the
patient’s cardiac rhythm but also the cardiovascular system.
Table 33-5 reviews vasoactive drugs more commonly used
during cardiac arrest.4,17,22,34 Refer to Table 33-6 for
overview of cardiovascular drugs that can be given via en-
dotracheal tube or interosseous route when IV access cannot
be established.10,38
Acute Coronary Syndromes
The broader terminology of acute coronary syndromes is
inclusive of Q wave myocardial infarction (full-thickness
myocardial necrosis), non–Q wave myocardial infarction,
now called non–ST elevation MI or non–STEMI (suben-
docardial or intramural wall damage), and unstable angina
(myocardial ischemia without necrosis). Approximately
1.5 million people experience acute myocardial infarction
(AMI) annually in the United States; 40% die before
reaching the hospital. The majority of patients die in the
first 2 hours after onset of infarction. Mortality from in-
farction can be reduced significantly if the patient receives
proper medical care in the early phases of infarction. All
these syndromes evolve from rupture or erosion of athero-
matous plaque. An estimated 5.5 million people over age
18 years in the United States have atherosclerosis. Patho-
genesis of atherosclerosis includes accumulation of lipids
on intimal lining of the arteries, calcific sclerosis of the
medial layer of arteries, and thickening of the walls of the
arteries (Figure 33-9 on p. 465). Generally, atherosclerosis
affects the aorta and the coronary, cerebral, femoral, and
other large or middle-size arteries. Risk factors for athero-
sclerosis include smoking, hyperlipidemia, hypertension,
diabetes mellitus, stress, lack of exercise, aging, diet high
 CHAPTER 33 Cardiovascular Emergencies 459

Table 33-4 DRUGS COMMONLY USED IN CARDIOPULMONARY RESUSCITATION

Drug Category Actions Indications Dose Comments
Adenocard Unclassified anti- Slows conduction PSVT SVT: 6 mg rapid IV push May cause brief
(Adenosine) dysrhythmic through the AV over 1 to 3 seconds; may heart block or tran-
node; also can in- give additional 12 mg sient asystole; may
terrupt the reentry rapid IV push if first dose cause other dys-
pathways through not effective, may repeat rhythmias (e.g.,
the AV node to 12 mg after 1 to 2 min PVC, PAC, sinus
decrease the heart It is helpful to rapidly bolus bradycardia, sinus
rate 10 ml normal saline after tachycardia) during
giving adenocard to clear time of conversion
IV tubing completely from PSVT
These symptoms are
usually brief be-
cause of the short
half-life of the drug
(i.e., 10 seconds)
Contraindications in-
clude: Second- or
third-degree AV
block, or sick sinus
syndrome
Amiodarone Combined Prolongs myocar- Recurring ven- Arrest: 300 mg IV push May cause hypoten-
(Cordarone) -adrenergic dial cell action tricular fibril- followed by 150 mg IVP if sion, nausea,
blocker and cal- potential duration lation and no response bradycardia
cium channel and refractory unstable ven- Nonarrest: Initial infusion:
blocker period; decrease tricular tachy- 150 mg over 10 min; can
AV conduction cardia repeat every 10-15 min as
and sinus node needed
function Early maintenance: 1 mg/
min for 6 hours
Late maintenance:
0.5 mg/min
Do not exceed 2.2 g in 24
hours, including initial
dose
Atropine Parasympa- Increases the rate Hemodynami- Bradycardia and AV May cause paradoxic
tholytic; anti- of SA node firing; cally signifi- blocks: 0.5 to 1.0 mg (IV slowing of heart
cholinergic increases conduc- cant bradycar- push) or intratracheally rate when given
tion through AV dia; asystole; every 5 min to maximum slowly or in doses
node; decreases high-degree dose of 0.04 mg/kg of less than 0.5 mg
vagal tone AV blocks Asystole: 1.0 mg IV push
or intratracheally; repeat
every 3-5 min up to a to-
tal of 0.04 mg/kg

PSVT, Paroxysmal supraventricular tachycardia; SVT, supraventricular tachycardia; IV, intravenous; PVC, premature ventricular con-
traction; PAC, premature atrial contraction; AV, atrioventricular; SA, sinoatrial; VF, ventricular fibrillation; VT, ventricular tachycar-
dia; D5W, 5% dextrose in water; gtt, drops.
Continued

in fat and cholesterol, gender, and family history. Multiple
existing risk factors increase a person’s chance of develop-
ing acute coronary syndromes.4,11,31
Overview of Acute Coronary Syndromes
The major cause of the final event leading to AMI is throm-
bosis formation in a narrowed coronary artery from rup-
tured or fissured atherosclerotic plaque. Subsequent vessel
occlusion and thrombosis cause myocardial hypoxia and
necrosis. Myocardial hypoxia may also be caused by coro-
nary artery spasm and dissecting aortic aneurysm. Com-
plete necrosis occurs in 4 to 6 hours. The area surrounding
the zone of necrosis is ischemic. Damage to the my-
ocardium predisposes the patient to pump failure and vari-
ous dysrhythmias secondary to conduction defects and irri-
tability of myocardial tissue. Location and size of the
infarct depend on which coronary artery is affected and
where the occlusion occurs (Table 33-7, p. 466). Most
Text continued on p. 464

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
460 CHAPTER 33 Cardiovascular Emergencies

Table 33-4 DRUGS COMMONLY USED IN CARDIOPULMONARY RESUSCITATION—cont’d

Drug Category Actions Indications Dose Comments
Epinephrine Sympathomimetic Both - and Allergic reac- Cardiac arrest: 1 mg IV Available as
(Adrenalin) -adrenergic ef- tion; cardiac push or intratracheally; 1:10,000 solution
fects; increases arrest; bron- repeat every 5 min when (1 mg in 10 ml)
mean arterial choconstric- needed May cause tachycar-
pressure; de- tion or bron- dia, palpitations,
creases fibrillatory chospasm PVCs, angina
threshold; stimu-
lates heart in asys-
tole and idioven-
tricular rhythms
Isoproterenol Sympathomimetic Nonspecific Hemodynami- Bradycardia: 1 mg in 250 Causes an increased
(Isuprel) -adrenergic cally signifi- ml D5W (4 g/ml); workload on the
stimulation cant bradycar- 2-20 g/min IV (30-300 heart; use with ex-
dia refractory -gtts/min); titrate to treme caution: ex-
to Atropine achieve heart rate of 60 acerbates ischemia
beats/min and extends infarct
Lidocaine Category IB anti- Decreases automa- PVCs, VT, VF, VF and VT with collapse: May cause central
(Xylocaine) dysrhythmic ticity; suppresses preintubation 1.5 mg/kg IV push or in- nervous system de-
ventricular ectopy; for patients tratracheally; repeat in pression, drowsi-
depresses conduc- with suspected 3-5 min; not to exceed ness, dizziness,
tion through re- increased in- 3 mg/kg confusion, anxiety
entry pathways; tracranial PVC’s and VT: 1 mg/kg Contraindications in-
elevates VF pressure or IV push or intratracheally; clude: Bradycardia-
threshold laryngospasm repeat at 0.5 mg/kg every related PVCs,
8-10 min not to exceed bradycardia, id-
3 mg/kg ioventricular
IV infusion: 1 g in 250 ml rhythm; if given
D5W (4 mg/ml) at 2-4 too rapidly, may
mg/min (30-60 gtts/min) cause seizures
Preintubation: 1.5 mg/kg
IV push, wait 90 seconds
then intubate
Procainamide Category IA anti- Suppresses PVCs; PVCs and VT IV push: 100 mg IV (slow May cause hypoten-
(Pronestyl) dysrhythmic suppresses reentry refractory to IV push—20 mg/min) re- sion, bradycardia
dysrhythmias; lidocaine; peat every 5 min; dose not Contraindications:
may elevate VF hemodynami- to exceed 1 g Third-degree AV
threshold; negative cally signifi- IV infusion: 1 g in 250 ml block, digoxin toxi-
chronotrope and cant SVT D5W (4 mg/ml) at 1 to 4 city
dromotrope; mild mg/min (15-60 gtt/min)
negative inotrope;
potent peripheral
vasodilator
Sodium Alkalotic agent Buffers or neutral- Suspected aci- 1 mEq/kg IV push; repeat May inactivate cate-
bicarbonate izes metabolic dosis in cases 0.5 mEq/kg every 10 to cholamines when
acidosis of cardiac 15 min when required given together in the
arrest same IV line; when
possible use arterial
blood gases to guide
administration
Verapamil Category IV anti- Blocks entry of SVT IV push: 0.075 to 0.15 May cause hypoten-
(Calan, dysrhythmic Ca into cells; mg/kg IV (slow IV push) sion
Isoptin) negative dromo- Elderly patients: give 2 mg
trope and de- over 3 to 4 min
presses atrial
automaticity; neg- Maximum dose 10 mg
ative chronotrope;
negative inotrope;
vasodilator

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
 CHAPTER 33 Cardiovascular Emergencies 461

Table 33-5 COMMONLY USED PARENTERAL VASOACTIVE DRUGS

FOR CARDIOVASCULAR EMERGENCIES
Drug Category Actions Indications Dose Comments
Brevibloc -adrenergic Depresses AV con- SVT (e.g., IV push: Initial loading dose May cause significant
(Esmolol) blocker duction and PAT, atrial of 500 mcg/kg given over bradycardia, hypo-
Class II antiar- myocardial auto- fibrillation/ 1 min, followed by 50 tension, broncho-
rhythmic maticity, especially flutter, sinus mcg/kg over 4 min spasm, heart failure
in the SA node; tachycardia) May repeat initial loading Contraindications:
prolongs the re- dose followed by the 4 min. Heart block, CHF,
fractory period infusion increased at incre- severe asthma
ments of 50 mcg/kg/min Has an immediate on-
Do not give over 200 set of action
mcg/kg/min Duration of action ap-
IV infusion: Follow loading prox 30 min after
dose with an infusion of end of infusion
100 mcg/kg/min

Calcium Electrolyte replace- Improves vascular Rapid electrolyte IV push: May cause hypoten-
chloride ment tone and myocar- replacement For Ca Replacement: 500 sion, bradycardia,
dial contractility In seriously mg to 1 g (i.e., 7 to 14 mEq) dysrhythmias
hypotensive For hyperkalemic ECG Contraindications:
patients who changes: 100 mg to 1 g Hypercalcemia, ven-
respond poorly For hypocalcemic tetany: 300 tricular fibrillation
to fluid/ mg to 1.2 g
vasopressors For hypotension associated
when hypocal- with Ca channel
cemia suspected blockers: 500 mg to 2 g
Administer slowly at a rate
not to exceed 0.7 to 1.4
mEq/min
IV infusion: Administer di-
luted solution over 30-60
min (i.e., dilute calcium
chloride in 50-100 ml D5W,
LR, or 0.9% NS)
Diazoxide Antihypertensive Direct relaxation of Significant IV push: 1-3 mg/kg (e.g., Inject drug rapidly as
(Hyperstat) vasodilator arteriolar smooth hypertension approx. 50-150 mg) slow administration
muscle May repeat every 5-15 min reduces hypotensive
Inhibits release of as needed effects
pancreatic insulin Maintenance Dose  50-150 Onset of action
mg every 4-24 hours 1 min, with peak
in 2-5 min
May cause hypoten-
sion CHF, dysrhyth-
mias, myocardial
and cerebral is-
chemia, and hyper-
glycemia

PAT, Paroxysmal atrial tachycardia; CHF, congestive heart failure; ECG, electrocardiogram; HCL, hydrochloride; BP, blood pres-
sure; AMI, acute myocardial infarction; PVC, polyvinyl chloride; ICP, intracranical pressure; see Table 33-4 for other definitions.
Continued

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
462 CHAPTER 33 Cardiovascular Emergencies

Table 33-5 COMMONLY USED PARENTERAL VASOACTIVE DRUGS

FOR CARDIOVASCULAR EMERGENCIES—cont’d
Drug Category Actions Indications Dose Comments
Diltiazem Calcium channel SA node automatic- SVT (e.g., atrial IV push: 0.25 mg/kg to be May cause hypoten-
HCL blocker ity decreased; fibrillation/ administered over 2 min sion, bradycardia,
(Cardizem) AV conduction flutter, PSVT) May give additional dose in AV heart block
prolonged; in- 15 min of 0.35 mg/kg if Has an immediate on-
creased refractori- initial dose inadequate to set when given IV,
ness of AV node; control HR with peak effect in
and vasodilation IV infusion: 5-15 mg/hr 15 min
including coronary Contraindications:
arteries Heart block, acces-
sory conduction
pathways or preexci-
tation syndromes
Dobutamine Sympathomimetic, Positive inotropic ef- To optimize car- IV infusion: Initially May cause tachycar-
HCL -1 adrenergic fects (e.g., in- diac output; 2.5 mcg/kg/min; continue dia, dysrhythmias
(Dobutrex) receptor agonist creases force of may be used as titration to maintain effec- (e.g. ventricular)
myocardial con- concurrent tive cardiac output Consider dose reduc-
traction); increases therapy with Maintenance dose usually tion of dobutamine
heart rate at higher afterload- 2.5-10 mcg/kg/min if heart rate 10%
doses reducing agents Maximum dose  above baseline
to also increase 40 mcg/kg/min
cardiac output
Dopamine Sympathomimetic, At low doses: Va- At low doses: To IV infusion: May cause dysrhyth-
HCL -1 and -adren- sodilates mesen- increase uri- low dose: 0.5-2 mcg/kg/min mias
(Intropin, ergic agent; also teric and cerebral nary output intermediate dose: 2-10 Extravasation of the
Dopastat) a dopaminergic blood flow mcg/kg/min drug may cause tis-
stimulator At intermediate At intermediate high dose: 10 mcg/kg/min sue sloughing and
doses: Increase doses: To in- Maximum dose  20 necrosis
myocardial con- crease cardiac mcg/kg/min
tractility and pe- output
ripheral vasodila-
tion
At high doses: In- At high doses:
creased peripheral/ To increase BP
renal vascular re- in nonhypo-
sistance and in- volemic shock
creased myocar-
dial contractility
Enalaprilat Angiotensin- Reduces vascular Significant IV push: Initial dose 0.625 May cause hypoten-
(Vasotec) converting en- tone hypertension mg IVP; may repeat in 1 sion, pulmonary
zyme (ACE) in- Adjunct to digi- hour edema
hibitor talis and diuret- Maintenance dose1.25 mg
ics for acute every 6 hours IVP
CHF
Ibutilide Class III antiar- Slows conduction; Recent onset IV: 60 kg: 1 mg adminis- May have proarrhyth-
(Corvert) rhythmic delays repolariza- atrial fibrilla- tered over 10 min, may re- mic effects—
tion by activation tion or atrial peat dose in 10 min if not monitor closely for
of slow, inward flutter effective in converting torsades de pointes
current (mostly rhythm or polymorphic ven-
sodium) resulting 60 kg: 0.01mg/kg over 10 tricular tachycardia;
in prolongation of min, may repeat dose in 10 especially within 4-6
atrial and ventricu- min if needed hours after adminis-
lar action potentials tration

PAT, Paroxysmal atrial tachycardia; CHF, congestive heart failure; ECG, electrocardiogram; HCL, hydrochloride; BP, blood pres-
sure; AMI, acute myocardial infarction; PVC, polyvinyl chloride; ICP, intracranical pressure; see Table 33-4 for other definitions.

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
 CHAPTER 33 Cardiovascular Emergencies 463

Table 33-5 COMMONLY USED PARENTERAL VASOACTIVE DRUGS

FOR CARDIOVASCULAR EMERGENCIES—cont’d
Drug Category Actions Indications Dose Comments
Labetalol Selective Blocks sympathetic Hypertension IV push: 20 mg (0.25 May cause hypoten-
(Normodyne, -adrenergic stimulation, mg/kg) IV to be adminis- sion, bradycardia,
Trandate) blocker and thereby causing tered over 2 min heart block, bron-
nonselective vasodilation Additional doses of 40-80 mg chospasm
-adrenergic of the drug can be given at
blocker 10-min intervals up to max-
imum dose of 300 mg total
Magnesium Electrolyte Adequate Mg is Supraventricular IV push: 1-3 g of magne- Rapid injection may
sulfate replacement needed for normal and ventricular sium sulfate (concentration cause hypotension,
cardiac automatic- dysrhythmias of magnesium should not heart block, cardiac/
ity, excitability, exceed 200 mg/ml respiratory arrest
conduction and Also Mg should not be Onset of action is
contractility administered faster than immediate when
150 mg/min) given IV
IV infusion: Follow initial Observe for hyper-
IV dose with 1-2 g of magnesemia: Flush-
Mg per hour ing, hypotension,
bradycardia, confu-
sion, weakness, de-
pressed deep tendon
reflexes, respiratory
depression
Metaprolol -adrenergic Selectively blocks Hypertension; IV push: 5 mg IVP for hy- May cause bradycar-
tartrate blocker -1 adrenergic re- AMI in hemo- pertension dia, hypotension,
(Lopressor) ceptors, which dynamically Treatment for AMI: 3 IV bronchospasm
slows sinus heart stable patient injections of 5 mg; give 50
rate, decreases car- mg metaprolol “orally”
diac output, de- every 6 hours after last
creases BP dose IV metaprolol
Nicardipine Calcium channel Significantly de- Hypertensive IV infusion: 5 mg/hr to be May cause tachycar-
(Cardene) blocker creases peripheral emergency titrated to desired effect— dia, angina,
vascular resistance up to 15 mg/hr hypotension
Nitroglycerin Vasodilator Relaxation of vascu- Angina, IV infusion: Initiate infusion May cause hypoten-
(Tridil) lar smooth muscle, hypertension at 5-10 mcg/min sion, headache,
promoting venous Increase infusion by 5-10 dizziness
and coronary mcg/min every 5-10 min Nitroglycerin is ab-
artery vasodilation; Maximum dose: 200 mcg/min sorbed by many soft
reduces venous plastics; therefore di-
return lute the concentrate
in a glass bottle and
consider using non-
absorbing, non-PVC
tubing or flush tubing
with 20-25 mls be-
fore starting infusion
Nitroprusside, Vasodilator Relaxes vascular Significant IV infusion: Initiate infusion May cause hypoten-
sodium smooth muscle— hypertension at 0.3-0.5 mcg/kg/min. sion, angina, in-
(Nipride) lowering both arte- Increase infusion by 1-2 creased ICP, seizures
rial and venous BP mcg/kg/min to attain de- The IV solution needs
sired hemodynamic effects to be protected from
Maximum infusion rate  the light by using a
10 mcg/kg/min light-resistant cover-
ing (e.g., aluminum
foil, opaque plastic)
Onset of action imme-
diate, with peak ac-
tion of 1-2 min

Continued

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
464 CHAPTER 33 Cardiovascular Emergencies

Table 33-5 COMMONLY USED PARENTERAL VASOACTIVE DRUGS

FOR CARDIOVASCULAR EMERGENCIES—cont’d
Drug Category Actions Indications Dose Comments
Norepinephrine Vasopressor Peripheral Short-term use IV infusion: Initiate infusion May cause ventricular
bitartrate venous/arterial for hypotension at 2 mcg/min and titrate to tachycardia/
(Levophed) vasoconstriction; or shock desired BP fibrillation (i.e., sec-
cardiac stimulation Usual range  2-12 mcg/min ondary to increased
myocardial oxygen
consumption)
Extravasation of the
drug may cause tis-
sue sloughing and
necrosis

Phenylephrine Vasopressor Potent postsynaptic Short-term IV push: 0.1-0.5 mg to be May cause hyperten-
(Neo- -adrenergic use for given over 1 min sion, dysrhythmias,
Synephrine) agonist hypotension/ IV infusion: Dilute to yield reflex bradycardia,
shock solution of 0.1/ml and cerebral hemorrhage
titrate gtt every 10-15 min Extravasation of the
to achieve and to maintain drug may cause tis-
BP 90 mm Hg sue sloughing and
necrosis

Propranolol Nonselective Blocks sympathetic Control of hyper- IV push: 0.5 to 3 mg May cause bron-
HCL -adrenergic stimulation of tension and Give slowly 1 mg/min; may chospasm, hypoten-
(Inderal) blocker and -1 adrenergic suppression of repeat dose after 2 min sion, heart block,
class II antidys- receptors rapid-rate angina
rhythmic cardiac dys-
rhythmias
Vasopressin Vasopressor Directly stimulates Short-term use IV infusion: Dilute with May cause hyperten-
(Pitressin) contraction of for hypotension 5% dextrose in water or sion, dysrhythmias
smooth muscles; or shock 0.9% NaCl to a concentra- Contraindicated in
causes vasocon- Alternative to tion of 0.1 to 1.0 U/ml preexisting CV dis-
striction wih re- epinephrine in titrate gtt every 10-15 min ease; IV dose same
duced blood flow cardiac arrest to achieve and to maintain as IO and ET dose
to coronary, pe- d/t VF or BP 90 mm Hg
ripheral, cerebral, pulseless VT in Cardiac arrest: 40 units IV
and pulmonary patients with- push
vessels out CV disease

AMIs are caused by blockage of the left anterior descend-
ing coronary artery, which causes involvement of the ante-
rior wall of the myocardium.11
Non–STEMI is usually related to intermittent occlusive
thrombosis causing distal myocyte necrosis of the region
supplied by the related coronary artery. As the clot enlarges
around the thrombus, it may embolize and eventually oc-
clude coronary microvasculature, which results in small el-
evations of cardiac enzymes. Underlying pathology for un-
stable angina is partial occlusion by thrombus of
atherosclerotic plaque. Patients with either non–STEMI or
unstable angina are at high risk for progression to trans-
mural myocardial infarction.2,29,32,33
When the coronary artery(s) becomes narrowed or oc-
cluded, myocardium becomes hypoxic, often resulting in
classic retrosternal chest discomfort or angina pectoris. Pain
is described as crushing, burning, sharp, heavy, or a variety
of other descriptors. The pain lasts several minutes to several
weeks and may vary in location. Local hypoxia, lactate
buildup, and sensory response of the hypoxic myocardium
contribute to pain. Pain may localize in the substernal area
or radiate to the jaw and down the left arm. Associated
symptoms include nausea, vomiting, diaphoresis, and hic-
cups if the phrenic nerve is stimulated.
Blood pressure decreases with AMI because poor pump
action decreases cardiac output. Sodium and water reten-
tion may occur as a result of decreased cardiac output and
increased venous pressure. When AMI occurs, ventricular
failure occurs. With severe ventricular failure, stroke vol-
ume decreases and ventricular diastolic pressure in-
creases, whereas the sympathetic response decreases
blood flow to the periphery. Decreased blood flow and
pressure to the kidneys slows glomerular filtration rate
(GFR). Decreased GFR stimulates renal cells to produce
renin so angiotensin levels rise and aldosterone is se-
creted. Increased aldosterone and decreased GFR cause
sodium and water retention and formation of interstitial
edema.11

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.

Table 33-6 ALTERNATE ROUTES FOR DRUG ADMINISTRATION IN CARDIOVASCULAR EMERGENCIES
Route
ENDOTRACHEAL (ET)
When IV access not available, can administer selected
emergency drugs:
Epinephrine
Atropine
Lidocaine
Naloxone
Consider dose 2.0 to 2.5 times recommended IV dose (for
above medications)
Vasopressin (ET dose same as IV dose)
INTRAOSSEOUS (IO)
Used most often in children age 6 years or younger
Intraosseous needle placed in proximal tibia
Can be placed in any portion of the tibia excluding the
epiphyseal plates (e.g., distal tibia, midanterior distal one third
of the femur, iliac crest, humerus); the sternum can be used as
a site in patients age 3 years or older
Use for medications, fluids, and blood and blood products
IV, Intravenous.
FIGURE 33-9 Major components of well-developed atheromatous plaque. From Cotran R, Kumar V, Collins T:
Pathologic basis of disease, ed 6, Philadelphia, 1999, WB Saunders.)
Patient Assessment for Acute Coronary Syndrome
Prompt assessment of the patient with acute coronary syn-
dromes is crucial because the incidence of ventricular fibril-
lation is 15 times greater during the first hour after onset of
AMI symptoms. On average, patients delay 2 or more hours
before seeking medical care for AMI symptoms.40 Most pa-
tients are resting or engaged in only moderate activity when
symptoms begin. Chest pain indicative of AMI is usually se-
vere, lasts longer than 30 minutes, and is not relieved with
rest or vasodilators such as nitroglycerin. Ironically, up to
20% of patients with AMI do not experience chest pain. Pa-
tients with diabetes mellitus are more prone to neuropathy
and may not experience pain. Among patients older than 85
years, the classic symptom of AMI is shortness of breath.
Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
CHAPTER 33 Cardiovascular Emergencies 465
Nursing management
Dilute drug in sterile saline or sterile water (i.e., 10 ml for adults
and 1 to 2 ml for children)
Administer medications as far down ET tube as possible; consider
inserting intracatheter in ET tube and advancing to give
medication
Administer drug quickly down ET tube, follow with three to four
rapid insufflations of ambu-bag to aerosolize medication in
tracheobronchial tree
Use sterile technique to insert an intraosseous needle; alternative
methods include using #16 or #18 gauge hypodermic, spinal, or
bone marrow needle
Confirm placement by aspiration of bone marrow, and freely flow-
ing IV without evidence of infiltration
Secure firmly with sterile dressing and tape to prevent dislodgement
Monitor for extravasation and patency
Flush with dilute saline or heparin to maintain patency
Dilute hypertonic-alkaline solutions before administration
Heart transplant patients do not experience chest pain be-
cause pain receptors are disconnected during transplant.
Obtaining a concise, brief history of chest pain is crucial;
the PQRST mnemonic is particularly useful for these pa-
tients (Table 33-8). Patients who have chest pain must have a
differential diagnosis made between angina pectoris and
AMI.8,19 There are two types of angina—stable and unstable
(Table 33-9). Stable angina, known as typical angina, occurs
as a predictable event after activities such as exercise or body
strain. Two categories of unstable angina are typical unstable
angina and Prinzmetal’s angina. Attacks of typical unstable
angina, also called preinfarction angina, are prolonged, occur
more frequently, and worsen with each episode. Typical un-
stable angina is associated with higher incidence of left main
466 CHAPTER 33 Cardiovascular Emergencies

and proximal left anterior descending coronary artery dis-
ease. Half the patients with typical unstable angina have to-
tal or near-total occlusion (70% to 100% stenosis) of a coro-
nary artery (Figure 33-10). Prinzmetal’s angina, or variant
angina, occurs when the patient is at rest, usually at the same
time each day. Prognosis with Prinzmetal’s angina is poor,
with 50% mortality during the first year.
In addition to assessing pain, assess for associated symp-
toms and pertinent medical history. Associated symptoms in-
clude diaphoresis, nausea, vomiting, indigestion, dyspnea, pal-
pitations, dizziness, or lightheadedness. Evaluate risk factors
for cardiac disease; for example, smoking, hypertension, hy-
perlipidemia, diabetes, and related medical history (i.e., previ-
ous angina, previous AMI or cardiac surgery, peripheral vas-
cular disease, and immediate family history of AMI).
Medication history may include antianginals, antidysrhyth-
mics, antihypertensives, anticoagulants, and digitalis prepara-
tions. Such drugs as H2 blockers, antacids, sucralfate, and non-
steroidal antiinflammatory drugs may assist in differentiating
gastrointestinal problems and/or musculoskeletal discomfort.
In addition to cardiac disease, other etiologies may be as-
sociated with chest pain (Table 33-10, p. 469). Hyperventila-
tion, a common condition in the ED, may occur as a result of
anxiety disorder or may be a response to disease processes
such as AMI, salicylate overdose, or intracerebral hemor-
rhage. Treat these patients with extreme caution and assess
carefully for signs and symptoms of an underlying disorder.
A patient with hyperventilation is a difficult diagnostic
problem. Hyperventilation may be a response to an organic
process in which having the patient breathe into a paper bag
may be detrimental. Hyperventilation is a sign of many ill-
nesses and conditions, including anxiety, pregnancy, fever,
liver disease, trauma, hypovolemia, pulmonary embolus,
stress, ketoacidosis, high altitude, thyrotoxicosis, pul-
monary hypertension, pulmonary edema, anemia, stroke,
central nervous system lesion, and fibrotic lung disease.
Hyperventilation causes partial arterial carbon dioxide
pressure to drop and cerebral vasculature to constrict, re-
sulting in respiratory alkalosis and tetany. Signs and symp-
toms include anxiety; panic; shortness of breath; paresthe-

Table 33-7 CORONARY ARTERIES IN MI

Right coronary artery Left coronary artery

Aorta
Superior vena cava
Pulmonary artery
Left coronary artery
Circumflex branch
Right coronary artery Circumflex branch– Right coronary
Descendent branch artery
left coronary artery
Posterior descending
branch–right coronary
artery

Anterior Lateral
Inferior
Lateral Posterior
Areas of infarct
Inferior
Areas of infarct
Supplies Left circumflex branch
Right atrium Supplies
Right ventricle Left atrium
Posterior surface left ventricle Free wall left ventricle
50%-60% sinoatrial node 40%-50% sinoatrial node
Bundle of His 8%-10% arteriovenous node
Block causes Bundle of His
Infarction posterior wall left ventricle Right bundle
Infarction posterior wall interventricular septum Block causes
Anticipate second-degree heart block, Mobitz type 1 block, Lateral wall infarction
and Wenckbach block in inferior MI Posterior wall infarction (near base)

Left anterior descending branch

Supplies
Interventricular septum
Block causes
Infarction anterior wall left ventricle
Affects papillary muscle, which attaches to mitral valve
Infarction anterior wall septum
Anticipate second-degree heart block and Mobitz type 2 block
in anterior MI

MI, Myocardial infarction.

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
 CHAPTER 33 Cardiovascular Emergencies 467

sia of the fingers, toes, and periorbital area; carpopedal
spasms; confusion; syncope; and, occasionally, chest pain.
Therapeutic intervention includes calming and reassuring
the patient. Have the patient talk; it is difficult to hyperven-
tilate when speaking. As a last therapeutic intervention,
have the patient breathe into a paper bag to facilitate carbon
dioxide rebreathing.
Chest pain may also be caused by abdominal illnesses
such as hiatal hernia, gastric or peptic ulcer, pancreatitis,
esophageal spasms, Mallory-Weiss syndrome, or Boer-
haave’s syndrome. Other problems that cause chest pain are
musculoskeletal disorders involving trauma, degenerative
Table 33-8 PQRST MNEMONIC FOR CHEST
PAIN ASSESSMENT
Factor Description questions
P Provokes, palliates, What provoked the pain?
precipitating What makes the pain better?
factors What makes the pain worse?
Have you had this type of pain be-
fore?
What were you doing when the pain
occurred?
Q Quality What does the pain feel like?
Is it burning? Crushing? Tearing?
Sharp?
R Region, radiation Show me where the pain is.
How large an area is involved?
Does the pain radiate? If so, where?
S Severity, associated How severe is the pain?
symptoms If you were to rate the pain on a
scale from 0 to 10 with 10 being
the most severe pain you can
imagine, how would you rate your
pain?
What else did you feel besides the
pain?
T Time, temporal When did the pain start?
relations How long did it last?
Does it come and go?
Were you awakened by the pain?
Is the pain always present?
disk disease, xiphoidalgia, costochondritis, Mondor’s dis-
ease, and postherpetic syndrome.
Physical findings associated with AMI are usually con-
sistent with a patient who is acutely ill. Because of hemody-
namic effects of AMI, the patient may have a variety of heart
rates and heart dysrhythmias. The patient may be hyperten-
sive secondary to low cardiac output and sympathetic stim-
ulation or hypotensive from pump failure. The first heart
sound may be decreased because of decreased myocardial
contractility, whereas the second heart sound may be in-
creased because of increased pulmonary artery pressure. An
S3 sound (gallop) may be present as the result of ventricular
dilation and increased ventricular fluid pressure. The pres-
ence of a new systolic murmur indicates ischemic mitral re-
gurgitation or ventricular septal defect.
A transient pericardial friction rub occurs secondary to
the inflammatory response to necrosis. There also may be an
alternating pulse rate caused by left-sided heart failure. In-
creased pressure from congestion causes backflow of blood
into jugular veins so jugular vein distention occurs when the
patient is sitting at a 45-degree angle. There may also be a
prominent V wave with rapid Y wave descent. The patient
may also have an elevated temperature caused by inflamma-
tion and necrosis of myocardial tissue.
The patient is often diaphoretic and anxious. Diaphoresis
is related to the autonomic nervous system response, where-
as anxiety may be due to pain and fever. Cyanosis may be
caused by decreased oxyhemoglobin concentration and de-
creased blood supply to the peripheral vascular system.
ECG
Changes in the ECG provide information about the site of
coronary artery occlusion, myocardial ischemia, and the pres-
ence of tissue necrosis. Lead placement of an ECG deter-
mines which area of the heart the ECG signal is representing
(Figures 33-11 and 33-12, p. 471). Changes in the ECG occur
because of changes in electrical current flow when there is
myocardial damage or ischemia (Figure 33-13, p. 471). When
current flows toward a lead (arrowhead, positive electrode),
an upward ECG deflection occurs. When current flows away
from a lead (arrowhead, positive electrode), downward de-
flection occurs. When current flows perpendicular to a lead

Table 33-9 DIFFERENTIAL DIAGNOSIS OF ANGINA

Characteristic Stable angina Unstable (preinfarction) angina
Location of pain Substernal; may radiate to jaws, neck, and down arms Substernal; may radiate to jaws, neck, and down arms
and back and back
Duration of pain 1-5 min 5 min; occurring more frequently
Characteristic of pain Aching, squeezing, choking, heavy burning Same as stable angina but more intense
Other symptoms Usually none Diaphoresis; weakness
Pain worsened by Exercise; activity; eating; cold weather; reclining Exercise; activity; eating; cold weather; reclining
Paine relieved by Rest; nitroglycerin; isosorbide Nitroglycerin, isosorbide may give only partial relief
ECG findings Transient ST depression; disappears with pain relief ST segment depression; often T wave inversion; ECG
may be normal

ECG, Electrocardiogram.

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
468 CHAPTER 33 Cardiovascular Emergencies
FIGURE 33-10 Thrombus formation. (From Roetting M, Tanabe P:
Emergency Management of acute coronary-syndromes, J Emerg
Nurs (suppl) 26(6):S1, 2000.)
(arrowhead), biphasic ECG deflection occurs.20 Figures 33-14
through 33-17 on p. 472 illustrate ECG changes with my-
ocardial infarction. Serial ECGs are used in conjunction with
patient assessment, history, and other diagnostic measures to
confirm the diagnosis of AMI. A single ECG cannot be used
exclusively. ECG findings are sensitive only 50% of the time,
and ECG changes occur with other conditions. Patients with
stable angina can have ST segment depression, and ST seg-
ment elevation can occur with unstable angina and
Prinzmetal’s angina. Pericarditis may cause ST segment ele-
vation in many leads, hemorrhagic stroke is associated with T
wave inversion, and ventricular aneurysms may be associated
with ST elevation.12,14,28
Elevation of the segment between the end of the S wave
and the beginning of the T wave (ST segment) is indicative
of myocardial injury and occurs minutes after occlusion of a
coronary artery. The ST segment can remain elevated for 24
hours. T wave inversion occurs 6 to 24 hours after occlusion,
may persist months to years, and is due to ischemia. (Hy-
poxia should also be considered with T wave inversion.)
Pathologic Q waves, measuring more than 0.04 seconds in
width and at least 25% or more of overall QRS height, oc-
cur within 24 hours and indicate irreversible myocardial cell
death. ST segment depression may also be associated with
AMI. Reciprocal changes (ST segment depression and
peaked T wave) may be seen in ECG leads that view regions
opposite the damaged area. Hyperkalemia should be elimi-
nated as a cause of tall, peaked T waves. Changes in ECG20
have an overall 79% sensitivity and 44% specificity in de-
tecting an AMI (Box 33-1, p. 473).
A Q wave has been associated with transmural AMI;
however, studies now demonstrate both Q wave and non–Q
wave (non–STEMI) infarcts can be transmural or subendo-
cardial. In general, Q wave infarctions are associated with a
larger region of myocardial necrosis, higher enzyme levels,
Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
fresh coronary thrombosis, frequent vomiting, congestive
heart failure, conduction defects, dysrhythmias, and less col-
lateral circulation. When ST segment depression occurs in
the inferior (II, III, aVF), lateral (I, aVL, V5, V6), or ante-
rior (V1 through V6) leads and cardiac enzymes are ele-
vated, diagnosis of non–STEMI is supported. ST elevation
is most frequently associated with Q wave infarctions and
almost 50% of non–STEMIs.12,14,28
All patients with suspected inferior or lateral AMI should
be evaluated for right ventricular infarction. Right ventricu-
lar infarct is present in up to 40% of patients with inferior
myocardial infarctions resulting from occlusion of the right
coronary artery. Changes noted on the ECG may include
isolated ST segment elevation in V1 or ST elevation in V1 to
V4. A more reliable method of determining right ventricular
infarct is use of right ventricular leads (V3R to V6R). Figure
33-18 and Box 33-2 on p. 473 illustrate right ventricular
lead placement. Use of lead V4R has 92% sensitivity for
right coronary artery occlusion.35
ECG changes in posterior infarct (ST depression in V1 to
V4) represent reciprocal changes of the anterior wall, the
portion of the heart opposite the posterior portion. Other
changes include R waves longer than 0.04 seconds in V1 and
V2 and R wave to S wave ratio larger in V1 and V2.35 Fur-
ther evaluation may include posterior ECG leads (V7 to V9)
(Figures 33-19 and 33-20, p. 474 and Box 33-2, p. 473).
Continuous ECG monitoring in one or more leads is es-
sential for the AMI patient. Dual lead or continuous ST seg-
ment monitoring is available to detect changes in the ECG
and identify dysrhythmias. The best lead to use for diagnos-
ing wide complex QRS rhythms is MCL-1 and MCL-6 (see
Figure 33-19). This combination of a limb lead and precor-
dial lead is valuable in detecting both ST segment changes
associated with further blockage of coronary arteries and for
dysrhythmia detection. If bedside monitoring permits, the
combination of leads V1, I, and aVF allows quick evaluation
of ECG axis. Figure 33-20 on p. 474 provides an overview
of axis based on leads I and aVF. Evaluation of axis during
wide-complex QRS rhythms or dysrhythmias assists in dif-
ferentiating supraventricular from ventricular dysrhythmias.
In one study, three lead combinations were 100% sensitive
for ischemic changes in the major coronary vessels. Leads
III, V2, and V5 reflect the coronary artery and left circum-
flex artery. Leads III, V3, and V5 reflect left anterior de-
scending artery. As technology evolves, multilead ECG
monitoring and continuous ST segment monitoring may be-
come increasingly common in the ED.13
Cardiac Markers
In addition to ECG monitoring, cardiac markers are mea-
sured as part of the diagnostic workup for acute coronary
syndromes.* Myoglobin is a nonspecific protein associated
with muscle oxygen transport. Myoglobin levels elevate
about 1 hour sooner than creatine kinase (CK) after myo-
cardial injury and peak in 2 to 4 hours, and are therefore
considered an early cardiac biomarker. Myoglobin is found
in striated muscle of the heart and skeletal muscle; thus, el-
*1,18,26,30,31,33,39
 CHAPTER 33 Cardiovascular Emergencies 469

Table 33-10 ETIOLOGIC FACTORS TO BE CONSIDERED IN THE DIFFERENTIAL DIAGNOSIS

OF CHEST PAIN
P Q R S T
Etiologic Precipitating/ Time/
factors Palliating Quality Radiating/Region Severity/Symptoms Temporal
Ischemic/ Precipitating factors: Tightness, Retrosternal, area af- Associated symptoms: Gradual onset
Anginal Effort-related activity, burning, deep, fected the size of the Profuse diaphoresis, of pain builds
large meals, emo- constrictive palm of the hand weakness, shortness up to maxi-
tional stress Pain may radiate to left of breath, nausea, mum pain in-
shoulder, left hand vomiting tensity; usu-
Palliation: Ceases with (e.g., especially the ally anginal
activity abatement, 4th and 5th fingers), pain lasts 1-5
relief with nitroglyc- epigastrium, trachea, minutes
erin, relief with rest larynx

Never involves region

above the level of the
eye
Myocardial Precipitating factors: Severe chest Chest pain; may have Associated symptoms: Usually pain
infarction Effort-related activity, pain radiation of pain to Palpitations, dysp- has lasted 30
large meals, emo- back, jaw, or left arm nea, diaphoresis, minutes or
tional stress nausea, vomiting, more
dizziness, weakness,
sense of impending
doom
Acute peri- Precipitating factors: Chest pain may Anterior chest pain Associated symptoms: May be hours
carditis May occur after AMI, be dull to se- with radiation to the Fever (i.e., between to days
may also be related to vere and neck, arms, or shoul- 101-102° F or 38.3-
viral, collagen, or crushing type ders; pain may be in- 38.9° C); pericardial
vascular disorders pain tensified by deep in- friction rub; ECG:
spiration ST segment eleva-
tion in all leads ex-
cept V1 and aVR
Dissecting Sudden onset Severe, ripping, Anterior and posterior Associated symptoms: Sudden
aortic tearing type chest Dyspnea, tachypnea, onset
aneurysm pain CHF (i.e., secondary
Often radiates from to aortic regurgita-
anterior chest to in- tion caused by dis-
trascapular region or section); also, CVA,
to abdomen syncope, paraplegia
and pulse loss asso-
Pain may move with ciated with dissect-
progression of aortic ing aneurysm
dissection
Esophageal dis- Precipitating factors: Burning or May radiate to neck, Associated symptoms: Minutes to days
orders (esoph- Often triggered by pressure-like ear, jaw or lower ab- Dysphagia, aspira-
ageal reflux, exercise, or by food pain domen tion
esophageal (large meal, spicy May be severe
spasm) foods, acidic foods,
cold foods) or ethanol
intake
Cocaine Precipitating factors: Sharp, heavi- Substernal location, Associated symptoms: Occurs from
induced Cocaine use ness, pressure with radiation to Tachycardia, palpita- 1-6 hours af-
of the chest both arms tions, diaphoresis, ter cocaine
nausea, dizziness, use
Palliation: Relieved Severe type syncope, dyspnea
with nitroglycerin pain

AMI, Acute myocardial infarction; ECG, electrocardiogram; CHF, congestive heart failure; CVA, Cerebrovascular accident; COPD,
chronic obstructive pulmonary disease.
Continued

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
470 CHAPTER 33 Cardiovascular Emergencies

Table 33-10 ETIOLOGIC FACTORS TO BE CONSIDERED IN THE DIFFERENTIAL DIAGNOSIS

OF CHEST PAIN—cont’d
P Q R S T
Etiologic Precipitating/ Time/
factors Palliating Quality Radiating/Region Severity/Symptoms Temporal
Postoperative Precipitating factors: Mild to severe Anterior chest, may Associated symptoms: Persistent type
coronary artery Use of IMA for graft chest pain, radiate over entire Numbness, tender- of pain
bypass graft of CABG patient burning, chest wall and partic- ness on palpation of Shooting type
(CABG) due prickling, and ularly over the site of the sternum, hyper- pain may last
to harvest of dull-type sen- the graft, may radiate esthesia along the for several
internal mam- sations to neck or axilla incisional line, de- seconds and
mary artery layed healing of the occur several
(IMA) sternum times per day
Mitral valve Palliation: Relief in re- Dull and Nonretrosternal chest Associated symptoms: Onset may be
prolapse cumbent position, no aching; al- pain Systolic murmur, sudden or re-
relief with nitroglyc- though may unexplained dysp- current
erin also be sharp nea, weakness,
midsystolic (apical) May last for a
click few seconds,
or be persis-
tent for days
5-Fluorouracil Precipitating factors: Mild to severe Central chest pain; ra- Associated symptoms: Occurs several
(FU) therapy Following infusion of pain diates to left shoul- Nausea, vomiting, hours after IV
5-FU der and left arm tachycardia, hyper- bolus or infu-
tension sion of 5-FU
Palliation: relief with No chest pain
nitroglycerin between treat-
ment
Spontaneous COPD, chronic asthma Sharp or stab- Usually pain of entire Associated symptoms: Continuous
pneumothorax bing; de- lung region Decreased or absent pain until
scribed as (hemithorax), may breath sounds; pneu- treated
moderate to rediate to back and mothorax per chest
severe neck radiograph
Tachydys- Precipitating factors: Sharp, stabbing Precordial chest pain Associated symptoms: Paroxysmal in
rhythmias anxiety, digitalis toxi- type of chest Weakness, fatigue, onset
city, exercise, organic pain lethargy, palpita-
heart disease tions, dizziness, Lasts briefly to
May have pal- vertigo hours
Palliation: terminated pitations,
by antiarrhythmics, “skipped
direct current shock, beats”
vagal maneuvers
Anxiety May have history of Pain may be Anterior chest and ab- Associated symptoms: Variable; often
disorders depression or anxiety vague, diffuse; domen Dyspnea, fatigue, continuous
may be fur- anorexia for hours to
ther described days
as disabling
Monosodium Occurs with food Burning type of Retrosternal chest pain Associated symptoms: Occurs shortly
glutamate ingestion high in chest pain Facial pain, nausea, after meals or
monosodium vomiting up to several
glutamate hours after
meal

Musculoskeletal Precipitating factors: Generalized Tenderness of the an- Persistent chest pain
pain with inspiration aching, stiff- terior chest wall without relief with
or with musculo- ness with rest
skeletal movement point tender-
ness, swelling

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
 CHAPTER 33 Cardiovascular Emergencies 471

aVL
aVR

III II
aVF

FIGURE 33-11 Six-limb lead (leads I, II, III, aVR, aVL, and aVF) normally appear as shown.

MCL
Posterior

Right Left
V6
V1 V2
V3
V4 V5 V6
V5
V4
V 1 V2 V3

FIGURE 33-12 Precordial or chest (V1-6) leads.

T ST ST

Q
Normal Ischemia Injury Infarct
Decreased blood supply Acute or recent; Significant Q wave
T wave inversion the more elevated greater than 1 mm
May indicate ischemia the ST segment, wide and half the
without myocardial infarction the more recent height  depth of
the injury the entire complex
indicates myocardial
necrosis

FIGURE 33-13 ECG changes.

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
472 CHAPTER 33 Cardiovascular Emergencies

evations can be associated not only with AMI but also with
conditions such as neuromuscular disorders, strenuous exer-
cise, and renal failure. Cardiac-specific troponin is also a
protein found in the myofibrils of muscle. Two subforms,
cardiac-specific troponin T (cTn T) and troponin I, are very
specific for the cardiac muscle because they have a role in
contraction of myocardial muscle. Some studies have found
not only that troponin elevations occur with AMI, but some
studies have reported cTn T is released from myocardial
cells in unstable angina. Troponin is detectable 4 to 6 hours
after AMI, peaks at 10 to 24 hours, and remains elevated 5
to 7 days. Other primary cardiac markers released from
necrotic myocardium are CK and the MB fraction of the CK
(CK-MB); with CK-MB once the “gold” standard for defin-
itive diagnosis of AMI. However, CK-MB may take 4 to 6
hours to elevate, so biomarkers such as myoglobin and tro-
ponins that elevate earlier can be useful to the clinician for a
more timely diagnosis. In addition, there are isoforms or
subforms of CK-MB: CK-MB1 and CK-MB2. Studies have
demonstrated that CK-MB2 of more than 1 U/L or a ratio of
CK-MB2 to CK-MB1 of 1.5 is also indicative of AMI.5,31
Lactate dehydrogenase (LDH), which is released by is-
chemic heart muscle, is elevated after AMI. Examine espe-
cially the isoforms LDH-1 and LDH-2; normally, LDH-2 is

Anterior wall MI
R L

I
FIGURE 33-14 Anterior myocardial infarction Limb and augmented
(V2, V3, and V4) leads Anterior wall MI

III II
V2 V3 V4

F Chest (V) leads

Inferior wall MI
R L

Inferior wall MI
I
Limb and augmented
FIGURE 33-15 Inferior myocardial infarction leads
(II, III, and aVF).
III II

F
Chest (V) leads

Lateral wall MI
R L
Lateral wall MI

I V6
FIGURE 33-16 Lateral myocardial infarction (I, Limb and augmented
aVL, V5, and V6). leads

III II V5

F Chest (V) leads

Posterior wall MI
R L
Posterior wall MI
I
FIGURE 33-17 Posterior myocardial Limb and augmented
leads
infarction (V1 and V2).
III II
Chest (V) leads
V1 V2 F

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
 CHAPTER 33 Cardiovascular Emergencies 473

higher but with AMI the ratio “flips” and the LDH-1 level
will be higher than LDH-2. Because of its lengthy time of
elevation, LDH can be useful for prolonged retrospective di-
agnosis of myocardial infarction. Table 33-11 on p. 475 de-
scribes markers released with myocardial tissue necrosis.
Further evaluation of the patient with acute coronary syn-
dromes includes a chest radiograph to rule out other causes of
chest pain such as pneumonia, pneumothorax, trauma, and
malignancy. A chest radiograph is also valuable in determining
the presence of cardiomegaly and pulmonary congestion. In
some situations, an echocardiogram may be used to evaluate
myocardial wall motion, valve abnormalities, and septal wall
defect. Although not diagnostic of AMI, an echocardiogram is
useful in determining the extent of damage to the myocardium.
Extensive myocardial damage puts the patient at risk for com-
plications such as heart failure and cardiogenic shock.
Patient Management
While obtaining the history and assessing the patient’s status,
the emergency nurse should convey a calm and reassuring
manner. Any patient with AMI or suspected AMI should have
low-flow oxygen (2 to 6 L/min) and the head of the bed
should be elevated. Maintain oxygen saturation greater than
95%. If oxygenation cannot be maintained or the patient is
acidotic, intubation and mechanical ventilation are indicated.
After oxygen therapy is initiated, establish IV access for
medications and fluid therapy. Insert at least two large-bore
(18-gauge) catheters and infuse normal saline as needed.
Ongoing assessment includes frequent determination of
blood pressure, continuous ECG monitoring, and continu-
ous pulse oximetry monitoring. Assessment of pain inten-
sity, location, radiation of pain, and applicable descriptors
establishes baseline. Assessment parameters should be re-
assessed after any intervention for chest pain. Nitroglycerin
is the initial drug of choice for treatment of chest pain re-
lated to angina pectoris and AMI. Nitroglycerin can be ad-
ministered sublingually in 0.3- or 0.4-mg tablets or in a
spray. One tablet or spray is administered every 5 minutes,
up to three doses. Nitroglycerin dilates coronary arteries,
reduces afterload by dilating peripheral venous circulation,
and reduces preload; that is, decreases venous return to the
heart. Nitroglycerin is not usually given unless systolic
blood pressure (SBP) is at least 100 mm Hg because of po-
tential decreased blood pressure that can occur. If sublin-
gual nitroglycerin is not effective, IV nitroglycerin (Tridil)
can be used. Initiate nitroglycerin infusion at 10 to 20
mcg/min and titrate in increments of 5 to 10 mcg/min up to
50 to 180 mcg/min.4,31
If nitroglycerin fails to relieve chest pain, the next drug of
choice is morphine sulfate. This narcotic analgesic relieves

Box 33-1 CRITERIA FOR SIGNIFICANT Box 33-2 LEAD PLACEMENT

ECG CHANGES FOR RIGHT VENTRICULAR
AND POSTERIOR LEADS
PROBABLE NEW TRANSMURAL AMI
1 mm ST segment elevation in two leads RIGHT VENTRICULAR LEADS
OR V3R  Between V1 and V4R
Abnormal Q waves in two leads V4R  Fifth intercostal space right midclavicular line
V5R  Fifth intercostal space right anterior axillary line
NEW STRAIN OR ISCHEMIA V6R  Fifth intercostal space right midaxillary line
1 mm ST segment depression in two leads
POSTERIOR LEADS
NEW ST OR T WAVE CHANGES OF ISCHEMIA OR STRAIN V7  Fifth intercostal space posterior axillary line
ST depression 1 mm and T wave inversions (can represent V8  Fifth intercostal space between V7 and V9
ischemia or strain) V9  Fifth intercostal space next to vertebral column

ECG, Electrocardiogram.

Posterior

V8R V8
V9R V9
V7R   V7
 
 

FIGURE 33-18 Right ventricular and posterior wall

V6R 
electrocardiogram lead placement. (Modified from Hearns
 V6
PA: Differentiating ischemia, injury, infarction: expanding the
12-lead electrocardiogram, Dimen Crit Care Nurs 13(4):176,
  1994.)
V5R V5
l
era

  
 
Lat

V4R  V1 V2
V4
V3
V3R

Anteroseptal

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474 CHAPTER 33 Cardiovascular Emergencies

MCl6 MCl1

 Midaxillary line  4th intercostal

at 5th intercostal space
space

Left arm

Left arm

G Anywhere
G Anywhere
 G

MCl6 MCl1

FIGURE 33-19Monitoring on three-lead electrocardiogram monitor. Leads MCl6 and MCl1 are the best leads for
monitoring dysrhythmias.

aVF
aVF

I I

I I

aVF aVF

Lead I

Lead aVF

Normal Right Left Northwest

Axis (0° - 90°) (90° - 180°) (0° -
90°) (
90° - 180°)

1 2 3 4 5

FIGURE 33-20 Determination of QRS axis. (1) Note predominant QRS polarity in leads I and aVF. (2) If QRS during
tachycardia is primarily positive in I and aVF, axis falls within normal quadrant from 0 degrees to 90 degrees. (3) If
complex is primarily negative in I and positive in aVF, right axis deviation is present. (4) If complex is
predominantly positive in I and negative in aVF, left axis deviation is present. (5) If QRS is primarily negative in
both I and aVF, markedly abnormal “northwest” axis is present that is diagnostic of ventricular tachycardia.
(Modified from Drew BJ: Bedside electrocardiographic monitoring, Heart Lung 20(6):610, 1991.)

chest pain and anxiety, which decreases myocardial oxygen
consumption.25 If SBP is greater than 100 mm Hg, adminis-
ter morphine 2 to 4 mg IV every 5 to 10 minutes until pain
is relieved. Monitor respiratory status and hemodynamic re-
sponse carefully after morphine administration.
After the patient is initially evaluated, aspirin should be
given orally (to be chewed) unless contraindicated (e.g., al-
lergy, active gastrointestinal [GI] bleeding). If the patient is
unable to tolerate oral aspirin, one rectal suppository can be
given. Recommended dosage ranges from 160 to 325 mg. If
the patient is “allergic” to aspirin, other antiplatelet agents
such as dipyridamol, ticlopidine, or clopidogrel can be con-
sidered.4,31
Primary Percutaneous Transluminal Coronary Angioplasty
Primary percutaneous transluminal coronary angioplasty
(PTCA) refers to use of angioplasty to reestablish blood flow
in the occluded coronary artery or arteries in the evolving

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
 CHAPTER 33
Table 33-11 CARDIAC MARKERS FOR ACUTE MYOCARDIAL INFARCTION
Initial elevation
Cardiac after acute
marker myocardial infarction
Myoglobin 1-4 hours
Troponin-I (cTn I) (cardiac specific) 3-12 hours
Troponin-T (cTn T) (cardiac specific) 3-12 hours
Creatine kinase-MB (CK-MB) 4-12 hours
CK-MB subforms: MB1 & MB2 1-6 hours
Lactate dehydrogenase (LDH) 8-12 hours
*LDH-1/LDH-2 ratio 0.76 is significantly associated
with acute myocardial infarction
AMI process and is considered potentially superior to fibri-
nolytic therapy.4,31 Current standards indicate that primary
angioplasty should be performed in tertiary care centers with
qualified clinicians. Targeted times from door to balloon
should be 90  30 minutes for patients with diagnosed AMI.
Thus early diagnosis and decision-making regarding optimal
treatment are necessary to facilitate primary PTCA.
Fibrinolytic Therapy
Fibrinolytic therapy for the patient with AMI is a crucial
component of overall therapy to reduce patient mortality and
morbidity. Patients benefit from therapy if the fibrinolytic
agent is initiated within 12 hours of onset of chest pain. The
goal of fibrinolytic therapy is to lyse coronary thrombi, re-
store blood flow to a hypoperfused myocardium, and abort
or prevent complete evolution of the infarction process.
When treatment begins within 3 hours of new symptoms,
the incidence of successful reperfusion is 60% to 70% for all
fibrinolytic agents.
Fibrinolytic therapy targets elements of the clotting
process to cause fibrinolysis, the process of clot degradation.
Lysis of the clot begins with activation of plasminogen, which
converts to plasmin. Plasmin degrades or breaks down fibrin
in the clot, circulating fibrinogen, factor V, and factor VIII.
Fibrinolytic agents are an exogenous source of plasminogen.
Refer to Table 33-12 for a comparison of fibrinolytic agents.31
Fibrinolytic agents have a significant potential for bleed-
ing complications. Absolute contraindications for fibri-
nolytic therapy include recent internal bleeding (less than 1
month before arrival), known bleeding diathesis, history of
cerebrovascular accident (CVA), recent surgery (e.g., in-
tracranial, intraspinal, intraocular), intracranial AV malfor-
mations, uncontrolled hypertension (SBP greater than 180
mm Hg, diastolic blood pressure [DBP] greater than 110
mm Hg), recent trauma (in the past 10 days), and CPR. Rel-
ative contraindications include minor trauma, diabetic
retinopathy, pregnancy, concurrent anticoagulation, severe
trauma (e.g., in the past 6 months), any previous central ner-
vous system event, and unsuccessful central venous punc-
ture. If the patient will receive streptokinase or anistreplase,
the patient should be screened for recent history of a strep-
tococcal infection (less than 6 months ago) or prior treat-
ment with streptokinase or anistreplase. Additional lab data
Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
Cardiovascular Emergencies 475
Time to return
Mean peak time to baseline
6-7 hours 18-24 hours
10-24 hours 3-7 days
12-48 hours 10-14 days
10-24 hours 48-72 hours
18 hours Unknown
24-48 hours 10-14 days
such as a complete blood cell count, prothrombin time, par-
tial thromboplastin time (PTT), fibrinogen, and platelet
count can assist with determining potential bleeding prob-
lems and serve as baseline data.
Additional nursing management for the patient receiving
fibrinolytic therapy focuses on assessing for potential com-
plications, monitoring for reperfusion, and minimizing tis-
sue trauma. The major complication for the patient receiving
fibrinolytic therapy is bleeding and hemorrhage. Bleeding
occurs most often at cut-down sites, arterial puncture sites,
and injection sites. Systemic bleeding, that is, GI, urinary,
vaginal, cerebral, or retroperitoneal, and neurologic impair-
ment (e.g., CVA) may also occur. Monitor for hypotension,
decreased hemoglobin and hematocrit, and tachycardia. The
other major complication that occurs is an allergic reaction,
particularly with use of streptokinase or anistreplase. Moni-
tor for respiratory distress, rash, or urticaria. Minimize tis-
sue trauma by keeping the patient on bed rest, limiting arte-
rial and venous punctures, and limiting use of noninvasive
blood pressure cuffs. Reperfusion cannot be absolutely de-
termined without benefit of cardiac angiography; however,
markers of reperfusion that can be assessed by the emer-
gency nurse include resolution of chest pain, normalizing of
ST changes, and occurrence of reperfusion dysrhythmias
such as accelerated idioventricular rhythms.
A heparin infusion is recommended in conjunction with
fibrinolytic therapy to prevent formation of a new clot and
reocclusion of the coronary vessel. The recommended dose
is 60 U/kg as a bolus at the same time as initiating fibri-
nolytic therapy. A maintenance infusion of 12 U/kg per
hour is titrated to maintain the patient’s PTT at 1.5 to 2
times the control levels. Heparin is also recommended for
patients who receive nonselective fibrinolytic agents (e.g.,
streptokinase, anistreplase); however, heparin should be
withheld 6 hours and activated PTT (aPTT) checked before
initiation of heparin to ensure aPTT is less than 2 times the
control.
Heparin is also indicated for use in patients with non-ST
elevation acute coronary syndromes. Options for heparin in-
clude IV heparin, subcutaneous unfractionated heparin
(7500 U twice daily), or low molecular weight heparin (e.g.,
enoxaparin [Lovenox], dalteparin [Fragmin]) at 1 mg/kg
twice daily.31
476 CHAPTER 33 Cardiovascular Emergencies

Table 33-12 COMPARISON OF FIBRINOLYTIC AGENTS

Agent Action
Streptokinase Exogenous plasminogen
(Steptase, Kabikinase) activator; not clot specific
Anistreplase Inactivated derivative of
(Eminase) thrombolytic enzyme syn-
thesized from streptoki-
nase and lysoplasminogen;
promotes thrombolysis af-
ter activation within the
body
Alteplase Proteolytic enzyme; direct
(Activase, activator of plasminogen;
Activase rt-PA) high degree of clot speci-
ficity
Reteplase Activates the conversion of
(Retavase) plasminogen to plasmin;
high degree of clot
specificity
TNK-tissue plasminogen Activates clot-bound
activator (TNKase) plasminogen to plasmin
Dose
IV: 1.5 million units IV over 1 hr
Intracoronary: 10,000 to 30,000
U; followed by maintenance in-
fusion of 2,000 to 4,000 U/min
until thrombolysis occurs (e.g.,
150,000 to 500,000 U total)
IV: 30 U over 2-5 min; dilute
only with 5 ml sterile water
IV: 15 mg IV bolus over 1-2 min;
then 50 mg over 30 min, then
35 mg over 60 min
IV: 10 U over 2 min; then repeat
10 U in 30 min after initiation
of first bolus
IV: 30-50 mg bolus over 5 sec
Dosing based on patient weight:
60 kg30 mg TNK
60 to 70 kg  35 mg TNK
70 to 80 kg  40 mg TNK
80 to 90 kg  45 mg TNK
90 mg  50 mg TNK
Comments
Half-life in plasma is 18 min; has a
prolonged effect on coagulaiton be-
cause of depletion of fibrinogen,
which persists for 18-24 hr; anti-
bodies to the drug may be present
in persons who have been exposed
to Streptococcus infection resulting
in: allergic reactions (e.g., rash,
fever, chills); patients should not be
retreated with streptokinase for a
period of 2 wk to 1 yr after initial
administration because of sec-
ondary resistance to development
of antibodies
Do not give to patients who are aller-
gic to streptokinase; may not be as
effective as usual when adminis-
tered more than 5 days after the
previous dose or after streptokinase
therapy or streptococcal infection;
discard if not used within 30 min of
mixing
Half-life in plasma is 5-7 min; may
cause sudden hypotension; inline
IV filters can remove as much as
47% of the drug
Give normal saline fluid before and
after administraiton of Reteplase
(Retevase)
Reconstitute just before administra-
tion and use within 4 hr after re-
constituting
More fibrin specificity and less inci-
dence of bleeding than rt-PA

IV, Intravenous; rt-PA, recombinant prurokinase.

Additional Pharmacologic Therapy
Nitroglycerin IV infusions are recommended for the first 24
to 48 hours after AMI, especially anterior AMI. Nitroglyc-
erin dilates coronary arteries, increases collateral blood
flow, and decreases preload and afterload. Recent studies
recommend additional pharmacologic agents to provide
further protection for the AMI patient from mortality and
morbidity. -Blocker therapy should be initiated within 12
hours after AMI or for non-ST elevation acute coronary
syndromes if there are no absolute contraindications, such
as severe left ventricular failure and pulmonary edema,
bradycardia (heart rate less than 60 bpm), hypotension
(SBP lower than 100 mm), signs of poor peripheral perfu-
sion, and second or third degree heart block. -Blockers
have proven especially useful in AMI patients with recur-
rent symptoms of ischemia, hypertension, sinus tachycar-
dia, and in patients younger than 65 years of age. Addi-
tional therapy that may be initiated in the ED includes
angiotensin-converting enzyme (ACE) inhibitor agents for
those patients with AMI (e.g., enalapril, captopril, lisino-
pril). These agents should be started within 24 hours of
AMI. Use of ACE inhibitors has been associated with re-
duced mortality. Known contraindications to ACE inhibitor
therapy include allergies, Killip class III and IV (classifica-
tion system for cardiac severity), history of renal failure, or
bilateral renal artery stenosis.4,31

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.

Table 33-13 OVERVIEW OF GLYCOPROTEIN IIB/IIIA INHIBITORS
Glycoprotein IIB/IIIA
inhibitor Dosage
Abciximab (ReoPro) 0.25 mg/kg over 10-60 min
0.125mg/kg/min for 12 hr
Eptifibatide (Integrilin) 180 mcg/kg over 1 to 2 min
2 mcg/kg/min for up to 72 hr
Tirofiban HCL (Aggrastat) 0.4 mcg/kg/min for 30 min
0.1 mcg/kg/min for 12-24 hr
Another aspect of management of non-ST elevation acute
coronary syndromes is the use of glycoprotein IIB/IIIA in-
hibitors. Platelet adhesion, activation, and aggregation play
major roles in development of thrombus, which can potenti-
ate evolution of these acute coronary syndromes into an
AMI. Glycoprotein IIB/IIIA inhibitors antagonize or inhibit
the receptor sites, which inhibits platelet aggregation. It has
been demonstrated that these reduce risk for development of
thrombus independent of aspirin and heparin therapies. Re-
fer to Table 33-13 for an overview of these agents.4,17,22,31,34
Dysrhythmias
Blood flow deprivation to the myocardium as a result of
AMI can affect the heart’s electrical conduction system,
causing various dysrhythmias. Table 33-14 summarizes dys-
rhythmias and categories of antidysrhythmics according to
modified Vaughan-Williams classification schema. By un-
derstanding drug classifications, the emergency nurse can
anticipate expected action of the drug and nursing implica-
tions for drug administration and patient assessment.17,22,34
PVCs are the most common dysrhythmia associated with
cardiac ischemia and AMI, occurring in approximately 85%
of patients with AMI. After initiation of oxygen therapy, li-
docaine is the drug of choice for symptomatic PVCs. Lido-
caine may be used prophylactically for AMI patients, even
without PVCs, because of the high incidence of ventricular
tachycardia and ventricular fibrillation that occurs without
warning dysrhythmias. Some studies suggest that prophy-
lactic use of lidocaine in patients with AMI may increase
mortality; therefore, lidocaine use must be considered with
respect to potential adverse effects. PVCs may also be
caused by hypoxemia, acidosis, alkalosis, electrolyte imbal-
ances, digoxin toxicity, and bradycardia.6 The underlying
mechanism responsible for the patient’s PVCs should be
evaluated and treated.
Bradycardia is defined as a heart rate less than 60 beats
per minute and occurs in approximately 65% of AMI pa-
tients, particularly those with inferior wall infarction.
Bradycardic dysrhythmias include AV blocks. Four different
types occur, depending on area and degree of damage to the
conduction system. These AV blocks are referred to as first-
degree, second-degree Mobitz I (Wenckebach), second-de-
gree Mobitz II, and third-degree or complete heart block.
Blocks in conduction may be caused by myocardial infarc-
Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
CHAPTER 33 Cardiovascular Emergencies 477
Potential side effects
Potential for increased bleeding, hypotension, bradycardia, nausea and
vomiting, diarrhea
Potential for increased bleeding, hypotension
Potential for increased bleeding, nausea, bradycardia
Box 33-3 SYSTEMATIC EVALUATION
OF CARDIAC RHYTHMS
RATE
Bradycardia: 60 beats/min
Normal rate: 60 to 100 beats/min
Tachycardia: 100 beats/min
RHYTHM
Is the rhythm regular or irregular?
P WAVES
Are P waves present? Does one P wave appear before each
QRS? Is P wave deflection normal?
QRS COMPLEX
Normal is 0.06 to 0.12 second. Are the QRS complexes nor-
mal shape and configuration?
P/QRS RELATIONSHIP
Does QRS complex follow every P wave?
PR INTERVAL
Normal is 0.12 to 0.2 second. Is the interval prolonged?
Shortened?
tion, infection, degenerative changes in the conduction sys-
tem, rheumatic heart disease, and medications such as beta
blockers, calcium channel blockers, and cardiac glycosides.
Management of symptomatic bradycardias and heart blocks
includes drugs such as atropine and epinephrine. An exter-
nal pacemaker or transvenous pacemaker may also be used.
Second-degree Mobitz I heart block, associated with a con-
duction defect through the AV node, is usually benign and
transient. This rhythm is commonly associated with inferior
infarction because the right coronary artery supplies this
area and the AV node. Second-degree Mobitz II AV block
occurs when conduction through the bundle branches is im-
paired, usually because of blockage of the left coronary
artery, which supplies the anterior wall and bundle
branches.6 This form of second-degree block is more likely
than the other form to progress to third-degree block.
Other dysrhythmias that commonly occur are supra-
ventricular tachycardias, which may be indicative of