C H A P T E R 33
CARDIOVASCULAR
Cardiovascular emergencies affect the heart and great ves-
sels. The event may be subtle or obvious, caused by pro-
gressive disease development or a sudden traumatic event.
Emergencies secondary to trauma are described in Chapter
23. Cardiovascular emergencies in children are discussed in
Chapter 48. This chapter describes cardiovascular emergen-
cies caused by progressive disease development or a sudden
nontraumatic cardiac event.
CARDIAC ANATOMY AND PHYSIOLOGY
The heart is a four-chambered, muscular structure with
valves between each chamber to prevent back flow with
pumping action of the heart (Figure 33-1). The heart works
in synchrony as a two-pump system. Deoxygenated blood
from the venous system enters the right atrium through the
inferior and superior vena cavae. Blood is pumped from the
right ventricle into the pulmonary vasculature. After oxy-
genation, blood returns to the left atrium via the pulmonary
veins. The left ventricle then pumps blood to the body via
the arterial system. Figure 33-2 illustrates blood flow
through the heart. The left side of the heart is the stronger
side, with the ability to pump 4 to 8 L of blood per minute.
Oxygenation of the heart muscle is provided by blood from
the right and left coronary arteries. Arteries arise from the
right and left sinuses of Valsalva of the aortic valve. Coro-
nary arteries lie on the surface of the heart and fill during
ventricular diastole.21
450
Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
EMERGENCIES
Susan Barnason
The heart is surrounded by a fibrous, fluid-filled sac
called the pericardium. Pericardial fluid lubricates the heart
and prevents friction with contraction. The heart is divided
into three distinct layers, the epicardium, myocardium, and
endocardium. Epicardium serves as the visceral surface of
the pericardium. Myocardium, the thickest portion of the
heart, is composed of concentric rings of muscle fibers.
Contraction of concentric rings facilitates blood flow up and
out of the ventricles. The endocardial layer is a smooth tis-
sue that is the inner layer of the atria and ventricles. Endo-
cardium also functions as the surface of the heart valves.
One of the unique characteristics of cardiac tissue is au-
tomaticity or intrinsic ability to initiate electrical activity.
Figure 33-3 shows the heart’s electrical conduction system.
The sinoatrial (SA) node has the highest rate of automatic-
ity, spontaneously depolarizing 60 to 100 times per minute.
Impulses generated by the SA node are carried to the atrio-
ventricular (AV) node by intraatrial tracts; that is, Bachmann,
Bundle, Wenckebach’s, and Thorel’s tracts. Electrical stim-
ulation of heart muscle at the level of the atria causes the
mechanical event of atrial contraction. At the AV node,
slight delay in impulse transmission allows completion of
atrial contraction before ventricular stimulation. From the
AV node, the electrical impulse is carried to the ventricles
by the right and left bundle branches of the His bundle.
Bundles terminate with Purkinje fibers, which deliver the
impulse to the ventricular muscle, causing ventricular con-
traction.27
 CHAPTER 33 Cardiovascular Emergencies 451

Pulmonic valve

Aorta
Aortic valve Pulmonary artery

Superior vena cava Left atrium

Pulmonary veins

Mitral valve

Papillary muscle
Right atrium
Left ventricle

Triscuspid valve

Inferior vena cava

Interventricular septum
Right ventricle

FIGURE 33-1Anatomy of the heart. (From Lounsberry P, Frye SJ: Cardiac rhythm disorders: a nursing process
approach, ed 2, St. Louis, 1992, Mosby.)

Aorta

Pulmonary artery

Superior vena
cava

Pulmonary valve Pulmonary veins

Right atrium Left atrium

Coronary sinus Mitral valve

Tricuspid valve
Left ventricle

Inferior vena cava

Right ventricle
Aortic valve

FIGURE 33-2 Circulation of blood through the heart. Arrows indicate direction of flow. (From Atkinson LJ, Fortunato
NM: Berry & Kohn’s operating room technique, ed 8, St. Louis, 1996, Mosby.)

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

SA node

AV node

Common bundle

Right bundle branches

Left bundle branches

FIGURE 33-3 Conduction system of the heart. (From Davis JH, Drucker WR et al: Clinical surgery, vol 1, St. Louis,
1987, Mosby.)

Ao
Ao
PA PA
A LA

A LA B

RA RA
LV
LV
RV
RV

FIGURE 33-4 Blood flow during (A) systole, and (B) diastole. (From Canobbio MM: Mosby’s clinical nursing series,
cardiovascular disorders, vol 1, St. Louis, 1990, Mosby.)

Mechanical events of the cardiac cycle are called diastole
and systole. Approximately 60% of the cardiac cycle is di-
astole, the time when the ventricles are filling. Diastole is
also the time when aortic and pulmonic valves close. Mitral
and tricuspid valves open during this time. Electrically, this
corresponds to electrical stimulation and mechanical con-
traction of the atria. With atrial contraction and opening of
AV valves, pressure in the atria is higher than pressure in the
ventricles.9 Therefore blood flows from an area of greater
pressure to an area of lesser pressure (Figure 33-4). The sys-
tolic phase of the cardiac cycle corresponds with ventricular
contraction and opening of pulmonic and aortic valves. Dur-
ing contraction, AV valves close and chordae tendineae con-
tract to prevent regurgitation. Figure 33-5 depicts the rela-
tionship between electrical and mechanical components of
the cardiac cycle.
Pressures within the cardiovascular system affect cardiac
output because of the effect on preload and afterload. After-

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.

AV node
Atrium H B P
S conduction system is superimposed on the surface ECG. SN,
I B
N S
P T
QRS
NORMAL
PRELOAD
Left
12 ventricular
filling pressure
Pulmonary
7 wedge
pressure
15 Pleural
pressure
FIGURE 33-6 The effects of normal pleural pressure on cardiac filling pressure. (From Davis JH, Drucker WR et al:
Clinical surgery, vol 1, St. Louis, 1987, Mosby.)
load refers to pressure in the arterial system, which opposes
blood flow from the left ventricle. Preload refers to blood
volume coming into the right side of the heart.21 Figure 33-6
illustrates the effect of these pressures on cardiac filling.
Cardiac activity is regulated by branches of the auto-
nomic nervous system. Specific effects of each branch are
described in Table 33-1. Receptors in the heart and great
vessels respond to signals from the sympathetic nervous sys-
tem (Table 33-2). Stimulation affects heart rate, contractil-
ity, automaticity, conduction, and vascular smooth muscle.
These receptors prepare the body to fight or flee perceived
threats, including loss of blood volume.
SPECIFIC CARDIOVASCULAR EMERGENCIES
Specific emergencies discussed are cardiac arrest, acute
coronary syndromes, dysrhythmias, heart failure, acute peri-
carditis, abdominal aortic aneurysm, and hypertensive crisis.
Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
CHAPTER 33 Cardiovascular Emergencies 453
FIGURE 33-5 Schematic drawing of cardiac activation related to the
surface ECG. The timing of activation of the components of the
Sinus node; HIS, common bundle of HIS; BB, bundle branches;
P, Purkinje network; ECG, electrocardiogram. (From Lounsberry
P, Frye SJ: Cardiac rhythm disorders; a nursing process
approach, ed 2, St. Louis, 1992, Mosby.)
AFTERLOAD
Arterial pressure 120
Systolic
left ventricular 120
pressure
Transventricular 125
pressure
Cardiac Arrest
Sudden cardiac arrest can be defined as nontraumatic death
resulting from cardiac causes that occurs within 1 hour of
onset of acute symptoms.16,36 More than 600 people experi-
ence sudden cardiac death daily, or an annual rate of ap-
proximately 365,000, which represents more than 50% of all
cardiovascular deaths.3,16 Common causes of sudden cardiac
arrest are ventricular tachycardia (VT) and ventricular fibril-
lation (VF). These lethal dysrhythmias are usually a late
complication of myocardial infarction, but they may also
be associated with aneurysm rupture, cardiomyopathies,
rheumatic heart disease, mitral valve prolapse, and cardiac
surgery. Sudden cardiac arrest can also be associated with
other conditions or events. Table 33-3 presents etiologic fac-
tors associated with other causes of cardiopulmonary arrest.
In patients ages 18 to 35 years, approximately 23% of sud-
den cardiac deaths are related to coronary artery disease.23
454 CHAPTER 33 Cardiovascular Emergencies

Table 33-1 PARASYMPATHETIC AND Table 33-2 SYMPATHETIC NERVOUS

SYMPATHETIC STIMULATION SYSTEM RECEPTORS
OF THE HEART Sympathetic Clinical
Nerve Cardiac Clinical receptor Location response
activation effect manifestations  Vascular smooth muscle Vasoconstriction
Parasympathetic Slows SA node dis- Symptomatic -1 Myocardium Increased heart
charge bradycardia rate, contraction,
Slows AV node Transient heart automaticity,
conduction and block and conduction
increases refrac- -2 Peripheral vasculature Vasodilation of
toriness and lungs peripheral vas-
Sympathetic Heart rate increases Tachycardia culature and
Enhances AV node Hypertension bronchodilation
function Dopaminergic Renal, mesenteric, Vasodilation
Shortens His-Purkinje Increased cardiac cerebral, and coronary
and ventricular output arteries
muscle refrac-
toriness
Increased ventricular
contraction uations, for example, reducing rescuer fatigue in prolonged
Increased peripheral resuscitation efforts. The most common mechanical com-
vascular resistance pression device is the compressed gas-powered plunger
mounted on a backboard. During use of such devices, re-
SA, Sinoatrial; AV, artrioventricular.
member to place the plunger in the correct location over the
sternum to provide maximum cardiac output and minimize
adverse events, for example, fractured ribs. Another me-
Another condition associated with death among young adults chanical device reported in the literature is a cardiopul-
is hypertrophic cardiomyopathy, which causes left ventricular monary resuscitation (CPR) vest; however, use of this de-
outflow obstruction or myocardial ischemia secondary to vice is still considered investigational.4,10
small intramural vessels, and may potentiate lethal dysrhyth- Open thoracotomy and cardiac massage may be required
mias. Other etiologic factors associated with sudden cardiac in cases of penetrating wounds to the heart, penetrating ab-
arrest6 in the young include congenital coronary artery anom- dominal trauma with deterioration and arrest, pericardial
alies, myocarditis, idiopathic concentric left ventricular hy- tamponade, tension pneumothorax, or crushing chest in-
pertrophy, Marfan’s syndrome, mitral valve prolapse, aortic juries. This technique may also be used for patients with
stenosis, idiopathic long QT syndrome, and miscellaneous chronic lung disease who have a barrel chest when other
causes (e.g., Wolff-Parkinson-White syndrome, high-risk be- more conservative measures for chest compression have
haviors inclusive of alcohol and drug use—cocaine, tricyclic failed. Studies have demonstrated that direct cardiac chest
agents, heroin, anabolic steroids). massage provides better hemodynamics than closed chest
Among people 30 years of age and older, an estimated compressions; however, this procedure must be performed
20% to 30% of sudden cardiac deaths are secondary to acute within 15 minutes of arrest to be effective.
myocardial infarction causing pump failure.16 Immediate in-
terventions include establishing an airway, supporting oxy- Defibrillation
genation, and providing circulation with chest compres- Advanced cardiac life support measures implemented in the
sions. Airway management and oxygenation are discussed emergency department (ED) augment basic life support
in greater detail in Chapter 32. Circulation for the pulseless measures with administration of drugs, fluids, and defibril-
patient is produced with chest compressions. Properly per- lation. Restoring normal circulation for the patient who has
formed chest compressions can produce 30% of the patient’s experienced sudden cardiac arrest or cardiopulmonary arrest
normal cardiac output, which is enough blood flow through requires vigilance to restore or stabilize cardiac rhythm. If
the heart and brain to sustain tissue viability for a short time. the patient has VF or pulseless VT, the intervention of
Cerebral blood flow must be at least 50% of normal volume choice is immediate defibrillation. For defibrillation to be ef-
to maintain consciousness.6 fective, an electric current sufficient to depolarize a critical
Chest compressions are best accomplished with the vic- portion of the left ventricle must pass through the heart.
tim on a firm surface to allow even compression of the tho- When treating VF and pulseless VT in adults, up to three
racic cavity. Compressions should be forceful enough to countershocks should be rapidly delivered, the first at 200
generate a carotid or femoral pulse. Mechanical chest com- joule (J), the second at 200 to 300 J, and the third at 360 J.
pression devices should be an adjunct to manual chest com- Check the pulse and ECG rhythm between shocks to deter-
pressions and used only by trained personnel in limited sit- mine if defibrillation has been effective.

Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.