Digiulio M., Keogh J. Medical-Surgical Nursing Demystified
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ABOUT THE AUTHORS
Mary DiGiulio is an Adult Nurse Practitioner on the faculty in the School of Nursing at
UMDNJ in Newark, NJ and in practice in Teaneck, NJ. She has taught nursing at the
graduate, baccalaureate and pre-licensure levels and presented for RN and PN review
courses and nurse refresher courses.
Donna Jackson is an Adult Nurse Practitioner currently in practice in Teaneck, NJ. She
is on the Advisory Board of the nursing program at Saint Peter’s College in Jersey City,
NJ. She has taught nursing courses at the graduate, baccalaureate and pre-licensure levels.
Jim Keogh is on the faculty of Saint Peter’s College in Jersey City and New York
University. He is the author of more than 70 books including Pharmacology Demystified,
Microbiology Demystified, Nurse Management Demystified, Medical Billing and Coding
Demystified, and Charting Demystified.
ACKNOWLEDGMENTS
Mary, Donna, and Jim are indebted to the dedication and work of Judy Bass, Maureen B.
Walker, Pamela A. Pelton, Joanna V. Pomeranz, Nancy W. Dimitry, Gabriella Kadar, Don
Pomeranz, and Don Dimitry who made this book possible.Ihanks to my nephew Tim
Boutelle, a student at the University of Chicago. He spent many hours helping me proof-
read the manuscript, and he offered insights and suggestions from the point of view of
the intended audience.
Copyright © 2007 by The McGraw-Hill Companies, Inc. Click here for terms of use.
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CHAPTER 1
Cardiovascular System
aorta ascendens
v. cava superior
a. coronaria dextra
a. pulmonalis
a. coronaria sinistra
v. cordis magna
Superior Vena Cava
Arch of the Aorta
Right Atrium
Inferior Vena Cava
Tricuspid Valve
Right Ventricle
Ventricular Septum
Pulmonary Trunk
Left Atrium
Pulmonary Vein
Mitral Valve
Papillary Muscle
Left Ventricle
Copyright © 2007 by The McGraw-Hill Companies, Inc. Click here for terms of use.
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Medical-Surgical Nursing Demystified
Learning Objectives
Key Terms
Aneurysm
Angina
Aortic valve
Atherosclerosis
Atria
Atrioventricular (AV) valves
Cholesterol
Diastolic
Embolism
Infarction
Ischemia
Mitral valve
Necrosis
Occlusion
Pericardium
Pulmonic valve
Septal wall
Stenosis
Systolic
Tamponade
Tricuspid valve
Ventricle
Aortic aneurysm
Angina (Angina pectoris)
Myocardial infarction (MI)
Coronary artery disease
(CAD)
Peripheral arterial disease
(PAD)
Cardiac tamponade
Cardiogenic shock
Cardiomyopathy
Endocarditis
Heart failure [Congestive heart
failure (CHF)]
Hypertension (HTN)
Hypovolemic shock
Myocarditis
Pericarditis
Pulmonary edema
Raynaud’s disease
Rheumatic heart disease
Thrombophlebitis
Atrial fibrillation
Asystole
Ventricular fibrillation
Ventricular tachycardia
Aortic insufficiency (AI)
Mitral insufficiency
Mitral stenosis
Mitral valve prolapse (MVP)
Tricuspid insufficiency
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CHAPTER 1 Cardiovascular System
How the Cardiovascular System Works
The cardiovascular system is responsible for delivery of blood, which carries oxy-
gen and other nutrients, to the tissues of the body. The heart pumps the blood to
the body where it delivers nutrients and oxygen, picks up waste products, and then
returns to the heart.
The heart has four chambers. The upper chambers are the atria; the lower cham-
bers are the ventricles. In the middle, there is a septum, a wall that separates the
right side of the heart from the left side of the heart. Atrioventricular (AV) valves
control the blood flow between the upper and lower chambers of the heart. The tri-
cuspid valve is on the right side, while the mitral valve is on the left side between
the atria and the ventricle. The pulmonic valve controls the flow between the right
ventricle and the pulmonary artery, while the aortic valve controls the flow between
the left ventricle and the aorta.
Unoxygenated blood empties into the right atrium from the systemic circulation
via the inferior vena cava and superior vena cava. As the right atrium contracts, the
tricuspid valve opens, allowing the blood to flow into the right ventricle. With con-
traction of the right ventricle, the pulmonic valve opens, allowing the unoxygenated
blood to enter the pulmonary artery to go to the lungs to pick up oxygen. Once
oxygenated, the blood returns to the heart via the pulmonary vein and enters the
left atrium. As the left atrium contracts, the mitral valve opens, allowing the blood
to flow into the left ventricle. As the left ventricle contracts, the aortic valve opens,
allowing the blood to flow into the aorta and systemic circulation. The blood will
return to the heart from the lower body via the inferior vena cava and from the
upper body via the super vena cava. The actions on the right side and left side of
the heart happen simultaneously. So when we listen to a normal heartbeat, the
sounds we hear are the sounds of the valves closing. The mitral and tricuspid valves
create the first heart sound (S1), while aortic and pulmonic valves create the sec-
ond heart sound (S2).
The electrical conduction system of the heart starts at the sino-atrial (SA) node,
which is located in the right atrium. It initiates the heart beat, ranging between 60
to 100 beats per minute, every day, for a lifetime. The electrical current travels
across both atria, then converges on the atrio-ventricular (AV) node, where the cur-
rent slows, allowing the atria to repolarize. The AV node is located in the superior
portion of the ventricular septum. In the bottom portion are located the right and left
Bundle of His, which is a group of special cardiac muscles that sends an electrical
impulse to the ventricle to begin cardiac contractions. These end in the Purkinje
fibers and spread out through the ventricles. The current passing through these
fibers causes ventricular contraction, forcing the blood from the right ventricle to
the lungs and from the left ventricle to the aorta, and thus, the systemic circulation.
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Medical-Surgical Nursing Demystified
Just the Facts
Aortic Aneurysm
WHAT WENT WRONG?
A weakening in the wall of a portion of the aorta results in a balloon-like bulge as
blood flows through the aorta. The blood flow within this bulging area of the aorta
becomes very turbulent. Over time this turbulence can cause the dilated area to
increase in size, creating an aneurysm. The aneurysm can rupture causing a dis-
ruption in blood flow to everything below the affected area, and may even result
in death.
This is commonly due to atherosclerosis where fatty substances, cholesterol,
calcium and the clotting material fibrin, referred to as plaque, build up in the inner
lining of an artery resulting in thickening and hardening of the arteries. It may also
be caused by degeneration of the smooth muscle layer (middle) of the aorta,
trauma, congenital defect, or infection. The aneurysm may be found incidentally
on radiographic studies done for other reasons, or the patient may have developed
symptoms indicating that something was wrong, such as severe back or abdomi-
nal pain, or a pulsating mass. Severe hypotension and syncope (fainting caused by
insufficient blood supply to the brain) may indicate rupture.
PROGNOSIS
Outcome will vary depending on size and location of aneurysm. Some patients
have aneurysms for months before a diagnosis is made, because they are asymp-
tomatic. Treatment decisions will depend on the size and location of the aneurysm.
Some patients with an aneurysm will have watchful waiting with periodic imag-
ing to monitor the size of the aneurysm while other patients may need emergent
surgery.
HALLMARK SIGNS AND SYMPTOMS
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Asymptomatic
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Abdominal pain
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Back pain that may radiate to posterior legs
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Abdominal pulsation
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CHAPTER 1 Cardiovascular System
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Diminished femoral pulses
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Anxiety
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Restlessness
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Decreased pulse pressure
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Increased thready pulse
INTERPRETING TEST RESULTS
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An aneurysm will be displayed in a chest x-ray, abdominal ultrasound, CT
scan, or MRI.
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Swishing sound over the abdominal aorta or iliac or femoral arteries because
the natural flow of blood is disturbed (bruit).
TREATMENT
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Surgery to resect the aortic aneurysm by removing the section containing the
aneurysm and replacing it with a graft.
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Administer antihypertensives, reducing the force of the pressure within the
aorta to decrease the likelihood of rupture.
•
Administer analgestics to treat patients who may be having pain from pres-
sure on nearby structures (nerves, etc.) or tearing of the vessel.
•
Administer oxycodone, morphine sulfate as needed to decrease oxygen
demand.
NURSING DIAGNOSES
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Ineffective peripheral tissue perfusion
•
Risk for deficient fluid volume
•
Acute pain
•
Anxiety
NURSING INTERVENTION
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Monitor vital signs—look for changes in blood pressure or elevated pulse
and respiratory rates. During aortic dissection the blood pressure (BP) may
initially increase due to severity of pain. It may then become difficult to
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Medical-Surgical Nursing Demystified
impossible to obtain both the BP and pulse in one or both arms because of
blood flow disruption to the arm(s). The patient may go into shock quickly
if the aneurysm ruptures.
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Monitor cardiovascular system by checking heart sounds, peripheral pulses
(upper and lower extremities), and checking for abdominal bruits, swishing
sounds heard over the blood vessel when flow is disturbed.
•
Measure intake and output.
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Hypovolemia is suspected if there is a low urine output and high specific
gravity of urine.
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Palpate abdomen for distention or pulsatile mass.
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Abdominal distention, which is an enlarged abdomen, may signify imminent
rupture of the aneurysm.
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Check for signs of severe decrease in blood or fluid (hypovolemic shock).
The BP decreases as less blood circulates. Pulse rate increases as the heart
tries to pump the blood faster to meet the oxygen demands of the body.
Respiratory rate increases to meet oxygen needs while peripheral pulse sites
are harder to find as BP lowers. The further away the pulse is from the heart,
the more difficult it will be to find; it will be harder to locate the dorsalis
pedis and posterior tibialis pulses earlier than the radial pulses.
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Pale, clammy skin will be present as circulation decreases.
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Severe back pain due to rupture or dissection.
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Anxiety due to uncertainty of what is happening.
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Restlessness due to anxiety, discomfort, and decreased oxygenation.
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Decreased pulse pressure due to less circulating volume, increased heart rate,
and less filling time between heartbeats.
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Increased thready pulse.
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Limit patient’s activity to a prescribed exercise and rest regimen.
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Be alert for decreased peripheral circulation.
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Numbness.
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Tingling.
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Decrease in temperature of extremities.
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Change in skin color in extremities.
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Absence of peripheral pulses.
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Reduce patient anxiety.
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Maintain a quiet place.
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Have the patient express his or her feelings.
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CHAPTER 1 Cardiovascular System
Angina (Angina Pectoris)
WHAT WENT WRONG?
A narrowing of blood vessels to the coronary artery, secondary to arteriosclerosis,
results in inadequate blood flow through blood vessels of the heart muscle, caus-
ing chest pain. An episode of angina is typically precipitated by physical activity,
excitement, or emotional stress. There are three categories of angina.
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Stable angina—pain is relieved by rest or nitrates and symptoms are con-
sistent.
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Unstable angina—pain occurs at rest; is of new onset; is of increasing inten-
sity, force, or duration; isn't relieved by rest; and is slow to subside in response
to nitroglycerin.
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Prinzmetal’s or vasospastic angina—usually occurs at rest or with minimal
formal exercise or exertion; often occurs at night.
Atherosclerotic heart disease occurs when there is a buildup of plaque within
the coronary arteries. Angina is often the first symptom that heart disease exists.
When the demand for oxygen by the heart muscle exceeds the available supply,
chest pain occurs.
PROGNOSIS
Patients can often be managed with lifestyle modifications and medications to
control symptoms of angina. The most important factor is patient education.
Patients need to understand the importance of their symptoms and when to seek
medical attention. The pain must be evaluated initially and whenever a change in
pattern or lack of response to treatment occurs.
HALLMARK SIGNS AND SYMPTOMS
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Chest pain lasting 3 to 5 minutes—not all patients get substernal pain; it may
be described as pressure, heaviness, squeezing, or tightness. Use the patient’s
words.
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Can occur at rest or after exertion, excitement, or exposure to cold—due to
increased oxygen demands or vasospasm.
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Usually relieved by rest—a chance to re-establish oxygen needs.
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Medical-Surgical Nursing Demystified
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Pain may radiate to other parts of the body such as the jaw, back, or arms—
angina pain is not always felt in the chest. Ask if the patient has had similar
pain in the past.
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Sweating (diaphoresis)—increased work of body to meet basic physiologic
needs; anxiety.
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Tachycardia—heart pumping faster trying to meet oxygen needs as anxiety
increases.
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Difficulty breathing, shortness of breath (dyspnea)—increased heart rate
increases respiratory rate and increases oxygenation.
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Anxiety—not getting enough oxygen to heart muscle, the patient becomes
nervous.
INTERPRETING TEST RESULTS
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Electrocardiogram during episode:
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T-wave inverted with initial ischemia, which is reduced blood flow due to
an obstructed vessel, usually first sign.
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ST-segment changes occur with injury to the myocardium (heart muscle).
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Abnormal Q-waves due to infarction of myocardium.
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Labs: troponins, CK-MB, which is an enzyme released by damaged cardiac
tissue 2 to 6 hours following an infarction, electrolytes.
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Chest x-ray to determine signs of heart failure.
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Holter monitoring: a portable EKG which the patient wears for 24 to 48 hours,
giving that many hours of continuous cardiac monitoring.
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Coronary arteriography to determine plaque build-up in coronary arteries.
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Cardiac PET (positron emission tomography) to determine plaque build-up
in coronary arteries.
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Stress testing to determine symptoms when at exercise or under pharmaco-
logic stress.
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Echocardiogram or stress-echo to determine any abnormality of wall motion
due to ischemia.
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Cardiology consult.
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Nonemergent labs: Complete Blood Count (CBC) used to determine the
general health status of the patient, chemistry (provides information about
the status of eletrolytes, kidneys, acid/base balance, blood sugar and calcium
levels), Prothrombin Time (PT/INR), Activated Partial Throboplastin Time