1. Nelia B. Perez RN, MSN
PCU – MJCN
NCM 103

5.  Chest pain or pressure
 Shortness of breath
 Edema and weight gain
 Palpitations
 Fatigue
 Dizziness or loss of consciousness

7.  S1 and S2
 S3 and S4
 Gallop sounds
 Snaps and clicks
 Murmurs
 Friction Rub

8.  Cardiac Enzyme Analysis
 Blood Chemistry
 Lipid profile
 Cholesterol levels
 Serum electrolyte
 Blood urea nitrogen
 Serum glucose
 Coagulation Studies
 Hematologic Studies

9.  Chest radiography and fluoroscopy
 Electrocardiography
 Cardiac stress testing
 Echocardiography
 Radionuclide Imaging
 Cardiac Catheterization
 Angiography
 Electrophysiologic testing

11.  Central Venous Pressure
 Pulmonary Artery Pressure
 Intra-arterial BP monitoring

15.  Ischaracterized by the accumulation
of plaque within coronary
arteries, which progressively
enlarge, thicken and calcify.
 This causes critical narrowing of the
coronary artery lumen (75%
occlusion), resulting in a decrease in
coronary blood flow and an
inadequate supply of oxygen to the
heart muscle.

17. Ischemia may be silent
(asymptomatic but evidenced by
ST depression of 1 mm or more
on electrocardiogram (ECG) or
may be manifested by angina
pectoris (chest pain).

18. Risk factor for Coronary Artery
Disease include
dyslipidemia, smoking, hypertensio
n, male gender (women are
protected until
menopause), aging, non-white
race, family
history, obesity, sedimentary
lifestyle, diabetes
mellitus, metabolic
syndrome, elevated

19. Acute coronary syndrome is a
complication of CAD due to lack
of oxygen to the myocardium.
Mnaifestations include unstable
angina, non ST-segment
elevation infarction, and ST-
segment elevation infarction.

20. Other causes of angina include
coronary artery spasm, aortic
stenosis, cardiomyopathy, severe
anemia, and thyrotoxicosis.

21.  Chest pain is provoked by exertion
or stress and is relieved by
nitroglycerin and rest.
 Character. Substernal chest
pain, pressure, heaviness, or
discomfort. Other sensations include
a
squeezing, aching, burning, choking,
strangling, or cramping pain.

23.  Severity.Pain maybe mild or severe and
typically present with a gradual buildup
of discomfort and subsequent gradual
fading away.
 Location.Behind middle or upper third of
sternum; the patient will generally will
make a fist over the site of pain (positive
Levine sign; indicates diffuse deep
visceral pain), rather than point to it with
fingers.

24.  Radiation. Usually radiates to
neck, jaw, shoulders, arms, hands, and
posterior intrascapular area. Pain occurs
more commonly on the left side than the
right; may produce numbness or weakness
in arms, wrist, or hands.
 Duration. Usually last 2 to 10 minutes
after stopping activity; nitroglycerin
relieves pain within 1 minute.

25.  Precipitating factors. Physical
activity, exposure to hot or cold
weather, eating a heavy meal, and sexual
intercourse increase the workload of the
heart and, therefore, increase oxygen
demand.
 Associated manifestation.
Diaphoresis, nausea, indigestion, dyspnea,
tachycardia, and increase in blood
pressure.

26.  Resting ECG may show left ventricular
hypertrophy, ST-T changes, arrhythmias, and
possible Q waves.
 Exercise stress testing with or without
perfusion studies shows ischemia.
 Fasting blood levels of cholesterol, low
density lipoprotein, high density
lipoprotein, lipoprotein A, homocysteine, and
triglycerides may be abnormal.
 Coagulation studies, hemoglobin
level, fasting blood sugar as baseline studies.

27.  Cardiac catheterization shows
blocked vessels.
 Position emission tomography may
show small perfusion defects.
 Radionuclide ventriculography shows
wall motion abnormalities and
ejection fraction.

28.  Fasting blood levels of
cholesterol, low density
lipoprotein, high density
lipoprotein, lipoprotein
A, homocysteine, and triglycerides
may be abnormal.
 Coagulation studies, hemoglobin
level, fasting blood sugar as baseline
studies.

29.  Antianginal medications (nitrates, beta-
adrenergic blockers, calcium channel
blockers, and angiotensin converting enzyme
inhibitors) to promote a favorable balance of
oxygen supply and demand.
 Antilipid medications to decrease blood
cholesterol and tricglyceride levels in
patients with elevated levels.
 Antiplatelet agents to inhibit thrombus
formation.
 Folic acid and B complex vitamins to reduce
homocysteine levels.

30.  Percutaneous transluminal coronary
angioplasty or intracoronary atherectomy, or
placement of intracoronarystent.
 Coronary artery bypass grafting.
 Transmyocardial revascularization.

31.  Monitor blood pressure, apical heart
rate, and respirations every 5 minutes during
an anginal attack.
 Maintain continuous ECG monitoring or
obtain a 12-lead ECG, as directed, monitor
for arrhythmias and ST elevation.
 Place patient in comfortable position and
administer oxygen, if prescribed, to enhance
myocardial oxygen supply.

32. 
Identify specific activities patient
may engage in that are below the
level at which anginal pain occurs.
 Reinforce the importance of
notifying nursing staff whenever
angina pain is experienced.
 Encourage supine position for
dizziness caused by antianginals.

33.  Be alert to adverse reaction related to
abrupt discontinuation of beta-adrenergic
blocker and calcium channel blocker therapy.
These drug must be tapered to prevent a
“rebound phenomenon”;
tachycardia, increase in chest pain, and
hypertension.

34.  Explain to the patient the
importance of anxiety reduction to
assist to control angina.
 Teach the patient relaxation
techniques.
 Review specific factors that affect
CAD development and progression;
highlight those risk factors that can
be modified and controlled to
reduce the risk.

35. a temporary chest pain that results from
inadequate oxygen flow to the myocardium.
 It’s usually described as
burning, squeezing, or a tight feeling in the
substernal or precordial chest. This pain may
radiate to the left arm, neck, jaw, or
shoulder blade.
 Typically, the patient clenches his fist over
his chest or rubs his left arm when describing
the pain, which may also be accompanied by
nausea, vomiting, fainting, sweating, and
cool extremities.

36.  Angina commonly occurs after
physical exertion, but may also
follow emotional
excitement, exposure to cold, or a
large meal. It may also develop
during sleep, and symptoms may
awaken the patient.

37.  When assessing for anginal
pain, older adults commonly have an
increased tolerance for pain, and
may be less likely to complain.
Instead, they may compensate by
slowing their activity levels. Older
adults may not experience chest
pain at all, but may report
dyspnea, faintness, or extreme
fatigue.

38.  The person’s health history may suggest a
pattern to the type and onset of pain. If
the pain is predictable and relieved by
rest or nitrates, it’s called stable angina. If
it increases in frequency and duration and
is more easily induced, it’s referred to as
unstable angina or unpredictable angina.
Unstable angina may occur at rest and
generally indicates extensive or worsening
disease that may progress to an MI. Variant
or Prinzmetal’s angina is caused by
coronary artery spasm, and commonly
occurs at rest without initial increased
oxygen demand.

39.  Administer oxygen to relieve ischemia at a
flow rate based on institutional policy and
the patient’s condition.
 Assess and document continuous ECG
rhythm, vital signs, mental status, heart and
lung sounds.
 Assess and document pain
characteristics: location, duration, intensity
(have patient grade pain on a scale from 1 to
10), precipitating factors, relief measures
and any symptoms that indicate changes in
these parameters.

40.  Assess vital signs with complaints of chest
pain, and compare to baseline.
 Begin IV nitroglycerin titrated until acute pain
is relieved; check blood pressure every 15
minutes or according to institutional policy;
maintain systolic blood pressure greater than
90 mm Hg or according to institutional
protocol; document the patient’s response to
therapy.
 Administer IV morphine in small doses to
relieve pain and decrease preload.

41.  Give sublingual, oral, or topical
nitroglycerin prophylactically for chronic
pain.
 Consider calcium channel blockers with
Prinzmetal’s angina to block the influx of
calcium into the cell; calcium channel
blockers produce vasodilation of coronary
and peripheral arteries.
 Use beta-adrenergic blockers to decrease
myocardial oxygen demand by decreasing
contractility, heart rate, and blood
pressure.
 Notify the doctor and obtain a 12-lead
ECG at the onset of recurring chest pain.

42.  Maintain activity restrictions based
on the patient’s activity tolerance to
reduce myocardial oxygen demands.
 Begin the patient on a low-
cholesterol, low-sodium diet to
alleviate the modifiable risk factors.
 Consider percutaneous transluminal
coronary angioplasty (PTCA) to
improve blood flow through the
stenotic coronary arteries.

43.  Remember that a coronary artery
bypass graft (CABG) may be indicated
when medical treatment has been
unsuccessful, based on the patient’s
symptoms and the cardiac
catheterization report.
 Provide patient education, and ensure
that the patient can recognize signs
and symptoms necessitating medical
attention (unrelieved chest pain after
taking three nitroglycerin tablets
sublingually 5 minutes apart).

44.  Work with the patient and family to
identify the patient’s risk factors
and necessary life style
modifications.
 Refer the family to appropriate
sources for cardiopulmonary
resuscitation (CPR) training.
 Ensure that the family can activate
the emergency medical system if
any problems occur at home.

45.  Refersto a dynamic process by
which one or more regions of the
heart muscle experience a severe
and prolonged decrease in oxygen
supply because of insufficient
coronary blood flow. The affected
muscle tissue subsequently becomes
necrotic.

47. Onset of Myocardial Infarction
may be sudden or gradual, and
the process takes 3 to 6 hours to
run its course.

48.  Itis the most serious manifestation of
acute coronary syndrome, a
complication of coronary artery
disease (CAD).
 Approximately 90% of Myocardial
Infarction are precipitated by acute
coronary thrombosis (partial or total)
secondary to severe CAD (greater than
70% narrowing of the artery).

49.  Other causative factors include
coronary artery spasm, coronary
artery embolism, infectious diseases
causing arterial
inflammation, hypoxia, anemia, and
severe exertion or stress on the
heart in the presence of significant
coronary artery disease.

50.  Chest pain
 Character: variable, but often
diffuse, steady substernal chest pain.
Other sensations include a crushing and
squeezing feeling in the chest. Other
sensations include a crushing and
squeezing feeling in the chest.
 Severity: pain may be severe; not
relieved by rest or sublingual vasodilator
therapy, requires opioids.

51.  Location: variable, but often pain
resides behind upper or middle
third of sternum.
 Radiation: pain may radiate to the
arms (commonly the left), and to
the shoulders, neck, back, or jaw.
 Duration: pain continues for more
than 15 minutes.

52.  Associated manifestations include
anxiety, diaphoresis, cool clammy
skin, facial pallor,hypertension or
hypotension, bradycardia or
tachycardia, premature ventricular
or atrial
beats, palpitations, dyspnea, disorie
ntation, confusion, restlessness, fain
ting, marked
weakness, nausea, vomiting, and
hiccups.

53.  Atypicalsymptoms of MI include
epigastric or abdominal distress, dull
aching or tingling
sensations, shortness of breath, and
extreme fatigue (more frequent in
women).

54.  Riskfactors for MI include male
gender, age over 45 for men, age
over 55 for men, smoking; high
blood cholesterol
levels, hypertension, family history
of premature CAD, diabetes and
obesity.

55.  Serial
12-lead electrocardiograms (ECGs)
detect changes that usually occur within 2 to
12 hours, but may take 72 to 96 hours
 ST-segment depression and T-wave inversion
indicate a pattern of ischemia; ST elevation
indicates an injury pattern.
 Q waves indicate tissue necrosis and are
permanent
 Nonspecific enzymes including aspartate
transaminase, lactate dehydrogenase, and
myoglobulin may be elevated
 More specific creatinine phosphokinase
isoenzyme CK-MB will be elevated.

56.  Triponin T and I are myocardial proteins that
increase in the serum about 3 to 4 hours
after an MI, peak in 4 to 24 hours, and are
detectable for upto 2 weeks; the test is easy
to run, can help diagnose an MI up to 2
weeks earlier, and only unstable angina
causes a false positive.
 White blood cell count and sedimentation
rate may be elevated.
 Radionuclide imaging, positron emission
tomography, and echocardiography may be
done to evaluate heart muscle.

57.  Pain control drugs to reduce catecholamine-
induced oxygen demand to injured heart
muscle.
 Opiate analgesics: Morphine
 Vasodilators: Nitroglycerin
 Anxiolytics: Benzodiazepines
 Thrombolytic therapy by I.V. or intracoronary
route, to dissolve thrombus formation and
reduce the size of the infarction.
 Anticoagulants or other anti-platelet
medications such as adjunct to thrombolytic
therapy.

58.  Reperfusion arrhythmias may follow
successful therapy.
 Beta-adrenergic blockers, to improve oxygen
supply and demand, decrease sympathetic
stimulation to the heart, promote blood flow
in the small vessels of the heart, and provide
antiarrhythmic effects.
 Calcium channel blockers, to improve oxygen
supply and demand.

59.  Monitor continuous ECG to watch for life
threatening arrhythmias (common within 24
hours after infarctions) and evolution of the
MI (changes in ST segments and T waves).
Be alert for any type of premature
ventricular beats- these may herald
ventricular fibrillation or ventricular
tachycardia.
 Monitor baseline vital signs before and 10 to
15 minutes after administering drugs. Also
monitor blood pressure continuously when
giving nitroglycerin I.V.

60.  Handle the patient carefully while
providing care, starting I.V.
infusion, obtaining baseline vital
signs, and attaching electrodes for
continuous ECG monitoring.
 Reassure the patient that pain relief is a
priority, and administer analgesics
promptly. Place the patient in supine
position during administration to
minimize hypotension.

61.  Emphasize the importance of reporting
any chest pain, discomfort, or epigastric
distress without delay.
 Explain equipment, procedures, and need
for frequent assessment to the patient
and significant others to reduce anxiety
associated with facility environment.

62.  Promote rest with early gradual
increase in mobilization to prevent
deconditioning, which occurs during
bed rest.
 Tell the patient that sexual relations
may be resumed on advise of health
care provider, usually after exercise
tolerance is assessed.

63.  Be alert to signs and symptoms of
sleep deprivation such as
irritability, disorientation, hallucinat
ions, diminished pain tolerance, and
aggressiveness.
 Take measures to prevent bleeding if
patient is thrombolitic therapy

65.  Interventional cardiology is a
branch of cardiology that deals
specifically with the catheter based
treatment of structural heart
diseases.

66.  AngioplastyAlso called percutaneous
transluminal coronary angioplasty
(PTCA), angioplasty is an
intervention for the treatment
ofcoronary artery disease.

68. Valvuloplasty
It is the dilation of narrowed
cardiac valves
(usually mitral, aortic, or pulmona
ry).

69.  Congenital heart defect correction
Percutaneous approaches can be
employed to correct atrial septal
and ventricular septal
defects, closure of a patent ductus
arteriosus, and angioplasty of the
great vessels.
Percutaneous valve replacement: An
alternative to open heart
surgery, percutaneous valve
replacement is the replacement of a
heart valve using percutaneous
methods.

70. Coronary thrombectomy
Coronary thrombectomy involves
the removal of
a thrombus (blood clot) from
the coronary arteries.[

71.  3]Cardiac ablation
A technique performed by clinical
electrophysiologists, cardiac
ablation is used in the treatment
of arrhythmias.

73. Disorders of the formation and/or
conduction of electrical impulses
in the heart
Cause disturbances of heart rate
and/or heart rhythm
May be evidenced by changes in
hemodynamics
Diagnosed by analyzing
electrocardiogram

75.  Sinus Bradycardia
 Sinus Tachycardia
 Sinus Arrhythmia

77.  Premature Atrial Complex
 Atrial Flutter
 Atrial Fibrillation

79.  Premature Junctional Complex
 Junctional Rhythm
 Atroventricular Nodal Reentry
Tachycardia
 Supraventricular tachycardia

80.  Premature Ventricular Complex
 Ventricular Tachycardia
 Ventricular Fibrillation
 Idioventricular Rhythm
 Ventricular Asystole

83.  First-Degree Atrioventricular Block
 Second-Degree Atrioventricular
Block, Type I
 Second-Degree Atrioventricular
Block, Type II
 Third-Degree Atrioventricular Block

84.  Monitoring and managing the
dysrhythmia
 Minimizing anxiety
 Teaching self-care

85.  Provides electrical stimuli to heart
muscle
 Used for slower-than-normal impulse
formation, to control some
tachycardias, or for advanced heart
failure
 May be permanent or temporary

86.  NASPE-BPEG code
 First letter identifies chambers
being paced
 Second letter describes the
chambers being sensed
 Third letter describes type of
response by pacemaker to what is
sensed

88.  Delivery of electrical current to depolarize
a critical mass of myocardial cells
 When cells repolarize the SA node, is
usually able to recapture its role as
pacemaker of heart
 Cardioversion involves use of “timed”
electrical current to terminate a
tachydysrhythmia

89. Defibrillation is used in
emergency situations as
treatment for ventricular
fibrillation and pulseless VT

90.  Chronic heart failure managed based
upon type, severity, and cause
 Diastolic heart failure
 Systolic heart failure
 Ejection performed to assist in
diagnosis

93.  Pulmonary congestion occurs when
left ventricle cannot pump well
 Dyspnea upon
exertion, orthopnea, and paroxysmal
nocturnal dyspnea
 Oliguria

94.  Congestion of viscera and peripheral tissues
when right ventricle fails
 Jugular vein distention
 Dependent edema
 Hepatomegaly
 Ascites
 Weakness, anorexia, and nausea
 Weight gain

96.  Eliminate or reduce contributing factors
 Reduce workload of heart by reducing afterload and
preload
 Pharmacologic Therapy
 ACE inhibitors and ARBs
 Hydralazine and isosorbide dinitrate
 Beta-blockers
 Diuretics
 Digitalis
 Calcium channel blockers
 Other: anticoagulants and antianginal
medications
 Low Sodium Diet

97.  I&O
 Weigh daily
 Auscultate lung sounds
 Determine degree of JVD
 Assess dependent edema
 Monitor VS

98. Exam skin turgor and mucous
membranes
Assess for symptoms of fluid
overload

99.  Pulmonary Edema is abnormal
accumulation of fluid in the
lungs, interstitial spaces and/or alveoli
 Increasing restlessness and anxiety
 Cyanosis
 Weak, rapid pulse
 Incessant coughing with mucoid sputum

100. Pharmacologic Therapy
 Oxygen
 Morphine
 Diuretics
 Dobutamine
 Milrinone
 Nesiritide

101.  Myocardial rupture is rare. Can occur as
result of MI, infectious process, cardiac
trauma, pericardial disease, or other
myocardial dysfunction
 Result is immediate death
 Cardiac arrest occurs when heart ceases
to produce effective pulse and blood
circulation
 Pulseless electrical activity
 Emergency Management is CPR