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MedSurg P.M > Acute Coronary Syndrome > Flashcards

Acute Coronary Syndrome Flashcards

1
Q

Evaluates specific and general ventricular performance, regional wall motion, and
ejection fraction

A

Cardiac blood imaging/Multiple-gated Acquisition (MUGA) Scan

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2
Q

includes the description of the presenting symptoms, the
history of previous cardiac and other illnesses, and the family history of heart
diseases.

A

Patient history

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3
Q

Because of increased oxygen demand and a decrease in the supply
of oxygen, ** occurs.

A

shortness of breath

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4
Q

present as a result of the stimulation of sympathetic nervous
system.

A

Indigestion.

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5
Q

To compensate for the decreased oxygen supply,

A

Tachycardia and tachypnea

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6
Q
A
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7
Q

Evaluates specific and general ventricle performance, regional wall motion, and
ejection fraction.

A

MUGA

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8
Q

CPK-MB (isoenzyme in cardiac muscle): Elevates within 4–8 hr, peaks in 12–20 hr,
returns to normal in 48–72 hr.

A

Cardiac enzymes and isoenzymes

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9
Q

May reveal abnormal valvular action as cause of chest pain.

A

Echocardiogram

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10
Q

CAUSES of MI

A

Atherosclerosis
Embolism

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11
Q

contraindication of nitroglycerin

A

Erection-enhancing medicine such as sildenafil
(Viagra), tadalafil (Cialis), and vardenafil (Levitra). Combining nitroglycerin

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12
Q

Thallium-201: Ischemic regions appear as areas of decreased thallium uptake.

A

Nuclear imaging studies (rest or stress scan)

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13
Q

reduce pain and anxiety, also has other
beneficial effects as a vasodilator and decreases the workload of the heart by
reducing preload and afterload.

A

Morphine

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14
Q
A
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15
Q
A
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16
Q
A
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17
Q

to avoid intense straining that may trigger arrhythmias or another cardiac
arrest.

A

Stool Softeners

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18
Q

s prevent thrombus formation

A

Anticoagulants

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19
Q

The patient may need reminders about follow-up
monitoring, including periodic blood laboratory testing

A

Follow-up monitoring.

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20
Q

Visualizes narrowing/occlusion of coronary arteries and is usually done in
conjunction with measurements of chamber pressures and assessment of left
ventricular function (ejection fraction). Procedure is not usually done in acute
phase of MI unless angioplasty or emergency heartsurgery

A

Coronary angiography

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21
Q

heart pumps more and more blood to compensate the decreased
oxygen supply, and the cardiac muscle would ultimately fail leading to ***

A

Cardiac arrest.

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22
Q
A

placed in a dark-colored (such as
brown), airtight, glass container that cannot see through. Keep the
container tightly closed. Keep nitroglycerin pills and liquid spray away from
heat or moisture

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23
Q

can precipitate an attack by increasing myocardial oxygen demand

A

Physical exertion

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24
Q

Imbalances of sodium andpotassiumcan alter conduction and compromise
contractility.

A

Electrolytes

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25
Q

o Evaluates myocardial blood flow and status of myocardial cells, e.g.,
location/extent of acute/previous MI.

A

Nuclear imaging studies: Persantine or Thallium

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26
Q

symptoms increase in frequency and severity and may not be
relieved with rest or nitroglycerin.

A

Unstable angina

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27
Q

prevents the formation of thromboxane A2 which causes platelets to
aggregate and arteries to constrict. The earlier the patient receives ASA after
symptom onset, the greater the potential benefit.

A

Aspirin

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28
Q

Leukocytosis (10,000–20,000) usually appears on the second day after MI because
of the inflammatory process.

A

WBC

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29
Q

ASSESSMENT AND DIAGNOTICS

A

ECG
24-hour ECG monitoring (Holter)
Cardiac enzymes
Chest x-ray
PCo2, potassium, and myocardial lactate
Serum lipids
MUGA
Echocardiogram
Ergonovine (Ergotrate) injection

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30
Q

Usually within normal limits (WNL); elevation indicates myocardial damage

A

Cardiac enzymes (AST, CPK, CK and CK-MB; LDH and Isoenzymes LD1, LD2)

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31
Q

five (5) classifications or types of angina:

A

Stable angina.
Unstable angina
Intractable or refractory angina.
Vasospastic Angina/Prinzmetal Angina/Variant angina
Silent ischemia

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32
Q

Usually normal; however, infiltrates may be present, reflecting cardiac
decompensation or pulmonary complications.

A

Chest x-ray

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33
Q

often felt deep in the chest behind the sternum and may radiate to
the neck, jaw, and shoulders. is usually relieved by rest unlike in MI.

A

chest pain

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34
Q

causes the release of catecholamines, which increased blood pressure, heart
rate, and myocardial workload.

A

Stress

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35
Q

A heme protein of small molecular weight that is more rapidly released from
damaged muscle tissue with elevation within 2 hr after an acute MI, and peak
levels occurring in 3– 15 hr.

A

Myoglobin

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36
Q

CAUSES of Angina pectoris

A

 Physical exertion
 Exposure to cold.
 Eating a heavy meal
 Stress.

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37
Q

A catheter is inserted into the
blood vessels either in the
***

A

groin or in the arm.

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38
Q

increase in oxygen demand could cause shortness of breath.

A

Shortness of breath

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39
Q

Rises on second or third day after MI, indicating inflammatory response

A

Erythrocyte Sedimentation Rate (ESR)

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40
Q

May be elevated (CAD risk factor).

A

Serum lipids (total lipids, lipoprotein electrophoresis, and isoenzymes cholesterols [HDL,
LDL, VLDL]; triglycerides; phospholipids)

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41
Q

These enzymes have increased
specificity for necrosis and are therefore useful in diagnosing postoperative MI
when MB-CPK maybe elevated related to skeletal trauma.

A

Troponin I (cTnI) and troponin T (cTnT):

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42
Q

health educations for angina

A

Reduce anginal attacks.
Follow-up monitoring
Adherence.

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43
Q

he cardinal symptom of MI. Persistent and crushing substernal pain
that may radiate to the left arm, jaw, neck, or shoulder blades.

A

Chest pain

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44
Q

MI can arise from any condition in which the myocardial oxygen supply can’t keep pace with
demand, including:

A

Coronary Artery Disease (CAD)
. coronary artery emboli
. thrombus
. congenital coronary artery anomalies.

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45
Q

May indicate hypoxia or acute/chronic lung disease processes.

A

ABGs/Pulse oximetry

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46
Q

ST elevation signifying ischemia; peaked upright or inverted T wave
indicating injury; development of Q waves signifying prolonged ischemia or
necrosis

A

ECG

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47
Q

First-line of treatment for angina pectoris and acute MI; causes vasodilation and
increases blood flow to the myocardium.

A

Nitroglycerine

48
Q

-plaques occlude the vessels, causing a decrease in blood flow to the heart.

A

Atherosclerosis -

49
Q

commonly known as a heart attack. The area of
infarction is often due to build-up of plaque over time
(atherosclerosis). It may also be due to a clot that
develops in association with the atherosclerosis within
the vessel.

A

MYOCARDIAL INFARCTION

50
Q

May be normal or show an enlarged cardiac shadow suggestive of HF or
ventricularaneurysm.

A

Chest x-ray

51
Q

Classification of acute coronary syndromes include:

A

o Unstable angina
o Myocardial Infarction
!
Non–ST-segment elevation myocardial infarction (NSTEMI)
!
ST-segment elevation myocardial infarction (STEMI)

52
Q

CLINICAL MANIFESTATIONS of angina

A

Chest pain
Numbness
Shortness of breath.
Pallor

53
Q

May be abnormal, depending on acute/chronic abnormal organ function/
perfusion.

A

Chemistry profiles

54
Q

Accumulates in ischemic cells, outlining necrotic area(s).

A

Technetium

55
Q

time of elevation, peak, and normalization of CPK-MB

A

Elevates within 4–8 hr, peaks in 12–20 hr,
returns to normal in 48–72 hr.

56
Q

There is pain at rest, with
reversible ST-segment elevation and thought to be caused by coronary artery vasospasm.
Usually occurs when a person is at rest, usually between midnight and early morning

A

Vasospastic Angina/Prinzmetal Angina/Variant angina

57
Q

Often normal when patient at rest or when pain-free; depression of the ST
segment or T wave inversion signifies ischemia. Dysrhythmias and heart block may
also be present. Significant Q waves are consistent with a prior MI.

A

ECG

58
Q

Determines cardiovascular response to activity (often done in conjunction with
thallium imaging in the recovery phase)

A

Exercise stress test

59
Q

lipid laden plaques that are soft tend to break off. A clot thenforms over that
area. This clot can partially or totally occlude the vessels.

A

Embolism

60
Q

time of elevation, peak, and normalization of Lactate dehydrogenase

A

Elevates within 8–24 hr, peaks within 72–144 hr, and may take as long as 14 days
to return to normal.

61
Q

increases the blood flow to the mesenteric area for
digestion, thereby reducing the blood supply available to the heart muscle; in a severely
compromised heart, shunting of the blood for digestion can be sufficient to induce anginal
pain.

A

Eating a heavy meal.

62
Q

chest pain is usually described as
heavy, squeezing, or crushing and may persist for **

A

12 hours or more.

63
Q

Inadequate blood supply to peripheral tissues cause it

A

pallor

64
Q

severe incapacitating chest pain.

A

Intractable or refractory angina.

65
Q

atient may experience such as coolness in extremities,
perspiration,anxiety, and restlessness.

A

Catecholamine responses

66
Q

Unusually occurs at the onset of MI, but a low-grade temperature elevation may
develop during the next few days.

A

fever

67
Q

r to limit the size of infarction and give rest to the patient. Valium or an
equivalent is usually g

A

Sedatives

68
Q

dissolve the thrombus in a coronary artery, allowing blood to flow through
again, minimizing the size of the infarction and preserving ventricular function;
given in some patients with MI.

A

Thrombolytic

69
Q

complications of angina

A

 Myocardial infarction
 Cardiac arrest.
 Cardiogenic shock

70
Q

usually initiated at the onset of chest pain in an
attempt to increase the amount of oxygen delivered to the myocardium and reduce pain

A

Oxygen therapy.

71
Q

On occasion, may be used for patients who have angina at rest to demonstrate
hyperspastic coronary vessels.
o Patients with resting angina usually experience chest pain, ST elevation, or
depression and/or pronounced rise in left ventricular end-diastolic pressure
[LVEDP], fall in systemic systolic pressure, and/or high-grade coronary artery
narrowing. Some patients may also have severe ventricular dysrhythmias.

A

Ergonovine (Ergotrate) injection

72
Q

Blood supply to the myocardium is interrupted for a
prolonged time due to the blockage of coronary arteries.
This results in insufficient oxygen reaching cardiac
muscle, causing cardiac muscles to die (necrosis).

A

MYOCARDIAL INFARCTION

73
Q

Activities should be planned to minimize the occurrence
of angina episodes.

A

o Reduce anginal attacks

74
Q

*** percent of patients with unstable angina have normal-appearing
coronary arteries.

A

Ten

75
Q

provide and improve oxygenation of ischemic myocardial tissue; enforced
together with bedrest to help reduce myocardial oxygen consumption. Given via
nasal cannula at 2 to 4 L/min.

A

Oxygen

76
Q

Side effects of nitroglycerin

A

a warm or flushed feeling, headache, dizziness, or
lightheadedness, burning sensation under the tongue.

77
Q

a special type of X-ray used in coronary angioplasty

A

fluoroscopy

78
Q

May be elevated during anginal attack (all play a role in myocardial ischemia and
may perpetuate it).

A

PCo2, potassium, and myocardial lactate

79
Q

. A rapid heart rate, thyrotoxicosis, or ingestion
ofcocainecauses an increase in the demand for oxygen.

A

Increased demand for oxygen

80
Q

cause is insufficient coronary blood flow, resulting in a decreased oxygen supply when
there is increased myocardial demand for oxygen in response to physical exertion or
emotional stress.

A

ANGINA PECTORIS

81
Q

time of elevation, peak, and normalization of troponin

A

elevated at 4– 6 hr, peak at 14– 18 hr, and return to baseline over 6–7 days

82
Q

prevent platelet aggregation

A

Antiplatelet medications

83
Q

RISK FACTORS of MI

A

 Family history of MI
 Gender (men are more susceptible)
 Hypertension
 Smoking
 Diabetes mellitus
 Obesity
 Sedentary lifestyle
 Aging,
 Stress,
 Menopause,

84
Q

An occlusion of a coronary artery. It’s one component of
acute coronary syndrome.

A

MYOCARDIAL INFARCTION

85
Q

have negative inotropic effects.

A

Calcium channel blockers

86
Q

Definitive test for CAD in patients with known ischemic disease with angina or
incapacitating chest pain, in patients with cholesterolemia and familial heart
disease who are experiencing chest pain, and in patients with abnormal resting
ECGs.
o Abnormal results are present in valvular disease, altered contractility, ventricular
failure, and circulatory abnormalities.

A

Cardiac catheterization with angiography

87
Q

a clinical syndrome usually characterized by episodes or paroxysms of
pain or pressure in the anterior chest.

A

ANGINA PECTORIS

88
Q

occurs from acute blood
loss,anemia, or low blood pressure.

A

Decreased oxygen supply

89
Q

Provides more diagnostic information, such as duration and level of activity
attained before onset of angina. A markedly positive test is indicative of severe
CAD. Note: Studies have shown stress echo studies to be more accurate in some
groups than exercise stress testing alone.

A

Exercise or pharmacological stress electrocardiography

90
Q

ASSESSMENT AND DIAGNOSTIC FINDINGS

A

Patient history
ECG
Troponins
Myoglobin
Electrolytes
WBC

91
Q

an emergent situation characterized by an acute onset of myocardial
ischemia that results in myocardial death (ie, myocardial infarction [MI]) if definitive interventions do not
occur promptly

A

ACUTE CORONARY SYNDROME (ACS)

92
Q

A feeling of weakness or numbness in the arms, wrists and hands.

A

numbness

93
Q

predictable and consistent pain that occurs on exertion and is
relieved by rest and/or nitroglycerin.

A

Stable angina.

94
Q
A
95
Q

May be done to determine dimensions of chambers, septal/ventricular wall
motion, ejection fraction (blood flow), and valve configuration/function.

A

Two-dimensionalechocardiogram

96
Q

Elevates within 8–24 hr, peaks within 72–144 hr, and may take as long as 14 days
to return to normal. An LDH1 greater than LDH2 (flipped ratio) helps
confirm/diagnose MI if not detected in acute phase.

A

Lactate Dehydrogenase (LDH)

97
Q

Technique used to visualize status of arterial bypass grafts and to detect peripheral
artery disease.

A

Digital subtraction angiography (DSA)

98
Q

PHARMACOLOGIC MANAGEMENT of MI

A

M: Morphine
O: Oxygen
N: Nitroglycerine
A: Aspirin
T: Thrombolytic
A: Anticoagulants
S: Stool Softeners
S: Sedatives

99
Q

Patients are typically (not always) symptomatic, but some
patients will not be aware of the event; they will have
what is called a ***

A

silent MI

100
Q

CLINICAL MANIFESTATIONS of MI

A

 Chest pain.
 Shortness of breath
 Indigestion
 Tachycardia and tachypnea.
 Catecholamine responses.
 Fever.

101
Q

time of elevation, peak of myoglobin

A

elevation within 2 hr after an acute MI, and peak
levels occurring in 3– 15 hr.

102
Q
A
103
Q

is the end result of angina pectoris if left
untreated.

A

Myocardial infarction

104
Q

MI also predisposes the patient to **

A

cardiogenic shock

105
Q

o It is a nonsurgical technique for treating
obstructive coronary artery disease,
including unstable angina, acute
myocardial infarction (MI), and multivessel
coronary artery disease (CAD).
o The procedure is used to open the
occluded coronary artery and promote
reperfusion to the area that has been
deprived of oxygen.

A

Percutaneous Transluminal Coronary Angioplasty (PTCA)/Percutaneous Coronary
Intervention (PCI)
o also known as coronary angioplasty

106
Q

Myocardial ischemia results

A

angina

107
Q

o prevent clots from becoming larger and block coronary arteries. They are
usually given with other anticlotting medicines to help prevent or reduce
heart muscle damage.

A

Anticoagulants

108
Q

Elevations may reflect arteriosclerosis as a cause for coronary narrowing or spasm.

A

Lipids (total lipids, HDL, LDL, VLDL, total cholesterol, triglycerides, phospholipids)

109
Q

cause vasoconstriction and elevated blood pressure, with
increased oxygen demand.

A

Exposure to cold.

110
Q

There is objective evidence of ischemia but patient reports no pain.

A

Silent ischemia

111
Q

ives long term and short term reduction of myocardial oxygen
consumption through selective vasodilation within three (3) minutes

A

nitoglycerin

112
Q

Allows visualization of blood flow, cardiac chambers or intraventricular septum,
valves, vascular lesions, plaque formations, areas of necrosis/infarction, and blood
clots.

A

Magnetic resonance imaging (MRI)

113
Q

This is the sudden constriction or narrowing of the coronary artery.

A

Vasospasm

114
Q

The causes of MI primarily stems from the vascular system.

A

 Vasospasm.
 Decreased oxygen supply.
 Increased demand for oxygen

115
Q

Done to see whether pain episodes correlate with or change during exercise or
activity. ST depression without pain is highly indicative of ischemia.

A

24-hour ECG monitoring (Holter)

116
Q

MEDICAL MANAGEMENT for angina

A

Oxygen therapy.
Nitroglycerin (NTG)
Beta-blockers
Calcium channel blockers
Antiplatelet medications
Anticoagulants

117
Q

reduces myocardial oxygen consumption by blocking beta-adrenergic
stimulation of the heart.

A

Beta-blockers

MedSurg P.M (6 decks)

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