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ACLS > Chapter 5 > Flashcards

Chapter 5 Flashcards

1
Q

what is a chronic disease of the arterial system characterized by abnormal thickening and hardening of the vessel walls?

A

Arteriosclerosis

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2
Q

What is a form of arteriosclerosis in which the thickening and hardening of the vessel walls are caused by a buildup of fat-like deposits in the inner lining of large and middle-sized muscular arteries?

A

Atherosclerosis

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3
Q

what is the usual cause of an acute coronary syndrome?

A

Rupture of an atherosclerotic plaque

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4
Q

Fatty streaks are thin, flat yellow lesions composed of lipids (mostly cholesterol) or smooth muscle cells that protrude slightly into the arterial opening. Do these cause a lot of problems?

A

NO! Fatty streaks do not obstruct the vessel and are not associated with any clinical symptoms

Progression from a fatty streak to an advanced lesion is associated with injured endothelium that activates the inflammatory response

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5
Q

how much of arterial stenosis should occur to produce angina symptoms?

A

70% stenosis of the vessel’s diameter

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6
Q

what are the 3 vulnerable sites for plaque disruption within the coronary arteries?

A
  1. the proximal portion of the LAD
  2. near the origin of the marginal branch on the RCA
  3. near the origin of the first obtuse marginal branc on the circumflex coronary artery
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7
Q

why is aspirin such a grand idea?

A

Aspirin blocks the formation of thromboxane A2 which is released by platelets. Thromboxane A2 causes vasoconstriction therefore reduced blood flow at the site - aspirin lowers the risk of complete blockage of a vessel

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8
Q

what’s the most common cause of an MI?

A

acute plaque rupture

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9
Q

what can result from a partial (incomplete) blockage of a coronary artery?

A
  • no clinical signs and symptoms (silent MI)
  • unstable angina
  • NSTEMI
  • sudden death
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10
Q

What can result from a complete blockage of a coronary artery?

A

STEMI or sudden death

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11
Q

How does cocaine cause MI?

A
  1. increasing myocardial oxygen demand by increasing heart rate, BP and contractility
  2. decreasing oxygen supply via vasoconstriction
  3. inducing a prothrombotic state by stimulating platelet activation and altering the balance between procoagulant and anticoagulant factors
  4. accelerating atherosclerosis
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12
Q

which type of angina is the result of intense spasm of a segment of a coronary artery and may occur in otherwise healthy individuals?

A

Prinzmetal’s angina AKA variant angina

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13
Q

when does Prinzmetal’s angina usually occur?

A

it usually occurs at rest, often occurs between midnight and 8 am and may awaken the patient from sleep
also it can be precipitated by exercise, emotional stress, hyperventilation or exposure to cold

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14
Q

What does Prinzmetal’s angina look like on EKG?

A

Prinzmetal’s angina produces ST segment elevation during periods of chest pain
After the episode of chest discomfort is resolved, the ST usually returns to baseline
so you may see no change in ST if you don’t have a pre-treatment EKG before you give nitroglycerin

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15
Q

what should you do when a patient presents with a possible ACS?

A

You should obtain a baseline 12-lead EKG before initiating treatment in any pt presenting with a possible ACS

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16
Q

what are the forms of acute coronary syndromes?

A

unstable angina, NSTEMI and STEMI

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17
Q

what is it called when chest discomfort occurs when the heart muscle doesn’t receive enough oxygen

A

Angina pectoris

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18
Q

what is the term given for squeezing or tightening rather than pain?

A

angina

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19
Q

describe ischemic chest discomfort

A

ischemic chest discomfort is usually not sharp, it’s NOT worsened by deep inspiration, it’s not affected by moving muscles in the area where the discomfort is localized nor is it positional

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20
Q

What angina is characterized by one or more of the following:

  • symptoms that occur at rest and usually last for more than 20 mins
  • symptoms that are severe and/or of new onset
  • symptoms that are increasing in duration, frequency or both; and intensity in a patient with a history of stable angina
A

unstable angina

note that the discomfort associated with unstable angina may be described as painful

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21
Q

what are the subdivisions of the myocardium?

A

the innermost half of the myocardium is called the subendocardial area and the outermost half is called the subepicardial area

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22
Q

what areas of the heart are most vulnerable to ischemia?

A

the endocardial and subendocardial areas of the myocardial wall because they have a high demand for oxygen and they are fed by the most distal branches of the coronary arteries

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23
Q

what provides the strongest evidence for the early recognition of MI?

A

patients history and symptoms, cardiac biomarkers, and the presence of ST segment elevation

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24
Q

at what time of the day are peak incidence of acute cardiac events?

A

between 6 AM and noon

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25
Q

a patient presents with an acute coronary syndrome - what mnemonics are included in the targeted history?

A
  • SAMPLE history

- OPQRST for pain presentation

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26
Q

What is included in the SAMPLE history?

A 
Signs and symptoms
Allergies
Medications
Past medical history
Last oral intake
Events leading to the incident
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27
Q

What is included in the OPQRST pain presentation?

A 
Onset
Provocation/Palliation/Position
Quality
Region/Radiation/Referral
Severity
Timing
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28
Q

What is the Levines signs?

A

When the patient describes their discomfort with a clenched fist held against the sternum

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29
Q

what are the typical symptoms with ACS?

A

chest discomfort
Levine’s sign
discomfort typically lasts longer than 30 minutes and it may be constant or come and go, occasionally it may be relieved with belching

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30
Q

what are angina equivalent symptoms?

A

Symptoms of MI other than chest pain or discomfort
examples would be difficulty breathing, dizzy, dysrhythmia, sweating, fatigue, weak, arm or jaw pain, palpitations, syncope or near syncope, N/V

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31
Q

what are the goals of reperfusion therapy?

A

to give fibrinolytics within 30 mins of patient arrival or provide percutaneous coronary intervention within 90 minutes of arrival

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32
Q

what can you expect to see on an EKG with myocardial infarction?

A

ST elevation in the leads facing the affected area and ST depression in leads OPPOSITE the affected area

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33
Q

What’s the threshold value for abnormal J point elevation in men 40 y and older?

A

2 mm in leads V2 and V3 and 1 mm in all other leads

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34
Q

what’s the threshold value for abnormal J point elevation in men younger than 40 yo?

A

2.5 mm in leads V2 and V3 and greater than 1 mm in all other leads

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35
Q

what’s the threshold for abnormal J point elevation in V3R and V4R for men and women?

A

0.5 mm except for males younger than 30 yo theirs is 1mm

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36
Q

what’s the threshold value for abnormal J point elevation in leads V7 through V9?

A

0.5 mm

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37
Q

what phase of an MI includes a tall T wave (tombstone) that typically measure more than 50% of the preceding R wave

A

Hyperacute phase

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38
Q

in what phase of an MI do you see ST segment elevation

A

Early acute phase - ST segment elevation may occur within the first hour or few hours of an MI

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39
Q

In what phase of an MI do you see the presence of T wave inversion

A

Later acute phase

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40
Q

In what phase of an MI do you see abnormal Q waves ?

A

Fully evolved phase

abnormal Q waves are .04 s or more wide (1 small box or more) or is more than one third of the amplitude of the R wave in that same lead

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41
Q

In what phase of an MI do you see a normal EKG except for a deep Q wave?

A

Healed phaes

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42
Q

What EKG changes are associated with ischemia?

A

ST segment depression and T wave inversion

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43
Q

What EKG changes are associated with myocardial injury?

A

ST segment elevation

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44
Q

What indicative changes will you see with a inferior MI?

A

II, III, aVF
views the inferior surface of the LV

Right coronary artery (most common) - posterior descending branch or left coronary artery (circumflex branch)

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45
Q

What indicative changes will you see with an anterior MI?

A

V3, V4

Left coronary artery - LAD - diagonal branch

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46
Q

What indicative changes will you see with a septal MI?

A

V1, V2
Left coronary artery - LAD - septal branch

can lead to a LBBB (more commone), RBBB, second degree AV block Type 2 and third degree AV block

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47
Q

What indicative changes will you see with a lateral MI?

A

I, aVL, V5, V6
this is a lateral wall of the left ventricle
left coronary artery - LAD - diagonal branch
- Circumflex branch (it’s circumflex esp if it’s an isolated lateral wall)
or right coronary artery

lateral wall infarctions often occur as extensions of anterior or inferior infarctions

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48
Q

What indicative changes will you see with a inferobasal (posterior) MI?

A

V7, V8, V9

Right coronary artery or circumflex artery (marginal branch)

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49
Q

What indicative changes will you see with an anteroseptal MI?

A

V1 - V4

Left coronary artery - LAD - either the diagonal or spetal branch

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50
Q

What indicative changes will you see with an anterolateral MI?

A

I, aVL, V3-V6
left coronary artery - LAD - diagonal branch
- Circumflex branch

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51
Q

what makes two leads contiguous?

A

If the leads look at the same or adjacent areas of the heart or if they are numerically consecutive chest leads

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52
Q

What is the result of a blockage of the RCA proximal to the marginal branch?

A

inferior wall MI AND RV MI

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53
Q

What’s the result of a blockage of the RCA distal to the marginal branch?

A

Inferior MI

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54
Q

T or F: Parasympathetic nervous system hyperactivity is common with inferior wall MIs

A

TRUE! it results in bradydysrhythmias (like first degree AV block and second degree AV block type I)

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55
Q

When should you suspect a RVI?

A

When EKC changes suggest an inferior infarction (II, III, aVF have ST elevation)

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56
Q

What is the blood supply to the right ventricle?

A

Right ventricular marginal branch of the RCA

57
Q

What are the clinical evidence of a RV infarction?

A

triad: Hypotension, JVD and clear breath sounds

58
Q

What are the cardiac biomarkers?

A 
Creatine kinase (CK)
creatine kinase myocardial band (CK-MB)
myoglobin
troponin I
Troponin T
59
Q

which biomarkers are highly sensitive and specific for myocardial necrosis?

A

Troponin I and Troponin T

These appear 8 to 12 hrs after onset of symptoms and remain elevated for 4-7 d for troponin I and 10 - 14 d for troponin T

60
Q

Should you have imaging studies done in a patient with an ACS?

A

Yes, a portable chest radiograph should be obtained for patients with a suspected ACS within 30 minutes of patient presentation

61
Q

if there’s a high clinical suspicion of a STEMI and your patient is symptomatic but there’s nothing seen on ECG what should you do?

A

obtain serial ECGs at 5-10 min intervals or continuous monitoring of the ST segment should be performed to detect the potential development of ST elevation

62
Q

What drug has the adverse side effects of headache, flushing, tachycardia, dizziness and orthostatic hypotension?

A

Nitroglycerin

63
Q

What does NTG do?

A

relaxes smooth muscle causing dilation of peripheral arteries and veins. Causes pooling of venous blood –> decreased preload.

Also dilates normal and atherosclerotic epicardial coronary arteries and reduces left ventricular systolic wall tension which decreases afterload

64
Q

Before NTG administration, what should you make sure the patient doesn’t have?

A

The patient should not have taken a phosphodiesterase inhibitor like sildenafil or tadalafil within past 48 hrs

NTG should also NOT be given in patients with a possible RVI – should suspect RVI if you give NTG to a patient with inferior wall MI and they become hypotensive after having the NTG

65
Q

what drug is a potent narcotic analgesic and anxiolytic that causes venodilation and can lower heart rate (through increased vagal tone) and systolic BP reducing myocardial oxygen demand?

A

Morphine

Adverse effects: N/V and respiratory depression - if respiratory or circulatory depression occurs you may need to give a narcotic antagonist

66
Q

When do you give morphine?

A

Morphine is the preferred analgesic for patients with STEMI who experience persistent chest discomfort unresponsive to nitrates

don’t use in NSTEMI bc its associated with increased mortality

you can use fentanyl instead of morphine

67
Q

What drug will reduce myocardial contractility, SA node rate and AV node conduction velocity thereby decreasing cardiac work and reducing myocardial oxygen demand?

A

Beta blockers

be careful! simultaneous IV administration with IV CCBs can cause severe hypotension!

68
Q

what’s the mnemonic for medications used for the management of ACS?

A 
MONA
Morphine
Oxygen
Nitroglycerin
Aspirin
69
Q

What do ACE inhibitors do?

A

Vasodilation and therefore decrease the myocardial workload
ACE inhibitors also increase renal blood flow which helps rid the body of XS sodium and fluid accumulation

Adverse effects: may cause a drop in BP following first dose or if used with diuretics

70
Q

When should aspirin be given and what do you do if the patient can’t have aspirin?

A

Aspirin should be given ASAP after presentation and continued indefinitely unless contraindicated.

You can use Clopidogrel if the pt can’t have aspirin

71
Q

What are Glycoprotein 2b/3a inhibitors?

A

Potent antiplatelet medications that are given IV, act on GP 2b/3a receptors and prevent platelets from binding with fibrinogen

72
Q

What prevents new clots from forming but does nothing to dissolve already made clots?

A

anticoagulants … heparin

73
Q

what do you monitor when a patient is on unfractionated heparin?

A

aPTT

74
Q

What’s the benefit of using low molecular weight heparin?

A

it’s dosed based on patients weight and you don’t have to monitor aPTT or tirate the dose

75
Q

What is meant by primary PCI?

A

WHen PCI is done alone as the primary treatment after diagnostic angiography

76
Q

What is meant by facilitated PCI?

A

When you use a combination of medications (fibrinolytics, GP 2b/3a inhibitors ) and PCI

77
Q

What is meant by contemporary PCI?

A

The use of GP 2b/3a inhibitors and a thienopyridine (clopidogrel)

78
Q

What is mean by rescue PCI?

A

If the procedure is performed after an unsuccessful reperfusion attempt with fibrinolytics

79
Q

what patients that have ACS are most likely to benefit from reperfusion therapy?

A

Those with a STEMI

“time is muscle” goal is to minimize total ischemic time (time from onset of symptoms of STEMI)

80
Q

What are your time goals in a patient with STEMI to initiation of reperfusion therapy?

A

30 minutes for fibrinolytics and 90 minutes for PCI

81
Q

What do fibrinolytics do?

A

These are your clot busters - they alter plasmin in the body which then breaks down fibrinogen and fibrin clots

  • watch for reperfusion dysrhythmias!
82
Q

Who is fibyrinolytic therapy indicated for?

A

patients with UA/NSTEMI who also have a true posterior MI as evidenced by ST depression in two contiguous anterior chest leads or isolated ST elevation in posterior chest leads

83
Q

What’s the most common SA node dysrhythmia after MI?

A

Sinus bradycardia, common with inferior wall infarctions, particularly in the first hour of inferior STEMI

84
Q

when is the incidence of VF the highest after a STEMI?

A

4 hrs after a STEMI and remains an important contributing factor to death during the first 24 hrs after a STEMI

85
Q

What are the most common complications of a ventricular aneurysm?

A

acute heart failure, systemic emboli, angina and recurrent ventricular dysrhythmia

86
Q

what is the most consistent physical finding of postinfarction ventricular septal rupture?

A

A new loud systolic murmur that is best heard at the left lower sternal border
- accompanied by a thrill in 50% of cases

87
Q

Where does a free wall rupture most commonly occur?

A

Lateral wall of the left ventricle

88
Q

what is the cardiovascular triad?

A
  1. conduction system (rate)
  2. myocardium (pump)
  3. tank or vascular system (volume)
89
Q

what should you do in severe hypotension that’s due to a volume problem?

A

IV fluid challenge - and if this doesn’t work you can try vsaopressors

90
Q

How do you know cardiogenic shock exists?

A

If pulmonary edema is associated with hypotension then cardiogenic shock exists

91
Q

as RV failure what might you see?

A

anasarca - complete generalized edema of the entire body

92
Q

what is the focus of treating ventricular failure?

A

correcting hypoxia, reducing preload, reducing afterload, and improving myocardial contractility

93
Q

List some medications that might be used to treat heart failure?

A
  • antiarrhythmics
  • analgesics if pain is present
  • diuretics like furosemide to reduce preload
  • venodilators like NTG to reduce preload
  • positive inotropic agents (dopamine, dobutamine) to increased myocardial contractility
  • ACE inhibitors or ARBS or beta blockers to reduce afterload
94
Q

digitalis, dopamine, dobutamine and epinephrine are examples of what kinds of drugs?

A

positive inotropic

95
Q

how does furosemide work?

A

inhibits the reabsorption of sodium and chloride in the ascending limb of the loop of henle

also causes venodilation decreasing preload

96
Q

What is a serious side effect of furosemide?

A

ototoxicity and resulting transient deafness can occur with rapid administration

97
Q

what is dressler’s syndrome?

A

pericarditis that occurs as a late complication of an acute MI, typically within 2-7 d after an MI and a low grade fever is common

98
Q

what is the pain with pericarditis like?

A

It can often be localized with one finger and it is a sharp or stabbing chest discomfort
it’s affected by movement, breathing and position - worse with inspiration and lessened by sitting forward

99
Q

what are the four phases of ECG changes seen with pericarditis?

A

phase 1 - diffuse ST segment elevation and PR segment depression
phase 2 - normalization of the ST and PR segments
Phase 3 - widespread T wave inversions
phase 4 - normalization of the T waves

give an aspirin

100
Q

what’s the most important risk factor for an embolic stroke?

A

Atrial fibrillation

101
Q

T or F: myocardial ischemia prolonged more than just a few minutes can result in myocardial injury

A

true

102
Q

T or F fibrinolytic therapy is an essential intervention in the treatment of all patients with unstable angina/non-STEMI

A

false only for UA/NSTEMI patients with a true posterior MI evidenced as ST segment depression in two contiguous anterior chest leads and/or idolated ST segment elevation in posterior chest leads

103
Q

T or F in the early acute phase, telling the difference between a pt with unstable angina and a patient having an acute MI is often impossible bc their clinical presentations and EKG may be identical

A

true

104
Q

T or F a patient experiencing atypical chest pain has discomfort that is localized to the chest area but may have musculoskeletal, positional or pleuritic features

A

true

not all patients present the same

105
Q

T or F in prehospital or ED settings, GP 2b/3a inhibitors should be routinely used in the management of ACS with and without ST elevation

A

False

106
Q

T or F decisions regarding the care of a pt experiencing an ACS are primarily based on his or her assessment findings and symptoms, oxygen saturation and presence of cardiac risk factors

A

false
decisions are primarily based on the assessment findings and symptoms, history, presence of risk factors, serial 12 lead EKG, lab results and other diagnostic tests

107
Q

T or F ACE inhibitors act on beta 1 and beta 2 receptors to slow sinus rate depress AV conduction and reduce blood pressure

A

false

108
Q

what is the correct ECG hallmark of ischemia?

A

ST segment depression, T wave inversion

109
Q

What do beta blockers do?

A

reduce myocardial contractility

110
Q

what’s the recommended initial dose of aspirin?

A

162 - 325 mg

111
Q

what does dopamine do?

A

It’s used to increase HR and BP

112
Q

The highest incidence of VF occurs about ___ hrs after STEMI symptom onset

A

4 hrs

113
Q

Examples for electrical complications of an acute MI include?

A

Sinus bradycardia and BBBs

114
Q

Sublingual NTG tablets or spray may be given….

A

at 3 to 5 minute intervals to a maximum of 3 doses

115
Q

when viewing the EKG of a patient experiencing an acute coronary syndrome, the presence of ST segment elevation in the leads facing the affected area suggests myocardial ____

A

injury

116
Q

If nitrates don’t work and you have to give morphine whats the dose?

A

Give morphine 2 mg IV, reassess vital signs and level of discomfort after each dose and give additional doses 5 to 15 minute intervals until the patient is pain free

117
Q

a patient is DX with anteroseptal MI. which complications may be anticipated?

A

heart failure and cadiogenic shock

118
Q

the time from onset of symptoms of STEMI to start of reperfusion therapy

A

total ischemic time

119
Q

a combination of meds (such as fibrinolytics and or GP 2b/3a inhibitors) and PCI

A

Facilitated PCI

120
Q

ECG changes seen in leads opposite the affected area are called ____ changes

A

reciprocal

121
Q

this type of angina is the result of intense spasm of a segment of a coronary artery

A

Prinzmetal’s

122
Q

A procedure in which a catheter is used to open a coronary artery blocked or narrowed by CAD

A

Percutaneous coronary intervention

123
Q

Contraindicated in the early period (less than 7-10d) after MI because they may predispose to cardiac rupture

A

nonsteroidal anti-inflammatory drugs (NSAIDs)

124
Q

memory aid used to recall the meds typically given in the management of ACS

A

MONA

125
Q

an actual fluid deficit is also called a ____ hypovolemia

A

absolute

126
Q

A classic initial finding in pts with acute pericarditis

A

pericardial friction rub

127
Q

vasopressor that stimulates dopaminergic, beta and alpha adrenergic receptor sites

A

dopamine

128
Q

examples of calcium channel blockers

A

diltiazem, verapamil

129
Q

prevents new clots from forming, but do not dissolve previously formed clots

A

Anticoagulants

130
Q

example of an antiplatelet agent

A

clopidogrel

131
Q

potent peripheral vasoconstrictor

A

norepinephrine

132
Q

PCI performed after an unsuccessful reperfusion attempt with fibrinolytics

A

rescue PCI

133
Q

treatment for sustained monomorphic and polymorphic VT that is not associated with hemodynamic compromise

A

Antiarrhythmics

134
Q

Treatment for sustained monomorphic ventricular tachycardia associated with hemodynamic compromise

A

synchronized cardioversion

135
Q

PCI performed alone as the primary treatment after diagnostic angiography

A

primary PCI

136
Q

the most common electrical complication in the first few hours following MI

A

dysrhythmias

137
Q

What’s the difference between myocardial injury and myocardial infarction?

A

Myocardial injury means the cells are still alive but will ide if the ischemia is not quickly corrected - if the blocked vessel can be opened quickly and restore blood flow and oxygen then no tissue death occurs

an MI occurs when blood flow to the hear muscle stops or is suddenly decreased long enough to cause cell death

138
Q

which leads look at tissue supplied by the RCA?

A

II, III, aVF

ACLS (5 decks)

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