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ACS/MI/HF Flashcards

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1
Q

ACS is progressive _______________ causing thrombosis formation that leads to imbalance of O2 _________ and ____________

A

Atherosclerosis; supply; demand

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2
Q

O2 supply to heart: determined by coronary ___________, cardiac _________, (systolic/diastolic) _____________ time, HgB, and _______

A

Arteries; output; diastolic filling; SaO2

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3
Q

O2 demand of heart is dependent on the factors that determine _________ ___________

A

Cardiac output

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4
Q

O2 demand of heart is based on ______, _________, afterload, and ______________

A

HR; preload; contractility

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5
Q

Troponin levels in ACS elevate within 3-___ hours, peak in 14-_____ hrs

A

6; 20

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6
Q

Females with ACS May commonly present with ______ symtoms, (chest/pleuritic/back) pain, or fatigue

A

GI; back;

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7
Q

DM pts experiencing ACS may not feel chest _____ - instead, the often present with _____________ of ________

A

Pain; shortness; breath

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8
Q

What symptom is a DM pt with ACS likely to present with?

A

Shortness of breath

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9
Q

What symptom/s is a female pt with ACS likely to present with?

A

GI symptoms; back pain

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10
Q

Causes of non-cardiac chest pain are from ____________ (pleuritic) pain or _____ conditions and associated pain

A

Respiratory; GI

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11
Q

True or False: Pain from GI conditions such as pancreatitis and stomach ulcers can cause non cardiac chest pain

A

True

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12
Q

Pleuritic pain - worse with ______________ and ________________

A

Inspiration; exhalation

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13
Q

Stable Angina is _____________ and symptoms predictably stop if ____________ stops

A

Exertional; exertion

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14
Q

Stable angina May have fixed ________ ____________ with ___________ ischemia - this is why exertion (increase in O2 ___________) causes exertional chest pain

A

Vessel stenosis; demand; demand;

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15
Q

Stable angina may require sublingual ________

A

NTG

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16
Q

Unstable angina is angina that is __________________ in onset/triggers - increasing _____________, _____________, and time/duration of pain. Pain may develop at _______

A

Unpredictable; frequency; intensity; rest

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17
Q

UA is pain that develops at _______, without exertion

A

Rest

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18
Q

In UA, pain developing at rest is due to an imbalance between O2 _________ and O2 ___________

A

Demand; supply

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19
Q

The NSTE-ACS that are anginas are _________ angina, __________ angina, and ____________ angina

A

Stable; unstable; variant’s

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20
Q

Variants angina is chest pain caused by coronary artery ___________ - occurs at ______ or when ______________

A

Vasospasm; rest; sleeping

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21
Q

Variants angina (vasospasm) should be treated with ______ and CCBs - ____________ dinitrate and _____________

A

NTG; isosobide;. Diltazem

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22
Q

With or without symptoms, get a ____-_______ _______ for pt with variant’s angina

A

12-lead EKG

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23
Q

UA - the _________ does not elevate

A

Troponin

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24
Q

UA May be a ____________ to an MI, consider ________________ therapy

A

Precursor; antiplatelet

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25
In NSTEMI there is ___________ _____________ of coronary ________, creating imbalance between supply and demand
Partial occlusion; artery
26
NSTEMI - pain/symptoms occur at ________, and last >_____ minutes
Rest; 20
27
Only in NSTEMI/STEMI does (EKG changes/troponin elevates)
Troponin elevates
28
Hallmark of nSTEMI 12-lead EKG - ST depression and ____ _______ ________________
T wave inversion
29
ST ____________ or ____ _______ __________________ are EKG indicators of ISCHEMIA
depression; T wave inversion
30
ECG changes in different _______ in nSTE-ACS are not ___________ __________, like in STEMI
Leads; artery specific
31
____ or more leads with ST depression/ T ______ _____________ along with ST elevation in lead _______: suspicion for multi-___________ disease, (proximal/distal) _______ occlusion, or _______ ________ artery occlusion
8; wave inverstion; aVR; vessel; proximal LAD; left main
32
Treatment for NSTEMI is _______ or ___________ _______, if pt is high risk
PCI; early PCI
33
nSTEMI has chest pain that does NOT ___________, even with administration of _______
Relieve; NTG
34
In both MI types - nSTEMI/MI - chest pain does _______ relieve, and _____________ are elevated
NOT; troponin
35
nSTEMI chest pain does NOT relieve - it is chest pain from __________ coronary artery occlusion and (reversible/irreversible) myocardial __________ and damage
Partial; Irreversible; injury
36
UA is unpredictable, but may be relieved with _______
NTG
37
UA pain is from ischemia, but is from (reversible/irreversible) myocardial ischemia
Reversible
38
Imbalance between coronary O2 __________ and ___________ (thus causing ______________) is reflected by ______ ______________ and T wave __________________ on EKG
Supply; demand; ischemia; ST depression; inversion
39
ST depression and T wave inversion on EKG : indication of ___________ between O2 supply and _________
Imbalance; demand
40
STEMI is a __________ occlusion of the coronary artery, caused by __________ rupture leading to ____________ formation
Complete; plaque; thrombus
41
Treatment for STEMU is immediate _______________ - either through _______ or administration of __________________ (followed by catheterization lab later on)
Reperfusion; PCI; fibrinolytic
42
NSTEMI Treatment - ______ or early _______ STEMI treatment - immediate/emergent _______ or ________________ therapy with cath lab later on
PCI; PCI; PCI; fibrinolytic
43
Hallmark of STEMI is chest pain >____ min, SOB, and ___________
20; diaphoresis
44
Post MI, if a pts EF is <40%, what medication class can be expected to be prescribed to them upon discharge?
ACEi/ARB/ANRI
45
Occlusion of the LAD/left ________ artery will cause an ________________ MI, with ST elevation in ____-______
Main; Anterospetal; V1-V4
46
Leads V1 - V4 are the (anterior/inferior/septal/anterolateral/posterolateral/anteroseptal) leads
Anteroseptal
47
The septal wall and any EKG changes it may have in MI is located in the leads _____-______
V1-V4
48
Occlusion of the LCX and possibly left ________ can cause a ____________ MI, with ST Elevation in I, aVL, and _____, ______
Main; lateral; V5; V6
49
Inferior MI is seen by ST elevation in the leads ____, III, and _______ - this is caused by occlusion of ________
II; aVF; RCA
50
A RV MI occurs usually when there is an occlusion of the ____________ ________
Proximal RCA
51
Occlusion of RCA - ___________ MI Occlusion of proximal RCA - _________ sided MI
Inferior; right
52
Other than an inferior or right ventricular MI, what is the other type of MI that can be caused by RCA occlusion?
Posterior MI
53
Posterior MI from RCA occlusion has ST elevation in posterior leads that are not seen in 12 lead - BUT, posterior MI has reciprocal changes (______ depression) in leads V1-____, as well as ______ __________ (T/P/R/Q) waves in ___-____
ST; V3; tall upright R; V1-V3
54
Inferior MI has reciprocal changes in the leads ____ and ______ leads
I; aVL
55
An anteroseptal MI has reciprocal changes in the leads _____, ______, and __________
II; III; aVF
56
Bedside monitor for Inferior wall MI is lead _____
III
57
In inferior wall MI, if ____ elevation is lead _____ > lead II, likely _______ occlusion
ST; III; RCA
58
What lead should be bedside monitored for an inferior MI?
Lead III
59
Administration in NTG with MI has to be cautious for what type of MI?
Inferior MI/RVMI
60
If patient has inferior MI/suspected RVMI, what two emergent MI medications should be avoided due to concern for _____________ and __________ reduction?
Hypotension; preload // NTG and Morphine
61
In a Right sided MI, avoid giving _________ or __________ for painQ
Nitroglycerin; morphine
62
Administer ___________ cautiously in _____/nSTEMI, as it can cause ________________
Morphine; UA; hypotension
63
Large “v” waves on PAOP waveform are caused by ___________ __________ rupture and/or ___________ regurgitation
Papillary muscle; mitral
64
Papillary muscle rupture is often diagnosed by
Echocardiogram
65
Papillary muscle rupture treatment is emergent _________ ________ or ________ replacement
Surgical repair; valve
66
Ventrical septal rupture (associated with ________ wall MI) results in a _______ to right _________
Septal; left; shunt
67
Ventricular septal rupture will appear as large “__” waves on _______ waveform
V; CVP
68
Clinical signs of cardiogenic shock (LV Failure) include ____ sound/pulmonary ________, tachycardia, ___________, decreased ______, and signs of decreased ______________ such as mottling
S3; edema; arrhythmias; UOP; perfusion
69
True or False: Arrythmias are a clinically presenting sign of oncoming cardiogenic shock
True
70
Hemodynamics of cardiogenic shock - decreased CO/____ and decreased _____ (<65%)
CI; SvO2
71
ABG in cardiogenic shock will show ____________ respiratory and ____________ _______________ and ______________
Mixed; metabolic acidosis; hypoxemia
72
Metabolic acidosis in cardiogenic shock is due to __________ acidosis that is occurring from decreased systemic ______________and ________________ metabolism
Lactic; perfusion; anaerobic
73
In cardiogenic shock, respiratory acidosis on ABG is ___________ in etiology, and is a result of ______________ __________
Hypercapnic; pulmonary edema
74
Echo in patient with cardiogenic shock will show decreased _______ __________, and reduced _______
Wall motion; EF
75
Mixed respiratory and metabolic acidosis in cardiogenic shock - respiratory acidosis from ____________ d/t pulmonary _________, metabolic acidosis d/t __________ acidosis from decreased ______________/CO
Hypercapnia; edema; lactic; perfusion
76
Treatment for cardiogenic pulmonary edema includes measures to decrease (preload/afterload), including ___________, NTG, and __________
Diuretics; morphine
77
In acute/flash cardiogenic pulmonary edema, treatment is the same (diuretics, _______), but in addition, there is admin of positive ___________ (increase contractility) and ______________ (decrease afterload)
NTG; inotropes; vasodilators

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