ACS Flashcards
1
Q
Spectrum of cardiac ischemic disorders
A
Acute Coronary Syndrome (ACS)
2
Q
Major trigger for coronary thrombosis; due to chemical/physical stresses on the lesion
A
Atherosclerotic plaque rupture
3
Q
Vasoconstriction and diminished anti-thrombotic function can exacerbate…
A
coronary thrombosis
4
Q
Examples of endogenous anti-thrombotics
A
Antithrombin III Protein C and S Tissue Factor Pathway Inhibitor tPA Prostacyclin NO
5
Q
Acute Coronary Syndromes that are partially occlusive
A
Unstable Angina
NSTEMI
6
Q
Approx. _____ minutes of ischemia can cause an infarct
A
30
7
Q
Myocardial infarctions are usually the result of…
A
plaque changes with coronary thombosis
8
Q
Frequently, coronary thrombi dissolute within _____ hours
A
24
9
Q
MIs affect the (LV/RV) more often
A
LV
10
Q
In a subendocardial infarct, why is it only the innermost layers of the myocardium affected?
A
Poor collateral flow and furthest from epicardial coronaries
11
Q
Factors that affect the amount of tissue infarcted
A
Mass of myocardium perfused by the artery Duration of ischemia Oxygen demand Adequacy of collateral flow Degree of reperfusion
12
Q
An occlusion in the LAD can infarct what areas of the heart
A
Anterior LV
Anterior septum
Apex
13
Q
An occlusion in the LCx can infarct what areas of the heart
A
Lateral LV
14
Q
An occlusion in the RCA can infarct what areas of the heart
A
Posterior LV
Posterior septum
Posterior papillary muscle
Inferior
15
Q
Why does an MI result in cellular edema and risk of arrhythmias?
A
Decreased ATP synthesis (anaerobic metabolism) makes it harder to regulate ions.
16
Q
Macroscopic features of infarction: <24 hours
A
Dark mottling
17
Q
Macroscopic features of infarction: 1-14 days
A
Yellow/tan necrotic center, with possible red borders
18
Q
Macroscopic features of infarction: 2-8 weeks
A
gray-white scar
19
Q
Microscopic features of infarction: <24 hours
A
Wavy fibers
Nuclear pyknosis
Early PMNs (intravascular)
Contractile proteins coagulate (band necrosis)
20
Q
Microscopic features of infarction: 1-3 days
A
Loss of nuclei and striations
Interstitial PMNs
21
Q
Microscopic features of infarction: 3-14 days
A
Macrophages and granulation tissue
22
Q
Microscopic features of infarction: 2-8 weeks
A
Loss of cellularity
Increased collagen
Surrounding myocytes are hypertrophied (to compensate)
23
Q
Examples of systolic dysfunction
A
Hypokinesis
Akinesis
Dyskinesis
24
Q
When a local region in the ventricle has reduced contraction
A
Hypokinesis
25
When a local region in the ventricle has no contraction
Akinesis
26
Akinesis
Dyskinesis
27
Prolonged, but gradually reversible period of contractile dysfunction; takes days to weeks to recover
Stunned myocardium
28
When brief ischemia renders tissue more resistant to future episodes of ischemia
Ischemic preconditioning
29
MI complication resulting in left-to-right flow of blood through the septum
Septal perforation
30
MI complication resulting in severe mitral regurgitation due to valve incompetence
Papillary muscle rupture
31
MI complication when the wall bulges outward during systole and the fibrous scar progressively stretches; predisposes to rupture and mural thombosis
Ventricular aneurysm
32
Symptoms of MI
```
Chest pain (persistent, substernal, can radiate)
Nausea, vomiting, weakness
Diaphoresis, cool/clammy skin
Fever (inflammatory response)
Shortness of breath
```
33
Differential diagnosis for chest pain
```
Ischemia
Pericarditis
Costochondritis
GERD
Peptic ulcers
Pneumonia
PE
```
34
EKG abnormalities that hint at ischemia (in the setting of chest pain)
New ST elevation >1mm
New ST depression >1mm
New T-wave inversion
35
If you have the reversal of EKG abnormalities (T wave inversion) shortly after treatment such as nitro, it is suggestive of...
Myocardial ischemia
36
Cardiac biomarker that is released following cell death (necrosis) or injury; typically present in extremely low levels due to slow turnover
Troponins
37
Cardiac biomarker that is a cytosolic enzyme for energy production in cardiac tissues; no longer used for diagnosing MI
Creatine Kinase-MB
38
Why must you collect serial samples to analyze cardiac biomarkers for chest pain patients?
Initial set of "negative" does not rule out MI
| Values begin to rise at ~3 hours, and fluctuate over days
39
Non-cardiac causes of Troponin elevation
```
PE
Shock
Aortic dissection
Myocarditis
Trauma
```
40
When does an elevated troponin indicate a MI?
>99th percentile
41
ST-Elevation in leads II, III and aVF indicate infarction in...
inferior portion of heart (RCA)
42
ST-Elevations in leads V2-V4 indicate infarction in...
anterior portion of heart (LAD)
43
ST-Elevations in lead V4R indicate infarction in...
Right ventricle (RCA)
44
ST-Depressions in leads V1-V2 indicate infarction in...
Posterior portion of the heart (RCA)
45
Diagnostic difference between unstable angina and NSTEMI
UA: negative troponin
NSTEMI: positive troponin
46
Risk score for outcomes and treatment guidelines for potential MIs
TIMI Risk Score
47
UA, NSTEMI or STEMI:
| ST elevations; positive troponins; completely occluded coronary artery
STEMI
48
UA, NSTEMI, or STEMI:
| No ST elevation; positive troponins; sub-totally occluded coronary artery
NSTEMI
49
UA, NSTEMI, or STEMI:
| No ST elevation; negative troponin; sub-totally occluded coronary artery
UA
50
General therapies for Acute Coronary Syndromes
```
Bed rest
Oxygen
Analgesic
Anti-ischemic (beta blockers, nitrates)
Antiplatelet/thrombotic
```
51
If you see a evidence of a STEMI....
Open the artery emergently
52
therapy that decreases sympathetic drive on the heart (reduces oxygen demand); enhances electrical stability; target heart rate is <60 bpm
Beta blockers (metoprolol)
53
Contraindications for beta blockers
Bradycardia
Bronchospam
Hypotension
Acute heart failure
54
therapy that induces venodilation, decreasing preload and wall stress; improves blood flow to coronary arteries; administered sublingual then IV
Nitrates
55
Contraindication for nitrates (nitro)
```
RV infarction (dependent on pre-load, so can cause hypotension)
Sexual enhancement drugs (Viagra)
```
56
therapy that induces vasodilation, decreased chronotropy/inotropy; used if beta-blockers contraindicated; can't use in LV systolic dysfunction
Non-dihydropyridine Calcium Channel blockers (verapamil, diltiazem)
57
therapy that inhibits platelet synthesis of TxA2, thus platelet activation; given immediately
Aspirin
58
therapy that inhibits P2Y12 (ADP receptor) on platelets; used for aspirin-allergic patients; prodrug, so need to measure liver metabolism
Clopidogrel (Plavix)
59
therapy that is the most potent antiplatelet agent; blocks fibrinogen linkage; adjunctive therapy with PCI
G IIb/IIa inhibitor
60
Anticoagulant therapy that can only be used for when NO PCI is planned
Fondaparinux
61
Anticoagulant therapy that is only used in the cath lab for PCI
Bivalirudin
62
PCI technique that involves passing a balloon into partially occluded artery and inflating it to widen the opening; faulty because the artery can collapse with time
Percutaneous Transluminal Coronary Angioplasty (PTCA) or Plain ol' balloon angioplasty (POBA)
63
PCI
Percutaneous Coronary Intervention
64
PCI therapy that involves a metal cage into an obstructed artery; decreases restenosis compared to balloon angioplasty
Bare-metal stent
65
PCI therapy that involves a bare-metal stent that elutes antiproliferative agent, markedly reducing restenosis
Drug-eluting stent
66
Goals for treating STEMIs
Restore blood flow quickly
Prevent further thombus formation
Restore balance between O2 and demand
67
therapy that accelerates clot lysis, restoring blood flow and salvaging myocardium; transforms plasminogen to active plasmin; if given within 2 hours of onset of symptoms, mortality significantly reduced
Fibrinolysis
68
Contraindications to fibrinolysis
```
Active ulcers
Recent CVA
Recent surgery
Uncontrolled HTN
Very elderly
```
69
Immediate cardiac catheterization and revascularization; greater survival and less bleeding than fibrinolysis; needs to be performed within 90 minutes of onset
PCI (Primary Percutaneous Coronary Intervention)
70
What it is called when you give PCI after fibrinolytics have failed to reperfuse
Rescue PCI
71
If the time to PCI is going to be more than ___ hour(s) beyond when lytics could be given, then lytics are favored with immediate transfer to facility
1
72
Largely responsible for sudden cardiac death within 48 hours after an MI; most fatalities prior to hospital arrival
V-tach
| V-fib
73
How can sinus bradycardia result from a MI
SA node ischemia (occlusion of RCA)
74
Occlusion in what coronary artery is considered a "widow-maker"
LAD (effects the Left Bundle Branch)
75
therapy that helps the left ventricle pump blood, and increases blood flow through coronary arteries
Intra-aortic balloon pump (IABP)
76
Signs of right-sided heart failure
Elevated jugular venous pressure
Hypotension
Clear lungs
77
A holosystolic murmur is indicative of...
(Mitral) Papillary muscle rupture
78
Persistent ST elevation weeks after a STEMI is indicative of...
Ventricular aneurysm
79
inflammation of pericardial surfaces; sharp, pleuritic pain, fever, friction rub
Acute pericarditis
80
Immune process against necrotic myocardium; develops week later
Dressler syndrome
81
Drugs that reduce incidence of heart failure and recurrent ischemia; greatest benefit in those with LV dysfunction
ACE inhibitors
82
"Sham" procedures for PCI, very similar to a "placebo", are only able to be done because..
PCI has no improvement of mortality
83
What causes transmural infarct to happen?
Prolonged ischemia or total occlusion of coronary artery causes the entire thickness of myocardium to die.
84
What causes subendocardial infarct to happen?
Since the innermost layer of myocardium is further away from epicardial coronary artery and collateral blood flow, it doesn't get enough oxygen supply.
85
What is the process called when there is a change in the size, shape, structure, and function of the heart? Leads to ventricular dilation; "slippage" of myocytes; increases wall stress
Ventricular remodeling
86
Ventricular remodeling may result in diminished
contractile function (systolic) and stroke volume
87
Examples of Diastolic dysfunction
1. Reduced compliance
| 2. Elevated ventricular (diastolic) filling pressure
88
What is the complication of AMI that is caused by large infarcts and is most likely to occur in days 3-7 of a MI when wall is weakest?
Myocardial Free Wall Rupture
89
What complication can arise from free wall rupture
Hemopericardium (blood from wall rupture filling up pericardial cavity), causing cardiac tamponade.
90
What is the complication of AMI that results in conduction disturbances and myocardial irritability leading to sudden death?
Arrhythmias
91
What is the complication of AMI that involves infarct in LV and is the result of high grade stenosis of all coronary vessels and can lead up to 90% mortality?
Acute left ventricular failure --> cardiogenic shock
92
What is the complication of AMI that results in ongoing/repeat ischemia
Extension of Infarct
93
What is the complication of transmural AMI that results in bulging of ventricular wall during systole?
Aneurysm
94
What causes aneurysm?
Fibrous scar progressively stretching as infarct matures.
| * Increased risk for myocardial rupture, causing mural thrombosis
95
What is the complication of AMI that predisposes patients to systemic embolization especially after apical infarcts?
Mural thrombosis
96
Chest pain that is pleuritic, positional, sharp, not associated with exertion and is reproducible with palpation is
Atypical (not likely to be AMI)
97
Chest pain that radiates to limbs or shoulders, associated with exertion, nausea, vomiting, sweating is
Typical (likely to be AMI)
98
Hints for a MI during a physical examination
1. Evidence of Systemic Hypoperfusion
| 2. Evidence of Heart Failure
99
What are evidences of systemic hypoperfusion?
hypotension, tachycardia, impaired cognition, cool extremities, end-organ injury
100
What are evidences of heart failure?
elevated JVP, pulmonary crackles, S3/S4 gallops, new murmurs
101
S4 (atrial gallop) indicates
compromised ventricular filling due to decreased ventricular wall compliance = increased resistance to filling of ventricle.
102
Ischemia makes the heart stiffer, thus compromising diastolic filling and producing a (S3 or S4) sound
S4
103
Change in T wave inversion in the setting of chest pain (from inverted T wave to upright normal T wave) after nitroglycerin treatment is suggestive of
Myocardial Ischemia
104
ST depression and T wave inversion is suggestive of
Subendocardial ischemia
105
ST elevation on EKG is suggestive of
Transmural ischemia
106
ST depression segment points ____ epicardial injury
toward
107
ST elevation segment points ____ epicardial injury
away from
108
What is the biomarker that was used in the past to diagnose MI?
Creatine Kinase-MB
109
What was the function of CK?
It was a cytosolic enzyme responsible for energy production in cardiac tissue
110
What are some non-cardiac causes of troponin elevation?
- PE, trauma, shock
- ICD discharge, myocarditis
- Heart failure, aortic dissection (tearing)
111
How do you diagnose STEMI?
Based on ECG
112
What are the requirements of STEMI diagnosis?
1. presence of >1mm ST elevation in at least two contiguous leads
OR
2. >2mm ST elevation in 2 contiguous precordial leads
OR
3. New LBBB
113
ST-elevations in leads V1-V4 indicate infarction in...
anteroseptal of heart (LAD)
114
ST-elevations in leads I, aVL, V5, V6 indicate infarction in...
lateral (LV) of heart (LCx)
115
LBBB indicate infarction in
anterior of heart (LAD)
116
Electrically silent ECG indicate infarction of
LCx
117
STEMI is treated with emergent
Cardiac Catheterization
118
Pathologic Q waves are indicative of...
Previous transmural STEMI
119
Diagnostic criteria for pathologic Q waves are
1. > or = 1mm wide
2. >25% of overall QRS complex
3. present in at least 2 contiguous leads
120
What can cause an unusual transient ST elevations?
Variant (Prinzmetal) angina
121
What causes Variant Angina?
It's caused by a spasm in the focal coronary artery in the absence of atherosclerotic lesions. The spasm is due to smooth muscle hyperactivity and endothelial dysfunction.
122
What can increase the risk of variant angina?
smoking
123
How do you diagnose Variant (Prinzmetal) Angina?
Intracoronary ACh to provoke spasm
*cardiac cath is required to do this.
124
What are ECG abnormalities of UA or NSTEMI?
T wave inversion, ST depression
125
What is the most important risk factors of UA or NSTEMI and is denoted on TIMI risk score?
1. ST changes >= 0.5mm
| 2. elevated cardiac marker
