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Foundations II > CHD and ACS > Flashcards

CHD and ACS Flashcards

1
Q

Differential dx for Chest Pain?

A
  • Non-ischemic cardiovascular CP: aortic dissection, expanding aortic aneurysm, pericarditis, PE
  • Non-cardiovascular causes: Pulmonary (PNA, pleuritis, pneumothorax), GI (GERD, esophageal spasm/ or perforation, PUD, pancreatitis, biliary dz), Musculoskeletal (costochondritis, cervical radiculopathy, rib fx), other (anxiety/panic attack, Munchausen, sickle cell crisis, Zoster)
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2
Q

What is the classic ACS initial therapy?

A

MONA:
- Morphine: pain, anxiety, & pulmonary edema
- Oxygen: for pt’s with SpO2 <90%, heart failure, or dyspnea
- Nitroglycerin: for pts w/ ongoing CP, HTN, or HF
- ASA: all pts w/out hypersensitivity, chewable or PR
+/- antiemetics

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3
Q

What percentage of people in the US who experience ACS will be NSTE-ACS?

A
  • 70%
  • M>F over 40 y/o
  • women and elderly w/ atypical sxs such as GI, lung, and fatigue
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4
Q

What is angina?

A

clinical syndrome characterized by jaw, shoulder, or arm discomfort attributable to coronary ischemia

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5
Q

What is typical angina?

A
  • substernal chest discomfort w/ characteristic quality and duration
  • provoked by exertion or emotional stress
  • relieved by rest or nitroglycerin
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6
Q

What is atypical angina?

A
  • having only 2 of the typical characteristics

- may be pleuritic, reproducible pain w/palpation or movement, constant and lasting days, fleeting pain lasting seconds

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7
Q

What is stable angina?

A
  • develops w/predictable amount of exertion
  • similar to typical angina
  • short duration (<5 mins)
  • resolves w/rest or antianginal med
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8
Q

What is unstable angina?

A
  • develops at rest or w/minimal exertion
  • change in typical pattern of angina
  • more severe, longer lasting up to 30 mins
  • may not resolve w/rest or antianginal medication
  • due to insufficient coronary blood flow, w/out evidence of myocardial necrosis
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9
Q

What is NSTE-ACS?

A
  • any condition compatible w/acute myocardial ischemia and/or infarction usually due to an abrupt reduction in coronary blood flow
  • imbalance of myocardial oxygen consumption and demand that may lead to ischemia/infarct
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10
Q

What is NSTEMI & STEMI

A
  • angina w/elevated cardiac biomarkers indicating MI w/ or w/out ST segment deviation
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11
Q

What is a myocardial infarction?

A

rise or fall of cardiac biomarker values (preferably Troponin) w/ at least one value above the 99% of upper reference limit + one of the following:
- sxs of ischemia, new ST-segment-T wave changes or new LBBB, pathological Q waves, new loss of viable myocardium or new RWMAs, intra-coronary thrombus by angiography or autopsy

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12
Q

What are pain descriptors that are characteristic of angina?

A
  • radiation to R arm or shoulder, both arms or shoulders, radiation to left arm, exertional, diaphoresis, N/V, pressure
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13
Q

Describe the coronary dz spectrum.

A

Ischemia: stable and unstable angina
infarction: NSTEMI, STEMI
ACS: unstable angina, NSTEMI, STEMI
stable > unstable angina > NSTEMI, STEMI (worst)

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14
Q

When would you do ischemia-guided (conservative) strategy vs. early invasive?

A
  • ischemia guided: low risk score (TIMI 0-1/2), pt/md preference, extensive comorbidities (hepatic, renal, pulmonary failure, CA)
  • early invasive: new ST depression, elevated Trop, recurrent angina at rest despite therapy, CHF sxs or low LV function, hemodynamic instability, arrhythmia, prior PCI/CABG w/in 6 mo’s
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15
Q

Etiology of NSTE-ACS?

A
  • Coronary a. obstruction (atherosclerosis –> plaque rupture and thrombosis)
  • vasospasm (Prinzmetal’s “pressure” angina, drugs)
  • coronary embolism (DVT w/ PFO, LV thrombus, endocarditis)
  • dissection (aortic or coronary)
  • non-obstructive (hyper/hypotension, anemia, hyperthyroid, arrhythmias)
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16
Q

What are some initial steps in evaluation for a pt with ACS?

A
  • Hx
  • PE: possible findings incl Levine’s sign (bring hand up to chest saying “tight”), new S4, splitting of s2, pericardial friction fub, 3 P’s (Palpable, positional, pleuritic)
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17
Q

What is pt’s baseline risk for ACS? aka what are the CAD risk factors?

A
  • M > F, age, prior hx CAD, kidney dz, DM, HLD, HTN, PAD, smoking
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18
Q

What should every patient undergo w/in 10 mins of arrival to ED for evaluation of ACS?

A
  • an ECG along w/ obtaining hx
  • may repeat q15-30 mins for 1st hour as sxs change
  • a normal ECG does not exclude ACS
  • ECG changes: peaked T waves, Q wave formation, T wave inversion
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19
Q

what changes would you see on ECG for NSTE- ACS?

A
  • ST-segment depression by 5mm in 2 contiguous leads and T-wave inversion of at least 1mm (0.1mV)
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20
Q

what are some ECG pitfalls?

A

False positives: pre-excitation, J-point elevation (Brugada syndrome), CNS dz, metabolic disturbance, drug-induced (digoxin)
False negatives: RV pacing, LBBB, prior MI w/ Q waves or persistent ST elevation

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21
Q

What diagnostic studies should you order when doing initial evaluation for ACS?

A
  • Serum biomarkers: CK, CK-MB, Trop
  • CBC, BMP, coagulation panel, cholesterol levels
  • B-type natriuretic peptide (BNP)
  • CXR
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22
Q

What are diagnostic studies you could order in addition to the initial diagnostic studies for ACS?

A
  • exercise stress testing
  • stress echocardiography
  • pharmacologic stress testing
  • Myocardial perfusion imaging
  • cardiac CT angiography
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23
Q

IF you do an ECG and ST is elevated =

A

STEMI

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24
Q

IF you do an ECG and ST is depressed or there are T-wave inversions =

A

NSTE-ACS

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25
Q

NSTE-ACS Troponin: when should you order? which pt’s?

A
  • all pt’s who p/w sxs c/w ACS to identify rising and/or falling pattern
  • at presentation and 3-6 hrs after sxs onset
  • obtain beyond 6 hrs for pt’s w/ normal Trop but ECG or clinical presentation confer intermediate/high index suspicion for ACS
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26
Q

Cardiac biomarkers: Troponins are elevated as early as ___, but may not be elevated for up to ____, and may persist _____ or longer.

A
  • 2-4 hrs
  • 12 hrs
  • 14 days

Note: normal levels does not mean there is no ischemia

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27
Q

How long does Troponin stay elevated after onset of AMI?

A
  • about 1 week
28
Q

False positive cardiac biomarkers

A
  • sepsis, burns, respiratory failure, drug toxicity, HTN, acute PE, CKD
29
Q

Causes of elevated troponin: injury related to supply/demand imbalance of myocardial ischemia?

A
  • tachy/brady arrhythmias
  • cardiogenic, hypovolemic, or septic shock
  • Hypertension w/ or w/out LVH
30
Q

Causes of elevated troponin: multifactorial or indeterminate myocardial injury?

A
  • heart failure
  • severe pulmonary embolism or pulmonary hypertension
  • sepsis and critically ill pt’s
  • renal failure
31
Q

Cardiac enzymes: CK-MB can be used for the dx of ___ and to ___. What is the difference between the enzyme CK-MB and Troponin?

A
  • reinfarction
  • assess reperfusion
  • Trop normalizes in 7-14 days while CK-MB normalizes in 1-3 days
32
Q

What are the 3 most common risk-stratification modules useful in management of NSTE-ACS?

A
  • TIMI risk score
  • GRACE risk model
  • HEART score for MACE
33
Q

Describe the TIMI UA/NSTEMI risk score.

A 
generates score up to 7 w/ yes answers.
1) age 65 y/o or greater
2) 3 or more risk factors for CAD
( fam hx, HTN, HLD, DM, current smoker)
3) known CAD (stenosis >50%)
4) ASA in past 7 days
5) severe angina >2 or + episodes w/in 24hrs 6) ST changes > 0.5mm (ST depression)
7) positive cardiac biomarker
- 0-2 = low risk
- 3-4 = intermediate risk
- 5-7 = high risk
34
Q

Who should be admitted to the hospital for initial inpatient management?

A
  • pt’s w/ recurrent sxs, ischemic changes on ECG, elevated Trop, intermediate to high risk pt’s (TIMI 3)
35
Q

NSTE-ACS standard medical therapies

A
  • supplemental O2
  • anti-platelet
  • Statin: high intensity (i.e. Atorvastatin 80mg)
  • obtain fasting lipid panel w/in 24 hrs
  • Nitroglycerin: for persistent angina, CHF, or HTN
  • Analgesics: IV morphine, NSAIDs contraindicated
36
Q

NSTE-ACS standard medical therapies: describe anti-platelet therapy

A
  • ASA (non-enteric coated, chewable) continue indefinitely
  • P2Y12 inhibitor in addition for up to 12 mo’s (i.e. plavix): Clopidogrel (300-600mg) then 75mg daily, Ticagrelor 180mg then 90mg daily
  • All pt’s should receive DAPT (dual antiplatelet therapy)
  • GP IIb/IIIa inhibitors (Abciximab, Eptifibatide, Tirofiban)
37
Q

How long should you continue anti-platelet therapy after NSTE-ACS?

A
  • ASA 81mg daily for life

- P2Y12 inhibitor for STEMI for 1 year

38
Q

All pt’s w/ NSTE-ACS w/out contraindications should receive a P2Y12 inhibitor. What 2 should you choose from?

A
  • Clopidogrel or Ticagrelor
39
Q

____ is recommended in addition to DAPT in pt’s with NSTE-ACS irrespective of initial treatment strategy?

A

Anticoagulation:
- indirect thrombin inhibitors –> UFH, Enoxaparin,
Fondaparinux
* increase ATIII activity but do not lyse existing clots
- direct thrombin inhibitors –> Bivalirudin, Argatroban

40
Q

For a NSTE-ACS which medication should you give w/in the 1st 24 hrs? When should you hold giving this medication? What med could you give instead if the previous med was contraindicated?

A
  • Betablockers: oral metoprolol, carbedilol, bisoprolol
  • if pt has acute CHF, hypotension, heart block or airway dz
  • Calcium Channel blockers
41
Q

When would you consider giving a NSTE-ACS an Angiotensin Converting Enzyme Inhibitor (ACE-I)? What would you use if pt has an intolerance to ACE-I?

A
  • all pt’s w/ a LV-EF <40%, HTN, DM, or stable CKD

- ARB (i.e. Losartan)

42
Q

When is an aldosterone antagonist recommended for NSTE-ACS?

A
  • for pts post-MI w/ no renal dysfunction (Cr) or hyperkalemia, who are on therapeutic ACE-I and BB & have… an LVEF <40%, DM, or CHF
43
Q

What are the steps to risk stratification?

A
  • clinical features: angina pattern, ECG, trop, CHF
  • consider risk factors: HTN, HLD, DM, FH, gender, tobacco use
  • combination: Diamond-Forrester angina scale, TIMI risk score, GRACE,etc)
  • is there coronary ischemia or not? Order noninvasive stress test
44
Q

When is it recommended to order a noninvasive stress test for evaluation of coronary ischemia?

A
  • if pt has had 2 negative Trop’s

- low or intermediate risk who are free of ischemia at rest for minimum of 12hrs

45
Q

What are the advantages and disadvantages to an exercise ECG?

A
  • A’s: simple, low cost, available

- D’s: doesn’t quantify ischemia, low sensitivity, prone to false positives in women

46
Q

Which pt’s need to undergo stress imaging?

A
  • abnormal baseline ECG (i.e. baseline ST abnormalitis, BBB’s, digoxin, etc)
47
Q

Advantages and disadvantages to a stress echocardiography?

A

D: subjective and not standardized
A: good specificity and sensitivity, localizes ischemia, fast results

48
Q

What are the advantages and disadvantages to a stress nuclear myocardial perfusion imaging test?

A
  • A: good sensitivity and specificity, if pt has CAD, info about viability of myocardium, quantity of involved myocardium
  • D: expensive, takes more time, radiation exposure
49
Q

Post-hospital care for pt’s that rule in and have an MI should be referred for…

A

cardiac rehab bc it decreases cardiac and overall mortality

50
Q

What TLC’s and medications should the patient receive post-hospital visit after having an MI?

A
  • ASA 75 - 162mg daily
  • ACE-I/ARB on discharge if LV systolic dysfunction
  • Beta blockers
51
Q

Provide a short summary of the management of NSTE-ACS.

A
  • pt p/w angina
  • EKG w/in 10 mins
  • H&P + biomarker (risk stratify)
  • if low risk then d/c home and consider outpt stress test
52
Q

Acute coronary syndromes w/ ST segment elevation =

A

STEMI, which results from a thrombus developing from a ruptured atherosclerotic plaque
- depicted by irreversible ischemia leading to death of the myocardium (infarction)

53
Q

Special considerations for Acute coronary syndromes w/ST segment elevation.

A
  • consider cocaine in young adults
  • Vasospasms (less common)
  • R-sided ECG if inferior AMI suspected
  • sxs are more severe
  • painless MI seen in 1/3 pt’s, esp. women, elderly, DM, and alcoholics
54
Q

What changes on ECG would you expect to see for a STEMI?

A
  • new ST-segment elevation (>1mm) in 2 contiguous leads
  • in leads V2-V3, 2mm or more in men and 1.5mm or more in women
  • in other leads 1mm or more
55
Q

If pt has a STEMI on ECG…

A
  • if FMC to device is 90 mins or less…do PCI if capable –> guideline-directed medical therapy
  • if greater than 120mins–> fibrinolytic therapy in 30 mins or less –> guideline-directed medical therapy
56
Q

What is a percutaneous coronary intervention?

A
  • coronary angiography: catheter inserted leg and up the aorta –> tip stops at left coronary a. –> contrast agent inject into aa. –> xray imaging shows stenosis in left coronary a.
57
Q

When do you do a CABG?

A
  • unsuccessful angioplasty or persistent ischemia
  • stent thrombosis
  • fibrinolysis and PCI contraindicated
  • Class I: signif L main stenosis over 70%
58
Q

STEMI Anti-platelet therapy: ASA, when & which dosages?

A
  • ASA 162-325mg at presentation then 81mg for life
59
Q

STEMI Anti-platelet therapy: P2Y12 inhibitor, when & which dosages?

A
  • P2Y12 inhibitor at presentation or time of PCI: Clopidgorel 600mg, Prasugrel 60mg (No if hx of TIA/CVA), Ticagrelor 90mg BID;
  • maintenance doses go down to Clopidgorel 75mg, Prasugrel 10mg, Tacagrelor 90mg for 1 year or until bleeding risk outweighs benefit
60
Q

STEMI Anti-platelet therapy: Fibrinolytic therapy & antiplatelet, when & which dosages?

A
  • Fibrinolytic therapy and anti-platelet therapy: load w/ ASA 162-325mg &… Clopidgorel 300mg for patients 75 y/o or younger or Clopidgorel 75mg for pt’s 75 y/o +
  • continue ASA for life; Clopidgorel at least 2 weeks
61
Q

STEMI Anti-platelet therapy: IIb/IIIa inhibitor, when & which dosages?

A
  • IIb/IIIa inhibitor at time of PCI: Abciximab, Tirofiban, Eptifibatide
62
Q

STEMI management- anticoagulation: PCI therapy

A
  • initiate ASAP

- UFH (unfractionated Heparin) w/ or w/out GP IIb/IIIa inhibitor

63
Q

STEMI management- anticoagulation:

Fribrinolytic therapy

A
  • iniate ASP
  • UFH (unfractionated Heparin)
  • Enoxaparin - if beyond 48 hrs
  • Fondaparinux
64
Q

Fibrinolytics/Thrombolytics

A
  • streptokinase, urokinase, and rtPA
  • earlier it is initiated more benefits
  • major contraindications: brain bleed
65
Q

STEMI management - routine medical therapy

A

MONS

Foundations II (3 decks)

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