Cardio Midterm 2

Front 1

Where do plaques involved in atherosclerosis accumulate?

Back 1

in medium and large sized arteries throughout the body

Front 2

Does atherosclerosis occur only the in the heart?

Back 2

no

Front 3

What do more than 1/3 of US deaths result from?

Back 3

CV disease

Front 4

What is claudication?

Back 4

blockages of arteries of the lower extremities

Front 5

What is initial diagnosis of ACS based on?

Back 5

-hx
-risk factors
-symptoms
-EKG
-lab findings (positive cardiac enzymes)

Front 6

3 diagnoses under umbrella of ACS

Back 6

-unstable angina
-NSTEMI
-STEMI

Front 7

ST depression=

Back 7

ischemia

Front 8

What is the leading cause of death in the US?

Back 8

ACS (1:5 deaths)

Front 9

How many Americans will have new or recurrent coronary attack/ACS each year?

Back 9

1.2 million

Front 10

Will there be cardiac enzymes changes in unstable angina?

Back 10

NO

Front 11

Between stable angina and MI, what exists?

Back 11

unstable angina or pre-infarction angina

Front 12

Patient with prior stable angina may develop what?

Back 12

angina with less exertion (may develop at rest or awaken the patient from sleep)

Front 13

What is angina at rest with EKG changes associated with?

Back 13

BAD prognosis

Front 14

What do you need to exclude in a patient with unstable angina?

Back 14

factors other than pure mechanical obstruction (anemia, heart failure, arrhythmias which all increase myocardial O2 demand)

Front 15

What are unstable plaques characterized by?

Back 15

-large, lipid-rich core
-only a thin fibrous cap
-vulnerable to rupture

Front 16

What is believed to be involved in destabilizing a plaque and fibrous cap?

Back 16

-inflammatory cells
-activated macrophages

Front 17

What other cells have an important role in ACS?

Back 17

-platelets which are activated and aggregate after plaque fissure/rupture
-results in near or total occlusion of the coronary artery

Front 18

What is unstable angina also known as?

Back 18

crescendo angina

Front 19

What is used to classify risk for patients with unstable angina?

Back 19

Braundwald classification

Front 20

The higher the TIMI score...

Back 20

the greater the risk of an adverse cardiac event

Front 21

Can TIMI be used for patients with NSTE-ACS?

Back 21

yes

Front 22

What are 4 goals in treating patients with ACS?

Back 22

-increase myocardial blood flow
-relieve pain
-prevent overt infarction
-increase survival

Front 23

What are 2 therapeutic goals in treating patients with ACS?

Back 23

-reduce oxygen demand
-decrease platelet aggregation
-*RESTORE PERFUSION

Front 24

Patient Evaluation: Unstable Angina

Back 24

-hx/PE
-OPQRST

Front 25

What questions should be asked in PE of unstable angina?

Back 25

-is the patient hypo/hypertensive
-pulse?
-signs/symptoms of CHF?
-new murmurs/gallops?
-does patient have aortic stenosis or mitral regurgitation?
-does the patient look ill?

Front 26

What are standard labs to order?

Back 26

CBC
chem-7
coagulation studies
cardiac enzymes

Front 27

If a 12 lead EKG shows no ST segment elevation, what are they possibly having?

Back 27

-either NSTEMI or unstable angina

Front 28

Do patients with ST segment depression have the same 6 month risk of mortality as patients with ST segment elevation?

Back 28

YES (stresses importance of aggressive in-hospital and post-d/c therapy)

Front 29

What is the most sensitive and specific marker for myocardial injury?

Back 29

troponin!

Front 30

What is each troponin complex composed of?

Back 30

troponin C, T, and I (troponin I has 3 subtypes)

Front 31

What can troponins be spuriously elevated in?

Back 31

renal failure

Front 32

When does CK-MB become positive?

Back 32

-6-8 hrs after event

Front 33

What should you be leary of with CK -MB?

Back 33

-false positives, i.e. in rhabdomyolysis

Front 34

What is CK-MB not as sensitive/specific as?

Back 34

troponin

Front 35

What did the results of the TIMI IIB study show?

Back 35

-the greater the troponin level in patients who present with NSTE-ACS, the greater the risk of future mortality

Front 36

For the low risk patient

Back 36

-chest pain probably NOT angina, use clinical judgement and take a detailed history
-no more than 1 traditional risk factor for CAD (other than DM)
-unremarkable EKG
-biomarkers are serially negative

Front 37

What should you also do for the low risk patient?

Back 37

-ADMIT and check serial enzymes and EKG/telemetry (to rule out MI)
-BP control
-check fasting lipids
-stress test with nuclear imaging
-aspirin/beta blocker/statin
-life style changes

Front 38

If a patient remains without recurrent angina or positive biomarkers during observation, what is next step?

Back 38

stress test (preferably a nuclear study)

Front 39

If the hospitalized patient develops recurrent angina, "rules in by cardiac enzymes." or has an abnormal stress test result, what is warranted?

Back 39

coronary angiography

Front 40

If a hospitalized patient "rules in" for myocardial infarction, develops ischemic EKG changes, or has an abnormal stress test, then what is next step?

Back 40

cardiac catheterization

Front 41

If a patient rules in for MI by cardiac enzymes in absence of STE on EKG, what is this referred to as?

Back 41

NSTEMI

Front 42

If a patient shows up to the ED with ST segment depression, T wave inversions, or both, what are they considered?

Back 42

high risk
-higher risk of developing an MI, dying, or needing urgent revascularization

Front 43

**What should be concerning to clinicians (5 things)?

Back 43

-a concerning or worrisome hx
-abnormal EKG
-biomarkers positive/NSTEMI
-TIMI risk score > or equal to 3
-hemodynamic instability or pulmonary edema

Front 44

Management of at risk patients with high risk features:

Back 44

-anti-platelet agents (aspirin, heparin)
-beta blockers
-nitrates
-statins
-morphine for pain

Front 45

Generally speaking, how is cardiac catheterization performed?

Back 45

-catheter introduced into femoral artery
-catheter advanced to the heart
-contrast dye released and special radiographs taken to create a "road map" of the coronary arteries, identifying blockages
-usually balloon angioplasty and stent deployment

Front 46

What is another option in case of anatomic or technical difficulties with cardiac cath/stent placement?

Back 46

CABG

Front 47

ACS Rx to be familiar with

Back 47

-anti-platelet agents
-nitrates
-statins (80 mg lipitor)
-beta blockers
-ACE inhibitors/ARB
-morphine
-oxygen

Front 48

What are 4 examples of anti-platelet agents?

Back 48

-aspirin
-clopidogrel (Plavix)
-heparin
-IIBIIIA inhibitors

Front 49

What is the single most important drug you can give someone who you are suspecting is having a heart issue?

Back 49

**ASPIRIN

Front 50

What does aspirin do?

Back 50

-antiplatelet
-should be taken IMMEDIATELY after heart attack or suspected heart attack
-*has been shown to reduce mortality
-MC antiplatelet drug, and most patients with heart disease take it on a daily basis

Front 51

What provides more rapid benefit, chewing aspirin or swallowing it?

Back 51

chewing it

Front 52

Heparin

Back 52

-potent anticoagulant
-IV available
-inhibits clot formation and prevents extension or existing clots within the coronary arteries
-NOT clot buster

Front 53

Who should thrombolytics NOT be given to?

Back 53

the elderly

Front 54

What are 2 thienopyridines?

Back 54

-another class of anti-platelet drugs
-clopidogrel (plavix)
-prasugrel (effient)

Front 55

When should thienopyridines be given?

Back 55

-after PCI (angioplasty and stent) along with aspirin)
-patients with unstable angina for whom aspirin is contraindicated
-patients with unstable angina who are about to undergo a procedure
-can be taken on an ongoing basis as well

Front 56

How long should patients who have undergone PCI take aspirin and a thienopyridine?

Back 56

at least a year

Front 57

Beta blockers

Back 57

-reduce myocardial oxygen demand by slowing down the heart rate and lowering BP
-DECREASE mortality

Front 58

When should long term oral beta blockers be given?

Back 58

for patients with symptomatic coronary artery disease, particularly after heart attacks

Front 59

What are the 2 meds that have been shown to decrease mortality?

Back 59

aspirin and beta blockers

Front 60

Nitrates

Back 60

-dilate coronary arteries and veins
-increased flow of blood to heart and relief of ischemic pain
-usually self administered as a spray or sublingually (also available as transdermal)

Front 61

3 ACE inhibitors

Back 61

-lisinopril (zestril)
-ramipril (altace)
-captopril (capoten)

Front 62

Indications for ACE inhibitors

Back 62

-patients who have had a STEMI/NSTEMI
-*for patients with left ventricular dysfunction
-patients at risk of CHF

Front 63

Actions of ACE inhibitors

Back 63

-afterload reduction
-benefit in LV remodeling
-treat HTN
-first line for patients with DM and renal insufficiency

Front 64

What is considered first-line agent for patients with DM and renal insufficiency?

Back 64

ACE inhibitors

Front 65

What do statins do?

Back 65

lower LDL (especially for patients with ACS; aggressive lipid management)

Front 66

How do statins work?

Back 66

-competitively inhibit HMG CoA reductase (enzyme needed for hepatic production of cholestrol)
-liver responds by upregulating LDL receptors which remove LDL from plasma

Front 67

What is the goal LDL for a patient post MI?

Back 67

70

Front 68

What are the 2 most commonly prescribed statins?

Back 68

Atorvastatin (Lipitor)
Simvastatin (Zocor)

Front 69

What 2 drugs have been shown to have mortality BENEFIT?

Back 69

statins, ACE inhibitors

Front 70

Who should aldosterone blockers be given to?

Back 70

patients with ACS who also have CHF or LV dysfunction EF less than 40%

Front 71

What is the post ACS patient care plan? (7 things)

Back 71

-glycemic control
-weight loss
-healthy diet
-smoking cessation
-BP control
-lipid management
-cardiac rehab (nutrition, exercise)

Front 72

Case study: there were EKG changes but did not specify that they were elevation...so diagnosis was:

Back 72

NSTEMI