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NP School > CAD, ACS > Flashcards

CAD, ACS Flashcards

1
Q

What are the risk non-modifiable risk factors for Coronary Artery Disease (CAD)?

A
  • increasing age
  • men > women
  • family history
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2
Q

What are the risk modifiable risk factors for Coronary Artery Disease (CAD)?

A
  • smoking, increases LDL and decreases HDL
  • HTN
  • uncontrolled DM
  • obesity
  • contraceptive use, usually if > 35 y/o
  • HLD
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3
Q

What does ASCVD stand for?

A

atherosclerotic cardiovascular disease

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4
Q

What is the dosage of atorvastatin when starting a patient in high-intensity statin therapy?

A

40 or 80mg

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5
Q

How do statins affect the patients lipid profile?

A
  • HMG-CoA reductase inhibitor
  • decreases LDL
  • modestly decreases TG
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6
Q

What are potential complications of hyperlipidemia?

A
  • atherosclerosis
  • pancreatitis
  • steatosis, fatty liver
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7
Q

What are the potential complications of statin therapy?

A
  • rhabdomyolysis
  • hepatitis
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8
Q

When should high intensity statin therapy be started?

A

1) clinical ASCVD (CAD, MI, etc)
2) LDL > 190
3) DM + 40 to 75yr + LDL >70
4) 40 to 75yr + LDL>70 + 10 ASCVD 10 risk of stroke/MI >7.5%

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9
Q

What is the dosage of rosuvastatin when starting a patient in high-intensity statin therapy?

A

20 or 40 mg

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10
Q

What baseline labs need to be drawn prior to starting high intensity statin therapy?

A
  • creatine kinase to monitor for rhabdomyolysis
  • LFT’s to monitor for hepatitis
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11
Q

How do bile acid sequestrants affect the patients lipid profile?

A
  • inhibits bile acid absorption in the GIT
  • lowers LDL
  • causes diarrhea
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12
Q

What is the class and MOA of Cholestyramine?

A
  • bile acid sequestrant
  • lowers LDL
  • inhibits bile acid absorption in the GIT
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13
Q

What is the class and MOA of Ezetimibe?

A
  • lowers LDL
  • inhibits cholesterol absorption in the GIT
  • causes diarrhea
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14
Q

What effect do Fibrate medications have on the lipid profile?

A

-decrease TG
- slightly decrease LDL
- poss increase HDL

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15
Q

What is the difference between angina and an acute myocardial infarction?

A
  • angina is discomfort or pressure in the chest with no myocardial damage
  • MI is necrosis of the myocardial tissue
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16
Q

What is the underlying cause of an acute myocardial infarction?

A
  • myocardial O2 demand is greater the ability of the coronary arteries to supply
  • blockage of blood supply to myocardial tissue
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17
Q

What are risk factors for the having an acute myocardial infarction?

A
  • CAD
  • HTN
  • metabolic syndrome
  • obesity
  • DM
  • male
  • sedentary lifestyle
  • diet
  • stress
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18
Q

How long should it take for a STEMI patient to receive fibrinolytics upon arrival to the hospital (door to fibrinolytics)?

A

within 30 min

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19
Q

How is the door to angioplast/heart cath time for a STEMI patient?

A

within 90 mins

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20
Q

What should be suspected if a patient presents with intermittent chest pain/discomfort that has the same onset, intensity and duration. It usually induced by exercise, exertion or stress and last between 5-20 mins?

A

Stable angina

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21
Q

Why is nitroglycerin given a patient with stable angina?

A

it causes vasodilation of the coronary arteries, which increases the blood and O2 supply to the myocardium

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22
Q

What is the term for chest comfort or pain at rest with transient ECG changes in the ST segment?

A

Prinzmetal angina
- aka: vasospastic or variant

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23
Q

What is Prinzmetal angina?

A
  • aka: vasospastic or variant
  • term for chest comfort or pain at rest with transient ECG changes in the ST segment
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24
Q

What is the difference between prinzmetal and stable angina?

A

1) Onset:
- prinzmetal (PM): usually occurs at rest
- stable angina is usually triggered by exertion
2) Symptoms:
- PM: chest pain or discomfort that can move to arm, shoulder, or head
- stable: feels like pressure or indigestion
3) Pattern:
- PM: last up to 30mins and can recur
- stable: lasts 5-30 mins and is regular, predictable
4) ECG
- PM: ST-segment elevation
- stable: ST depression

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25
Q

What is/are the main causes of Prinzmetal angina?

A

coronary arterial spasms
- may be precipitated by sumatriptan, amphetamines, EtoH, cocaine

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26
Q

What is/are the treatment(s) for Prinzmetal angina?

A

Calcium channel blockers to manage the coronary arterial spasms

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27
Q

What is/are the treatment(s) for stable angina?

A
  • lifestyle modifications (diet, exercise, smoking cessation)
  • nitrates
  • beta blockers
  • calcium channel blockers
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28
Q

What are common symptoms a woman would report if having an myocardial infarction?

A
  • GI like symptom
  • pain that radiates to the back
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29
Q

Lack of pain during an Myocardial Infarction is common in what patient population?

A

diabetics and elderly secondary to neuropathies

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30
Q

Should a cardiac workup be completed on an woman presenting with GI-like symptoms, fatigue, SOB and pain radiating to their back?

A

Yes, these are common presentations in women experiencing a myocardial infarction or unstable angina

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31
Q

What are the 3 subclassifications of acute coronary syndrome?

A
  • unstable angina
  • NSTEMI
  • STEMI
32
Q

What ECG changes, if any, would be seen in a patient experiencing a Non-ST segment elevation MI?

A

may see:
- ST segment depression
- T-wave inversion

33
Q

What are the symptoms of Acute Coronary Syndrome?

A
  • chest pain
  • N/V
  • diaphoresis
  • cool, clammy skin
  • dyspnea
  • feeling of impending doom
34
Q

How do you differentiate an MI from unstable angina?

A

chest pain associated with MI is not relieved by nitroglycerin

35
Q

ST segment depression seen on a 12-lead ECG is indicative of what?

A

myocardial ischemia

36
Q

The following are indicative of what?
- T-wave inversion
- peaked T-waves
- ST segment depression

A

myocardial ischemia

37
Q

Which vessels are involved if a ST-segment elevation seen in leads II, III and aVF?

A

Inferior MI involving the:
- right coronary artery (80-90%
- left circumflex (10-20%)

38
Q

Which vessels are involved if a ST-segment elevation seen in leads II, III, aVF, V5 and V6?

A

Inferolateral MI involving:
- left circumflex artery

39
Q

Which vessels are involved if a ST-segment elevation seen in leads V3 and V4?

A

Anterior MI involving the left anterior descending artery

40
Q

Which vessels are involved if a ST-segment elevation seen in leads I, aVL, V5 and V6?

A

Anterolateral and lateral MI involving:
- left anterior descending artery
- left circumflex artery

41
Q

Which vessels are involved if a ST-segment elevation seen in leads V1, V2 and V3?

A

Posterior MI involving:
- right coronary artery
- left cirumflex

42
Q

How often should serial cardiac enzymes be drawn on a suspected MI patient?

A

q6-8 hrs

43
Q

What is the preferred biomarker for identifying Acute Coronary Syndromes (UA, STEMI, NSTEMI)

A

Troponin (T and I)

44
Q

What serum cardiac enzymes should be drawn in a patient suspected of having experiencing Acute Coronary Syndrome?

A
  • Troponin T
  • Troponin I
  • myoglobin
  • CK-MB
  • total CK
  • B-type natriuretic peptide (BNP)
45
Q

What BNP serum levels are associated with an MI?

A

100-400 pg/ml

46
Q

What labs should be drawn on a patient suspected of experiencing Acute Coronary Syndrome?

A
  • BNP
  • CBC
  • prothrombin time (PT)
  • partial prothrombin time (PTT)
  • BMP
  • Lipoprotein profile (lipid panel)
47
Q

How is the treatment/management of acute coronary syndrome?

A
  • aspirin 162-325 mg (chew)
  • nitroglycerin 0.4 mg
  • morphine (2-4mg)
  • O2
  • 12 lead
  • telemetry
  • labs
    admit to hospital
  • start beta-blocker if hemodynamically stable
  • consider anticoagulation
  • high intensity statin
  • fibrinolytic therapy for STEMI
  • cardiac catheterization
48
Q

What is the dosage of aspirin prescribed to a suspected MI patient?

A

162-325mg PO chewable

49
Q

What is the dosage for nitroglycerin when prescribed for a suspected MI patient?

A

0.4mg sublingual
- q5 min x 3

50
Q

What is aspirin’s MOA?

A
  • non-selective irreversible inhibition of COX-1 (primarily) and COX-2 (in high doses) enzymes
  • results in the inhibition of platelet aggregation and production of pain-causing prostaglandins.
  • stops the conversion of arachidonic acid to thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation
51
Q

What is the average lifespan of a platelet cell?

A

7-10 days

52
Q

For hemodynamically stable ACS patients, starting oral beta-blocker therapy should be done within what timeframe?

A

within the 24hrs of admission

53
Q

Which medication should be started within 24hrs of admission for a hemodynamically stable ACS patients?

A

oral beta-blocker
- metoprolol 25-50mg, then titrate to maintenance dose of 50-100mg BID

54
Q

What is the reversal agent for heparin?

A

protamine sulfate

55
Q

Which lab value should be monitored when a patients is receiving scheduled heparin (fractionated) or lovenox (low-molecular weight heparin)?

A

prothrombin time (PTT)
- normal range = 11-13.5 secs

56
Q

What medication should be given if a patient is allergic or cannot tolerate aspirin?

A

clopidogrel (plavix)

57
Q

What does t-Pa stand for and why is the risk of bleeding less than than other fibrinolytics?

A
  • Tissue plasminogen activator
  • less risk because it is fibrin specific and does not deplete clotting factors
  • converts plasminogen into plasmin which breaks down fibrin clots
58
Q

What is plasmin?

A

protein enzyme that breaks down fibrin in clots

59
Q

What is the normal ACT range?

A

70-120 secs

60
Q

Drug eluting stents require 12 months of dual antiplatelet therapy with which meds?

A

aspirin and plavix (clopidogrel)

61
Q

What is the term for the accumulation of blood and/or fluid in the pericardial space?

A

cardiac tamponade
- causes decreased CO

62
Q

What is Beck’s Triad?

A

1) jugular vein distention
2) narrowing pulse pressure
3) distant/muffled heart tones
- indicative of cardiac tamponade

63
Q

What is the term for a patient presenting with jugular vein distention, narrowing pulse pressure and distant/muffled heart sounds?

A

Beck’s Triad
- indicative of cardiac tamponade or fluid/blood accumulation in the pericardial space

64
Q

What is the gold standard to confirm the diagnosis of cardiac tamponade?

A

echocardiogram

65
Q

What is the management for a patient with cardiac tamponade?

A

pericardiocentesis
- symptom management with fluids, chronotropic and inotropic agents PRN

66
Q

What are the 2 categories of Peripheral Vascular Diseases?

A
  • Peripheral arterial disease
  • Chronic venous insufficiency
67
Q

What are the 2 biggest risk factors for PVD?

A
  • DM
  • smoking
68
Q

What are the six “Ps” r/t PAD symptoms?

A
  • Pain/intermittent claudication
  • Pallor
  • Pulse absent/diminished distal to occlusion
  • Paresthesia
  • Paralysis
  • Poikilothermia: inability to maintain core temp
69
Q

What are the s/s of PAD?

A
  • Pain/intermittent claudication
  • Pallor
  • Pulse absent/diminished distal to occlusion
  • Paresthesia
  • Paralysis
  • Poikilothermia
  • loss of hair on LE
  • shiny, think, cool, dry skin
  • dependent rubor/blushing
  • slow wound healing
70
Q

how is the ankle brachial index calculated?

A
  • need doppler
  • highest BP in arms / highest in foot
  • Normal > 1.0
  • PAD < 1.0
71
Q

What are the 2 tools used to diagnose PAD?

A
  • Rutherford’s categories
  • Ankle brachial index
72
Q

What is the med Cilostazol (Pletal) used to treat?

A
  • treats claudication in patients with PAD
  • inhibits platelet aggregation and induces vasodilation
73
Q

What are the s/s of chronic venous insufficiency?

A
  • leg ache that improves with elevation
  • tingling, burning, cramps, throbbing
  • restless leg
  • fatigue
  • dependent edema
  • shiny, taut, hyperpigmented skin
  • varicosities/varicose veins
74
Q

What exam confirms the diagnosis of chronic venous insufficiency (CVI)?

A

venous duplex imaging/ultrasound

75
Q

What is Virchow’s triad?

A

risk factors for DVT development
1) stasis of blood flow
2) endothelial injury
3) hypercoagulability

76
Q

What is the treatment for a DVT?

A
  • bed rest with extremity elevated
  • anticoagulation for 3-6 months for first, then for life if recurrent
  • Inferior vena cava (IVC) filter if anticoagulation is contraindicated
77
Q

What medications are used for anticoagulation therapy for a patient with a DVT?

A
  • heparin: 80mg bolus, gtt 18units/kg/hr
  • lovenox (enoxaparin)
  • direct thrombin inhibitor: dabigatran
  • factor Xa inhibitor: Eliquis (apixaban)
  • xarelto
  • warfarin (coumadin)

NP School (19 decks)

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