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OU Module Cardio Spring 2018 > Hospital Course of Treatment for ACS > Flashcards

Hospital Course of Treatment for ACS Flashcards

1
Q

Define Coronary Artery Disease (CAD)

A
  • Inadequate supply of blood and oxygen to a specific part(s) of the myocardium, usually due to coronary plaque
  • Imbalance between myocardial oxygen supply and demand
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2
Q

pathophysiology of CAD

A

Disruption of myocardial oxygen supply and demand within coronary anatomy

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3
Q

cardinal signs/symptoms of CAD

A
  • ECG changes
  • Presence of biomarkers
  • Angina pectoris (chest pain)
  • Others: Diaphoresis, Syncope, Hypotension, Hypertension, Tachycardia, Bradycardia, Pain radiating to left arm, Nausea, Vomiting, Dyspnea upon exertion, Dyspnea at rest, Atypical Symptoms
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4
Q

ECG changes

A
  • Blood supply to cardiac conduction system mostly supplied by coronary arteries to the SA node, AV node, and Bundle of His so if there is a blockage there, ECG will be abnormal
  • ST segment changes, T-wave inversions, Q-waves (indicative of pervious MI in the past), bundle brand blocks
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5
Q

Biomarkers

A
  • Troponin: Most specific, Troponin INT is specific -> only found in myocardium
  • Myoglobin
  • Creatine Kinase (CK)-MB
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6
Q

Angina pectoris (chest pain)

A
  • Ischemic manifestation
  • Substernal chest discomfort with a characteristic quality and duration, that can be provoked by exertion or emotional stress
  • Things to think about: quality of chest pain, location, duration, precipitating factors, relieving factors
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7
Q

pathophysiologic manifestations of CAD

A
  • Coronary artery with unstable plaque that resulted in formation of partial occlusive thrombus can lead to ischemia or infarction
  • Coronary artery with unstable plaque that resulted in formation of TOTAL occlusive thrombus can lead to infarction
  • All about plaque stability and degree of thrombus occlusion!!!
  • Thrombus Occlusion
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8
Q

Thrombus Occlusion

A
  • Partial Occlusion of Coronary Artery -> unstable angina (UA) or NSTEMI
    ▪ UA: unstable plaque causing ischemia
    ▪ NSTEMI: unstable plaque causing infarction
  • Total Occlusion of Coronary Artery -> STEMI
    ▪ Unstable plaque causing infarction
    ▪ Requires immediate intervention to clear plaque from coronary artery
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9
Q

assessment for CAD

A
  • Risk factors
  • Ischemic chest pain
  • Stress testing
  • Electrical conduction abnormalities in the ECG
  • Biomarkers (as a rule OUT)
  • Cardiac catheterization
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10
Q

Stress testing

A
  • causing ischemia to help diagnose CAD
  • if pt cannot reach peak heart rate (220-age) and is experiencing chest pain and ECG changes = CAD
  • can also be done via pharmacologic intervention: dobutamine injected -> vasodilates and steal oxygen from the vessels
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11
Q

How does electrical conduction abnormalities in the ECG relate to ischemia?

A

when pts experience ischemic symptoms, it will show in the ECG

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12
Q

CSA

A

chronic stable angina

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13
Q

SIHD

A

stable ischemic heart disease

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14
Q

CSA or SIHD

A
  • Stable coronary plaque
  • Angina precipitated by exertion or emotional stress and relieved by rest
  • Do not have biomarkers
  • Transient ST-segment changes that develop during symptomatic episodes that resolves when the patient becomes asymptomatic
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15
Q

UA

A
  • unstable angina
  • Unstable coronary plaque
  • Angina can precipitate by exertion or emotional stress or at rest, and is NOT relieved by rest
  • Do not have biomarkers
  • ST-segment changes that may develop during symptomatic episodes that do not resolve
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16
Q

AMI

A
  • acute myocardial infarction
  • Unstable coronary plaque
  • Angina can precipitate by exertion or emotional stress or at rest and is NOT relieved by rest
  • Presence of biomarkers
  • ST-segment changes that do not resolve when the patient becomes asymptomatic or that develop at rest
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17
Q

empiric treatment of agents used to restore balance of myocardial oxygen supply and demand for patients who are hospitalized for ACS

A

MONA-B

  • Morphine
  • Oxygen
  • Nitroglycerin
  • Aspirin
  • Beta blocker
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18
Q

Morphine

A
  • Decrease pain (when pts feel pain, they put more work on their heart) -> decrease work of breathing -> decrease HR -> decrease myocardial oxygen demand
  • Also increase in venodilation
  • Administration: 2-4mg IV; Titrate by 2-8 mg q. 5-15 min
  • NO EFFECT ON MORTALITY
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19
Q

morphine adverse effects

A
  • Hypotension
  • Nausea/vomiting
  • Respiratory depression
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20
Q

Oxygen

A
  • Only get oxygen if your O2 saturation (SaO2) is < 90%
  • Increase myocardial oxygen supply
  • NO EFFECT ON MORTALITY
  • Administer only for the first 6 hours
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21
Q

Nitroglycerin

A
  • decrease myocardial oxygen demand (reduce preload; reduce afterload at higher doses)
  • 0.4 mg PO SL q. 5 minutes x 3 doses maximum
  • Assess for IV nitroglycerin (5-10 mcg/min then 5-20 mcg/min until symptoms are relieved)
  • NO EFFECT ON MORTALITY
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22
Q

Nitroglycerin contraindications

A
  • have a SBP ≤ 90 mmHg or SBP drop 30 mmHg below baseline
  • have a HR < 50 bpm
  • have a suspected RV infarct
  • have taken sildenafil or vardenafil within the past 24 hours or taken tadalafil within the pat 48 hours
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23
Q

Aspirin

A
  • If have not received ASA in ambulance or at home, administer 325mg non-enteric coated tablet (ask them to chew)
  • Produces a rapid anti-thrombotic effect via immediate and neartotal inhibition of thromboxane A2 production
  • DECREASES MORTALITY
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24
Q

Beta blocker

A
  • Decrease heart rate = decreased myocardial demand = heart remains in diastole longer = increase in myocardial perfusion
  • Reduces magnitude of infarction and associated complications
  • Reduces life-threatening ventricular tachyarrhythmias
  • DECREASES MORTALITY
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25
Q

oral beta blockers is recommended within 24 hours to patients who do not present with what?

A
  • Signs of heart failure
  • Evidence of low output state
  • Increased risk for cardiogenic shock
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26
Q

Beta blocker contraindications

A
  • Prolonged PR interval on ECG (> 240 ms)
  • 2nd or 3rd degree AV block
  • Active asthma or reactive airway disease – relative CI; if you’re treating the asthma or COPD, you CAN use beta blockers
27
Q

if pt has contraindications to beta blockers, what can you do?

A

If pt does NOT have heart failure with reduced ejection fraction or an AV node block, can administer non-DHP CCB for the angina relief but do not affect mortality

28
Q

time to elevation and peak for cTnI (Cardiac Troponin I)

A
  • > 1.5 ng/mL
  • Time to initial elevation: 3-12 hours; seen more after 6 hours
  • Mean time to peak elevations: 24 hours
  • Time to return to normal range: 5-10 days
29
Q

time to elevation and peak for cTnT (Cardiac Troponin T)

A
  • > 0.1 ng/mL
  • Time to initial elevation: 3-12 hours; seen more after 6 hours
  • Mean time to peak elevations: 12-48 hours
  • Time to return to normal range: 5-14 days
30
Q

What intervals should you measure troponin levels?

A

Measure within 6 hours, remeasure every 6-8 hours until levels have peaked (2-3 times)

31
Q

Reperfusion Strategy goal

A
  • Occlusion of infarcted artery can occur from 6-12 hours while affected myocardial zone is undergoing necrosis
  • Restore perfusion to coronary vasculature by attenuating thrombus burden
32
Q

What are the reperfusion strategies?

A
  • Pharmacologic (Fibrinolysis)

- Percutaneous Coronary Intervention (PCI)

33
Q

Percutaneous Coronary Intervention (PCI)

A
  • Using a stent or balloon to open up artery
  • performed in the cardiac catheterization lab
  • associated with the best outcomes because have less risk of bleeding but is more invasive
  • two types: Drug-Eluting Stent (DES), Bare Metal Stent (BMS)
34
Q

role of high-intensity statin therapy in the treatment of ACS

A
  • Reduces rate of recurrent MI, CAD mortality, revascularization, and stroke
  • Decrease in anginal symptoms (?)
  • Lowering of LDL-C
  • Decrease in ischemic symptoms
  • Pleiotropic effects
  • Plaque stabilization
  • Regression of atheroma
  • Reduced inflammation
35
Q

When should high-intensity statins be used?

A

High-intensity statin therapy should be initiated or continued in all patients with ACS and no contraindications to its use

36
Q

pharmacogenomic considerations with the use of clopidogrel

A
  • Needs to be activated by CYP2C19
  • Avoid PPI’s; they will inhibit CYP2C19 -> Nexium and Prilosec; Can use H2 blockers -> Dexlansoprazole, lansoprazole and pantoprazole
  • P-glycoprotein can kick it out
  • People also have polymorphism of CYP2C19
37
Q

P2Y12 receptor antagonists

A
  • Ticlopidine (Ticlid®)
  • Clopidogrel (Plavix®)
  • Prasugrel (Effient®)
  • Ticagrelor (Brilinta®)
  • Cangrelor (Kengreal®)
38
Q

Ticlopidine doses

A

250 mg PO twice daily

39
Q

Clopidogrel doses

A
  • LD: 300-600 mg

- MD: 75 mg once daily

40
Q

Prasugrel doses

A
  • LD: 60 mg

- MD: 10 mg once daily

41
Q

Ticagrelor doses

A
  • LD: 180 mg

- MD: 90 mg twice daily

42
Q

Cangrelor doses

A

30 mcg/kg IV bolus prior to PCI followed immediately by an infusion of 4 mcg/kg/minute continued for at least 2 hours or for the duration of the PCI

43
Q

pearls for Ticlopidine

A
  • Black box warning: Hematologic Toxicity

- Avoid in patients with thienopyridine

44
Q

pearls for Clopidogrel

A
  • Bleeding
  • Avoid in patients with thienopyridine hypersensitivity
  • CI: active bleeding
45
Q

pearls for Prasugrel

A
  • Only to be used in UA/NSTEMI or STEMI patients managed with PCI
  • CI in pts with history of stroke and active bleeding
  • Should not be used in pts ≥ 75 years of age or < 60 kg due to increased risk of bleeding -> Has better outcomes but comes with increased risk of bleeding
  • Avoid in patients with thienopyridine hypersensitivity
46
Q

pearls for Ticagrelor

A
  • Greater platelet inhibition compared to prasugrel
  • greater, and more consistent platelet inhibition than clopidogrel -> better outcomes but comes with increased risk of bleeding (not as much as effient)
  • Maintenance doses of ASA > 100 mg reduces the effectiveness of ticagrelor
  • AE: bleeding, dyspnea, increased uric acid, CV events (Ventricular pauses, Bradycardia)
  • CI: history or HPI of intracranial hemorrhage, active bleeding
  • Drug-drug interaction with morphine: decreases the rate and extent of absorption
47
Q

pearls for Cangrelor

A
  • First IV; reversible; half life of 3-6 min
  • Platelets returns to normal function within an hour
  • Avoid in pts receiving GP IIb/IIIa receptor antagonists, prasugrel or clopidogrel
48
Q

Which medications should you avoid that has a thienopyridine allergy?

A
  • Clopidogrel
  • Prasugrel
  • Ticlopidine
49
Q

Describe the role of antiplatelet therapy (ASA, P2Y12 receptor antagonists, and GP IIb/IIIa receptor antagonists in the treatment of ACS.

A
  • ASA: 81mg now; prevents TxA2
  • P2Y12 receptor antagonists: for ADP inhibition
  • GP IIb/IIIa receptor antagonists: temporarily inactivate platelet cascade by promoting crosslinking of fibrinogen
50
Q

Risk Factors for Bleeding

A
  • Age ≥ 65 years
  • Body weight < 60 kg
  • Recent trauma/surgery (ex. CABG)
  • Anemia
  • Uncontrolled HTN
  • Recent or recurrent GI bleeding
  • Active Peptic Ulcer Disease (PUD)
  • Moderate-severe renal impairment
  • Severe hepatic impairment
  • Concomitant drugs that increase risk of bleeding
51
Q

What are the GP IIb/IIIa receptor antagonists?

A
  • Abiciximab
  • Eptifibatide
  • Tirofiban
  • more often used IN the cathlab, not so much after the procedure in the cathlab
  • Mostly administered in setting of no pretreatment with ASA/P2Y12 inhibitor
  • “Bail-out” therapy
52
Q

Why should you always treat chest pain seriously?

A

because it could be a sign of:

  • Aortic Dissection
  • Aortic Aneurysm
  • Peptic Ulcer Disease (PUD)
  • Gastroesophageal Reflux Disease (GERD)
  • Pericarditis
  • Pulmonary Embolism (PE)
  • Panic Disorder (“Panic Attack”)
53
Q

What is an acronym for the assessment of CAD in the ER?

A

“The Three Ds”

  • Door
  • Data
  • Decision
54
Q

How soon should you revascularize the coronary vasculature?

A

as soon as possible

55
Q

What is ischemic time?

A

the time it takes for the pt to get to the hospital until treatment

56
Q

When should you perform an ECG?

A
  • within 10 min of ED arrival
  • one every 15-30 min for first hour (ECG changes are only captured 30% of the time) if pt is symptomatic and initial ECG is not diagnostic
57
Q

Anticoagulation Therapy to Support Reperfusion

A
  • Unfractionated Heparin (UF)
  • Low Molecular Weight Heparin (LMWH): Enoxaparin, Dalteparin
  • Direct Thrombin Inhibitors (DTIs): Bivalirudin, Argatroban
  • Factor Xa Inhibitor: Fondaparinux
58
Q

Bare Metal Stent (BMS)

A
  • risk of repeat revascularization and restenosis
  • lower bleed risk
  • used over DES when issues with adherence arises, high risk bleeding with dual DAPT, surgery is about to happen
59
Q

Drug Eluting Stent (DES)

A
  • Anti-proliferative agents coated on the stent to decrease restenosis
  • increased risk of bleeding
  • delayed healing
60
Q

What are the drugs used in drug eluting stents?

A
  • Sirolimus
  • Everolimus
  • Zatarolimus
  • Paclitaxel
61
Q

What should be done after a drug eluting stent?

A

patient should be on P2Y12 receptor antagonists for at least 12 months

62
Q

Management/Inpatient Pharmacotherapy

A
  • MONA-B (administered in the ED)

- MONA-BAAS (administered in catheterization lab and/or cardiac intensive care unit)

63
Q

What are the anti-platelet therapies?

A
  • ASA
  • ADP inhibition: clopidogrel, prasugrel, ticagrelor, cangrelor
  • GP IIb/IIIa Receptor Antagonists: Abciximab, Eptifibatide, Tirofiban
64
Q

What is the purpose of AAS in MONA-BAAS?

A
  • have to keep artery open
  • temporarily inactivate platelet cascade
  • temporarily keep artery potent and keep thrombogenic material from moving downstream

OU Module Cardio Spring 2018 (16 decks)

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