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NRS 271B > CAD & ACS > Flashcards

CAD & ACS Flashcards

1
Q

Define Ischemic Heart Disease

A

narrowing of 1 or more of the coronary arteries

-this impedes coronary blood flow → deprives the tissues of oxygen supply → increases the oxygen demand

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2
Q

what is the leading cause of death for both men & women in the US?

A

Heart Disease

Middle aged men > women

post-menopausal women → increased incidence 2-3x

50% manifest as chronic stable angina

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3
Q

What is under the umbrella of Ischemic Heart Disease

A
  • IHD:
    • Chronic Stable Angina
    • Acute Coronary Syndromes (ACS)
      • Unstable angina
      • Non-STEMI
      • STEMI
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4
Q

Cardiac Conditions that are associated with Angina

A
  • Most common = atherosclerotic plaques
  • Vasospasm
    • less common → no atherosclerotic disease = Prinzmetal’s angina (beta-blockers worsen this)
  • Aortic Dissection
  • Aortic Stenosis
  • Pericarditis
  • Severe Uncontrolled HTN
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5
Q

Non-Cardiac Conditions Associated with Angina

A
  • anxiety
  • anemia
  • carbon monoxide poisoning
  • PUD, GERD
  • PE, pneumothorax, pulmonary HTN, thryotoxicosis
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6
Q

Symptoms of Chronic Stable Angina

A
  • predictable
  • associated with exercise or emotional stress
  • last a short amount of time (≤ 5 min)
  • disappears with rest or use of nitro
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7
Q

Symptoms of Unstable Angina

A
  • occurs even at rest
  • change in usual pattern of angina
  • unexpected
  • more severe and lasts longer than stable angina (~30min)
  • may not disappear with rest or use of angina medication
  • might signal a heart attack
  • no biomarkers (i.e. troponin is not elevated)
  • Abnormal EKG but no ST elevation
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8
Q

Types of Troponin

A
  • Troponin-T: 0-0.2ng/ml
    • binds to Tropomyosin
    • onset in 3-4 hours ***USED MOST OFTEN**
    • return to normal after 10-14 days
  • Troponin-I: 0-0.1ng/mL
    • Inhibits actomyosin ATPase
    • levels return to normal after 4-7 days
  • Troponin-C
    • binds to calcium to initiate contraction
    • can’t differentiate between cardiac and smooth muscle troponin-C
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9
Q

Types of STEMIs

A
  • Type I:
    • caused by atherothrombotic coronary artery
  • Type II:
    • mismatch of O2 supply/demand
  • Type III:
    • MI with unexpected death before drawing biomarkers
  • Type IV:
    • 4a: associated with PCI complications from procedure
    • 4b: PCI related due to stent/scaffold thrombosis
  • Type V:
    • MI associated with CABG
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10
Q

Primary Prevention vs Secondary Prevention

A
  • Primary Prevention:
    • before the person has the disease
  • Secondary Prevention:
    • managing the disease, preventing an event from happening AGAIN
  • BAAAS:
    • Beta-blocker
    • Anti-platelet therapy
    • ACE-I or ARB
    • Statin
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11
Q

General Meds/Factors to prevent ACS and death

A
  • Control modifiable risks
    • dyslipidemia
    • HTN
    • DM
  • antiplatelet agents
  • ace-i/ARBs
  • Statins
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12
Q

Meds to Prevent Recurrent Ischemic Symptoms

A
  • Beta-blockers
  • CCB
  • -long-acting nitrates
  • Ranolazine
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13
Q

Meds to Relieve acute symptoms

A

Short Acting Nitrates

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14
Q

Antiplatelet Classes

A

ASA and P2Y12 inhibitors

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15
Q

ASA

A

aspirin (NSAID)

inhibits cyclooxygenase (COX enzyme) → reduces thromboxane synthesis → inhibits the activation of platelets

  • Not for adults <50 or >70
  • 81-162 mg Qday
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16
Q

P2Y12 Inhibitors

A

inhibit platelet activation and aggregation!!

  • Clopidogrel
    • prodrug (activated by 2C19) + irreversible inhibition
    • DDI with PPI (espec omeprazole)
    • Qday
  • Prasugrel
    • highest Potency
    • prodrug (unaffected by 2c19) + irreversible inhibition
    • Qday
  • Ticagrelor
    • not a prodrug
    • REVERSIBLE inhibition
    • dosing BID not Qday (so less popular)
  • SEs:
    • cough, HTN, dizziness, HA, bleeding, edema, bradycardia, dyspnea
17
Q

Nitrates MOA, DDI & SEs

A
  • MOA:
    • nitrates → nitric oxide → activates guanylate cyclase in smooth muscle → increased cGMP → release of Ca2+ from muscle cells → smooth muscle relaxation
    • primarily cause VENODILATION which reduces preload
      • but higher doses can cause arterial dilation which reduces afterload and BP
        • dilating the coronary arteries = increase oxygen supply
  • DDI: CONTRAINDICATED:
    • PDE5 inhibitors → ***severe hypotension, syncope or MI****
      • sildenafil/tadalafil
    • lidocaine → increased risk of methemoglobinemia
    • dihydroergotamine (DHE = migraine med) → decrease nitrate efficacy, increase DHE level → vasoconstriction → angina
    • EtoH → severe hypotension
  • SEs:
    • Severe hypotension
    • methemoglobinemia
      • (heme can no longer carry o2 because it has be oxidized by NO)
    • HA
    • dizziness
    • Can develop tachyphylaxis so must allow up to 14 hours of nitro free intervals Qday
18
Q

Short Acting and Long Acting Nitrates

A
  • Short-Acting Nitrates:
    • Topical:
      • nitro-bid – 2% ointment
        • need 10-12h nitrate free interval Qday
      • nitro-dur – transdermal
    • Sublingual spray:
      • nitrolingual → 1-2 sprays q5min PRN
      • Nitromist
    • Sublingual Tab:
      • nitrostat = 0.4mg SL q5min prn
  • Long Acting:
    • isosorbide mononitrate
      • dosing 1-2x/day
    • isosorbide dinitrate
      • dosing 1-3x/day
19
Q

Use of Beta-Blockers in CAD & ACS and what to avoid

A
  • Why:
    • reduce the HR → decrease myocardial oxygen demand
    • slow HR → prolong diastole → increased coronary blood flow
    • stabilize the membrane to prevent arrhythmias
    • decrease risk of reinfarction → improves survival
      • metoprolol, propranolol, carvedilol
  • Avoid:
    • the ISA + Agents (carteolol, acebutolol) because they have intrinsic sympathomimetic activity → produces a lesser reduction of oxygen demand
    • non-selective agents for asthmatic patients
    • avoid beta-blockers in treating prinzmetal angina → can WORSEN SXS
20
Q

CCB and preventing recurrent ischemic symptoms: MOA, Efficacy, & ContraIndications

A
  • MOA:
    • decrease wall tension (afterload)
    • decrease contractility → decreased myocardial demand for oxygen
    • non-dihydropyridine slow SA & AV node conduction → further decreases the oxygen demand
      • more effect as antianginal than dihydropyridine
    • dilate coronary arteries (all CCBs) → increase oxygen supply and relieve spasm
  • Efficacy:
    • same as beta blockers
    • good alternative if BB is contraindicated
    • Dihydropyridines + CCB = relieve sx better than either one alone
      • CI: do not give non-dihydropyridine + BB → SEVERE bradycardia
  • Contraindication for IHD:
    • pre-existing conduction disease without pacemaker (non-dihydropyridines)
    • concurrent use with negative inotropic agent (beta blockers)
    • short acting dihydropyridine (ie nifedipine, nicardipine)
      • high risk for hypotension
21
Q

CCB and preventing recurrent ischemic symptoms: MOA, Efficacy, & ContraIndications

A
  • MOA:
    • decrease wall tension (afterload)
    • decrease contractility → decreased myocardial demand for oxygen
    • non-dihydropyridine slow SA & AV node conduction → further decreases the oxygen demand
      • more effect as antianginal than dihydropyridine
    • dilate coronary arteries (all CCBs) → increase oxygen supply and relieve spasm
  • Efficacy:
    • same as beta blockers
    • good alternative if BB is contraindicated
    • Dihydropyridines + BB = relieve sx better than either one alone
      • CI: do not give non-dihydropyridine + BB → SEVERE bradycardia
  • Contraindication for IHD:
    • pre-existing conduction disease without pacemaker (non-dihydropyridines)
    • concurrent use with negative inotropic agent (beta blockers)
    • short acting dihydropyridine (ie nifedipine, nicardipine)
      • high risk for hypotension
22
Q

Non-dihydropyridines

A

Diltiazem & Verapamil

  • slow SA & AV node conduction → further decrease oxygen demand
  • best for antianginal use
    • better than dihydropyridines
  • decrease contractility → decreased oxygen demand
  • dilate the coronary arteries
  • good alternative if beta blockers are contraindicated
  • contraindications:
      • beta blockers → risk of SEVERE bradycardia
    • preexisting conduction disease without a pacemaker
      • short acting dihydropyridines (ie nifedipine, nicardipine)
        • high risk of Hypotension
23
Q

Ranolazine (Ranexa)

A

Approved as first line for CHRONIC STABLE ANGINA but normally reserved for refractory angina

  • Minimal effects on HR & BP
  • MOA:
    • inhibits sodium channel opening during phase 0 → prevents influx of sodium into the ICF
  • SEs:
    • QT prolongation, syncope, bradycardia
    • hypotension, tinnitus, blurred vision, vertigo
  • Contraindications:
    • liver cirrhosis
    • tx with CYP3A4 inhibitors (ketoconazole, clarithromycin, nelfinavir)
    • tx with CYP 3a4 inducers
24
Q

Summary for Stable IHD

A
25
Q

Treatment Algorithm for Stable Angina

A
26
Q

Tx of Prinzmetal Angina

A

AVOID BETA-BLOCKERS

  • For Sx relief: Nitroglycerin IR
  • if HTN = CCB effective as monotherapy +/- Long acting nitrates
    • if hypotension → LA nitrates
27
Q

Unfractionated Heparin (UFH): MOA, indications, & contraindications

A

longer sugar chain so inhibits Factor Xa + Thrombin (IIa)

  • Indications:
    • STEMI: pts undergoing PCI and pts txed with fibrinolytics
    • NSTEMI: in combo with antiplatelet therapy for conservative or invasive approach PCI
  • Contraindications:
    • active bleeding, hx of heparin-induced thrombocytopenia, severe bleeding risk, recent stroke
28
Q

Low-Molecular Weight Heparin: MOA, indications, contraindications

A

Enoxaparin**

Shorter sugar chain so only inhibits factor Xa NOT thrombin (IIa)

  • indications:
    • STEMI:in pts receiving fibrinolytics
    • NSTEMI: in combo with aspirin for conservative or invasive approach
  • Contraindications:
    • active bleeding
    • hx of heparin-induced thrombocytopenia, severe bleeding risk
    • recent stroke
    • if CrCl < 15mL/min
    • avoid if CABG surgery planned
29
Q

Bivalirudin (Angiomax)

A

Direct thrombin inhibitor → binds 2 of 3 sties on Thrombin

used when pt has heparin-induced thrombocytopenia

  • indications:
    • NSTEMI: for invasive strategy
    • PCI in STEMI
  • Contraindications:
    • active bleeding, severe bleeding risk
30
Q

Initial Tx in STEMI & NSTEMI

A

oxygen (if O2 sat <90%), SL NTG, aspirin, morphine sulfate, IV NTG

31
Q

After initial tx: STEMI ≤ 12 hours

A
  • Reperfusion Therapy:
    • Option 1:
      • higher-dose statin before primary PCI
        • then clopidogrel, prasugrel or ticagrelor (P2Y12 inhibitors → inhibit activation and aggregation of platelets
        • then Bivalirudin (thrombin inhibitor) alone or UFH + GP IIb/IIIa receptor blocker
        • then Beta-blocker, ACE-i/ARB, eplerenone (spironolactone)
    • Option 2:
      • Fibrinolysis
      • clopidogrel, statin
      • then IV UFH or IV & SC enoxaparin
      • then Beta-blocker, ACE-i/ARB, eplerenone (spironolactone)
32
Q

After initial Tx: STEMI ≥ 12 hours

A

Secondary PCI or CABG or fibrinolysis then BAAAS (beta-blocker, ACE-i/ARB, aspirin, eplerenone (spironolactone)

  • for secondary PCI during hospitalization, admin bivalirudin alone or UFH or enoxaparin with optional GP IIb/IIIa inhibitor at time of PCI
33
Q

NSTEMI tx Chart = early conservative therapy or Early invasive strategy

A
34
Q

Glycoprotein IIb/IIIa receptor inhibitors

A

MOA: prevent aggregation

  • abciximab
  • eptifibatide
  • tirofiban
  • Contraindications:
    • active bleeding, thrombocytopenia, prior stroke, renal dialysis (eptifibatide)
35
Q

PCI

A

also called percutaneous coronary intervention, is a procedure that uses a catheter (thin, flexible tube) and small balloon threaded through a blood vessel in the groin or arm and guided to heart to open a blocked or narrowed coronary artery

36
Q

CABG

A

Surgery in which a healthy blood vessel taken from another part of the body is used to make a new path for blood around a blocked artery leading to the heart. This restores the flow of oxygen and nutrients to the heart. Also called aortocoronary bypass and coronary artery bypass grafting

NRS 271B (10 decks)

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