CAD Flashcards

1
Q

ischemic heart disease (IHD)

A

-Complication that occurs secondary to CAD (atherosclerosis)
-2 primary forms of IHD
-1. Angina pectoris – chronic condition characterized by episodic chest discomfort that occurs during transient coronary ischemia
-Typical angina:
-stable angina – attacks have similar characteristics and occur under same circumstances
-unstable angina – attacks increase in frequency and severity (often preclude MI)
-Variant angina (unstable) (aka Prinzmetal angina)- Due to acute coronary vasospasm and often occurs during rest or sleep

  1. myocardial infarction
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2
Q

angina

A

-pain secondary to ischemia
-can be sudden, severe, substernal, and radiating to the left shoulder
-can be induced by exercise, emotions, eating, or cold temperature
-waste products build

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3
Q

rationale of tx of angina: restore balance b/w myocardial O2 supply and demand

A

-increase O2 supply
-determined by coronary blood flow, regional blood flow and O2 extraction
-vasodilators (nitrates and CCBs) used to increase total coronary flow
-beta blockers can improve distribution of coronary flow by reducing intraventricular pressure (slow it down)

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4
Q

tx of angina: decrease myocardial O2 demand

A

-determined by HR, cardiac contractility and myocardial wall tension
-beta blockers and CCBs decrease HR, decrease BP and decrease contractility
-vasodilators reduce wall tension via their effects on ventricular volume and pressure
-decrease pre and after load

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5
Q

angina tx: differences in treating typical angina vs variant angina

A

-typical - vasodilators and beta-blockers work to decrease O2 demand via mechanism outlined above
-typical- increase O2 demand with limited O2 supply

-variant – vasodilators increase O2 supply by relaxing coronary smooth muscle and restoring normal coronary flow
-Beta-blockers NOT effective b/c they can’t counteract vasospasm
-variant- O2 supply is low (its a spasm) -> spasm is causing less O2 to tissue not
-can present weirdly

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6
Q

angina: adjunct tx

A

-Stabilize atherosclerotic plaques to prevent ACS
-Manage/treat the modifiable risk factors
-i. HTN
-ii. Hyperlipidemia
-iii. DM – optimize glycemic control
-iv. Smoking cessation

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7
Q

non pharm tx for angina

A

Revascularization (PCI and CABG)

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8
Q

stable ischemic heart disease tx chart

A
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9
Q

tx of angina: beta blockers

A

-“OLOL” drugs; (pregnancy category C/D) (first-line for typical angina if no contraindications)*
-MOA - decrease HR, decrease BP and decrease contractility -> myocardial O2 demand
-Indications – HTN, CHF, typical angina, MI, certain arrhythmias, migraine (certain agents)
-NOT used for variant/prinzmetal angina or acute angina attacks.
-Contraindications – sinus bradycardia (HR < 60), SBP < 100, heart block, cardiogenic shock, ADHF.
-Non-selective agents are contraindicated in COPD, asthma, DM.
-Precautions, Reactive airway disease, DM, PVD
-ADRs – fatigue, insomnia, dizziness, bradycardia, CHF, edema, hypotension, mental depression, hypercholesterolemia, sexual dysfunction
-DDIs – Verapamil (greatest potential for decrease contractility and decrease CO, other CCBs safer to combine), see HTN handout for other DDIs.
-Monitoring Parameters – BP, HR (titrate to HR 50-60) **
-Specific drugs used: (beta1 specific/cardioselective and non-ISA preferred)

-beta 1 specific/cardioselective*
-Metoprolol succinate (Toprol XL)
-Atenolol (Tenormin)
-Nebivolol (Bystolic)

-Non selective:
-Propranolol (Inderal)
-Nadolol (Corgard)

-α1/beta blockers:
-Carvedilol (Coreg)
-Labetalol (Trandate)

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10
Q

beta blocker

A

-improve mortality post MI
-titrate HR to 50-60

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11
Q

tx of angina: CCB

A

-MOA – bind to calcium ion channels in smooth muscle and cardiac tissue -> smooth muscle relaxation & suppression of cardiac activity -> increase O2 supply and/or decrease myocardial O2 demand
-indications – HTN, angina (esp useful for variant angina); arrhythmias (diltiazem and verapamil)
-Contraindications (mostly for non-DHPs) – SBP < 100, HR < 60, ADHF, EF < 40%, AV block
-ADRs – constipation
, fatigue, headache, flushing, dizziness, hypotension, bradycardia, reflex tachycardia, edema. Immediate release forms of nifedipine and other short-acting CCBs have increased risk of MI, CHF and death due to coronary heart disease.
-DDI – see HTN handout
-Monitoring Parameters – BP, HR, EKG (w/ certain agents)

-Role in angina management:
-Use non-DHPs as initial therapy when BBs are contraindicated
-Use DHPs as add on therapy to BBs
-Use in combo w/ nitrates
-Non-DHP preferred for variant angina

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12
Q

specific CCB used

A

-Non-DHPs
-Verapamil (Calan, Isoptin)
-Diltiazem (Cardizem, Tiazac)

-DHPs
-Amlodipine (Norvasc)
-Felodipine (Plendil)
-Nifedipine (Procardia XL) – avoid IR formulation

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13
Q

angina tx: organic nitrites and nitrates

A

-tolerance develops*
-MOA: release of nitric oxide -> diffusion into vascular smooth muscle cells -> formation of cyclic GMP -> venous dilation -> venous pooling -> decrease preload, decrease ventricular diastolic volume and decrease ventricular pressure -> decrease myocardial wall tension and decrease myocardial O2 demand.
-At higher doses: arterial dilation -> decrease PVR and left ventricular ejection pressure (afterload).
-Indications: angina, MI, CHF
-Contraindications: aortic valve stenosis, concurrent use with Sildenafil, Vardebafil, Tadalafil; angle-closure glaucoma, head trauma or cerebral hemorrhage, severe anemia and severe hypotension (SBP < 90)
-ADRs: H/A, dizziness, weakness, postural hypotension, rash, tolerance and anxiety. With overdose – reflex tachycardia and arrhythmias.
-DDI: PDE 5 inhibitors (Sildenafil, Vardebafil, Tadalafil) – severe hypotension and death have occurred; isosorbide is CYP3A4 substrate
-Monitoring parameters – blood pressure, heart rate
-Role in angina management:
-SL/PO to prevent effort-induced angina (prophylaxis)
-Long acting formulations for maintenance therapy (if CIs to BBs and CCBs or as add on to BB or CCB to optimize angina control)

-Formulations
-Amyl nitrate (INH) (X)
-nitroglycerin
-isosorbide

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14
Q

Organic Nitrites and nitrates: nitroglycerin

A

-IV, PO, SL, buccal, topical, transdermal
-SL form (Nitroquik, Nitrostat) and buccal form (Nitrogard) - Deteriorates in sunlight. Replace bottle every 3-6 months after opening
-Ointment form (Nitro-Bid 2% or Nitrol 2%) -messy only inpatient
-Patch form (NitroDur, Nitrek) – available in several doses -> 12 hr intervals to prevent tolerance
-PO form (Nitro-Time ER) – must be administered QD or BID only to minimize tolerance
-IV form – contains propylene glycol, need special tubing
-cool dry place, fridge, keep in container
-0.4mg every 5mins (3 doses max) - sublingual
-if first does doesnt provide any relief call 911

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15
Q

Amyl nitrate (INH) (X)

A

i. Rapid onset and brief DOA.
ii. Used for cyanide poisonings
-poppers

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16
Q

Organic Nitrites and nitrates: isosorbide

A

-PO, SL
-not as much tolerance
-dinitrate form (Isordil) – available PO or SL, give TID at 8am, 1pm, and 6pm.
-mononitrate form – available PO only -> Longer acting metabolite of dinitrate form:
-Ismo: BID – give 7 hrs apart
-Imdur: Once daily

17
Q

ranolazine

A

-MOA – sodium current inhibitor
-last choice
-Indications – Used for chronic stable angina in combination with CCB, beta-blockers or nitrates.
-Contraindications – pre-existing QT prolongation, uncorrected hypokalemia, hepatic failure, if taking drugs that prolong QT interval or drugs that are potent CYP3a4 inhibitors.
-Precautions - can prolong QT interval and induce torsades de pointes
-ADRs – dizziness, headache, constipation. Less effects on HR and BP than other classes. Prolongs QT interval
-DDIs – CYP450 substrate

18
Q

adjunct treatment: antiplatelets

A

-Aspirin
-MOA – inhibits synthesis of prostacyclin and thromboxane A2 -> prevent platelet aggregation -> decrease thrombosis.
-Role in angina - primarily used to prevent ACS in patients with unstable angina.
-Other agents:
-Clopidogrel (Plavix)- same efficacy as aspirin
-Prasugrel (Effient) – for UA
-Ticagrelor (Brilinta) – for UA

19
Q

optimize manageable risk factors

A

key
-htn, smoking, diet, lifestyle, exercise, lipids, diabetes

20
Q

adjunct tx: ACE inhibitors

A

-Role in angina:
-Use in all pts w/ CAD to help delay progression of CAD
-Do not relieve angina symptoms b/c do not directly affect O2 supply and demand

21
Q

overall management of angina

A

-1. Modification of cardiac risk factor
-2. Goals of treatment:
-Relieve acute symptoms
-Prevent ischemic attacks
-Reduce risk of MI and other cardiovascular problems

-3. Consider Type and severity of angina:
-Occasional episode- SL nitroglycerin
-Predictable episodes upon exertion - prophylaxis (mono,nitro,iso)
-Frequent episodes requiring regular SL NTG – beta blocker, CCB, nitrate + SL nitrate
-Angioplasty, stents or bypass may be necessary

-4. Consideration of Concomitant disease states:
-Asthma – non-DHP CCB or cardioselective BB most preferred
-DM – non-DHP CCB most preferred, nitrates/cardioselective BB are alternatives
-Heart failure – BBs and nitrates most preferred, non-DHP CCB least preferred
-HTN – BB & non-DHP CCB most preferred
-Prior MI – BB most preferred
-Bradycardia/heart block – DHP CCB preferred

22
Q

management of acute STEMI (ACCF/AHA STEMI guidelines)

A

-Goals of Therapy
-limit infarct size
-reperfuse obstructed coronary arteries
-reduce morbidity and mortality
-prevent post-MI complications

23
Q

pharm management of acute STEMI: aspirin

A

-antiplatelet agent.
-Dose: 162 - 325mg STAT, then 81-325mg QD
-Use for all MI patients unless contraindicated. Start ASAP, continue indefinitely
-reduces morbidity and mortality associated with MI

24
Q

pharm management of acute STEMI: IV nitroglycerin

A

-Recommended for the first 24 to 48 hours in patients with acute MI. Do not give if SBP < 90 or HR < 50
-NTG alleviates ischemic myocardial pain
-can take it prophylactically if you know you do something and get pain

25
Q

pharm management of acute STEMI: analgesics

A

-Intravenous morphine - 2 to 4 mg every 5 minutes, with some patients requiring as much as 25 to 30 mg before pain relief is adequate
-Pain control also includes – vasodilation, anxiety

26
Q

pharm management of acute STEMI: beta blockers

A

-Recommended to start IV dose ASAP and continue post MI with PO doses unless contraindicated
-Reduction in morbidity and mortality - immediate beta-blocker therapy appears to reduce (1) the magnitude of infarction and incidence of associated complications in subjects not receiving concomitant thrombolytic therapy and (2) the rate of reinfarction in patients receiving thrombolytic therapy

27
Q

pharm management of acute STEMI: ACE inhibitors

A

-Recommended for all post-MI patients with substantial left ventricular dysfunction and/or clinical CHF

28
Q

pharm management of acute STEMI: CCB

A

-Controversial in MI – do NOT affect morbidity and mortality.
-May be given to pts intolerant to beta-blockers
-Diltiazem – may be useful in pts w/ non-Q-wave MI without LV dysfunction
-can add on if on ACE and beta

29
Q

pharm management of acute STEMI: anticoagulants: duration of therapy depends on type of reperfusion therapy (PCI vs fibrinolytics)

A

-Weight-based Unfractionated heparin
-Low molecular weight heparins – (Enoxaparin or Dalteparin)
-Bivalrudin (Angiomax)
-Fondaparinux

30
Q

pharm management of acute STEMI: P2Y-12 inhibitors- antiplatelets agent

A

-(clopidogrel, prasugrel or ticagrelor)
-dose and duration depends on revascularization therapy*
-Usually continued w/ aspirin as Dual Antiplatelet therapy as maintenance

31
Q

pharm management of acute STEMI: fibrinolytics

A

-Fibrinolytics are used to achieve rapid thrombolysis. Usually used in institutions without PCI capability or if patient cannot be transferred to an institution with PCI capability
-Fibrinolytic therapy provides a survival benefit for patients with acute MI, based on large, well-controlled clinical trials
-MOA – plasminogen activators. Dissolve existing clots

-Absolute Contraindications in pts with MI*:
-Previous hemorrhagic stroke
-Other strokes or CVA within 1 year
-Intracranial neoplasm
-Suspected aortic dissection

-relative contraindications in pts with MI*:
-Severe uncontrolled HTN (> 180/110)
-Recent trauma, head trauma or major surgery
-Recent internal bleeding
-Pregnancy
-Active peptic ulcer
-History of chronic severe HTN

32
Q

examples of fibrinolytics

A

-Streptokinase – 1.5 million units over 30-60 minutes
-Alteplase (TPA) – 100 mg over 90 minutes total
-Reteplase (Retavase) – 10 units x 2 doses over 30 minutes total
-Anistreplase (Eminase) – 30 mg over 5 minutes total
-Tenecteplase (TNKase) - 30-50 mg (based on pt weight) over 5 seconds* -> time is tissue

33
Q

pharm management of acute STEMI: statins

A

Patient should be started on statins post-MI if not already receiving for long term reduction in CV events, morbidity and mortality
-anti-inflammatory affect - everywhere (including inside vasculature)

34
Q

reperfusion vs fibrinolytics for acute MI: STEMI pts

A

-If present to hospital w/ PCI capability, they should be treated with primary PCI (stent placement) within 90 minutes of first medical contact (Class IA rec)
-If present to hospital w/o PCI capability and cannot be transferred to PCI center within 90 minutes, they should be treated with fibrinolytics within 30 minutes of hospital presentation unless contraindicated (Class IB rec)

35
Q

management of other acute coronary syndrome: UA/NSTEMI pts

A

-PCI – stent placement (some pts require CABG therapy. If CABG therapy indicated, antiplatelets should be held for 5-7 days if possible)*
-ASA
-BBs
-Nitrates
-Antithrombotic regimens

-Anticoagulants - Options include:
-Weight-based unfractionated heparin
-LMWH
-Bivalrudin
-fondaparinux

-Antiplatelets
-ASA
-P2Y12 inhibitor (Clopidogrel, Prasugrel or Ticagrelor)
-IV Glycoprotein IIb/IIIa inhibitors (In most recent guidelines, the use of these agents is being diminished due to the efficacy of the P2Y 12 inhibitors + anticoagulants*
-On discharge: Dual oral antiplatelet therapy with aspirin and a P2Y12 inhibitor depending on type of stent placed; i.e. – drug eluting stents vs. bare metal stent)

-Statins – long term to delay progression, improve mortality
-ACE inhibitors – long term to delay progression, improve mortality
-A major difference in therapy between STEMI and NSTEMI is that fibrinolytics are NOT used in NSTEMI patients

36
Q

NSTEMI vs STEMI

A

-NSTEMI- white thrombus -> fibrinolytics dont work
-white thrombus is platelets
-STEMI- red thrombus

-NSTEMI enzymes are +
-NSTEMI ST depressions

37
Q

UA

A

-enzymes- negative