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Pharmacology > CAD, ischemic heart ds, angina, MI > Flashcards

CAD, ischemic heart ds, angina, MI Flashcards

1
Q

Angina pectoris: 3 classes

A

Typical angina/stable angina:
- attacks have similar characteristics
- occur under same circumstances (walk one block then pain)

Unstable angina
- attacks increase in frequency and severity
-often preclude MI

Variant angina/Prinzmetal angina:
- Due to acute coronary VASOSPASM
- often occurs during rest or sleep

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2
Q

Angina management with concomitant ds

A
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3
Q

Ischemic Heart Disease

A

Complication that occurs secondary to coronary artery disease= artherosclerosis

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4
Q

2 Primary Forms of IHD

A

Angina Pectoris
Myocardial Infarction

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5
Q

angina pectoris pain is secondary to what? what is it induced by?

A

Pain secondary to ischemia:**
- O2 deprivation
- nutrient deficiency
- build up of METABOLIC WASTE

Induced by:
- exercise
- emotions
- eating
- cold temperature

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6
Q

Goals of tx of angina:

A
  • Increase O2 SUPPLY
  • Decrease myocardial O2 DEMAND
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7
Q

Increase/Restore O2 SUPPLY: angina tx goal; what factors involved, and what drugs

A

Can increase O2 supply by modifying:
- coronary blood flow
- regional blood flow
- O2 extraction

Drugs:
-Vasodilators (nitrates and CCBs): increase total coronary flow
-Beta blockers: reduces preload + afterload = greater perfusion to coronaries

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8
Q

Decrease O2 DEMAND: angina tx goal; what factors do you modify and what drugs

A

Decrease myocardial O2 demand by modifying:
- HR
- contractility
- myocardial wall tension
- outcome: ↓ Preload & Afterload**

Drugs:
- BBs and CCBs: ↓ HR, ↓ BP, ↓ contractility
- Vasodilators: ↓ myocardial wall tension by lowering ventricular volume + pressure (preload + afterload)

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9
Q

angina tx: differences in treating typical angina vs variant angina

A

Typical: goal - DECREASE O2 demand
- vasodilators
- beta-blockers

Variant: goal - INCREASE myocardial O2 supply
- vasodilators: increase O2 supply by restoring normal coronary flow
-Beta-blockers = NOT effective b/c they can’t counteract vasospasm**
-variant: spasm is causing less O2 to tissue

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10
Q

Adjuct tx for angina: manage what risk factors? + stabilize what?

A

HTN
Hyperlipidemia
DM – optimize glycemic control
Smoking cessation

+ stabilize atherosclerotic plaque to prevent ACS (moderate to high dose statin)

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11
Q

non pharm tx for angina

A

Revascularization:
- PCI
- CABG

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12
Q

tx of angina: beta blockers monitoring parameters

A
  • BP
  • HR (titrate to HR 50-60) **
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13
Q

tx of angina: beta blockers MOA

A

MOA: lowers myocardial O2 demand *
- decrease HR + contractility -> decrease CO -> decrease BP *
- Less important for angina: inhibits renin secretion for renal juxtaglomerular cells -> decrease formation of angiotensin II -> decrease aldosterone secretion -> decrease blood volume -> decrease SV -> decrease CO -> decrease BP

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14
Q

What type of beta blocker is preferred for tx of typical angina?

A

beta1 specific/cardioselective and non-ISA preferred!!!

Beta 1: typical angina tx, post MI, asthma, DM
-Metoprolol *
-Atenolol*
-Nebivolol: additional vasodilating properties b/c it stimulates nitric oxide*
- Bisoprolol
- Betaxolol

OTHERS:

Non selective:
-Propranolol
-Nadolol
- Timolol

BBs with ISA activity: not good for angina
-less bradycardia than other BBS
- acebutolol
- penbutolol
- pindolol

α1/beta blockers:
-Carvedilol: CHF gold standard
-Labetalol: indicated for pregnancy

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15
Q

Beta Blockers: DDis

A

DDIs
- digoxin & BB (increase bradycardia risk)
- NSAIDs: decrease anti-HTN effect
- Verapamil: combo causes excessive decrease in contractility and CO

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16
Q

Angina: beta blockers ADR

A

ADRs
- bradycardia*
- hypotension*
- CHF/edema *
- dizziness *
- sexual dysfunction
- fatigue
- insomnia
- cold extremities: BBs cause reflex peripheral vasoconstriction
- hypercholesterolemia: lipid metabolism effects
- mask Sx of hypoglycemia (tachycardia & nervousness)
- CNS side effects: confusion, nightmares, depression (MC w/ lipid soluble BB)

“CHEF’S CBD MICHigan”
CHF*
Hypotension*
Edema
Fatigue
Sexual dysfunction
Cold extremities
BRADYCARDIA *
Dizziness *
Mask sx of hypoglycemia
Insomnia
CNS side effects: confusion, depression, nightmares
Hypercholesterolemia

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17
Q

Angina: Beta blockers indications and CI/precautions

A

Indications:
- typical angina: first line tx
– HTN: second line tx
- CHF: stage A or B
- Post -MI: IMPROVES MORTALITY
- atrial arrhythmias
- migraine
-NOT used for variant/prinzmetal angina or acute angina attacks

CI
– sinus bradycardia (HR < 60)
- SBP < 100
- heart block
- cardiogenic shock
- acute decompensentory HF
-Non-selective agents are contraindicated in COPD, asthma, DM.

Precautions:
- Reactive airway disease
- DM
- PVD

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18
Q

What is the first line treatment for typical angina if no contraindications?

A

BETA BLOCKERS: beta 1 and non-ISA

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19
Q

tx of angina: CCB MOA

A

MOA
– blocks calcium ion channels in smooth muscle and cardiac tissue -> smooth muscle relaxation + suppression of cardiac activity -> slows HR + decrease contractility + increase vasodilation

Outcome of MOA:
- increase O2 supply: increase coronary blood flow
- and/or decrease myocardial O2 demand: lower HR and reduces systemic vascular resistance

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20
Q

CCB monitoring parameters

A

– BP
- HR
- EKG (non-DHP): check for heart block

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21
Q

CCBs role in angina management

A

First line tx for VARIANT angina:
- Non-DHP CCBs

Initial therapy when BBs are CI:
- non-DHP CCBs

Add on therapy to BBs:
- DHP CCBs -> don’t want to use non-DHP CCBs and BBs at the same time -> could drop the HR

Use in combo w/ nitrates

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22
Q

CCB ADR

A
  • constipation: give them stool softeners; we DON’T want them to strain*
  • peripheral edema*
  • reflex tachycardia)* (compensation if too much vasodilation)
  • flushing*
  • heart block and hypotension* (w/ diltiazem and verapamil)
    -bradycardia
  • fatigue
  • headache, dizziness
  • CHF

Immediate release forms of nifedipine and other short-acting CCBs:
- increased risk of MI, CHF and death due to CAD

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23
Q

CCBs indications

A
  • angina: Non-DHP first line tx for VARIANT angina
    – HTN: first line tx (non-DHP)
  • atrial arrhythmias: diltiazem and verapamil
  • Raynaud’s disease: cold in response to temp or stress
  • AFRICAN AMERICAN population: HTN first line tx
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24
Q

CCBs contraindications, precaution

A

Contraindications (mostly for non-DHPs)
– SBP < 100: hypotension
- HR < 60: bradycardia
- Acute decompensated HF
- EF < 40%
- cardiogenic shock
- sick sinus syndrome
- 2nd or 3rd degree heart block

Precautions:
- sudden drop in PVR from CCBs can cause peripheral edema and reflex tachycardia
-need to slowly titrate dose
- be careful with use of verapamil/ diltiazem + beta-blockers with HR

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25
Q

CCB drug names: non-dhp vs dhp

A

Non-DHPs: first line variant angina, initial tx if BBs CI, DM, Asthma, HTN first line tx
-Verapamil
-Diltiazem

DHPs: “-pines”; preferred if pt has heart block/bradycardia
-Amlodipine
-Felodipine
-Nifedipine– avoid IR formulation
- Nicardipine

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26
Q

which CCB do we avoid immediate release? why

A

IR nifedipine: increases risk of MI, CHF, and death due to CAD

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27
Q

angina tx: organic nitrites and nitrates monitoring parameters

A

– blood pressure
- heart rate

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28
Q

angina tx: organic nitrites and nitrates MOA

A

MOA:
- nitrates release nitric oxide -> diffusion into vascular smooth muscle cells -> increase cGMP -> smooth muscle relaxation -> venous dilation -> venous pooling
- decrease PRELOAD, decrease ventricular diastolic volume and decrease VENTRICULAR PRESSURE

outcome:
-decrease myocardial wall tension
- decrease myocardial O2 demand

At higher doses:
- causes ARTERIAL dilation -> decrease PVR and decreases left ventricular ejection pressure (AFTERLOAD)

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29
Q

organic nitrites and nitrates indications

A
  • SL: relieve acute sx of MI
  • SL/PO prophylaxis for effort induced angina
  • Long acting formulations for maintenance therapy (if CIs to BBs and CCBs OR as add on to BB or CCB to optimize angina control)
  • IV Nitrates: ADHF without hypotension
30
Q

organic nitrites and nitrates CI

A
  • aortic valve stenosis
  • concurrent use with Sildenafil, Vardebafil, Tadalafil (PDE 5 inhibitors) -> severe hypotension/death*
  • angle-closure glaucoma
  • head trauma or cerebral hemorrhage
  • severe anemia*
  • severe hypotension (SBP < 90)*
31
Q

organic nitrites and nitrates ADR

A

“Tired Dwarfs Wobble Past Rocks And use NTG to blow it up”
- Tolerance **
- dizziness
- weakness
- postural hypotension
- rash
- anxiety

With overdose – reflex tachycardia and arrhythmias

32
Q

organic nitrites and nitrates DDIs

A
  • PDE 5 inhibitors (Sildenafil, Vardebafil, Tadalafil): severe hypotension and death have occurred
  • isosorbide: CYP3A4 substrate
33
Q

angina tx: organic nitrites and nitrates - what are you concerned about

A

-tolerance develops*

34
Q

Organic Nitrites and nitrates: nitroglycerin

A

SL form:
- Deteriorates in sunlight. Replace bottle every 3-6 months after opening
-relieves acute sx of MI/angina
- prophylaxis for typical effort induced angina
- 0.4mg every 5mins (3 doses max)
-if first dose doesnt provide any relief call 911

Ointment form:
- messy only inpatient

Patch form
-> 12 hr intervals to prevent tolerance

PO form:
– must be administered QD or BID only to minimize tolerance

IV form – contains propylene glycol, need special tubing - propylene glycol can bind to tubing and lose med

35
Q

Amyl nitrate

A

Rapid onset and brief DOA.
Used for cyanide poisoning
-poppers

(INH) (X)

36
Q

Organic Nitrites and nitrates: isosorbide

A

Doesn’t require nitrate free periods because of personalized dosing schedule -> less likely to develop tolerance

Dinitrate form (Isordil):
- give TID

Mononitrate form:
- Longer acting
-Ismo: BID
-Imdur: QD

37
Q

ranolazine MOA, indication

A

MOA
– sodium current inhibitor

Indications
– Used for chronic stable angina in combination with CCB, beta-blockers or nitrates
-last choice

38
Q

ranolazine CI

A

– pre-existing QT prolongation *
- if taking drugs that prolong QT interval
- if taking drugs that are potent CYP3a4 inhibitors
- uncorrected hypokalemia
- hepatic failure

39
Q

ranolazine ADR, precaution

A

Precautions
- can prolong QT interval and induce torsades de pointes*

ADRs
- Prolongs QT interval (CAN INDUCE TORSADES DE POINTES)*
– dizziness, headache, constipation

40
Q

ranolazine DDI

A
  • Has lots of DDI with non-DHP*
    – CYP450 substrate
41
Q

adjunct treatment: antiplatelets MOA and indications

A

MOA:
– inhibits synthesis of prostacyclin and thromboxane A2 -> prevent PLATELET AGGREGATION -> decrease thrombosis/clots

Indications:
- primarily used to prevent ACS/MI in patients with unstable angina

42
Q

antiplatelet drugs

A
  • Aspirin!! MONOtherapy or dual therapy best

others:
-Clopidogrel (Plavix)- same efficacy as aspirin
-Prasugrel (Effient) – for UA
-Ticagrelor (Brilinta) – for UA

43
Q

optimize manageable risk factors

A

Step 1: Lifestyle modifications to lower cardiac risk factors
-HTN
-smoking
- diet
- lifestyle/exercise
- lipids + DM

44
Q

ACE inhibitors - what is its role in angina/when is it indicated?

A

-Use in all pts w/ CAD to help delay progression of CAD
-Does NOT relieve angina symptoms b/c it doesn’t affect O2 supply and demand
- give in all post-MI pts to reduce mortality and slow progression

45
Q

overall management of angina: what is step 1 and what are goals of treatment

A

Step 1: Lifestyle modifications to lower cardiac risk factors

Goals of treatment:
-Relieve acute symptoms
-Prevent ischemic attacks
-Reduce risk of MI and other cardiovascular problems

46
Q

Severity of angina: what treatment for frequent episodes requiring regular SL NTG

A

beta blocker
CCB
nitrate

+ SL nitrate

47
Q

Severity of angina: what treatment for predictable episodes upon exertion?

A

prophylaxis with SL/PO nitrates

48
Q

Severity of angina: what treatment for occasional episodes of angina?

A

SL nitroglycerin
- 0.4 mg SL dose: use every 5 minutes x 3
- call 911 if you dont feel better after 1st dose

49
Q

management of acute STEMI: Goals of Therapy

A

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

50
Q

Management of Acute STEMI
Pharmacological management includes:

A

“MANABS”

Morphine IV *
Aspirin: ASAP; reduce morbidity and mortality
IV Nitroglycerin
ACE Inhibitors * -> should give to all post-MI pts
Beta-blockers *: ASAP; reduce morbidity and mortality
Statins -> should give post-MI

Calcium Channel blockers: controversial, second line

Anticoagulants
P2Y-12 Inhibitors
Fibrinolytics -> if no PCI

51
Q

pharm management of acute STEMI: aspirin

A

-antiplatelet agent
-Use for all MI patients unless contraindicated. Start ASAP, continue indefinitely*
-reduces morbidity and mortality associated with MI*

Dose: 162 - 325mg STAT, then 81-325mg QD
- Ideally: want to give at least one tablet of aspirin or 2 baby aspirin
- 1 baby aspirin = 81 mg

52
Q

pharm management of acute STEMI: IV nitroglycerin

A

Recommended for the first 24 to 48 hrs in pts with acute MI!!!
-NTG alleviates ischemic myocardial pain
- Do not give if SBP < 90 or HR < 50

53
Q

pharm management of acute STEMI: IV morphine (analgesics)

A

IV morphine:
-Pain control + anxiety relief
- vasodilation: helps with cardiac reperfusion
- takes away pain that IV NTG didn’t take away

54
Q

pharm management of acute STEMI: beta blockers

A

Start IV dose ASAP and continue post MI with PO meds
-Reduction in morbidity and mortality*

  • reduces magnitude of infarction and incidence of associated complications in subjects not receiving concomitant thrombolytic tx
    -reduces the rate of reinfarction w/ thrombolytic tx
55
Q

pharm management of acute STEMI: ACE inhibitors

A

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

56
Q

pharm management of acute STEMI: CCB

A

Controversial in MI – do NOT affect morbidity and mortality*

Indication:
-May be given to pts intolerant to beta-blockers
-can add on if on ACE and beta blocker
-Diltiazem: may be useful in pts w/ non-Q-wave MI without LV dysfunction

57
Q

pharm management of acute STEMI: anticoagulants

A

duration of therapy depends on type of reperfusion therapy (PCI vs fibrinolytics)

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

58
Q

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

A

Dose and duration depends on revascularization therapy*
-Usually continued w/ aspirin indefinitely as Dual Antiplatelet therapy as maintenance

Drugs:
-clopidogrel
-prasugrel
- ticagrelor

59
Q

pharm management of acute STEMI: fibrinolytics

A

Fibrinolytics: used for rapid thrombolysis using drug tx -> + survival benefit if pt is not able to get PCI

Indication:
- used in institutions without PCI capability -> TREAT within 30 min of entering hospital
- pt cannot be transferred to an institution with PCI capability within 90 minutes

MOA:
- plasminogen activators dissolve existing clots

60
Q

Absolute vs relative CI to thrombolytics in pts with MI*

A

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

61
Q

Fibrinolytics: drug names

A

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

“can use any of these drugs, no preference”

62
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)

63
Q

If present to hospital w/ PCI capability, they should be treated with primary PCI (stent placement) within ____ minutes

A

within 90 minutes!!!

64
Q

management of other acute coronary syndrome: UA/NSTEMI pts which meds

A

-ASA
-BBs
-Nitrates: sx relief
- Anticoagulants: heparin
- Antiplatelets
- Statins: long term to delay progression and improve mortality
- ACEi: long term to delay progression and improve mortality

65
Q

Antiplatelets: UA/NSTEMI

A

-P2Y12 inhibitor (Clopidogrel, Prasugrel or Ticagrelor)
-IV Glycoprotein IIb/IIIa inhibitors: Usage has decreased with the effectiveness of P2Y12 inhibitors and anticoagulants*

On discharge:
- dual oral antiplatelet therapy with aspirin + P2Y12 inhibitors
- duration depending on drug vs bare stent

66
Q

CABG indications + NSTEMI caution

A
  • 70% in left main coronary artery
  • > 50% in triple vessel disease

if NSTEMI/UA:
- stop antiplatelet tx 5-7 days before CABG to decrease bleeding risk

67
Q

management of other acute coronary syndrome: UA/NSTEMI pts on discharge

A

On discharge: Dual oral antiplatelet therapy
- aspirin + P2Y12 inhibitor
- choose P2Y12 inhibitor based on drug eluting stents vs. bare metal stent

Long term meds: to delay progression
- Statins: improve mortality
- ACE inhibitors: improve mortality

68
Q

management of other acute coronary syndrome: UA/NSTEMI: surgical intervention

A

PCI – stent placement
CABG

If CABG therapy indicated:
- antiplatelets should be held for 5-7 days if possible!!!*
- to reduce bleeding risk

69
Q

UA vs STEMI/NSTEMI

A

-enzymes- negative in UA

70
Q

A major difference in therapy between STEMI and NSTEMI is ______ tx is not used in NSTEMI.

A

A major difference in therapy between STEMI and NSTEMI is that FIBRINOLYTICS are NOT used in NSTEMI patients
- NSTEMI: white thrombus
More platelet predominant -> antiplatelets tx more helpful
- STEMI: red thrombus
fibrinolytics therapy more helpful

Pharmacology (15 decks)

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