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CDM 2 Exam 1 > Ischemic Heart Disease (IHD) > Flashcards

Ischemic Heart Disease (IHD) Flashcards

1
Q

Coronary Artery Disease (CAD) = Coronary Heart Disease (CHD)

A

Any vascular disorder that narrows or occludes coronary arteries

Usually a manifestation of atherosclerosis

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2
Q

Ischemic Heart Disease (IHD)

A

Blanket term for a number of syndromes

Occurs due to increase myocardial O2 demand or decrease in O2 supply to heart

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3
Q

Angina Pectoris

A

Clinical syndrome, characterized by pain or discomfort primarily in the chest, but may also be described in the jaw, shoulder, back or arm

Most commonly due to ischemic heart disease; a symptom of IHD

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4
Q

Subsets of Angina

A

Prinzmetal’s “Variant” Angina

Silent myocardial ischemia

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5
Q

Prinzmetal’s “Variant” Angina

A

Occurs at rest

Due to coronary spasm

Reversed with nitroglycerin and calcium channel blockers

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6
Q

Silent myocardial ischemia

A

Type I (Less common)
–> Defective anginal warning system
Type II (more common)
–> Angina may be a poor indicator of ischemia
–> Autonomic neuropathy, higher threshold for pain, excess endorphins
–> Indicates higher risk patient

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7
Q

Stable or Exertional Angina

A

Exertional pain lasting < 20 min, relieved by rest

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8
Q

ACS (unstable Angina, STEMI, or NSTEMI)

A

Pain occurring at rest lasting > 20 minutes

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9
Q

Modifiable Risk Factors

A 
Cigarette smoking
Dyslipidemia (elevated LDL or total; reduced HDL)
Diabetes mellitus
Hypertension
Physical inactivity
Obesity (BMI >30 kg/m2)
Low daily fruit and vegetable consumption
Alcohol overconsumption
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10
Q

Non-modifiable Risk Factors

A

Gender (men and postmenopausal women)

Age (Men >45; Women >55)

Family History (1st degree relative Father <55; Mother <65)

Environment (climate, air pollution, drinking water)

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11
Q

Signs and symptoms associated with angina (Subjective)

A

Shortness of breath (SOB), dyspnea on exertion
(DOE), diaphoresis, palpitations, chest pain (CP),
lightheadedness

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12
Q

Signs and Symptoms associated with angina (Objective)

A

BP, HR, decreased oxygen saturation on ABG,
ECG changes: ST segment elevation or
depression, or T wave inversions, troponins

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13
Q

PQRST

A

Precipitating factors and palliative measures

Quality of pain

Region and radiation of pain

Severity of pain

Temporal pattern

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14
Q

Non-invasive measure of MVO2:

A

Double product (DP) = HR x SBP

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15
Q

IHD is the result of an _____ in myocardial

oxygen demand and _____ supply

A

increase, decreased

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16
Q

IHD oxygen supply

A

decrease arterial PO2

decrease diastolic filling time

decrease coronary blood flow

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17
Q

IHD oxygen demand

A

increase HR

increase myocardial contractility

increase ventricular wall tension

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18
Q

increased demand (non-cardiac)

A 
Hyperthermia
Hyperthyroidism
Sympathomimetic toxicity
Hypertension
Anxiety
B- agonists
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19
Q

increased demand (cardiac)

A 
Hypertrophic 
cardiomyopathy
Aortic stenosis
Dilated cardiomyopathy
Tachycardia
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20
Q

decreased supply (non-cardiac)

A 
Anemia
Hypoxemia
Sickle cell disease
Sympathomimetic toxicity
Hyperviscosity
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21
Q

decreased supply (cardiac)

A

Aortic stenosis
Hypertrophic
cardiomyopathy

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22
Q

Short term treatment goals

A

Reduce or prevent
symptoms that limit
exercise capability and
impair quality of life

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23
Q

Long term treatment goals

A

Prevent CHD events (MI,
HF, stroke, death) and
extend the patient’s life

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24
Q

Treatment outcomes

A 
Prevent ACS and death
Alleviate acute symptoms of 
myocardial ischemia
Prevent progression of the disease
Reduce complications of IHD
Avoid or minimize adverse 
treatment effects
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25
Q

Class 1

A

is recommended/is indicated

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26
Q

Class 2 a

A

should be considered

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27
Q

Class 2 b

A

may be considered

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28
Q

Class 3

A

is not recommended

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29
Q

Level of Evidence A

A

Data derived from multiple randomized clinical trials or meta-
analysis

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30
Q

Level of Evidence B

A

Data derived from a single randomized clinical trial or large non-
randomized studies

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31
Q

Level of Evidence C

A

Consensus of opinion of the experts and/or small studies,

retrospective studies, registries

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32
Q

Non-pharm treatment options

A

Lifestyle modification
PCI (symptom relief no mortality benefit)
CABG (symptom relief and mortality benefit)

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33
Q

Medication treatment

Acute pain relief

A

SL NTG

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34
Q

Medication treatment

Maintenance

A

Nitrates
B-blockers with prior MI
CA blockers or long-acting nitrates
Ranolazine
Aspirin or clopidogrel if aspirin is contraindicated
ACE inhibitor to pts w/ CAD and DM or LV systolic dysfunction
LDL lowering therapy

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35
Q

Treatment Algorithm:

Lipid lowering therapy

A

Consider in all patients; especially those with elevated LDL/ASCVD risk: statin

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36
Q

Treatment Algorithm:

Lifestyle modification

A

Diet, exercise, weight loss, smoking cessation

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37
Q

Treatment Algorithm:

Immediate release nitrate

A

NTG SL or spray

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38
Q

Treatment Algorithm:

Select appropriate anti-platelet therapy

A

Aspirin 81 mg +/- clopidogrel

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39
Q

Treatment Algorithm:
Assess Comorbidities
If DM, HTN, and/or CKD

A

ACEi or ARB

40
Q

Treatment Algorithm:
Assess Comorbidities
If prior MI and/or LV dysfunction

A

ACEi or ARB +BB

41
Q

Treatment Algorithm:
Assess Comorbidities
if prinzmetal or variant angina

A

consider CCB or LA nitrate

42
Q

Treatment Algorithm:

Select Antianginal therapy

A

BB, CCB, or LA nitrate

if ineffective, add CCB or BB (if not first line) or LA nitrate or ranolazine

if still ineffective, consider triple therapy

43
Q

Effect of Drug Therapy on MVO2: Nitrates

A

HR: increase
contractility: 0
systolic pressure: decrease
LV volume: large decrease

44
Q

Effect of Drug Therapy on MVO2: BB

A

HR: large decrease
contractility: decrease
systolic pressure: decrease
LV volume: increase

45
Q

Effect of Drug Therapy on MVO2: Nifedipine

A

HR: increase
contractility: 0 or decrease
systolic pressure: 0 or decrease
LV volume: 0 or decrease

46
Q

Effect of Drug Therapy on MVO2: Verapamil

A

HR: decrease
contractility: decrease
systolic pressure: decrease
LV volume: 0 or decrease

47
Q

Effect of Drug Therapy on MVO2: Diltiazem

A

HR: large decrease
contractility: 0 or decrease
systolic pressure: decrease
LV volume: 0 or decrease

48
Q

Ways to reduce Myocardial Ischemia/Angina

Pharmacotherapy with Anti-Ischemics

A

• Reduce workload of heart
Three major categories:
• Nitrates, Beta-blockers, Calcium Channel Blockers
–> Additionally, Ranolazine

49
Q

Ways to reduce Myocardial Ischemia/Angina

Improve Coronary Blood Flow Mechanically

A 
Percutaneous Coronary Intervention (PCI)
• Placement of coronary stent
--> Bare-metal (BMS)
--> Drug-eluting (DES)
• Bypass Graft Surgery (CABG)
50
Q

Nitrates (O2 supple and demand)

A

O2 supply
–> increase coronary blood flow

O2 demand

  • -> no charge HR
  • -> no change contractility
  • -> decrease ventricular wall tension
51
Q

Nitrates immediate use

A

Nitroglycerin (Nitrostat)

Formulation SL tab, spray

52
Q

Nitrates Immediate Release

A

ISDN (isordil)

ISMN (Ismo Monoket)

53
Q

Nitrates Sustained Release

A

ISDN (Isordil Titradose Dilatreate- SR)

ISMN (Imdur)

54
Q

ISMN has (high/low) bioavailability and a longer/shorter half-life than ISDN

A

high

longer (4-6 hours)

55
Q

Rationale for Nitrate use

A

Restore balance between supply and demand
Prevent morbidity and mortality
Isosorbide third line for chronic prophylaxis/treatment
Use BB and CCB first
May use in combination with BB or CCB
Should not be used as monotherapy due to the lack of 24-hour coverage

56
Q

Nitrate mechanism of action

A

Converted to nitric oxide
Venous vasodilation predominantly
Coronary artery vasodilation
May increase supply and reduce demand

57
Q

Nitrates ADR/monitoring

A

ADR: Hypotension, headaches, flushing

Monitor: BP, HR, PRN usage, anginal symptoms

58
Q

Nitrates drug interactions

A

Contraindicated with PDE5 inhibitors

  • -> within 24 hours of sildenafil, vardenafil
  • -> within 48 hours of tadalafil
59
Q

Nitrate-free interval

A

for chronic use with isosorbide
dinitrate or mononitrate due to loss of effectiveness with
continuous exposure

Nitrate free period: at least 10-14 hours

Typically dosed ~7am and no later than 5pm

60
Q

NTG is the only anti-ischemic used for ____outpatient relief

A

immediate

61
Q

Nitrate Acute treatment

A

Sublingual tablet or Lingual spray

62
Q

Nitrates

For non-trauma-related chest discomfort/pain:

A

One NTG dose, if pain unimproved or worsening after
5 minutes, call 911. May take second dose of NTG.

Store in original container

63
Q

Nitrate

Prophylaxis

A

Take immediately before planned exercise/exertion

64
Q

Limited evidence to support use of long-acting nitrates

A

Tolerance → oxidative stress, endothelial

dysfunction, and sympathetic activation

65
Q

NTG storage considerations

A 
keep in original container 
Do not store in bathroom
Remove cotton plug prior to use 
Keep with patient at all times 
Take 1, if not working within 5 minutes call 911, take second
66
Q

Beta Blockers (O2 supply and O2 demand)

A 
O2 supply
--> no change in coronary blood flow
O2 demand 
--> decrease HR 
--> decrease contractility 
--> decrease ventricular wall tension
67
Q

rationale for BB

A

Decrease mortality
Effective in improving anginal symptoms
Decreased silent ischemia episodes
First line for post-MI as well as no prior MI

68
Q

BB mechanism of action

A

Decrease cardiac workload

Reduce heart rate by β-1 blockade

69
Q

BB ADR/monitoring

A

ADR: Hypotension, bradycardia, impaired glucose
metabolism, bronchospasm, peripheral
vasoconstriction/intermittent claudication

Monitor: HR, BP, PRN nitrate usage, anginal
symptoms, rescue inhaler use (asthmatics), glucose
intolerance (DM)

70
Q

____ reduction is the best predictor of efficacy
as an anti-ischemic agent (50-60 bpm resting HR, ≤
100 bpm exercise HR)

A

Heart Rate

71
Q

Non-selective beta-blockers additionally block β-2

receptors in the periphery

A

May result in blood vessel vasoconstriction and
pulmonary bronchospasm

Maximum doses of β-1 selective agents can also
cause these effects

72
Q

Beta-blockers with intrinsic sympathomimetic activity

(ISA) are inappropriate for chronic ischemia

A

Stimulate β-1 receptors (increase HR)

73
Q

All beta-blockers are INAPPROPRIATE for

Prinzmetal’s (variant) angina

A

Not vasodilators. Inappropriate for vasospasms

Caution in cocaine induced angina

74
Q

All beta-blockers are INAPPROPRIATE for

Prinzmetal’s (variant) angina

A

Not vasodilators. Inappropriate for vasospasms

Caution in cocaine induced angina

75
Q

Abrupt discontinuation of beta-blockers should be

avoided

A

May result in reflex tachycardia and ischemia

76
Q

Calcium Channel Blockers (O2 supple and O2 demand)

A

O2 supply
–> increase coronary blood flow
O2 demand
–> decrease HR (Verapamil/Ditilazem only)
–> decrease contractility (Verapamil/Ditilazem only)
–> decrease Ventricular wall tension

77
Q

Rationale for CCB

A

Second line to beta-blocker use if they are contraindicated or stopped due to ADR

May use in combination with BB when BB alone is not effective

Drug of choice in Prinzmetal’s (variant) angina

78
Q

CCB mechanism of action

A

Decrease coronary vasospasm via blocking calcium receptors in vascular smooth muscle

79
Q

CCB ADR/Monitoring

A

ADR: Constipation, lower extremity edema, hypotension, bradycardia

Monitor: HR (non-dihydropyridine CCBs), BP, PRN nitrate usage, anginal symptoms

80
Q

Non-dihydropyridines are more likely to ___ HR

bradycardia

A

slow

Verapamil, Diltiazem

81
Q

Rationale for Ranolazine

A

Inadequate response with other anti-anginal agents

In combination with standard therapy

82
Q

Ranolzaine MOA

A

Reduces calcium overload through inhibition of the late
sodium current

Minimal effects on HR and BP

83
Q

Ranolzaine Dosing

A

Start: 500 mg po BID & may titrate up to 1000 mg po BID

84
Q

Ranolazine ADR/monitoring

A

ADR: Constipation, headache, nausea, dizziness

Monitor: QT interval, hepatic function

85
Q

Ranolazine contraindications

A

Contraindications:
 Significant hepatic disease
 Potent CYP 3A4 inhibitors
 (ketoconazole, clarithromycin, protease inhibitors)
 Potent CYP3A4 inducers
 (rifampin, phenobarb, phenytoin, carbamazepine, St. Johns wort)
 Caution w/ potent/ moderate potent CYP3A4 inhibitors
 Diltiazem or verapamil: Limit ranolazine dose to 500mg bid
 Simvastatin max dose of 20mg daily
 (any ranolazine dose)
 Metformin max dose of 1700mg daily
 (only for max dose ranolazine 1000mg po bid)
 P-glycoprotein substrate
 Increased digoxin levels – monitor closely

86
Q

Rationale for Aspirin

A

Reduces stroke, MI, or vascular death in patient with ASCVD

First line choice in patients with CAD, Class I recommendation

87
Q

Aspirin MOA

A

Irreversibly blocks COX-1 activity for life of platelet

Inhibits thromboxane A2 production

88
Q

Aspirin dosing

A

81mg po once daily

Pearl: Rivaroxaban 2.5 mg bid + Asa 81 mg daily led to 24% RR CV death,
MI, stroke vs Asa alone

May consider in patients with vascular disease, HF, DM, moderate renal
impairment

Not in AHA guidelines/in ADA guidelines; clinical updates &uptake slow

89
Q

Aspirin

Adverse Drug Reactions/Monitoring:

A

ADR: bleeding, bruising, hemorrhage

Monitoring: hemoglobin, hematocrit, sx of bleeding

90
Q

NSAID timing

A 
Take ibuprofen/ 
naproxen  at least 30 
minutes after ASA 
dose or at least 8 
hours prior to ASA 
dose
91
Q

Rationale for clopidogrel

A

For patients unable to take aspirin due to allergy or intolerance

Reduces stroke, MI, or vascular death in patient with ASCVD

Second line choice in patients with CAD

92
Q

Clopidogrel MOA

A

Inhibits ADP receptor-mediated platelet activity

Must be metabolized to active metabolite

93
Q

Clopidogrel dosing

A

75mg once daily

94
Q

Clopidogrel ADR/monitoring

A

ADR: bleeding, bruising, hemorrhage

Monitoring: hemoglobin, hematocrit, sx of bleeding

95
Q

Risk factors that increase bleed risk

A

A history of previous gastrointestinal bleeding or peptic ulcer
disease or bleeding from other sites

Age >70 years

Female sex

Lean body weight

Thrombocytopenia

Coagulopathy

CKD; DM

Warfarin use

96
Q

ONLY add a third anti-anginal drug if:

A

2 drugs do not control symptoms

Patient is awaiting revascularization

Revascularization is not appropriate or acceptable

CDM 2 Exam 1 (3 decks)

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