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ST Health Assessment > Ischemic Heart Disease (Exam IV) > Flashcards

Ischemic Heart Disease (Exam IV) Flashcards

1
Q

Risk Factors for Ischemic Heart Disease (IHD)

A
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2
Q

What percentage of patients will have a risk factor for ischemic heart disease?

A

30%

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3
Q

What are the manifestations of IHD?

A
  • Angina Pectoris
  • Acute MI
  • Sudden Death
  • Dysrhythmias
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4
Q

What is Angina Pectoris

A

Chest pain d/t imbalance between coronary blood flow and myocardial oxygen consumption.

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5
Q

Stable angina typically develops in the setting of partial occlusion or significant (>______%) chronic narrowing of a segment of the coronary artery.

A
  • > 70%
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6
Q

Angina pectoris reflects the intracardiac release of what two substances during ischemia?

A
  • Adenosine
  • Bradykinin
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7
Q

What are the CV effects of adenosine and bradykinin release?

A
  • Stimulate Cardiac nociceptors whose afferent neurons converge with the T1 to T5 sympathetic ganglia resulting in chest pain.
  • Slow AV conduction
  • Decrease Contractility
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8
Q

How would a patient describe angina pectoris?

A
  • Retrosternal chest discomfort
  • Elephant sitting on their chest
  • Chest discomfort radiates to left shoulder/jaw
  • SOB and dyspnea
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9
Q

Angina Pectoris affect which dermatomes?

A
  • C8 to T4
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10
Q

What factors can induce angina pectoralis?

A
  • Physical exertion
  • Emotional tension
  • Cold weather
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11
Q

Differentiate Chronic vs Unstable Angina

A

Chronic stable: Chest pain that does NOT change in frequency or severity in a 2-month period

Unstable: Chest pain increasing in frequency and/or severity without an increase in cardiac biomarkers

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12
Q

During myocardial ischemia, the standard 12-lead ECG demonstrates ST-segment _______ that coincides with the anginal chest pain. This may be accompanied by transient symmetric _________ inversion.

A

During myocardial ischemia, the standard 12-lead ECG demonstrates ST-segment depression that coincides with the anginal chest pain. This may be accompanied by transient symmetric T-wave inversion.

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13
Q

What does the Exercise Stress Test evaluate on the EKG?

A
  • Degree of ST-segment depression

The greater the degree of ST-segment depression, the greater the likelihood of significant coronary artery disease.

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14
Q

What does nuclear stress imaging assess?

A
  • Assesses coronary perfusion (greater sensitivity than other tests)
  • Tracer activity in perfused vs ischemic areas
  • Estimates LV systolic size and function
  • Differentiates new perfusion abnormality vs. old MI

The size of perfusion abnormality will correlate with the significance of CAD.

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15
Q

What drugs can be administered to produce a rapid HR to create cardiac stress?

A
  • Atropine
  • Dobutamine
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16
Q

What is the chemical tracer used to analyze cardiac blood flow?

A
  • Thallium
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17
Q

These drugs dilate normal coronary arteries but evoke no change in the diameter of atherosclerotic coronary arteries.

A
  • Adenosine
  • Dipyridamole
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18
Q

What does an ECHO assess in IHD patients?

A
  • Wall motion abnormalities
  • Valvular functions
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19
Q

Purpose of coronary angiography.

A
  • Determines the location of occlusive disease
  • Diagnose Prinzmetal (variant/spasm) angina
  • Assess results of angioplasty/stenting
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20
Q

Coronary angiography does NOT measure what?

A
  • Stability of the plaque.
  • Does not tell you when the plaque will rupture.
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21
Q

Treatment for angina pectoralis?

A
  • Cessation of smoking
  • Ideal body weight
  • Low-fat, low-cholesterol diet (Statins)
  • Regular aerobic exercise
  • Treatment of hypertension
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22
Q

Patients are placed on statins when LDL levels are above ________ mg/dL.

A

160 mg/dL

Providers would like a 50% reduction in LDL during statin therapy.

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23
Q

Drug therapy for angina pectoralis

A
  • Antiplatelet drugs
  • Nitrates
  • β-blockers
  • Ranolazine
  • CCB
  • ACE inhibitors
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24
Q

Aspirin inhibits the enzyme _________. This results in the inhibition of ________, which plays an important role in platelet aggregation.

A

Aspirin inhibits the enzyme COX-1. This results in the inhibition of thromboxane A2, which stimulates activations for new platelets and is a potent vasoconstrictor.

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25
Q

Are the effects of aspirin reversible?

What is the dose for aspirin?

A
  • No, COX-1 inhibition will last for the duration of platelet lifespan (7 days)
  • 75-325 mg/day
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26
Q

How do platelet glycoprotein IIb/IIIa receptor antagonists work?

What are examples of these antiplatelet drugs?

A
  • Inhibit platelet aggregation
  • Abciximab, Eptifibatide, Tirofiban
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27
Q

Name a Thienopyridines (P2Y12inhibitors) drug.

A
  • Clopidogrel (Plavix)
  • Prasugrel
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28
Q

Is Clopidogrel reversible?

A

No, Clopidogrel is irreversible.

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29
Q

MOA of Clopidogrel

A
  • Blocks ADP from binding to P2Y12 receptor, which will inhibit platelet aggregation.
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30
Q

7 days after cessation of clopidogrel, ____% of platelets will have recovered normal aggregation function.

A
  • 80%
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31
Q

Clopidogrel is a _______ that is metabolized into an active compound in the liver.

A
  • Prodrug
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32
Q

________ % of patients taking clopidogrel demonstrate resistance or hyperresponsiveness.

A
  • 10-20%
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33
Q

_________ can affect the enzyme that metabolizes clopidogrel to its active compound and thereby can reduce the effectiveness of clopidogrel.

A
  • PPI
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34
Q

What drug has a similar mechanism action as clopidogrel, more predictable pharmacokinetics, and a higher risk of bleeding?

A
  • Prasugrel
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35
Q

How does Nitrate treat myocardial ischemia?

A
  • Decrease the frequency, duration, and severity of angina pectoris.
  • Dilate Coronary Arteries and Collaterals
  • Decrease peripheral vascular resistance
  • Decrease Preload
  • Anti-thrombotic effects

Nitrates will increase the amount of exercise required to produce ST-segment depression.

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36
Q

Nitrates are contraindicated with what heart conditions?

A
  • Severe aortic stenosis
  • Hypertrophic cardiomyopathy

The decrease in preload in these conditions will not be good.

37
Q

Nitrates are synergistic with what drugs?

A
  • β-Blockers and CCB
38
Q

The only drug to prolong life in CAD patients and decrease the risk of death and reinfarction in MI pts.

A

β blockers

39
Q

Effects of β1 antagonist (atenolol, metoprolol, acebutolol, bisoprolol).

A
  • ↓ HR
  • ↑ Diastolic Time, ↑ Coronary Perfusion
  • ↓ Myocardial contractility
  • ↓ Myocardial O2 demand
40
Q

Effects of β2 antagonist (propranolol, nadolol).

A
  • ↑ Bronchospasm

Do not give this drug to asthma patients.

41
Q

__________ are uniquely effective in decreasing the frequency and severity of angina pectoris due to coronary artery spasm (Prinzmetal or variant angina).

A
  • CCB
42
Q

Effects of CCB

A
  • Dilation of coronary artery
  • ↓ Vascular smooth muscle tone
  • ↓ Contractility
  • ↓ O2 Consumption
  • ↓ Systemic BP
43
Q

CCB is not as effective as β-blockers in what aspect?

A
  • β-blockers are more effective in decreasing the incidence of MI.
44
Q

Functions of ACE-inhibitors

A
  • Tx HTN
  • Tx HF
  • Cardioprotective
45
Q

What does ANG II increase?

A
  • Blood Pressure
  • Myocardial Hypertrophy
  • Interstitial Myocardial Fibrosis
  • Coronary Vasoconstriction
  • Inflammatory Response
46
Q

What drug is used for coronary plaque stabilization?

A

Statins

47
Q

What do statins decrease?

A
  • Lipid oxidation
  • Inflammation
  • Matrix metalloproteinase
  • Cell death
48
Q

When will revascularization be indicated?

A
  • Revascularization by CABG or PCI is indicated when optimal medical therapy fails to control angina pectoris.
49
Q

Revascularization is indicated when there is:
Stenosis of left main coronary artery stenosis of > _____%
Stenosis of epicardial coronary artery > _______%
Impaired EF < ______%

A
  • Stenosis of left main coronary artery stenosis of > 50%
  • Stenosis of epicardial coronary artery >70%
  • Impaired EF <40%
50
Q

When will CABG be preferred over a PCI?

A
  • Significant left main CAD
  • 3-vessel CAD
  • DM pts who have 2 or 3-vessel CAD
51
Q

What is ACS?

What is it caused by?

A
  • Acute or worsening imbalance of myocardial oxygen supply to demand
  • Plaque rupture → Coagulation cascade → Thrombin generation → Arterial occlusion
52
Q

ACS → 12-Lead EKG → No ST-elevation → Troponin/CK-MB negative → ________

ACS → 12-Lead EKG → No ST-elevation → Troponin/CK-MB positive → ________

ACS → 12-Lead EKG → ST-elevation → Troponin/CK-MB postivie → ________

A
  • Unstable Angina
  • NSTEMI → MI
  • STEMI → MI
53
Q

STEMI occurs when coronary blood flow decreases abruptly. This decrease in blood flow is attributable to acute thrombus formation. This creates a local environment that favors ________.

When plaques rupture, various chemical mediators such as ______, _______, _______, and _______ stimulate platelet aggregation.

The potent vasoconstrictor ________ is released, which further compromises coronary blood flow.

A
  • Thrombogenesis
  • Colloagen, ADP, Epi, Serotonin
  • Thromboxane A2
54
Q

_________ receptors on the platelets are activated, which enhances the ability of platelets to interact with adhesive proteins and other platelets and causes growth and stabilization of the thrombus.

Further activation of coagulation leads to the strengthening of the clot by _______. This makes the clot more resistant to thrombolysis.

A
  • Glycoprotein IIb/IIIa
  • Fibrin
55
Q

Criteria chart for diagnosing an MI

A
56
Q

Dx studies for ACS

A
  • Troponin Lab
  • Imaging
57
Q

Troponin is a cardiac-specific protein and biochemical marker for AMI.

Levels of cardiac troponins increase within _____ hours after myocardial injury and remain elevated for 7–10 days.

A
  • 3 hours

Troponins are more specific than CK-MB

58
Q

Patients with typical ECG evidence of AMI do not require evaluation with echocardiography.

However, echocardiography is useful in patients with _____ or an abnormal ECG in whom the diagnosis of AMI is uncertain.

A
  • LBBB

ECHO will demonstrate regional wall motion abnormalities in most patients with AMI.

59
Q

Drug therapy for ACS

A
  • MONA
  • P2Y12inhibitors (clopidogrel)
  • Platelet glycoprotein IIb/IIIa inhibitors
  • Unfractionated heparin
  • β-blockers
  • ACE-inhibitors/ARBs
60
Q

What drugs can be used for Reperfusion Therapy to restore normal antegrade blood flow?

When can these be initiated for IHD?

A
  • tPA, Streptokinase, Reteplase, Tenecteplase
  • 30–60 min of hospital arrival and within 12 hours of symptom onset.
61
Q

Indications for PCI

A
  • Contraindication to thrombolytic therapy
  • Severe HF and/or pulmonary edema
  • Symptoms present for 2 - 3 hours
  • Mature clot
62
Q

Indication for CABG

A
  • Bad coronary anatomy
  • Failed angioplasty
  • Evidence of infarction-related ventricular septal rupture or mitral regurgitation
63
Q

Causes Unstable Angina/NSTEMI

A
  • Rupture or erosion of a coronary plaque
  • Dynamic obstruction d/t vasoconstriction
  • Worsening coronary luminal narrowing
  • Inflammation
  • Myocardial ischemia
64
Q

Presentation of Unstable Angina/NSTEMI

A
  • Angina at rest, lasting >10 minutes
  • Chronic angina pectoris … more frequent and more easily provoked
  • New-onset angina severe, prolonged, or disabling
65
Q

Treatment of Unstable Angina/NSTEMI.

What treatment is NOT indicated?

A
  • Bed rest, oxygen, analgesia, and β-blocker therapy
  • Sublingual or IV nitroglycerin
  • Calcium channel blockers
  • Aspirin, clopidogrel, prasugrel, or ticagrelor and heparin therapy (unfractionated heparin or LMWH
  • Thrombolytic therapy NOT indicated
66
Q

What is a PCI?

A
  • Alternative to CABG
  • 3 types: Balloon angioplasty, bare-metal stent, drug-eluting stent
  • PCI will damage endothelium
67
Q

Risk of PCI

A
  • Thrombosis
  • Bleeding
68
Q

Re-endothelialization Time of the following:
Balloon Angioplasty
Bare-Metal Stent
Drug-Eluting Stent

A
  • Balloon Angioplasty: 2-3 weeks
  • Bare-Metal Stent: 12 weeks
  • Drug-Eluting Stent: 1 year

Important to stay on dual antiplatelet therapy (DAPT) - ASA w/ Plavix.

69
Q

When do you want to d/c DAPT before surgery?

Clopidogrel or Ticagrelor
Prasugrel
ASA

A
  • 5 days - Copidogrel or Ticagrelor
  • 7 days – Prasugrel
  • Continue ASA if possible
70
Q

Time to wait for Elective Surgery for the following procedures:
Angioplasty w/o stent:
Bare-metal stent placement:
Coronary artery bypass grafting:
Drug-eluting stent placement:

A
  • Angioplasty w/o stent: 2-4 weeks
  • Bare-metal stent placement: 30 days - 12 weeks
  • Coronary artery bypass grafting: 6-12 weeks
  • Drug-eluting stent placement: 6-12 months
71
Q

Pre-operative Assessment for Cardiac Procedures

A
  • Determine the presence of risk factors
  • Evaluate METs (>4)
  • Co-existing non-cardiac disease
  • Physical Exam
  • Specialize testing (EKG)
72
Q

Meds to continue before surgery for IHD pt.

A
  • β blocker
  • α2-agonist
  • control hyperglycemia (<180 mg/dL)
73
Q

Meds to d/c before surgery for PCI/IHD patients.

A
  • ACE inhibitor (d/c 24 hours before surgery)
  • Statins
  • DAPT (continue ASA if possible)
74
Q

What is given to a patient experiencing bradycardia in the OR?

A

Glycopyrrolate.

Atropine is not used d/t the increased risk of dysrhythmias.

75
Q

Revised Cardiac Risk Index (RCRI)

A
76
Q

What is MET?

What does 1 MET equal?

What do you want a patient’s MET to be above?

A
  • Metabolic equivalent of task - tool used to assess cardiopulmonary fitness.
  • 1 MET = 3.5 mL of O2/kg/min
  • > 4 METs (Can climb at least one flight of stairs).
77
Q

What is considered an emergency surgery?

A
  • Life or limb would be threatened if the surgery did not proceed within 6 hours or less
  • Proceed directly to emergency surgery w/o pre-op cardiac assessment
78
Q

Urgent Surgery

A

Urgent – life or limb would be threatened if the surgery did not proceed within 6 to 24 hours.

79
Q

Time Sensitive Surgery

A

Delays exceeding 1 to 6 weeks would adversely affect patient outcomes

80
Q

Active Cardiac Conditions that can cancel a surgery.

A
  • Unstable coronary syndromes
  • Unstable or severe angina
  • Decompensated HF
  • Severe valvular heart disease
  • Significant dysrhythmias
  • Age = Fraility (depends)
81
Q

Unstable Coronary Syndrome
It is suggested that more than _____ days should elapse after a recent MI before noncardiac surgery is undertaken (in the absence of coronary intervention).

A
  • 60 days
82
Q

Anesthetic Goals for IHD

A
  • Prevent myocardial ischemia
  • Monitor for ischemia
  • Treat ischemia
  • Maintain BP and HR within the normal awake baseline (20%)
83
Q

Anesthetic Preventions for IHD

A
  • Persistent tachycardia
  • Systolic HTN
  • SNS stimulation
  • Arterial hypoxemia
  • Hypotension
84
Q

DL should be less than ______ seconds.

A

15 seconds

85
Q

Anesthetic Considerations for IHD Patients
Severe LV function drug induction consideration:
Why avoid neuraxial anesthesia in DAPT pt?:
What type of NMBD to avoid:?

A
  • Severe LV function: Consider Opioid only induction
  • Avoid neuraxial anesthesia can cause bleeding.
  • Avoid NMBD that can release excessive histamine: atracurium
86
Q

Lead: I and aVL
Coronary Artery Responsible for Ischemia:
Area Involved:

A

Lead: I and aVL
Coronary Artery Responsible for Ischemia: Circumflex
Area Involved: Lateral aspect of LV

87
Q

Lead: V3-V5
Coronary Artery Responsible for Ischemia:
Area Involved:

A

Lead: V3-V5
Coronary Artery Responsible for Ischemia: LAD
Area Involved: Anterolateral aspect of LV

88
Q

Lead: II, III, aVF
Coronary Artery Responsible for Ischemia:
Area Involved

A

Lead: II, III, aVF
Coronary Artery Responsible for Ischemia: RCA
Area Involved: RA, RV, SA & AV Node, Inferior Aspect of LV

89
Q

In general, myocardial _______ is represented by ST depression and symmetric T-wave inversion (TWI), while myocardial ________ may be indicated by ST elevation with or without T wave changes.

A

In general, myocardial ischemia is represented by ST depression and symmetric T-wave inversion (TWI), while myocardial injury may be indicated by ST elevation with or without T-wave changes.

ST Health Assessment (26 decks)

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