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IHD Flashcards

1
Q

Risk factors for IHD

A

Dm, obesity, male, increasing age, hypercholesterolemia, htn, smoking, sedentary life, genetics

dysrhythmias, angina, acute MI, sudden death

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2
Q

Stable angina develops…..

A

Develops in the setting where CA is partiall or sig occluded greater than 70%. Chronic narrowing of CA.

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3
Q

Angina Pectoris releases what?

A

Release of adenosine and bradykinin

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4
Q

Release of adenosine and bradykinin cause…..

A

Cardiac nociceptors->
Afferent neurons->
send pain?
arrises at T1-T5 sympathetic ganglia

slow AV conduction
decrease cardiac contractility

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5
Q

dermatomes for angina/ other diagnosis

A

C8 – T4 dermatome,
C8 = hands
T4 = nipple line

Retrosternal chest pain, pressure, heaviness
Radiates to neck, left shoulder, left arm, or jaw
Occasionally to back or down both arms. chest pain with physical exertion cold weather or emotional tension

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6
Q

Chronic stable CP

A

Chest pain that does NOT change in frequency or severity in 2-month period

doesn’t hurt more or happening more often

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7
Q

Unstable CP

A

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

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8
Q

12 lead ECG changes look for

A

ST segment depression
Associated T wave inversion
ST elevation
order biomarkers to correlate

previous MI changes

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9
Q

Exercise stress test assess….

A

Assessing the Relationship of cardiac stressor/ movement to chest pain

assess supply and demand balance

looking for greater degree of ST changes with stress, greater depression = increased CAD

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10
Q

What dx cardiac test has greater sensitivity for assessing CAD?

A

nuclear stress imaging

tracers accumulating = good flow
dark area = no tracer = ischemia

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11
Q

Nuclear stress imaging
measures…..

A

Size of perfusion abnormality = significance of CAD detected
Estimates LV systolic size and function
Differentiates new perfusion abnormality vs. “old” MI

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12
Q

Tracers for nuclear stress imaging used with/without exercise

A

Thallium

Atropine, dobutamine, and pacing- used to help increase hr and cause the stress.

Adenosine, dipyridamole- Help with dilating the areas after we induce stress, only dilate normal CA not going to evoke change in arteries that are atherosclerotic. Poor arteries/ inflamed from atherosclerosis, these wont dilate them anymore

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13
Q

Get Echo when….

A

patho Q wave and new BBB

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14
Q

Echo assesses….

A

Wall motion abnormalities
Valvular function

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15
Q

Function of Coronary angiography

A

Determines location of occlusive disease

Diagnose Prinzmetal (variant/spasm) angina

Assess results of angioplasty/stenting

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16
Q

Coronary angiography does not measure…..

A

Does NOT measure stability of plaque; when it will rupture

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17
Q

Gen treatment for IHD

A

Cessation of smoking
Ideal body weight
Low-fat, low-cholesterol diet; Statins;
Regular aerobic exercise
Treatment of hypertension

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18
Q

When are statins prescribed

A

increased trig
LDL > 160 mg/dl, 50% reduction is what they are looking for

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19
Q

ASA moa

A

inhibits cox 1 = inhibits thromboxane A2= decreased clotting.

Irreversible, plat life span = 7 days

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20
Q

Platlets given to plavix pts is effective….

A

24 hours after the last dose / 5 half lives

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21
Q

Platelet glycoprotein IIb/IIIa receptor antagonists meds and MOA

A

(abciximab, eptifibatide, tirofiban)

Inhibit platelet activation, adhesion, and aggregation

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22
Q

Plavix metabolite increases clearance by….

A

6-8 hrs

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23
Q

Thienopyridines (P2Y12inhibitors)
medications

A

Clopidogrel and Prasugrel

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24
Q

Clopidogrel MOA

A

Inhibits ADP receptor P2Y12 and platelet aggregation

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25
Q

when clopidogrel is DC’s platlets….

A

D/C ~ 80% of platelets recover to normal function , takes time and we are always making plat

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26
Q

clopidogrel hypo/hyper responsive percentage

A

10 - 20% of people hypo/hyper-responsive = less predictable pharmacodynamics

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27
Q

Clopidogrel and PPI’s

A

reduce the effectiveness of the drug

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28
Q

Pragusul compared to clopidogrel

A

More predictable pharmacokinetics; more potent than Plavix.
Higher risk of bleeding

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29
Q

Nitrates effect

A

Decrease frequency, duration, and severity of CP

Increase exercise to produce ST-segment depression

Dilate coronary arteries and collaterals

Decrease peripheral vascular resistance

Decreases preload

Potential anti-thrombotic effects; not well researched

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30
Q

Nitrates are contraindicated in……

A

Contraindicated with aortic stenosis and hypertrophic cardiomyopathy

AS = need more venous return for forward motion
HC = outflow obstructed

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31
Q

Nitrates drug interactions

A

Synergistic with beta-blockers/calcium channel blockers; if given in addition then the effect is more profound.

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32
Q

Only drug to prolong life in CAD pts

A

Beta blockers

Decreases risk of death and reinfarction in MI pts

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33
Q

Beta blockers effects

A

Anti-ischemic, anti-hypertensive, anti-dysrhythmic

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34
Q

medication that Increased risk of bronchospasm in reactive airway disease

A

Beta 2 adrenergic blockers
(propranolol, nadolol)

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35
Q

Beta 1 blockers

A

Blockade of β1- receptors (atenolol, metoprolol, acebutolol, or bisoprolol)

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36
Q

Beta blockers effect

A

Decrease Heart rate
Inrease Diastolic time
Reduce Myocardial contractility
Decrease Myocardial oxygen demand
Helping heart to relax and refill, when increasing diastolic time = increases coronary perfusion time.

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37
Q

medication that is Uniquely effective for decreasing frequency/severity of spasm in coronary arteries (prinzmental)

A

CCB

Dilate coronary arteries,

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38
Q

CCB decrease ……

A

Vascular smooth muscle tone
Contractility
Oxygen consumption
Systemic BP

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39
Q

Beta blockers compared to CCBs

A

Not as effective as beta blockers in decreasing incidence of myocardial reinfarction

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40
Q

Angiotensin II increases….

A

Myocardial hypertrophy
Interstitial myocardial fibrosis
Coronary vasoconstriction
Inflammatory responses

ace i

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41
Q

ACE i treat

A

Hypertension
Heart failure

Cardioprotective ; reduce the workload to decrease demand and prevent vent remodeling and stabilize the repercussed heart and prevent the reoccurrence of reperfusion arrhythmias.

42
Q

Medication that helps with coronary plaque stabilization

A

statins by Decreases, Lipid oxidation, Inflammation, Matrix metalloproteinase, Cell death

43
Q

Statins reduce the mortality noncardiac surgery and vascular surgery by….

A

Reduces mortality noncardiac surgery (44%) and vascular surgery (59%)

44
Q

Revasularization for what pts….

A

Failure of medical therapy
> 50% L main coronary artery
> 70% epicardial coronary artery
Impaired EF <40%

45
Q

CABG > PCI when……

A

L main disease; 2 or 3 vessel CAD, DM and have 2 or 3 Vessels

46
Q

what is Acute Coronary Syndrome

A

Acute or worsening imbalance of myocardial oxygen supply to demand

47
Q

Events leading to ACS

A

Atheromatous plaque
Coagulation cascade
Thrombin generation
Arterial occlusion (partial or complete)

48
Q

No st seg elevation and negative biomarkers

A

unstable angina

49
Q

No st seg elevation with positive biomarkers

A

NSTEMI

50
Q

St elevation with positive biomarkers

A

STEMI

51
Q

What forms at the site of the ruptured plaque

A

plat monolayer and Vulnerable plaques; likely to ruputure.

52
Q

Chemicals that stim plat aggregation

A

Collagen, ADP, epinephrine, serotonin-> stim plat aggregations

TXA2 = vasoconstriction

53
Q

Glycoprotein 2b/3a function

A

Glycoprotein IIb/IIIa receptors; activated on plat and that enhances the ability to interact with adhesive proteins/ make stickier and make clot bigger -> growth-> stabilize thrombus

54
Q

Troponin increases within….

A

3 hours after myocardial injury , stay elevated for 7 to 10 days

More specific than CK-MB

55
Q

STEMI Dx

A

evidence of myocardial necrosis with myocardial ischemia; troponin, st changes, patho q wave,

56
Q

reperfusion medical therapy

A

Tissue plasminogen activator (tPA), streptokinase, reteplase, or tenecteplase- started within 30 min of hospital arrival/ 12 hr or symptom onset.

catalyze plasminogen-> plasmin to break down the clot

Restores normal antegrade blood flow

57
Q

When are imaging studies ordered

A

new LBB or abnormal ECG

Regional wall motion abnormalities
Ad look at valves, if pt has evidence of EKG with an MI. echo is not warranted. Only indictive if the pt needs an echo. Not everyone with an MI will have an echo.

58
Q

Indications for PCI

A

-Contraindications to thrombolytic therapy
-Severe HF and/or pulmonary edema
-Symptoms present for 2 - 3 hours
-Mature clot

59
Q

Indications for CABG

A

CABG recommended based on Coronary anatomy

failed angioplasty

Evidence of infarction-related ventricular septal rupture or mitral regurgitation

60
Q

Drug therapy for ACS

A

MONA; morphine, oxygen, nitrates, asa
P2Y12inhibitors (clopidogrel, prasugrel, or ticagrelor)
Platelet glycoprotein IIb/IIIa inhibitors
Unfractionated heparin (esp for PCI/ thrombolytic therapy is planned)
βblockers
RAAS; ACEi, ARB, prevent vent remodeling.

61
Q

Causes of unstable angina

A

Rupture or erosion of a coronary plaque
Dynamic obstruction due tovasoconstriction(prinzmental/ cold temp)
Worsening coronary luminal narrowing (atherosclerosis/ stent restenosis)
Inflammation (vasculitis)
Myocardial ischemia due to increased oxygen demand

62
Q

Unstable Angina/ NSTEMI

A

Angina at rest, lasting >10 minutes

63
Q

Chronic angina pectoris

A

Cp thats more frequent and more easily provoked
Crescendo pattern; gaining momentum

64
Q

New-onset angina

A

severe,prolonged, or disabling cp

65
Q

Treatment for unstable angina/ NSTEMI

A

Bed rest, oxygen, analgesia, andβ-blocker therapy
Sublingual or IV nitroglycerin
Calcium channel blockers
Aspirin, clopidogrel, prasugrel, or ticagrelor and heparin therapy (unfractionated heparin or LMWH)

66
Q

Thrombolytic therapy not indicated in what pts

A

unstable angina/ NSTEMI because the fibin is not there and pts still have flow

67
Q

Types of PCI

A

Balloon angioplasty, bare-metal stent, drug eluding stent……Destruction of endothelium of the vessel

68
Q

Reendovasualrization post balloon angioplasty can take…..

A

2-3 weeks- 2-3 weeks of therapy

69
Q

Reendovasualrization post baremetal stend angioplasty can take…..

A

12 weeks- 6 weeks of therapy

70
Q

Reendovasualrization post DES angioplasty can take…..

A

1 year

71
Q

DC clopidogrel or ticagrelor….

A

5 days to reduce bleeding risk

continue asa if possible

72
Q

DC prasugrel ……

A

7 days

73
Q

Angioplasty without stenting time to wait for elective sx

A

2-4 weeks

74
Q

Bare metal stent placement time to wait for elective surgery

A

at least 30 days ; 12 weeks preferable

75
Q

CABG time to wait for elective surgery

A

at least 6 weeks; 12 weeks preferable

76
Q

DES time to wait for elective surgery

A

at least 6 months; at least 12 months after acute coronary syndrome

77
Q

what anesthetic to avoid with post-cardiac intervention pts

A

Anesthetic technique; avoid spinal/ epidural

78
Q

Pre op beta blockers

A

continue throughtout peri- op

79
Q

treatment for bradycardia with beta blockers

A

Glycopyrrolate > atropine

80
Q

____ has less potential to cause arrhythmias

A

glycopyrrolate

81
Q

α2-Agonists MOA

A

Decrease sympathetic outflow, blood pressure, and heart rate

Continue because of rebound effects.

Rebound effects; tachycardia/ htn

82
Q

DC ACEi…..

A

D/C 24 hours before surgery

Sympathomimetics to treat hypotension

83
Q

Control hyperglycemia to…

A

< 180mg/dL

84
Q

Components of RCRI

A

High risk sx; intraperiotoneal, intrathoracic, subringuinal vasular procedure

ischemic heart dz
hx of CHF
hx of CVA
Dm w/ insulin
Creat > 2.0

85
Q

RCRI score

A

0=0.4%
1= 1%
2 = 2.4$
>3 = 5.4%

Low risk - <1%= ≤1 RCRI risk factor
Elevated risk - >1%= >2 RCRI risk factors

86
Q

Functional capacity assesses….

A

cardiopulmonary fitness
Poor functional capacity = increased peri-operative risk

87
Q

Mets

A

metabolic equivalent of task

Rate of energy consumption at rest

1 MET = 3.5 mL/kg/min
want > 4 METs

88
Q

Emergency surgery

A

life or limb would be threatened if surgery did not proceed within 6 hours or less
-Proceed directly to emergency surgery w/o pre-op cardiac assessment
-Focus on surveillance and early treatment

89
Q

Urgent surgery

A

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

90
Q

Time-sensitive surgery

A

delays exceeding 1 to 6 weeks would adversely affect patient outcomes

91
Q

2, 3, avF artery

A

RCA

areas; RA, RV, SA node, interior LV, AV node

92
Q

1, AVL artery

A

circumflex

area; lateral aspect of the LV

93
Q

V3-V5 artery

A

LAD

area; anterolateral aspect of LV

94
Q

Goals of IHD with anesthesia

A

Prevent myocardial ischemia
Monitor for ischemia
Treat ischemia

Prevent
Persistent tachycardia
Systolic HTN
SNS stimulation
Arterial hypoxemia
Hypotension

Maintain BP and HR w/in normal awake baseline 20%

95
Q

Causes of decrease oxygen delivery

A

decrease coronary blood flow
tachycardia
hypotension
hypocapnia
Coronary artery spasm
decreased oxygen content
anemia
arterial hypoxemia
shift of the oxyghbg dissociation cure to the L

96
Q

Increased oxygen requirements

A

symathetic nervous sytem stimulation
tachycardia
htn
increase Mypocardial contraciltiy
increased afterload
increased preload

97
Q

Anesthetic considerations for induction

A

Succinylcholine, vecuronium, rocuronium, & cisatracurium—avoid histamine release

DL ≤15 seconds
Laryngotracheal lidocaine, IV lidocaine, esmolol, fentanyl, remifentanil, and dexmedetomidine

Volatile anesthetics
Nitrous oxide
Opioids; Severe LV function
Neuraxial anesthesia- avoid if ont DAPT therapy

98
Q

med to give for tachycardia

A

esmolol

99
Q

Tx for hypotension

A

Fluid bolus
Sympathomimetic drugs (ephedrine, phenylephrine)

100
Q

Pragusul compared to clopidogrel

A

More predictable pharmacokinetics; more potent than Plavix.
Higher risk of bleeding

101
Q

What forms at the site of the ruptured plaque

A

plat monolayer and Vulnerable plaques; likely to ruputure.

102
Q

New-onset angina

A

severe,prolonged, or disabling cp

HA (15 decks)

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