Ischemic Heart Disease Flashcards

1
Q

What are the risk factors for ischemic heart disease?

A

30% surgical pts​

Angina pectoris, acute MI, and sudden death​

Dysrhythmias​

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2
Q

The two most important risk factors for the development of atherosclerosis involving the coronary arteries are _____ and increasing ______

A

male gender; increasing age

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3
Q

Angina pectoris is caused by ____

A

Imbalance between coronary blood flow (supply) and myocardial oxygen consumption (demand)​

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4
Q

Stable angina typically develops in the setting of _____ occlusion or significant (>70%) chronic narrowing of a segment of coronary artery.​

A

partial

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5
Q

_______ is the most common cause of impaired coronary blood flow resulting in angina pectoris, but it may also occur in the _____ of coronary obstruction as a result of myocardial hypertrophy, severe aortic stenosis, or aortic regurgitation

A

atherosclerosis ; absence

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6
Q

What can induce angina?

A

Physical exertion, emotional tension, and cold weather may induce angina​

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7
Q

Which statement best describes chronic stable angina?​

A

Chronic stable angina refers to chest pain or discomfort that does not change appreciably in frequency or severity over 2 months or longer.
chronic angina pectoris that becomes more frequent and more easily provoked​ ​

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8
Q

Describe unstable angina

A

angina at rest (typically lasting >10 minutes unless interrupted by antianginal medication), ​

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9
Q

Do patients with typical ECG evidence of AMI need an echo?

A

no

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10
Q

Troponin levels remain elevated for bumps in ___ hours, elevated for up to 2 weeks​

A

3-4 hours
Cardiac labs​

Troponin levels remain elevated for: bumps in 3-4 hours, elevated for 7-10 days
Greater the level of troponin the larger the MI

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11
Q

The greater the degree of _________ , the greater the likelihood of significant coronary artery disease.

A

ST-segment depression

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12
Q

Look at Picture

A

:) you can do it

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13
Q

What results in sudden cardiac death

A

overdose, cardiomyopathy, atherosclerosis

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14
Q

What results in coronary bloodflow being decrease?

A

reduction in lumen size, MI, hypotension
- we cause hypotension

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15
Q

What are signs you’ll see during anesthesia that they are having low coronary blood flow?

A

EKG changes

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16
Q

Stable angina is chest pain that ____ _____ with rest

A

goes away

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17
Q

When you have angina you’ll see slow ___ _____ and _____ cardiac contractility
What causes these changes?

A

AV conduction; decrease
Adenosine and bradykinin release

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18
Q

There are weird presentations of cardiac pain in ___ and _____

A

diabetics and women

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19
Q

How to differentiate cardiac from other pain?

A

touch it, give GI cocktail, if its pericarditis they will feel better with sitting up
- could be PE and you will see it on a blood gas. They could be confused and air hungry
- AAA: tearing pain in the back and chest

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20
Q

Unstable​ angina

A

Chest pain increasing in frequency and/or severity without increase in cardiac biomarkers​
- no increase in CKP
-chronic angina pectoris that becomes more frequent and more easily provoked​
- new-onset angina that is severe, prolonged, or disabling

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21
Q

chronic stable chest pain can be caused by

A
  • distal occlusions
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22
Q

After a EKG and labs are done for a chest pain patient, what else would you do?

A

Stress test

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23
Q
  1. ____ stress test is more accurate because it provides nuclear imaging
  2. The greater the size of perfusion abnormality = ??????
  3. What does a nuclear stress test show us?
A
  1. Chemical
  2. Size of perfusion abnormality = significance of CAD detected​
  3. Assesses coronary perfusion​

Tracer activity in perfused vs ischemic areas​

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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24
Q

what abnormality can you see on an ultrasound with chest pain?

A
  • valve function
  • wall motion abnormalities
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25
Q

gold standard for looking at coronary blood flow is

A

angiography
- can see little. occlusions that result in hypoperfusion

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26
Q

How do we treat stable angina?

A
  • reverse reversible factors (DM, weight, get off the couch, GLP-1)
  • treatment of HTN
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27
Q

What is the dose for daily aspirin?

A

75-325mg/day
“Baby aspirin” is 81mg/day

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28
Q

What is the life span of a platelet

A

7-14 days

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29
Q

Platelet glycoprotein IIb/IIIa receptor antagonists (abciximab, eptifibatide, tirofiban) ​ work by…..

A

Inhibit platelet activation, adhesion, and aggregation​
- given IV

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30
Q

Clopidogrel is _____

A

irreversible
- just like the other drugs

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31
Q

How do you assess platelet function?

A

Platelet function panel and TEG (thromboelastagram)

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32
Q

Effient is very ___

A

predictable
- cardiologist will use this pre or post intervention for a cath

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33
Q

Patients who take chronic nitrates ____________ respond well to doses

A

do not
- they wont respond

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34
Q

what is the only medication that prolongs life span with CAD?

A

beta blockers
- when you induce anesthesia you will see an induced hypotension

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35
Q

With beta 2 blockers we would worry about what complications?

A

pulmonary

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36
Q

propranolol is used for __ and ____

A

anxiety and tremors

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37
Q

describe the difference in metoprolol, esmolol, and labetolol

A

metoprolol is more for contractility and esmolol is more for HR
labetolol is in the middle

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38
Q

When do you start a patient on a CCB?

A

when the BB doesn’t work

39
Q

ACE inhibitors are very ____

A

cheap
- patients will be put on this early because it isnt expensive

40
Q

Why do we put patients on statins

A

Small reduction in mortality in patients undergoing surgical procedures
- coronary plaque stabilization

41
Q

2 primary interventions for revascularization are

A

CABG and PCI
- over 50% LAD occlusion = CABG
- over 70% epicardial coronary artery = CABG
- impaired EF < 40% = CABG

42
Q

What do we do in PCI?

A
  • angioplasty: balloon into the plaque and pushing it against the wall
  • placement of a stent and then use the balloon to open the stent
  • transluminal interventions: grinds the plaque off the walls of the vessels
43
Q

ACS is

A

Acute or worsening imbalance of myocardial oxygen supply to demand​

44
Q

ACS chart

45
Q

STEMI Diagnosis

46
Q

How do you know if the patient has a new LBBB?

A

must have an old 12 lead

47
Q

Troponin is more specific for ____ than CK-MG

A

cardiac damage

48
Q

Troponin​

Increase within ___ hours after myocardial injury ​

49
Q

Drug therapy for ACS

A

MONA????​

Oxygen​

Aspirin​

Morphine causes hypotension – fentanyl is starting to be used​

Torodol – decreased ???​

Nitrates​

P2Y12 inhibitors (clopidogrel, prasugrel, or ticagrelor)​

Platelet glycoprotein IIb/IIIa inhibitors​

Unfractionated heparin​

β blockers​

RAAS​

50
Q

What medications are in reperfusion drug therapy

A

TPA, streptokinase, reteplase, tenecteplase

51
Q

What is the time frame for thrombolytics

A

should be initiated within 30 to 60 minutes of hospital arrival and within 12 hours of symptom onset. Thrombolytic therapy restores normal antegrade blood flow in the occluded coronary artery.​

52
Q

indications for PCI

A

Indications​

Contraindication to thrombolytic therapy​

Severe HF and/or pulmonary edema​

Symptoms present for 2 - 3 hours​

Mature clot ​

53
Q

Causes of unstable angina

54
Q

chronic angina patients will have very ____ blood flow through their vessels

55
Q

Do we use thrombolytics for NSTEMI?

56
Q

What is DAPT therapy

A

Dual antiplatelet therapy
ASA and P2y12 inhibitor

57
Q

if a patient has had coronary intervention you dont want to take them to the OR for ____ to a _____

A

6 months to a year

Reendothelialize after balloon angioplasty - 2–3 weeks ​

bare-metal stent placement - 12 weeks​

drug-eluting stent - a full 1 year or longer

58
Q

You can give a 1:1 ratio of glycopyrrolate and neostigmine to reduce ____

A

reduce the bradycardia with neostigmine

59
Q

RCRI test

60
Q

What are the active cardiac conditions we worry about?Unstable coronary syndromes​

A
  • Acute (MI ≤ 7 days) or recent MI (>7 days but ≤ 1 month ago) with evidence of important ischemic risk ​
  • > 60 days post MI ideal​

Unstable or severe angina ​

Decompensated heart failure​

Severe valvular heart disease ​
- Severe aortic stenosis or severe mitral stenosis​

Significant dysrhythmias​
- High-grade atrioventricular block, Mobitz type II atrioventricular block, third-degree heart block, and symptomatic supraventricular and ventricular tachydysrhythmias ​

Age​

61
Q

How do you prevent ischemia in the OR?

A

Prevent​
- Persistent tachycardia​
- Systolic HTN​
- SNS stimulation​
- Arterial hypoxemia​
- Hypotension​
Etomidate will be induction of choice
May want an arterial line before induction

62
Q

What is the first manifestations of ischemic heart disease? (there are 3)

A

angina pectoris
acute MI
sudden death

63
Q

explain how adenosine and bradykinin release cause chest pain?

A

These substances stimulate cardiac nociceptive and mechanosensitive receptors whose afferent neurons converge with the upper five thoracic sympathetic ganglia and somatic nerve fibers in the spinal cord and ultimately produce thalamic and cortical stimulation that results in the typical chest pain of angina pectoris.​

64
Q

Describe EKG changes associated with ischemic heart disease?

A

12 lead ECG – GOLD standard​

ST segment depression ​

Associated T wave inversion​

ST elevation​

ST-segment depression (characteristic of subendocardial ischemia) that c

**resting electrocardiogram (ECG) may be normal in patients with angina, or it may show nonspecific ST–T-wave changes or abnormalities related to an old MI.​

65
Q

Patients with chronically inverted T waves resulting from previous MI may show a return of the _____ to the normal upright position (pseudonormalization of the T wave) during myocardial ischemia

66
Q

during an exercise stress test how would you know the patient have IHD?

A

At least 1 mm of horizontal or downsloping ST-segment depression during or within 4 minutes after exercise. The greater the degree of ST-segment depression, the greater the likelihood of significant coronary artery disease.​

67
Q

what are the tracers involved in a nuclear stress test?

how do the tracers work?

A

Tracers - thallium and technetium​
- A significant coronary obstructive lesion causes a reduction in blood flow, and thus less tracer activity is present in that area.​
- Exercise increases the difference in tracer activity between normal and underperfused regions because coronary blood flow increases markedly with exercise except in those regions distal to a coronary artery obstruction​

Administration of atropine, infusion of dobutamine, or institution of artificial cardiac pacing produces a rapid heart rate to create cardiac stress.​

cardiac stress can be produced by administering a coronary vasodilator such as adenosine or dipyridamole. These drugs dilate normal coronary arteries but evoke minimal or no change in the diameter of atherosclerotic coronary arteries. ​

68
Q

The _____ of the perfusion abnormality is the most important indicator of the significance of the coronary artery disease detected. in nuclear imaging

68
Q

what are the indications for cardiac angiography?

A

It is indicated in patients with
- known or possible angina pectoris who have survived sudden cardiac death
- those who continue to have angina pectoris despite maximal medical therapy,
- those who are being considered for coronary revascularization,
- those who develop a recurrence of symptoms after coronary revascularization,
- those with chest pain of uncertain cause, and those with a cardiomyopathy of unknown cause​

provides the best information about the condition of the coronary arteri

Does NOT measure stability of plaque​

69
Q

The most vulnerable plaques are those with a ____ core and lots of _____

A

lipid; macrophages
Vulnerable plaques (i.e., those most likely to rupture and form an occlusive thrombus) have a thin fibrous cap and a large lipid core containing a large number of macrophages. The presence of vulnerable plaque predicts a greater risk of MI regardless of the degree of coronary artery stenosis. Indeed, AMI most often results from rupture of a plaque that had produced less than 50% stenosis of a coronary artery. Currently there is no satisfactory test to measure the stability of plaques.​

70
Q

how does HTN increase the risk of IHD?

A

Hypertension increases the risk of coronary events as a result of direct vascular injury, left ventricular hypertrophy, and increased myocardial oxygen demand​

71
Q

when is drug treatment for IHD reccomended?

A

strongly recommended in patients with clinical atherosclerosis or when the low-density lipoprotein (LDL) cholesterol level exceeds 160 mg/dL (goal is >50% reduction or <70 mg/dL).​

72
Q

what does TXA2 do?

A

it stimulates activation of new platelets as well as increases platelet aggregation

Thromboxane A2 (TXA2) is a type of thromboxane that is produced by activated platelets during hemostasis and has prothrombotic properties:.​

73
Q

list all the possible drug therapy for IHD
* 8 were listed in lecture

A
  • Aspirin
  • Platelet glycoprotein IIb/IIIa receptor antagonists (abciximab, eptifibatide, tirofiban)
  • P2Y12 inhibitors (clopidegrel and Effient)
  • nitrates
  • beta blockers (B1 and B2 specific)
  • CCB
  • ACE inhibitors
  • Statins
74
Q

Tell me about clopidogrel?

A
  • prodrug
  • irreversible affect to platelets
  • Inhibits ADP (activates the platelets and makes them sticky) receptor P2Y12 and platelet aggregation​
75
Q

Effient poses a higher risk of ____ than plavix

A

bleeding

Prasugrel (Effient)​

Similar mechanism​

More predictable pharmacokinetics​

Higher risk of bleeding​

76
Q

Nitrates are contraindicated in what two diseases?

A

Contraindicated with aortic stenosis and hypertrophic cardiomyopathy​

77
Q

What do nitrates do? How do they help the angina?

A

Decrease frequency, duration, and severity​

Increase exercise to produce ST-segment depression​

Dilate coronary arteries and collaterals​

Decrease peripheral vascular resistance​, which reduces left ventricular afterload and myocardial oxygen consumption.

Decreases preload​ —> decrease stress on LV

Potential anti-thrombotic effects​

78
Q

antianginal effects of nitrates are greater when these drugs are used in combination with______ or _____

79
Q

What drugs block only beta 1?
What does that produce?

A

atenolol, metoprolol, acebutolol, or bisoprolol
decrease in:
Heart rate​

Diastolic time​

Myocardial contractility ​

Myocardial oxygen demand​

80
Q

propranolol & nadolol activate beta 1 and _____

A

beta 2
watch for pulmonary complicatio

81
Q

what do CCB do for IHD patients? 5 things

A

decrease:

Vascular smooth muscle tone​

Contractility​

Oxygen consumption​

Systemic BP​

and dilate coronaries

82
Q

statins decrease what 4 things

A

Decreases​: Lipid oxidation​, Inflammation​, Matrix metalloproteinase​, Cell death​

Reduces mortality noncardiac surgery and vascular surgery ​

83
Q

describe what is happening in this picture

A

Acute or worsening imbalance of myocardial oxygen supply to demand​

Atheromatous plaque ​—> Coagulation cascade—-> Thrombin generation​—-> Arterial occlusion ​

84
Q

Coronary angiography has documented that the majority of STEMIs are caused by ______ occlusion of a coronary artery.

A

thrombotic

In rare cases STEMI may be due to coronary occlusion caused by coronary emboli, congenital abnormalities, coronary spasm, or inflammatory diseases.

85
Q

Which substances contribute to thrombogenesis?​

A

​Collagen, ADP, epinephrine, serotonin​, Thromboxane A2​, Glycoprotein IIb/IIIa receptors​, Fibrin deposit

A platelet monolayer forms at the site of ruptured plaque, and various chemical mediators such as collagen, ADP, epinephrine, and serotonin stimulate platelet aggregation.​

The potent vasoconstrictor thromboxane A2 is released, which further compromises coronary blood flow. ​

Glycoprotein IIb/IIIa 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 strengthening of the clot by fibrin deposition. This makes the clot more resistant to thrombolysis​

86
Q

Contemporary studies using MRI suggest that the development of a Q wave on the ECG is more dependent on the ____ of the infarcted tissue than the transmurality of the infarction.​

87
Q

The primary goal in management of STEMI is to reestablish ____ in the obstructed coronary artery as soon as possible​

A

blood flow

88
Q

what is the time frame for PCI

A

angioplasty should be performed within 90 minutes of arrival at the healthcare facility and within 12 hours of symptom onset​

89
Q

_____ __________ discontinuation is the most significant independent predictor of stent thrombosis​

A

P2Y12 inhibitor

90
Q

This _______ myocardial ischemia usually occurs at a heart rate and blood pressure substantially lower than that present during exercise-induced ischemia. ​

A

silent
Some patients can have ischemia but it doesnt cause pain

91
Q