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Circulation Part 2 > Ischemic Heart Disease- Lecture > Flashcards

Ischemic Heart Disease- Lecture Flashcards

1
Q

More than 90% of acute coronary syndrome events (angina, NSTEMI, STEMI) result from the disruption of _

A

More than 90% of acute coronary syndrome events (angina, NSTEMI, STEMI) result from the disruption of atherosclerotic plaque followed by platelet aggregation and thrombus formation

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2
Q

Atherosclerotic plaques may rupture due to _ or _

A

Atherosclerotic plaques may rupture due to chemical factors that destabilize the lesion or physical stress on the lesion
* Triggers include strenuous physical activity, emotional stress, SNS activation

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3
Q

Coronary thrombosis following atherosclerotic plaque rupture is often exacerbated by _

A

Coronary thrombosis following atherosclerotic plaque rupture is often exacerbated by endothelial dysfunction –> leads to vasoconstriction and diminished anti-thrombotic function

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4
Q

The 90% lesions have lots of _ and are not as common to rupture; the 30-40% lesions are soft with _ and are more commonly the ones to rupture

A

The 90% lesions have lots of calcium and are not as common to rupture; the 30-40% lesions are soft with cholesterol and are more commonly the ones to rupture

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5
Q

Atherosclerotic plaque rupture will stimulate thrombosis via activation of _

A

Atherosclerotic plaque rupture will stimulate thrombosis via activation of hemostasis
* Endothelial damage –> exposure of the thrombogenic connective tissue to the cirulating blood
* Triggers soft platelet plug (1) and then fibrin clot (2)

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6
Q

The ACS pathologies that are characterized by partially occlusive thrombus are _

A

The ACS pathologies that are characterized by partially occlusive thrombus are unstable angina and NSTEMI

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7
Q

The ACS pathology that is characterized by completely obstructive thrombus is _

A

The ACS pathology that is characterized by completely obstructive thrombus is STEMI

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8
Q

The difference between unstable angina and NSTEMI is _

A

The difference between unstable angina and NSTEMI is NSTEMIs have enough blockage that there is necrosis of the tissue
* Troponin is normal in unstable angina, abnormal in NSTEMI

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9
Q

A common result of acute plaque rupture and coronary artery thrombosis is _

A

A common result of acute plaque rupture and coronary artery thrombosis is myocardial infarction

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10
Q

With an MI event, blood flow can be spontaneously restored within _ hours

A

With an MI event, blood flow can be spontaneously restored within 12-24 hours
* Endothelium is working to dissolve the thrombus
* However, this is often too late because ischemia can result very quickly

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11
Q

Only _ minutes of ischemia can cause irreversible myocyte injury called infarct

A

Only 20-30 minutes of ischemia can cause irreversible myocyte injury called infarct

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12
Q

Name some of the factors that determine the severity of an infarction

A
  1. Magnitude and duration of ischemia
  2. Is there collateral coronary flow?
  3. Mass of the myocardium perfused by the blocked coronary artery
  4. Oxygen demand of the myocardium at risk
  5. Degree and timing of reperfusion (good)
  6. Once you do reperfuse, how big is the inflammatory response (reperfusion injury)
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13
Q

Within 20-30 minutes irreversible cell injury ensues; marked by _ cellular change

A

Within 20-30 minutes irreversible cell injury ensues; marked by loss of nuclei
* An MI occurs when the ischemia is severe enough for long enough to cause irreversible injury and necrosis

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14
Q

During reversible myocyte injury, there is a rapid shift from _ –> _ metabolism

A

During reversible myocyte injury, there is a rapid shift from aerobic –> anaerobic metabolism
* Lactic acid accumulates
* Reduction in ATP

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15
Q

Reversible myocyte injury is also associated with abnormal electrolyte ion shifts that can result in _ or _

A

Reversible myocyte injury is also associated with abnormal electrolyte ion shifts that can result in arrhythmias or edema (rising intracellular Na+)

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16
Q

Infarctions begin in _ layer of the heart and can progress to the entire thickness of the myocardium due to prolonged, total occlusion of _

A

Infarctions begin in subendocardial layer of the heart and can progress to the entire thickness of the myocardium due to prolonged, total occlusion of epicardial coronary artery

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17
Q

The subendocardial layer is susceptible to ischemia due to _

A

The subendocardial layer is susceptible to ischemia due to poor collateral flow, being adjacent to high-pressure ventricles, and being furthest from epicardial coronary arteries

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18
Q

Two possible ECG findings that might suggest subendocardial ischemia:

A
  1. ST depression
  2. T wave inversion
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19
Q

The most suggestive finding on the ECG for an MI is _ ; however, _ or _ can also be signs

A

The most suggestive finding on the ECG for an MI is ST segment elevation ; however, ST segment depression or T wave inversion can also be signs

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20
Q

Labile T wave inversions in the setting of chest pain are likely to suggest _

A

Labile T wave inversions in the setting of chest pain are likely to suggest myocardial infarction

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21
Q

The ST segment represents _

A

The ST segment represents the period between depolarization and repolarization of the left ventricle
* In a normal state, the ST segment should be isoelectric to the PR segment

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22
Q
A

ST depression in multiple leads; suggestive of ischemia/ infarction

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23
Q

What medications are adminstered in the setting of unstable angina/ NSTEMI?

A
  1. Beta blockers (metoprolol)
  2. Nitrates (nitroglycerin)
  3. Anti-platelet therapies (aspirin, clopidogrel)
  4. Anticoagulant Therapy (heparin)
  5. ACE inhibitor (lisinopril)
  6. Statin (atorvastatin)
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24
Q

Beta blockers are administered for ischemic heart disease for the purpose of _

A

Beta blockers are administered for ischemic heart disease for the purpose of decreasing oxygen demand
* Lower the heart rate –> enhances electrical stability and decreases oxygen demand

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25
Beta blockers should be administered in the first 24 hours post MI and should be continued indefinitely because _
Beta blockers should be administered in the first 24 hours post MI and should be continued indefinitely because **reduces long-term mortality**
26
Beta blockers should almost always be used for ACS unless patient has _
Beta blockers should almost always be used for ACS unless patient has **marked bradycardia**, **severe bronchospasm**, **hypotension**, **acute heart failure**
27
Nitrates are used in the setting of ACS for the purpose of _
Nitrates are used in the setting of ACS for the purpose of **venodilation** --> decreases preload --> less wall stress --> lower oxygen demand *Additionally, coronary vasodilation improves blood flow, reduces vasospasm, and improves O2 supply*
28
Be cautious when using nitrates for right ventricle infarctions because these patients are often _
Be cautious when using nitrates for **right ventricle infarctions** because these patients are often **preload-dependent** --> nitrates can cause hypotension
29
Anti-platelet therapies in the context of ACS are very important because _
Anti-platelet therapies in the context of ACS are very important because they **reduce mortality** * Give them immediately and continue indefinitely * Often combine aspirin + clopidogrel
30
Aspirin works as an anti-platelet therapy by _
Aspirin works as an anti-platelet therapy by **inhibiting synthesis of TXA2** --> inhibits platelet activation
31
Clopidogrel, Ticagrelor, Prasugrel all function as _ inhibitors
Clopidogrel, Ticagrelor, Prasugrel all function as **P2Y12** inhibitors (they block ADP)
32
Heparins are also used in the context of ACS and work by _
Heparins are also used in the context of ACS and work by **enhancing antithrombin effects** * LMW heparin is technically more effective but is harder to monitor compared to unfractionated heparin
33
Severe occlusions require intervention via _
Severe occlusions require intervention via **percutaneous coronary intervention** (PCI)
34
All patients who receive a stent need to take a dual platelet therapy of _ + _
All patients who receive a stent need to take a dual platelet therapy of **aspirin (ASA)** + **clopidogrel**
35
To diagnose a STEMI on ECG, we must see ST segment elevation > _ mm in at least two anatomically contiguous leads
To diagnose a STEMI on ECG, we must see ST segment elevation > **1 mm** in at least two **anatomically contiguous leads**
36
Or we can diagnose STEMI if there is > _ mm elevation in 2 contiguous precordial leads
Or we can diagnose STEMI if there is > **2 mm** elevation in two **contiguous precordial leads**
37
We also proceed with STEMI treatment if we see _
We also proceed with STEMI treatment if we see **new left bundle branch block** * LBBB can hide the ST elevation so we proceed with treatment
38
ST elevation in lead II, III, aVF
Lead II, III, aVF: **inferior** infarction
39
ST elevation in lead V2-V4
Lead V2-V4: **anterior** infarction
40
ST elevation in lead V1-V4
Lead V1-V4: **anteroseptal** infarction
41
ST elevation in I, aVL, V5, V6
Lead I, aVL, V5, V6: **lateral** infarction
42
A left bundle branch block on ECG suggests _ MI
A left bundle branch block on ECG suggests **anterior** MI
43
ST elevation in V4R
V4R: **right ventricle** infarction
44
ST depressions in V1, V2
ST depressions in V1, V2: **posterior** infarction
45
"Electrically silent" on ECG
"Electrically silent" on ECG: **Left circumflex occlusion**
46
Infarction on the anterior or anteroseptal portion of the heart is a problem at the _
Infarction on the anterior or anteroseptal portion of the heart is a problem at the **left anterior descending artery (LAD)**
47
Infarction on the lateral portion of the heart is most often a problem of the _
Infarction on the lateral portion of the heart is most often a problem of the **left circumflex**, can sometimes be LAD
48
Infarction in the inferior portion of the heart is a problem of the _
Infarction in the inferior portion of the heart is a problem of the **right coronary artery**
49
ST elevation in V4R, which suggests a right ventricle MI is usually a problem of the _
ST elevation in V4R, which suggests a right ventricle MI is usually a problem of the **right coronary artery**
50
V1 and V2 ST depressions, which suggest posterior MI, is a problem of _
V1 and V2 ST depressions, which suggest posterior MI, is a problem of **right coronary artery (usually)** can sometimes be the left circumflex
51
Pathologic Q waves are indicative of _
Pathologic Q waves are indicative of **prior transmural MI**
52
3 criteria for Q waves to be "pathologic"
Criteria for Q waves to be pathologic: 1. Q waves > 1 mm wide 2. Q waves > 25% of QRS amplitude 3. Pathologic Q waves should be present in at least 2 contiguous leads
53
Two immediate treatment options in treating a STEMI are _ or _
Two immediate treatment options in treating a STEMI are **primary PCI** or **fibrinolytic therapy** * PCI is the ideal treatment option; fibrinolytics are used when there is no access to a cath lab * The goal is to restore flow to the epicardial vessels as soon as possible
54
Goals in STEMI treatment
1. Restore epicardial blood flow (salvage muscle) 2. Prevent further thrombus formation (antiplatelets, anticoagulants) 3. Restore the balance between O2 supply and demand (nitrates, beta blockers)
55
Name 3 major complications post MI
1. **Decreased contractility** (inc risk of thrombus) 2. **Electrical instability** (arrhythmias) 3. **Tissue necrosis** (papillary muscle tear, VSD, ventricular rupture)
56
The most common complication of an MI (both during and after) is _
The most common complication of an MI (both during and after) is **arrhythmias** * Impaired perfusion to the conduction system * Accumulation of toxic metabolic products * Autonomic stimulation * Sometimes even caused by the drugs that we give
57
Ventricular fibrillation
58
Ventricular tachycardia
59
Ischemia from a myocardial infarction results in: impaired contractility which is _ dysfunction & increased myocardial stiffness which is _ dysfunction
Ischemia from a myocardial infarction results in: impaired contractility which is **systolic** dysfunction & increased myocardial stiffness which is **diastolic** dysfunction
60
Left heart failure is a major complication of MI that presents with _ and can be treated with _
Left heart failure is a major complication of MI that presents with **dyspnea, rales, S3, peripheral edema, orthopnea** and can be treated with **ACE inhibitors, beta blocks, diuretics**
61
Left heart failure can progress to cardiogenic shock if the cardiac output reduces enough and SBP drops below _
Left heart failure can progress to cardiogenic shock if the cardiac output reduces enough and SBP drops below **90**
62
Recall, that if you administer nitroglycerin to a patient and they become very hypotensive, you probably have _ involvement
Recall, that if you administer nitroglycerin to a patient and they become very hypotensive, you probably have **right ventricular** involvement * About 1/3 of patients with LV inferior wall infarction will *also have RV involvement*
63
What does a right ventricular infarction look like on ECG?
ST elevation in lead III > II and ST elevation in V4R
64
What are the signs of right heart failure (possibly from RV infarction)
Elevated JVP, hypotension, clear lungs
65
What is the treatment plan for right ventricular infarction?
Lots of VOLUME!
66
Mitral papillary muscle rupture is a post-MI complication that can occur _ days post MI and can lead to _
**Mitral papillary muscle rupture** is a post-MI complication that can occur **3-5** days post MI and can lead to **severe mitral regurgitation** (holosystolic murmur)
67
The most common site of mitral papillary muscle tear is the _ muscle
The most common site of mitral papillary muscle tear is the **posteromedial papillary muscle** * Recall, it only has one single arterial blood supply (the RCA)
68
Ventricular septal rupture is a post MI complication that can occur _ days post MI and causes _
**Ventricular septal rupture** is a post MI complication that can occur **3-7** days post MI and causes **VSD** * A hole forms in the interventricular septum: causes shunting from LV --> RV * This causes a holosystolic murmur * Diagnosis with echo * This can lead to heart failure due to an overload of pulmonary circulation
69
Ventricular free wall rupture is a post MI complication that can occur within _ days of an MI
**Ventricular free wall rupture** is a post MI complication that can occur within **14** days of an MI * Blood fills the pericardial splace --> cardiogenic shock/ tamponade * This can form a pseudoaneurysm if the thrombus forms to plug the rupture
70
Describe the most common acute findings/ complication after an MI
**Pericarditis** involves inflammation extending from the injured myocardium to the pericardium * Patients experience sharp, pleuritic pain, fever, pericardial friction rub on auscultation * We treat with aspirin and avoid anticoagulants
71
As opposed to acute pericarditis which happens early on, _ is a pericarditis that occurs weeks later
As opposed to acute pericarditis which happens early on, **Dressler syndrome** is a complication that occurs weeks later
72
Dressler syndrome, which develops weeks after an MI is _
Dressler syndrome, which develops weeks after an MI is **immune process directed against necrotic myocardium** * We treat with aspirin and NSAIDs
73
* **QRS duration is prolonged** beyond normal (.10 seconds) * The normal Q wave in **lead V5 or V6** that represents septal depolarization is absent * There is **no secondary R’ wave** in VI as occurs in RBBE Several other ECG changes that may occur in LBBB are seen in this ECG although they are not essential to make the diagnosis. The QRS complexes in leads facing the left ventricle (I, aVL and V6) show an M shaped pattern and there are secondary changes in the ST segments which are depressed and accompanied by T wave inversion. The initial R waves that are normally seen in the right sided precordial leads are absent in this record and the complexes in these leads are changes in these leads – the ST segments are elevated and the T waves are tall. As explained elsewhere these changes should not be interpreted to indicate ischaemia in the presence of LBBB
74
Describe what to look for in a left bundle branch block on ECG
1. Prolonged QRS (more than 3 small boxes) 2. rS or QS wave in V1 3. Broad and notched/slurred R wave in lead I and V6
75
76
_ is a sudden increase in the tempo or severity of anginal episodes that occur at less exertion or at rest
**Unstable angina** is a sudden increase in the tempo or severity of anginal episodes that occur at less exertion or at rest * Result of rupture of unstable atherosclerotic plaque with subsequent platlet aggregation and thrombosis * Can progress to NSTEMI
77
_ is a predictable transient chest discomfort during exertion or emotional stress
**Chronic stable angina** is a predictable transient chest discomfort during exertion or emotional stress * Generally caused by fixed obstructive atherosclerotic plaque in at least one coronary artery * Caused by mismatch between oxygen supply and demand * Not associated with cardiomyocyte death
78
Recall that the most important factor in oxygen supply and demand is the _
Recall that the most important factor in oxygen supply and demand is the **radius of coronary arteries**
79
Metabolic factors that contribute to vascular tone:
Metabolic factors that contribute to vascular tone: * **Acidosis** --> vasodilation * **Hypoxia** --> vasodilation * **Citrate** --> vasodilation * **Adenosine** --> vasodilation
80
Endothelial factors that contribute to vascular tone:
Endothelial factors that contribute to vascular tone: * **Nitric oxide** --> vasodilation * **Endothelin-1** --> vasoconstriction
81
The humoral factors that contribute to vascular tone:
The humoral factors that contribute to vascular tone: * **Angiotensin II** --> vasoconstriction * **Prostaglandins** --> vasodilation
82
The neural factors that contribute to vascular tone:
The neural factors that contribute to vascular tone: * **alpha1, alpha2** --> vasoconstriction * **beta2** --> vasodilation * **serotonin** --> vasodilation * **acetylcholine** --> vasodilation
83
The most important factors for determining vascular tone and vascular resistance are _ and _
The most important factors for determining vascular tone and vascular resistance are **metabolic molecules** and **nitric oxide** (from the endothelial cells)
84
Endothelial-dependent vasodilators like NO work via a _ mechanism
Endothelial-dependent vasodilators like NO work via a **paracrine** mechanism
85
_ is the most potent known endogenous vasodilator; it tends to get disrupted by atherosclerosis
**NO** is the most potent known endogenous vasodilator; it tends to get disrupted by atherosclerosis * Atherosclerosis causes endothelial dysfunction --> depletes NO
86
Atherosclerosis decreases oxygen supply through 2 mechanisms:
Atherosclerosis decreases oxygen supply through 2 mechanisms: 1. **Fixed decrease in radius** (coronary stenosis) 2. **Decrease in dynamic vasodilation** (endothelial dysfunction --> decreases NO)
87
The primary intervention for stable angina is _
The primary intervention for stable angina is **beta bocker, nitrate, aspirin, statin**
88
The three major determinants of myocardial oxygen demand are _ , _ , and _
The three major determinants of myocardial oxygen demand are **heart rate** , **wall tension** , and **contractility** * These are all proportional to oxygen demand
89
Define wall stress
Wall stress = pressure * radius / 2 * wall thickness
90
Chronic stable angina is mostly a (supply/ demand) problem
Chronic stable angina is mostly a **demand** problem * Treatment is mostly directed at reducing demand
91
Atherosclerosis causes a (supply/ demand) problem
Atherosclerosis causes a **supply** problem
92
The major circulating mediators of demand are _
The major circulating mediators of demand are **catecholamines** * Physical or emotional stress --> NE, E * B1 stimulation Increase in contractility and heart rate --> increases myocardial oxygen demand
93
William Marrow
V1 and V6 LBBB: William RBBB: Marrow
94
Beta blockers block B1 on ventricular myocytes to _
Beta blockers block B1 on ventricular myocytes to **decrease contractility**
95
Beta blockers block B1 on nodal cells to _
Beta blockers block B1 on nodal cells to **decrease heart rate**
96
Additionally, beta blockers increase the time spent in _
Additionally, beta blockers increase the time spent in **diastole** --> increases myocardial oxygen supply
97
How can we blunt the reflex tachycardia associated with the administration of nitrates?
Nitrates --> arteriodilation --> reflex tachycardia to compensate for drop in BP --> **we can give beta-blockers to blunt this**
98
Nitrates are contraindicated for patients taking _
Nitrates are contraindicated for patients taking **phosphodiesterase inhibitors** like **viagra**
99
Nitrate tolerance develops over _ weeks
Nitrate tolerance develops over **1-3** weeks * Can be prevented by daily withdrawal of nitrates at night

Circulation Part 2 (15 decks)

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