isxaimiki nosos- ekseliksi efragmatos - diagnosi- typoi - entopisi sto ekγ- epiplokes -therapia Flashcards

1
Q

What are the characteristics of stable angina?

A

Chest pain occurring with exertion and improving with rest, ST depressions often seen on ECG, usually secondary to atherosclerosis

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2
Q

How does the etiology of Prinzmetal (variant) angina differ from other forms of angina?

A

It is 2° to coronary artery spasm at rest w/transient ST elevations on ECG, triggers are tobacco, cocaine, triptans (but often unknown)

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3
Q

How do the symptoms of unstable angina differ from those of stable angina?

A

Chest pain →↑in frequency or intensity, or occurs on minimal/no exertion, a result of incomplete coronary artery occlusion due to thrombosis

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4
Q

A 55-year-old man with angina takes a vasodilator. How may this actually aggravate his ischemia?

A

Blood is shunted within the coronaries to areas of higher perfusion, away from those of critical stenosis/ischemia (coronary steal syndrome)

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5
Q

At what point is ischemic heart disease given the term myocardial infarction rather than unstable angina?

A

When acute thrombosis due to coronary artery atherosclerosis results in myocyte necrosis with cardiac biomarker elevation

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6
Q

What are the five possible manifestations of ischemic heart disease?

A

Angina, coronary steal syndrome, myocardial infarction, sudden cardiac death, and chronic ischemic heart disease

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7
Q

What usually causes sudden cardiac death? How soon after onset of symptoms do people die?

A

Lethal arrhythmias, such as ventricular fibrillation; within 1 hour

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8
Q

What is chronic ischemic heart disease?

A

Progression to congestive heart failure over many years due to chronic ischemic damage from coronary atherosclerosis

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9
Q

What electrocardiogram change are you likely to see with stable angina during an exercise stress test? With Prinzmetal angina?

A

ST depressions; ST elevations

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10
Q

You suspect that your patient has unstable angina. What ECG changes may be seen with unstable angina? Would biomarkers help with diagnosis?

A

Possible ST depression and/or T-wave inversion; cardiac biomarkers are uninformative (but are useful for diagnosis of myocardial infarction

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11
Q

What test would you perform to diagnose whether a myocardial infarction is transmural or subendocardial?

A

ECG (transmural infarcts may show ST elevations, subendocardial infarcts may show ST depressions)

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12
Q

Your patient is a heavy smoker who complains of chest pain at rest. His ECG shows transient ST elevations. What could you treat him with?

A

Treat with calcium channel blockers, nitrates, and smoking cessation (he most likely has Prinzmetal angina)

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13
Q

What do most myocardial infarctions arise from?

A

Acute thrombosis from ruptured coronary artery atherosclerotic plaques

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14
Q

What diseases and conditions are associated with sudden cardiac death?

A

CAD (up to 70% of cases), hypertrophic/dilated cardiomyopathies, hereditary ion channelopathies (e.g., Brugada and long QT syndromes)

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15
Q

A 60-year-old man has crushing chest pain that radiates to his left arm. Which coronary arteries may be occluded (most to least likely)?

A

Left anterior descending, right, circumflex

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16
Q

A 65-year-old man comes to the ED, because he thinks he is having a heart attack. What symptoms may he have?

A

Diaphoresis, nausea, vomiting, severe retrosternal pain, left arm/jaw pain, dyspnea (shortness of breath), fatigue

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17
Q

How long after a myocardial infarction does the infarcted myocardium show extensive coagulative necrosis?

A

1–3 days

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18
Q

How long after an MI does the infarcted myocardium appear normal both grossly and on light microscopy? Can complications occur at this time?

A

In the first 4 hours; yes, as there is still risk for arrhythmias, heart failure, or cardiogenic shock

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19
Q

How long after a myocardial infarction does the infarcted myocardium first show contraction bands? What are contraction bands?

A

4–24 hours after injury; contraction bands are due to free radical damage in reperfusion injury

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20
Q

How long after a myocardial infarction does early coagulative necrosis begin? What changes are seen on light microscopy at this time?

A

After 4 hours; one sees edema, hemorrhages, neutrophils, and wavy fibers begin to appear

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21
Q

A patient has a myocardial infarction and is stabilized. A day later, the cardiologist is still worried about the patient. Why?

A

Patients are still at risk for arrhythmias, heart failure, and cardiogenic shock for up to 1 day after the myocardial infarction occurs

22
Q

During what period of time after a myocardial infarction is there the greatest risk for ventricular pseudoaneurysm formation?

A

From 3–4 days after myocardial infarction

23
Q

Describe the appearance and coloring of the affected myocardium 2 months after a myocardial infarction.

A

The myocardium appears gray-white, demonstrating a completely contracted scar

24
Q

At the cellular level, what happens to the infarcted myocardium on the first day of a myocardial infarction?

A

Intracellular contents of necrotic cells are released into the blood and neutrophil migration starts

25
As a result of macrophage-mediated structural degeneration, what are some possible dangerous sequelae of an MI 3–14 days after it occurs?
Free wall rupture, tamponade, papillary muscle rupture, mitral regurgitation, LV pseudoaneurysm, interventricular septal rupture
26
A man with severe CAD suddenly drops dead. Cardiac biopsy is performed an hour later. Is a normal appearance on light microscopy surprising?
No, as there are often no abnormal light microscopy findings for up to 4 hours after an MI has occurred
27
A 65-year-old man presents to the ED with 1 hour of crushing retrosternal pain radiating to his jaw. What is the diagnostic gold standard?
Electrocardiography is the gold standard diagnostic test for MI within 6 hours of onset of symptoms
28
Describe the time period of cardiac troponin I elevation after acute myocardial infarction.
Troponin I rises 4 hours after a myocardial infarction and is elevated for 7 to 10 days (more specific than other protein markers)
29
Which protein marker is the most specific during the early stages of myocardial infarction?
Troponin I
30
In which tissue other than the myocardium is CK-MB found? What is it useful for diagnosing?
Skeletal muscle; useful for diagnosing reinfarction on top of acute myocardial infarction, as levels return to normal in 48 hours
31
ST-segment elevations on ECG indicate what type of damage to the myocardium?An ST depression? Pathologic Q waves? Poor R wave progression?
Transmural infarct (STEMI); subendocardial infarct (NSTEMI); evolving or old transmural infarct; evolving or old transmural infarct
32
Hyperacute (peaked) T waves, inverted T waves, or a new left bundle branch block on an ECG could all indicate what type of infarct?
Transmural infarct (evolving or old)
33
Describe the time period of CK-MB elevation after acute myocardial infarction.
CK-MB rises 6–12 hours after a myocardial infarction and returns to normal after 48 hours (unless there is reinfarction)
34
A 50-year-old man with myocardial infarction symptoms has ST depressions on electrocardiogram. How much of his ventricular wall is necrotic?
His ECG suggests a subendocardial infarct, where
35
A 50-year-old man has a transmural myocardial infarction. What does his electrocardiogram show? How much of the cardiac wall is affected?
ST elevations and Q waves; the entire wall is affected
36
A 43-year-old woman comes to the ED with chest pain. Electrocardiogram shows ST elevations in V5 and V6. What territory is occluded?
Left circumflex artery or left anterior descending artery, as the infarct is anterolateral
37
A 43-year-old woman comes to the ED with chest pain. Electrocardiogram shows ST elevations in V3 and V4. What vessel is occluded?
Left anterior descending artery in the distal segments, causing an anteroapical infarction
38
A 43-year-old woman comes to the ED with chest pain. Electrocardiogram shows ST elevations in leads I and aVL. Where is the infarct?
The left circumflex artery, causing a lateral wall infarction
39
A patient with substernal chest pain is en route to the hospital. You are terrified that the patient may die. Why?
Cardiac arrhythmia is a major cause of death in MI patients before they reach the hospital—also common in the first few days after an MI
40
What complication of myocardial infarction can result in cardiac tamponade?
Ventricular free wall rupture
41
What is the cause of the friction rub that can be heard 1–3 days after a myocardial infarction?
Postinfarction fibrinous pericarditis
42
What three complications can result from ventricular pseudoaneurysm formation after a myocardial infarction?
Mural thrombus embolization, arrhythmia, and decreased cardiac output (CO) (greatest risk is 3–14 days after myocardial infarction)
43
What is Dressler syndrome?
An autoimmune syndrome resulting in fibrinous pericarditis several weeks after myocardial infarction
44
An 83-year-old man with recent myocardial infarction has worsening dyspnea. He has bibasilar rales and jugular venous distention. Diagnosis?
Pulmonary edema due to left ventricular failure as a complication of recent myocardial infarction
45
An 80-year-old man with sudden-onset chest pain and ST elevation on electrocardiogram has hypotension and tachycardia. Diagnosis?
Cardiogenic shock (high risk of mortality due to a large infarct)
46
A ventricular septal defect can result from which post-MI complication? When is the period of greatest risk for this complication?
Interventricular septum rupture; like all other ruptures, greatest risk is 3–14 days post-MI
47
Which post-MI complication is associated with fibrosis and causes a dyskinetic, outward bulge during contraction?
True ventricular aneurysm, which could arise 2 weeks to several months after MI
48
What are the standard treatments for unstable angina and non-ST-segment–elevation myocardial infarction?
Anticoagulation (e.g., heparin), antiplatelet therapy (e.g., aspirin + clopidogrel), β-blockers, statins, ACE inhibitors
49
You suspect that a patient has unstable angina. What medications could you provide for symptom control?
Nitroglycerin, morphine
50
A patient was just diagnosed with a transmural myocardial infarction. What is the most important therapy for this patient?
Reperfusion therapy is the most important therapy for a STEMI, as percutaneous coronary interventions are preferred over fibrinolysis
51
A woman with a STEMI is rushed to the cardiac catheterization lab. On returning to the floor, do you initiate therapies typical for NSTEMIs?
Yes, as such patients, in addition to reperfusion, benefit from these (anticoagulation, antiplatelets, β-blockers, ACE inhibitors, statins)