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
Q

As a result of macrophage-mediated structural degeneration, what are some possible dangerous sequelae of an MI 3–14 days after it occurs?

A

Free wall rupture, tamponade, papillary muscle rupture, mitral regurgitation, LV pseudoaneurysm, interventricular septal rupture

26
Q

A man with severe CAD suddenly drops dead. Cardiac biopsy is performed an hour later. Is a normal appearance on light microscopy surprising?

A

No, as there are often no abnormal light microscopy findings for up to 4 hours after an MI has occurred

27
Q

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?

A

Electrocardiography is the gold standard diagnostic test for MI within 6 hours of onset of symptoms

28
Q

Describe the time period of cardiac troponin I elevation after acute myocardial infarction.

A

Troponin I rises 4 hours after a myocardial infarction and is elevated for 7 to 10 days (more specific than other protein markers)

29
Q

Which protein marker is the most specific during the early stages of myocardial infarction?

A

Troponin I

30
Q

In which tissue other than the myocardium is CK-MB found? What is it useful for diagnosing?

A

Skeletal muscle; useful for diagnosing reinfarction on top of acute myocardial infarction, as levels return to normal in 48 hours

31
Q

ST-segment elevations on ECG indicate what type of damage to the myocardium?An ST depression? Pathologic Q waves? Poor R wave progression?

A

Transmural infarct (STEMI); subendocardial infarct (NSTEMI); evolving or old transmural infarct; evolving or old transmural infarct

32
Q

Hyperacute (peaked) T waves, inverted T waves, or a new left bundle branch block on an ECG could all indicate what type of infarct?

A

Transmural infarct (evolving or old)

33
Q

Describe the time period of CK-MB elevation after acute myocardial infarction.

A

CK-MB rises 6–12 hours after a myocardial infarction and returns to normal after 48 hours (unless there is reinfarction)

34
Q

A 50-year-old man with myocardial infarction symptoms has ST depressions on electrocardiogram. How much of his ventricular wall is necrotic?

A

His ECG suggests a subendocardial infarct, where

35
Q

A 50-year-old man has a transmural myocardial infarction. What does his electrocardiogram show? How much of the cardiac wall is affected?

A

ST elevations and Q waves; the entire wall is affected

36
Q

A 43-year-old woman comes to the ED with chest pain. Electrocardiogram shows ST elevations in V5 and V6. What territory is occluded?

A

Left circumflex artery or left anterior descending artery, as the infarct is anterolateral

37
Q

A 43-year-old woman comes to the ED with chest pain. Electrocardiogram shows ST elevations in V3 and V4. What vessel is occluded?

A

Left anterior descending artery in the distal segments, causing an anteroapical infarction

38
Q

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?

A

The left circumflex artery, causing a lateral wall infarction

39
Q

A patient with substernal chest pain is en route to the hospital. You are terrified that the patient may die. Why?

A

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
Q

What complication of myocardial infarction can result in cardiac tamponade?

A

Ventricular free wall rupture

41
Q

What is the cause of the friction rub that can be heard 1–3 days after a myocardial infarction?

A

Postinfarction fibrinous pericarditis

42
Q

What three complications can result from ventricular pseudoaneurysm formation after a myocardial infarction?

A

Mural thrombus embolization, arrhythmia, and decreased cardiac output (CO) (greatest risk is 3–14 days after myocardial infarction)

43
Q

What is Dressler syndrome?

A

An autoimmune syndrome resulting in fibrinous pericarditis several weeks after myocardial infarction

44
Q

An 83-year-old man with recent myocardial infarction has worsening dyspnea. He has bibasilar rales and jugular venous distention. Diagnosis?

A

Pulmonary edema due to left ventricular failure as a complication of recent myocardial infarction

45
Q

An 80-year-old man with sudden-onset chest pain and ST elevation on electrocardiogram has hypotension and tachycardia. Diagnosis?

A

Cardiogenic shock (high risk of mortality due to a large infarct)

46
Q

A ventricular septal defect can result from which post-MI complication? When is the period of greatest risk for this complication?

A

Interventricular septum rupture; like all other ruptures, greatest risk is 3–14 days post-MI

47
Q

Which post-MI complication is associated with fibrosis and causes a dyskinetic, outward bulge during contraction?

A

True ventricular aneurysm, which could arise 2 weeks to several months after MI

48
Q

What are the standard treatments for unstable angina and non-ST-segment–elevation myocardial infarction?

A

Anticoagulation (e.g., heparin), antiplatelet therapy (e.g., aspirin + clopidogrel), β-blockers, statins, ACE inhibitors

49
Q

You suspect that a patient has unstable angina. What medications could you provide for symptom control?

A

Nitroglycerin, morphine

50
Q

A patient was just diagnosed with a transmural myocardial infarction. What is the most important therapy for this patient?

A

Reperfusion therapy is the most important therapy for a STEMI, as percutaneous coronary interventions are preferred over fibrinolysis

51
Q

A woman with a STEMI is rushed to the cardiac catheterization lab. On returning to the floor, do you initiate therapies typical for NSTEMIs?

A

Yes, as such patients, in addition to reperfusion, benefit from these (anticoagulation, antiplatelets, β-blockers, ACE inhibitors, statins)