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396 Cards in this Set
- Front
- Back
|
Ischemic Heart Disease results from:
|
Imbalance between myocardial O2 demand and supply from the coronary arteries
|
|
|
Coronary artery blood flow provides oxygen to:
|
Cardiac muscle
|
|
|
Coronary vessels fill in:
|
Diastole
|
|
|
Tachycardia (>180 bpm) _____ ____ ____, leading to ischemia
|
Decreases filling time
|
|
|
Left anterior descending (LAD) coronary artery distribution:
|
(1) Anterior portion of the left ventricle
|
|
|
Site for 40% to 50% of coronary artery thromboses:
|
Left anterior descending (LAD) coronary artery
|
|
|
Most common site of coronary artery thrombosis:
|
Left anterior descending (LAD) coronary artery
|
|
|
Right coronary artery (RCA) distribution:
|
(1) Posteroinferior part of the left ventricle
|
|
|
Left circumflex coronary artery distribution:
|
Lateral wall of the left ventricle
|
|
|
Site for 15% to 20% of coronary artery thromboses:
|
Left circumflex coronary artery
|
|
|
Major cause of death in the United States:
|
Ischemic heart disease
|
|
|
Ischemic heart disease is more common in:
|
Men
|
|
|
Ischemic heart disease incidence peaks in man after ___ years of age and woman after ___ years of age:
|
60;70
|
|
|
Types of ischemic heart disease:
|
(a)Angina pectoris (most common type)
|
|
|
Ischemic heart disease risk factors:
|
(1)Age
|
|
|
Angina pectoris is more common in:
|
Middle-aged males and elderly males
|
|
|
Angina pectoris in females usually occurs after:
|
Menopause
|
|
|
Within 1 year of a diagnosis of stable angina, 10% to 20% will develop:
|
An acute myocardial infarction or unstable angina.
|
|
|
Most common variant of angina pectoris:
|
Chronic (stable) angina
|
|
|
Causes of stable angina:
|
(1) Fixed, atherosclerotic coronary artery disease (most common)
|
|
|
Chronic (stable) angina pathogenesis:
|
Subendocardial ischemia due to decreased coronary artery blood flow or thick muscle wall
|
|
|
In Chronic (stable) angina due to fixed, atherosclerotic coronary artery disease its likely that:
|
(a) One or more vessel obstructions.
|
|
|
In Chronic (stable) angina due to aortic stenosis or hypertension with concentric LVH O2 supply:
|
Is not adequate for the thickened muscle wall
|
|
|
Chronic (stable) angina clinical findings:
|
(1) Exercise-induced substernal chest pain lasting 30 seconds to 30 minutes
|
|
|
Prinzmetal's angina pathogenesis:
|
(1) Intermittent coronary artery vasospasm at rest with or without superimposed coronary artery atherosclerotic disease
|
|
|
Prinzmetal's angina:
|
Stress test shows ST-segment elevation (transmural ischemia).
|
|
|
Unstable angina pathogenesis:
|
(1) Severe, fixed, multivessel atherosclerotic disease
|
|
|
Unstable angina clinical findings:
|
(1) Frequent bouts of chest pain at rest or with minimal exertion
|
|
|
Chronic ischemic heart disease is a:
|
Progressive CHF resulting from long-term ischemic damage to myocardial tissue
|
|
|
In Chronic ischemic heart disease there is a replacement of:
|
Myocardial tissue with noncontractile scar tissue
|
|
|
Chronic ischemic heart disease:
|
Biventricular CHF
|
|
|
Sudden cardiac death (SCD) is:
|
Unexpected death within 1 hour after the onset of symptoms
|
|
|
Sudden cardiac death (SCD) risk factors:
|
Obesity
|
|
|
Sudden cardiac death (SCD) occurs more frequently in the morning hours when:
|
Hypercoagulability is at its peak
|
|
|
Sudden cardiac death (SCD) pathogenesis:
|
Severe atherosclerotic coronary artery disease
|
|
|
In >80% of cases Sudden cardiac death (SCD) there is absence of:
|
Occlusive vessel
|
|
|
In Sudden cardiac death (SCD) the cause of death is:
|
Ventricular fibrillation
|
|
|
Sudden cardiac death (SCD) is a diagnosis of exclusion after the following causes are ruled out:
|
Mitral valve prolapse (MVP)
|
|
|
Mitral valve prolapse (MVP) sudden death occurs by:
|
Arrhythmias from mitral regurgitation or CHF
|
|
|
Most common cause of death in adults in the United States:
|
Acute myocardial infarction (AMI)
|
|
|
Acute myocardial infarction (AMI) is proeminent in:
|
Males between 40 and 65 years old
|
|
|
Acute myocardial infarction (AMI) has no proeminent sex after the age of:
|
65 years old.
|
|
|
At least __% of AMIs are clinically unrecognized
|
25%
|
|
|
Acute myocardial infarction (AMI) pathogenesis sequence:
|
Rupture of disrupted plaque → platelet thrombus → AMI
|
|
|
Role of thromboxane A2 in acute myocardial infarction (AMI) pathogenesis:
|
(1) Contributes to formation of the platelet thrombus
|
|
|
Less common causes of AMI:
|
(a) Vasculitis
|
|
|
AMI with normal coronary arteries cause:
|
Cocaine use
|
|
|
AMI can be cause by embolization of plaque material from:
|
Atheromatous plaques in the aorta or coronary artery
|
|
|
AMI caused by vasculitis examples:
|
Polyarteritis nodosa, Kawasaki disease
|
|
|
AMI caused by thrombosis syndrome examples:
|
Antithrombin III deficiency, polycythemia
|
|
|
AMI caused by Dissection into the wall of coronary arteries examples:
|
Revascularization procedure, aortic dissection
|
|
|
Types of myocardial infarction:
|
Transmural infarction (Q wave infarction)
|
|
|
Transmural infarction (Q wave infarction) are:
|
New Q waves develop in an electrocardiogram (ECG
|
|
|
Transmural infarction (Q wave infarction) involves:
|
Full thickness of the myocardium
|
|
|
In Subendocardial infarction (non-Q wave infarction) Q waves are:
|
Absent
|
|
|
Subendocardial infarction (non-Q wave infarction) involves:
|
The inner third of the myocardium
|
|
|
Reperfusion injury follows:
|
Thrombolytic (fibrinolytic) therapy
|
|
|
Early reperfusion salvages some injured but viable myocytes but:
|
Destroys myocytes that are irreversibly damaged.
|
|
|
Removal of irreversibly damaged myocytes improves:
|
short- and long-term function and survival.
|
|
|
Early reperfusion:
|
Prevents any further damage to myocardial cells
|
|
|
Early reperfusion:
|
Limits the size of the infarction
|
|
|
Reperfusion histologically alters:
|
Irreversibly damaged cells.
|
|
|
Reperfusion histologically produces contraction band necrosis by:
|
Hypercontraction of myofibrils in dying cells due to the influx of Ca2+ into the cytosol
|
|
|
Gross and microscopic findings of AMI during 0 to 24 hours:
|
(1) No gross changes are evident until 24 hours.
|
|
|
Gross and microscopic findings of AMI during 1 to 3 days:
|
(1) Pallor of the infarcted tissue
|
|
|
Gross and microscopic findings of AMI during 3 to 7 days:
|
(1) Red granulation tissue surrounds the area of infarction.
|
|
|
Gross and microscopic findings of AMI during 7 to 10 days:
|
(1) The necrotic area is bright yellow
|
|
|
Gross and microscopic findings of AMI during 2 months:
|
Infarcted tissue replaced by white, patchy, noncontractile scar tissue
|
|
|
Acute myocardial infarction (AMI) clinical findings:
|
(a) Sudden onset of severe, crushing retrosternal pain
|
|
|
Caracterize the sudden onset of severe, crushing retrosternal pain in Acute myocardial infarction (AMI):
|
(1) Lasts >30 minutes
|
|
|
"Silent" AMIs may occur in the elderly and in individuals with diabetes mellitus due to:
|
High pain threshold or problems with nervous system
|
|
|
Q wave AMI has ______ early mortality rate compared to non-Q wave AMI:
|
Increased
|
|
|
Non-Q wave AMI has increased risk for:
|
(1) Increased risk of reinfarction
|
|
|
Acute myocardial infarction (AMI) complications:
|
(a) Cardiogenic shock occurs in ∼7% of cases.
|
|
|
In cardiogenic shock due to Acute myocardial infarction (AMI) _______ improves survival:
|
Revascularization
|
|
|
Acute myocardial infarction (AMI) arrhythmias:
|
(1) Ventricular premature contractions (most common)
|
|
|
Heart block occurs in 5% of ____ AMIs and 3% of _____ AMIs
|
Inferior; anterior
|
|
|
Congestive heart failure due to Acute myocardial infarction (AMI) usually occurs within:
|
The first 24h
|
|
|
Acute myocardial infarction (AMI) ruptures:
|
(1) Most commonly occurs between days 3 and 7
|
|
|
Anterior wall rupture due to Acute myocardial infarction (AMI) cause:
|
Cardiac tamponade
|
|
|
Anterior wall rupture due to Acute myocardial infarction (AMI) is associated with:
|
Thrombosis of the LAD coronary artery
|
|
|
Posteromedial papillary muscle rupture or dysfunction due to Acute myocardial infarction (AMI) is associated with:
|
(a) RCA thrombosis(most often with inferiror AMI)
|
|
|
Interventricular septum rupture due to Acute myocardial infarction (AMI) is most associated with:
|
LAD coronary artery thrombosis
|
|
|
Interventricular septum rupture due to Acute myocardial infarction (AMI) produces:
|
A left-to-right shunt causing RHF (Increased O2 saturation and pressure in right ventricle)
|
|
|
Mural thrombus due to Acute myocardial infarction (AMI) occurs in:
|
10% of AMI
|
|
|
Mural thrombus due to Acute myocardial infarction (AMI) is most often associated with:
|
LAD coronary artery thrombosis
|
|
|
In mural thrombus due to Acute myocardial infarction (AMI) there is the danger of:
|
Embolization
|
|
|
Fibrinous pericarditis (with or without effusion) due to Acute myocardial infarction (AMI) occurs when?
|
Days 1 to 7 of a Q wave AMI
|
|
|
Fibrinous pericarditis (with or without effusion) due to Acute myocardial infarction (AMI) can cause whan kind of pain? What other symptom?
|
Substernal chest pain is relieved by leaning forward and aggravated by leaning backward. Can also cause a A precordial friction rub.
|
|
|
In fibrinous pericarditis (with or without effusion) due to Acute myocardial infarction (AMI) the precordial friction rub is caused by:
|
Increased vessel permeability in the pericardium; exudate of acute inflammation
|
|
|
Fibrinous pericarditis (with or without effusion) due to Acute myocardial infarction (AMI) can be due a Q wave AMI or:
|
Autoimmune pericarditis 6 to 8 weeks after an acute MI
|
|
|
In Autoimmune pericarditis due to Acute myocardial infarction (AMI) there are antibodies directed against:
|
Damaged pericardial antigens
|
|
|
Autoimmune pericarditis due to Acute myocardial infarction (AMI) clinical findings include:
|
Fever and a precordial friction rub
|
|
|
Ventricular aneurysm due to Acute myocardial infarction (AMI) is clinically recognized within __ to __ weeks but start developing in the first ___ hours:
|
4;8;48
|
|
|
Ventricular aneurysm due to Acute myocardial infarction (AMI) ______ _____ occurs during systole because blood enters the aneurism causing ______ _____ _____ movement:
|
Precordial bulge; anterior chest wall
|
|
|
Ventricular aneurysm due to Acute myocardial infarction (AMI) complications:
|
(a) CHF occurs due to the lack of contractile tissue.
|
|
|
Ventricular aneurysm due to Acute myocardial infarction (AMI) rupture is uncommon because:
|
Scar tissue has good tensile strength
|
|
|
Right ventricular AMI due to Acute myocardial infarction (AMI) is associated with ___ thrombosis:
|
RCA
|
|
|
Right ventricular AMI due to Acute myocardial infarction (AMI) occurs in one third of _____ AMIs and clinically significant in __% of cases.
|
Inferior; 30%
|
|
|
Right ventricular AMI due to Acute myocardial infarction (AMI) clinical findings:
|
Hypotension, RHF, and preserved left ventricle function
|
|
|
Laboratory diagnosis of AMI include:
|
(a) Serial testing for creatine kinase isoenzyme MB (CK-MB)
|
|
|
CK-MB appears within __ to __ ___; peaks at __ ____; disappears within ___ to ___ ____ and has Sensitivity and specificity of ___%.
|
4 to 8 hours; 24hours; 1.5 to 3 days; 95%
|
|
|
Reinfarction occurs in ___% of AMIs and reapperance of CK-MB after __ days:
|
10%; 3 days
|
|
|
Cardiac troponins I (cTnI) and T (cTnT) normally regulate:
|
Calcium-mediated contraction
|
|
|
cTnI and cTnT appear within __ to __ ___; peaks at __ ____; disappears within ___ to ___ ____; has Sensitivity of __% to __% and specificity of ___% to __%
|
3 to 12 hours; 24hours; 7 to 10 days; 84% to 96%; 80% to 95%
|
|
|
Serial testing for cardiac troponins I (cTnI) and T (cTnT) false positive results are usually related to:
|
Ischemia (e.g., unstable angina).
|
|
|
cTnI, cTnT is gold standard for diagnosis of:
|
AMI
|
|
|
CK-MB is used in conjunction with troponins to diagnose an AMI because:
|
(a) Detects reinfarction (troponins cannot)
|
|
|
Normally, ___ is higher than ___ but in AMI, ____ in cardiac muscle is released, causing the "flip."
|
LDH2; LDH1; LDH1
|
|
|
Lactate dehydrogenase (LDH)1-2 "flip" appears within __ ___; peaks at __ to ___ ___; disappears within __ ___.
|
10 hours; 2 to 3 days; 7days
|
|
|
Lactate dehydrogenase (LDH)1-2 "flip" test has been replaced by:
|
Troponins I and T
|
|
|
In Acute myocardial infarction (AMI) inverted T waves in ECG correlate with:
|
Areas of ischemia at the periphery of the infarct
|
|
|
In Acute myocardial infarction (AMI) elevated ST segment correlate with:
|
Injured myocardial cells surrounding the area of necrosis
|
|
|
In Acute myocardial infarction (AMI) new Q waves correlate with:
|
Area of coagulation necrosis
|
|
|
Q waves in leads V1-V4 is a classic ECG patterns in AMI for:
|
LAD coronary artery anterior wall infarction
|
|
|
Q waves in leads V1-V2 is a classic ECG patterns in AMI for:
|
Anteroseptal infarction due to proximal LAD occlusion
|
|
|
Q waves in leads V4-V6, I, aVL is a classic ECG patterns in AMI for:
|
Anterolateral infarction due to mid-LAD or circumflex coronary arteries
|
|
|
Q waves in leads I, aVL is a classic ECG patterns in AMI for:
|
Lateral wall infarction due to left circumflex artery
|
|
|
Q waves in leads II, III, aVF is a classic ECG patterns in AMI for:
|
RCA inferior wall infarction
|
|
|
Q wave in lead V6 is a classic ECG patterns in AMI for:
|
Posterior wall infarction due to posterior descending artery occlusion
|
|
|
R wave > S wave in lead V1 is a classic ECG patterns in AMI for:
|
Posterior wall infarction due to posterior descending artery occlusion
|
|
|
Ischemic Heart Disease results from:
|
Imbalance between myocardial O2 demand and supply from the coronary arteries
|
|
|
Coronary artery blood flow provides oxygen to:
|
Cardiac muscle
|
|
|
Coronary vessels fill in:
|
Diastole
|
|
|
Tachycardia
>180 bpm) _____ ____ ____, leading to ischemia |
Decreases filling time
|
|
|
Left anterior descending
LAD) coronary artery distribution: |
1) Anterior portion of the left ventricle |
|
|
Site for 40% to 50% of coronary artery thromboses:
|
Left anterior descending
LAD) coronary artery |
|
|
Most common site of coronary artery thrombosis:
|
Left anterior descending
LAD) coronary artery |
|
|
Right coronary artery
RCA) distribution: |
1) Posteroinferior part of the left ventricle |
|
|
Left circumflex coronary artery distribution:
|
Lateral wall of the left ventricle
|
|
|
Site for 15% to 20% of coronary artery thromboses:
|
Left circumflex coronary artery
|
|
|
Major cause of death in the United States:
|
Ischemic heart disease
|
|
|
Ischemic heart disease is more common in:
|
Men
|
|
|
Ischemic heart disease incidence peaks in man after ___ years of age and woman after ___ years of age:
|
60;70
|
|
|
Types of ischemic heart disease:
|
a)Angina pectoris most common type) |
|
|
Ischemic heart disease risk factors:
|
1)Age |
|
|
Angina pectoris is more common in:
|
Middle-aged males and elderly males
|
|
|
Angina pectoris in females usually occurs after:
|
Menopause
|
|
|
Within 1 year of a diagnosis of stable angina, 10% to 20% will develop:
|
An acute myocardial infarction or unstable angina.
|
|
|
Most common variant of angina pectoris:
|
Chronic
stable) angina |
|
|
Causes of stable angina:
|
1) Fixed, atherosclerotic coronary artery disease most common) |
|
|
Chronic
stable) angina pathogenesis: |
Subendocardial ischemia due to decreased coronary artery blood flow or thick muscle wall
|
|
|
In Chronic
stable) angina due to fixed, atherosclerotic coronary artery disease its likely that: |
a) One or more vessel obstructions. |
|
|
In Chronic
stable) angina due to aortic stenosis or hypertension with concentric LVH O2 supply: |
Is not adequate for the thickened muscle wall
|
|
|
Chronic
stable) angina clinical findings: |
1) Exercise-induced substernal chest pain lasting 30 seconds to 30 minutes |
|
|
Prinzmetal's angina pathogenesis:
|
1) Intermittent coronary artery vasospasm at rest with or without superimposed coronary artery atherosclerotic disease |
|
|
Prinzmetal's angina:
|
Stress test shows ST-segment elevation
transmural ischemia). |
|
|
Unstable angina pathogenesis:
|
1) Severe, fixed, multivessel atherosclerotic disease |
|
|
Unstable angina clinical findings:
|
1) Frequent bouts of chest pain at rest or with minimal exertion |
|
|
Chronic ischemic heart disease is a:
|
Progressive CHF resulting from long-term ischemic damage to myocardial tissue
|
|
|
In Chronic ischemic heart disease there is a replacement of:
|
Myocardial tissue with noncontractile scar tissue
|
|
|
Chronic ischemic heart disease:
|
Biventricular CHF
|
|
|
Sudden cardiac death
SCD) is: |
Unexpected death within 1 hour after the onset of symptoms
|
|
|
Sudden cardiac death
SCD) risk factors: |
Obesity
|
|
|
Sudden cardiac death
SCD) occurs more frequently in the morning hours when: |
Hypercoagulability is at its peak
|
|
|
Sudden cardiac death
SCD) pathogenesis: |
Severe atherosclerotic coronary artery disease
|
|
|
In >80% of cases Sudden cardiac death
SCD) there is absence of: |
Occlusive vessel
|
|
|
In Sudden cardiac death
SCD) the cause of death is: |
Ventricular fibrillation
|
|
|
Sudden cardiac death
SCD) is a diagnosis of exclusion after the following causes are ruled out: |
Mitral valve prolapse
MVP) |
|
|
Mitral valve prolapse
MVP) sudden death occurs by: |
Arrhythmias from mitral regurgitation or CHF
|
|
|
Most common cause of death in adults in the United States:
|
Acute myocardial infarction
AMI) |
|
|
Acute myocardial infarction
AMI) is proeminent in: |
Males between 40 and 65 years old
|
|
|
Acute myocardial infarction
AMI) has no proeminent sex after the age of: |
65 years old.
|
|
|
At least __% of AMIs are clinically unrecognized
|
25%
|
|
|
Acute myocardial infarction
AMI) pathogenesis sequence: |
Rupture of disrupted plaque → platelet thrombus → AMI
|
|
|
Role of thromboxane A2 in acute myocardial infarction
AMI) pathogenesis: |
1) Contributes to formation of the platelet thrombus |
|
|
Less common causes of AMI:
|
a) Vasculitis |
|
|
AMI with normal coronary arteries cause:
|
Cocaine use
|
|
|
AMI can be cause by embolization of plaque material from:
|
Atheromatous plaques in the aorta or coronary artery
|
|
|
AMI caused by vasculitis examples:
|
Polyarteritis nodosa, Kawasaki disease
|
|
|
AMI caused by thrombosis syndrome examples:
|
Antithrombin III deficiency, polycythemia
|
|
|
AMI caused by Dissection into the wall of coronary arteries examples:
|
Revascularization procedure, aortic dissection
|
|
|
Types of myocardial infarction:
|
Transmural infarction
Q wave infarction) |
|
|
Transmural infarction
Q wave infarction) are: |
New Q waves develop in an electrocardiogram
ECG |
|
|
Transmural infarction
Q wave infarction) involves: |
Full thickness of the myocardium
|
|
|
In Subendocardial infarction
non-Q wave infarction) Q waves are: |
Absent
|
|
|
Subendocardial infarction
non-Q wave infarction) involves: |
The inner third of the myocardium
|
|
|
Reperfusion injury follows:
|
Thrombolytic
fibrinolytic) therapy |
|
|
Early reperfusion salvages some injured but viable myocytes but:
|
Destroys myocytes that are irreversibly damaged.
|
|
|
Removal of irreversibly damaged myocytes improves:
|
short- and long-term function and survival.
|
|
|
Early reperfusion:
|
Prevents any further damage to myocardial cells
|
|
|
Early reperfusion:
|
Limits the size of the infarction
|
|
|
Reperfusion histologically alters:
|
Irreversibly damaged cells.
|
|
|
Reperfusion histologically produces contraction band necrosis by:
|
Hypercontraction of myofibrils in dying cells due to the influx of Ca2+ into the cytosol
|
|
|
Gross and microscopic findings of AMI during 0 to 24 hours:
|
1) No gross changes are evident until 24 hours. |
|
|
Gross and microscopic findings of AMI during 1 to 3 days:
|
1) Pallor of the infarcted tissue |
|
|
Gross and microscopic findings of AMI during 3 to 7 days:
|
1) Red granulation tissue surrounds the area of infarction. |
|
|
Gross and microscopic findings of AMI during 7 to 10 days:
|
1) The necrotic area is bright yellow |
|
|
Gross and microscopic findings of AMI during 2 months:
|
Infarcted tissue replaced by white, patchy, noncontractile scar tissue
|
|
|
Acute myocardial infarction
AMI) clinical findings: |
a) Sudden onset of severe, crushing retrosternal pain |
|
|
Caracterize the sudden onset of severe, crushing retrosternal pain in Acute myocardial infarction
AMI): |
1) Lasts >30 minutes |
|
|
"Silent" AMIs may occur in the elderly and in individuals with diabetes mellitus due to:
|
High pain threshold or problems with nervous system
|
|
|
Q wave AMI has ______ early mortality rate compared to non-Q wave AMI:
|
Increased
|
|
|
Non-Q wave AMI has increased risk for:
|
1) Increased risk of reinfarction |
|
|
Acute myocardial infarction
AMI) complications: |
a) Cardiogenic shock occurs in ∼7% of cases. |
|
|
In cardiogenic shock due to Acute myocardial infarction
AMI) _______ improves survival: |
Revascularization
|
|
|
Acute myocardial infarction
AMI) arrhythmias: |
1) Ventricular premature contractions most common) |
|
|
Heart block occurs in 5% of ____ AMIs and 3% of _____ AMIs
|
Inferior; anterior
|
|
|
Congestive heart failure due to Acute myocardial infarction
AMI) usually occurs within: |
The first 24h
|
|
|
Acute myocardial infarction
AMI) ruptures: |
1) Most commonly occurs between days 3 and 7 |
|
|
Anterior wall rupture due to Acute myocardial infarction
AMI) cause: |
Cardiac tamponade
|
|
|
Anterior wall rupture due to Acute myocardial infarction
AMI) is associated with: |
Thrombosis of the LAD coronary artery
|
|
|
Posteromedial papillary muscle rupture or dysfunction due to Acute myocardial infarction
AMI) is associated with: |
a) RCA thrombosis most often with inferiror AMI) |
|
|
Interventricular septum rupture due to Acute myocardial infarction
AMI) is most associated with: |
LAD coronary artery thrombosis
|
|
|
Interventricular septum rupture due to Acute myocardial infarction
AMI) produces: |
A left-to-right shunt causing RHF
Increased O2 saturation and pressure in right ventricle) |
|
|
Mural thrombus due to Acute myocardial infarction
AMI) occurs in: |
10% of AMI
|
|
|
Mural thrombus due to Acute myocardial infarction
AMI) is most often associated with: |
LAD coronary artery thrombosis
|
|
|
In mural thrombus due to Acute myocardial infarction
AMI) there is the danger of: |
Embolization
|
|
|
Fibrinous pericarditis
with or without effusion) due to Acute myocardial infarction AMI) occurs when? |
Days 1 to 7 of a Q wave AMI
|
|
|
Fibrinous pericarditis
with or without effusion) due to Acute myocardial infarction AMI) can cause whan kind of pain? What other symptom? |
Substernal chest pain is relieved by leaning forward and aggravated by leaning backward. Can also cause a A precordial friction rub.
|
|
|
In fibrinous pericarditis
with or without effusion) due to Acute myocardial infarction AMI) the precordial friction rub is caused by: |
Increased vessel permeability in the pericardium; exudate of acute inflammation
|
|
|
Fibrinous pericarditis
with or without effusion) due to Acute myocardial infarction AMI) can be due a Q wave AMI or: |
Autoimmune pericarditis 6 to 8 weeks after an acute MI
|
|
|
In Autoimmune pericarditis due to Acute myocardial infarction
AMI) there are antibodies directed against: |
Damaged pericardial antigens
|
|
|
Autoimmune pericarditis due to Acute myocardial infarction
AMI) clinical findings include: |
Fever and a precordial friction rub
|
|
|
Ventricular aneurysm due to Acute myocardial infarction
AMI) is clinically recognized within __ to __ weeks but start developing in the first ___ hours: |
4;8;48
|
|
|
Ventricular aneurysm due to Acute myocardial infarction
AMI) ______ _____ occurs during systole because blood enters the aneurism causing ______ _____ _____ movement: |
Precordial bulge; anterior chest wall
|
|
|
Ventricular aneurysm due to Acute myocardial infarction
AMI) complications: |
a) CHF occurs due to the lack of contractile tissue. |
|
|
Ventricular aneurysm due to Acute myocardial infarction
AMI) rupture is uncommon because: |
Scar tissue has good tensile strength
|
|
|
Right ventricular AMI due to Acute myocardial infarction
AMI) is associated with ___ thrombosis: |
RCA
|
|
|
Right ventricular AMI due to Acute myocardial infarction
AMI) occurs in one third of _____ AMIs and clinically significant in __% of cases. |
Inferior; 30%
|
|
|
Right ventricular AMI due to Acute myocardial infarction
AMI) clinical findings: |
Hypotension, RHF, and preserved left ventricle function
|
|
|
Laboratory diagnosis of AMI include:
|
a) Serial testing for creatine kinase isoenzyme MB CK-MB) |
|
|
CK-MB appears within __ to __ ___; peaks at __ ____; disappears within ___ to ___ ____ and has Sensitivity and specificity of ___%.
|
4 to 8 hours; 24hours; 1.5 to 3 days; 95%
|
|
|
Reinfarction occurs in ___% of AMIs and reapperance of CK-MB after __ days:
|
10%; 3 days
|
|
|
Cardiac troponins I
cTnI) and T cTnT) normally regulate: |
Calcium-mediated contraction
|
|
|
cTnI and cTnT appear within __ to __ ___; peaks at __ ____; disappears within ___ to ___ ____; has Sensitivity of __% to __% and specificity of ___% to __%
|
3 to 12 hours; 24hours; 7 to 10 days; 84% to 96%; 80% to 95%
|
|
|
Serial testing for cardiac troponins I
cTnI) and T cTnT) false positive results are usually related to: |
Ischemia
e.g., unstable angina). |
|
|
cTnI, cTnT is gold standard for diagnosis of:
|
AMI
|
|
|
CK-MB is used in conjunction with troponins to diagnose an AMI because:
|
a) Detects reinfarction troponins cannot) |
|
|
Normally, ___ is higher than ___ but in AMI, ____ in cardiac muscle is released, causing the "flip."
|
LDH2; LDH1; LDH1
|
|
|
Lactate dehydrogenase
LDH)1-2 "flip" appears within __ ___; peaks at __ to ___ ___; disappears within __ ___. |
10 hours; 2 to 3 days; 7days
|
|
|
Lactate dehydrogenase
LDH)1-2 "flip" test has been replaced by: |
Troponins I and T
|
|
|
In Acute myocardial infarction
AMI) inverted T waves in ECG correlate with: |
Areas of ischemia at the periphery of the infarct
|
|
|
In Acute myocardial infarction
AMI) elevated ST segment correlate with: |
Injured myocardial cells surrounding the area of necrosis
|
|
|
In Acute myocardial infarction
AMI) new Q waves correlate with: |
Area of coagulation necrosis
|
|
|
Q waves in leads V1-V4 is a classic ECG patterns in AMI for:
|
LAD coronary artery anterior wall infarction
|
|
|
Q waves in leads V1-V2 is a classic ECG patterns in AMI for:
|
Anteroseptal infarction due to proximal LAD occlusion
|
|
|
Q waves in leads V4-V6, I, aVL is a classic ECG patterns in AMI for:
|
Anterolateral infarction due to mid-LAD or circumflex coronary arteries
|
|
|
Q waves in leads I, aVL is a classic ECG patterns in AMI for:
|
Lateral wall infarction due to left circumflex artery
|
|
|
Q waves in leads II, III, aVF is a classic ECG patterns in AMI for:
|
RCA inferior wall infarction
|
|
|
Q wave in lead V6 is a classic ECG patterns in AMI for:
|
Posterior wall infarction due to posterior descending artery occlusion
|
|
|
R wave > S wave in lead V1 is a classic ECG patterns in AMI for:
|
Posterior wall infarction due to posterior descending artery occlusion
|
|
|
Ischemic Heart Disease results from:
|
Imbalance between myocardial O2 demand and supply from the coronary arteries
Coronary artery blood flow provides oxygen to: |
|
|
(2) Anterior two thirds of the interventricular septum
Site for 40% to 50% of coronary artery thromboses: |
Left anterior descending (LAD) coronary artery
Most common site of coronary artery thrombosis: |
|
|
(5) Primary supply for atrioventricular and sinoatrial nodes
Left circumflex coronary artery distribution: |
Lateral wall of the left ventricle
Site for 15% to 20% of coronary artery thromboses: |
|
|
(d) Myocardial infarction
Ischemic heart disease risk factors: |
(1)Age
|
|
|
(6) Subtract 1 from the total number of risk factors if HDL > 60 mg/dL.
Angina pectoris is more common in: |
Middle-aged males and elderly males
Angina pectoris in females usually occurs after: |
|
|
(4) Cocaine-induced coronary artery vasoconstriction
Chronic (stable) angina pathogenesis: |
Subendocardial ischemia due to decreased coronary artery blood flow or thick muscle wall
In Chronic (stable) angina due to fixed, atherosclerotic coronary artery disease its likely that: |
|
|
(b) Severity of stenosis is >70%.
In Chronic (stable) angina due to aortic stenosis or hypertension with concentric LVH O2 supply: |
Is not adequate for the thickened muscle wall
Chronic (stable) angina clinical findings: |
|
|
(4) Stress test shows ST-segment depression > 1 mm
Prinzmetal's angina pathogenesis: |
(1) Intermittent coronary artery vasospasm at rest with or without superimposed coronary artery atherosclerotic disease
|
|
|
(2) Vasoconstriction is due to platelet thromboxane A2 or an increase in endothelin.
Prinzmetal's angina: |
Stress test shows ST-segment elevation (transmural ischemia).
Unstable angina pathogenesis: |
|
|
(2) Disrupted plaques with or without platelet nonocclusive thrombi
Unstable angina clinical findings: |
(1) Frequent bouts of chest pain at rest or with minimal exertion
|
|
|
(2) May progress to acute myocardial infarction (MI)
Chronic ischemic heart disease is a: |
Progressive CHF resulting from long-term ischemic damage to myocardial tissue
In Chronic ischemic heart disease there is a replacement of: |
|
|
May develop dilated cardiomyopathy
Sudden cardiac death (SCD) is: |
Unexpected death within 1 hour after the onset of symptoms
Sudden cardiac death (SCD) risk factors: |
|
|
Smoking
Sudden cardiac death (SCD) occurs more frequently in the morning hours when: |
Hypercoagulability is at its peak
Sudden cardiac death (SCD) pathogenesis: |
|
|
Cause of death is ventricular fibrillation.
In >80% of cases Sudden cardiac death (SCD) there is absence of: |
Occlusive vessel
In Sudden cardiac death (SCD) the cause of death is: |
|
|
Cocaine abuse
Mitral valve prolapse (MVP) sudden death occurs by: |
Arrhythmias from mitral regurgitation or CHF
Most common cause of death in adults in the United States: |
|
|
(3) Platelets adhere to the exposed material and eventually form an occlusive platelet thrombus.
Role of thromboxane A2 in acute myocardial infarction (AMI) pathogenesis: |
(1) Contributes to formation of the platelet thrombus
|
|
|
(2) Causes vasospasm of the artery to reduce blood flow
Less common causes of AMI: |
(a) Vasculitis
|
|
|
(e) Dissection into the wall of coronary arteries
AMI with normal coronary arteries cause: |
Cocaine use
AMI can be cause by embolization of plaque material from: |
|
|
Subendocardial infarction (non-Q wave infarction)
Transmural infarction (Q wave infarction) are: |
New Q waves develop in an electrocardiogram (ECG
Transmural infarction (Q wave infarction) involves: |
|
|
(3) Neutrophils begin to enter the area of infarction from the periphery
Gross and microscopic findings of AMI during 1 to 3 days: |
(1) Pallor of the infarcted tissue
|
|
|
(3) Neutrophils are abundant and lyse dead myocardial cells.
Gross and microscopic findings of AMI during 3 to 7 days: |
(1) Red granulation tissue surrounds the area of infarction.
|
|
|
(2) Macrophages begin to remove necrotic debris.
Gross and microscopic findings of AMI during 7 to 10 days: |
(1) The necrotic area is bright yellow
|
|
|
(2) Granulation tissue and collagen formation are well developed.
Gross and microscopic findings of AMI during 2 months: |
Infarcted tissue replaced by white, patchy, noncontractile scar tissue
Acute myocardial infarction (AMI) clinical findings: |
|
|
(b) "Silent" AMIs in ∼20% of cases
Caracterize the sudden onset of severe, crushing retrosternal pain in Acute myocardial infarction (AMI): |
(1) Lasts >30 minutes
|
|
|
(4) Associated with sweating (diaphoresis), anxiety, and hypotension
"Silent" AMIs may occur in the elderly and in individuals with diabetes mellitus due to: |
High pain threshold or problems with nervous system
Q wave AMI has ______ early mortality rate compared to non-Q wave AMI: |
|
|
(2) Increased risk for sudden cardiac death post-MI
Acute myocardial infarction (AMI) complications: |
(a) Cardiogenic shock occurs in ∼7% of cases.
|
|
|
(h) Right ventricular AMI
In cardiogenic shock due to Acute myocardial infarction (AMI) _______ improves survival: |
Revascularization
Acute myocardial infarction (AMI) arrhythmias: |
|
|
(3) Heart block
Heart block occurs in 5% of ____ AMIs and 3% of _____ AMIs |
Inferior; anterior
Congestive heart failure due to Acute myocardial infarction (AMI) usually occurs within: |
|
|
(4) Interventricular septum rupture
Anterior wall rupture due to Acute myocardial infarction (AMI) cause: |
Cardiac tamponade
Anterior wall rupture due to Acute myocardial infarction (AMI) is associated with: |
|
|
(b) Acute onset of mitral valve regurgitation and LHF
Interventricular septum rupture due to Acute myocardial infarction (AMI) is most associated with: |
LAD coronary artery thrombosis
Interventricular septum rupture due to Acute myocardial infarction (AMI) produces: |
|
|
(c) Rupture
Ventricular aneurysm due to Acute myocardial infarction (AMI) rupture is uncommon because: |
Scar tissue has good tensile strength
Right ventricular AMI due to Acute myocardial infarction (AMI) is associated with ___ thrombosis: |
|
|
(c) Lactate dehydrogenase (LDH)1-2 "flip"
CK-MB appears within __ to __ ___; peaks at __ ____; disappears within ___ to ___ ____ and has Sensitivity and specificity of ___%. |
4 to 8 hours; 24hours; 1.5 to 3 days; 95%
Reinfarction occurs in ___% of AMIs and reapperance of CK-MB after __ days: |
|
|
(b) Improves overall sensitivity and specificity in diagnosing an AMI
Normally, ___ is higher than ___ but in AMI, ____ in cardiac muscle is released, causing the "flip." |
LDH2; LDH1; LDH1
Lactate dehydrogenase (LDH)1-2 "flip" appears within __ ___; peaks at __ to ___ ___; disappears within __ ___. |
|
|
"Silent" AMIs may occur in the elderly and in individuals with diabetes mellitus due to:
|
High pain threshold or problems with nervous system
|
|
|
Acute myocardial infarction (AMI) arrhythmias:
|
(1) Ventricular premature contractions (most common)
|
|
|
Acute myocardial infarction (AMI) clinical findings:
|
(a) Sudden onset of severe, crushing retrosternal pain
|
|
|
Acute myocardial infarction (AMI) complications:
|
(a) Cardiogenic shock occurs in ∼7% of cases.
|
|
|
Acute myocardial infarction (AMI) has no proeminent sex after the age of:
|
65 years old.
|
|
|
Acute myocardial infarction (AMI) is proeminent in:
|
Males between 40 and 65 years old
|
|
|
Acute myocardial infarction (AMI) pathogenesis sequence:
|
Rupture of disrupted plaque → platelet thrombus → AMI
|
|
|
Acute myocardial infarction (AMI) ruptures:
|
(1) Most commonly occurs between days 3 and 7
|
|
|
AMI can be cause by embolization of plaque material from:
|
Atheromatous plaques in the aorta or coronary artery
|
|
|
AMI caused by Dissection into the wall of coronary arteries examples:
|
Revascularization procedure, aortic dissection
|
|
|
AMI caused by thrombosis syndrome examples:
|
Antithrombin III deficiency, polycythemia
|
|
|
AMI caused by vasculitis examples:
|
Polyarteritis nodosa, Kawasaki disease
|
|
|
AMI with normal coronary arteries cause:
|
Cocaine use
|
|
|
Angina pectoris in females usually occurs after:
|
Menopause
|
|
|
Angina pectoris is more common in:
|
Middle-aged males and elderly males
|
|
|
Anterior wall rupture due to Acute myocardial infarction (AMI) cause:
|
Cardiac tamponade
|
|
|
Anterior wall rupture due to Acute myocardial infarction (AMI) is associated with:
|
Thrombosis of the LAD coronary artery
|
|
|
At least __% of AMIs are clinically unrecognized
|
25%
|
|
|
Autoimmune pericarditis due to Acute myocardial infarction (AMI) clinical findings include:
|
Fever and a precordial friction rub
|
|
|
Caracterize the sudden onset of severe, crushing retrosternal pain in Acute myocardial infarction (AMI):
|
(1) Lasts >30 minutes
|
|
|
Cardiac troponins I (cTnI) and T (cTnT) normally regulate:
|
Calcium-mediated contraction
|
|
|
Causes of stable angina:
|
(1) Fixed, atherosclerotic coronary artery disease (most common)
|
|
|
Chronic (stable) angina clinical findings:
|
(1) Exercise-induced substernal chest pain lasting 30 seconds to 30 minutes
|
|
|
Chronic (stable) angina pathogenesis:
|
Subendocardial ischemia due to decreased coronary artery blood flow or thick muscle wall
|
|
|
Chronic ischemic heart disease is a:
|
Progressive CHF resulting from long-term ischemic damage to myocardial tissue
|
|
|
Chronic ischemic heart disease:
|
Biventricular CHF
|
|
|
CK-MB appears within __ to __ ___; peaks at __ ____; disappears within ___ to ___ ____ and has Sensitivity and specificity of ___%.
|
4 to 8 hours; 24hours; 1.5 to 3 days; 95%
|
|
|
CK-MB is used in conjunction with troponins to diagnose an AMI because:
|
(a) Detects reinfarction (troponins cannot)
|
|
|
Congestive heart failure due to Acute myocardial infarction (AMI) usually occurs within:
|
The first 24h
|
|
|
Coronary artery blood flow provides oxygen to:
|
Cardiac muscle
|
|
|
Coronary vessels fill in:
|
Diastole
|
|
|
cTnI and cTnT appear within __ to __ ___; peaks at __ ____; disappears within ___ to ___ ____; has Sensitivity of __% to __% and specificity of ___% to __%
|
3 to 12 hours; 24hours; 7 to 10 days; 84% to 96%; 80% to 95%
|
|
|
cTnI, cTnT is gold standard for diagnosis of:
|
AMI
|
|
|
Early reperfusion salvages some injured but viable myocytes but:
|
Destroys myocytes that are irreversibly damaged.
|
|
|
Early reperfusion:
|
Limits the size of the infarction
|
|
|
Early reperfusion:
|
Prevents any further damage to myocardial cells
|
|
|
Fibrinous pericarditis (with or without effusion) due to Acute myocardial infarction (AMI) can be due a Q wave AMI or:
|
Autoimmune pericarditis 6 to 8 weeks after an acute MI
|
|
|
Fibrinous pericarditis (with or without effusion) due to Acute myocardial infarction (AMI) can cause whan kind of pain? What other symptom?
|
Substernal chest pain is relieved by leaning forward and aggravated by leaning backward. Can also cause a A precordial friction rub.
|
|
|
Fibrinous pericarditis (with or without effusion) due to Acute myocardial infarction (AMI) occurs when?
|
Days 1 to 7 of a Q wave AMI
|
|
|
Gross and microscopic findings of AMI during 0 to 24 hours:
|
(1) No gross changes are evident until 24 hours.
|
|
|
Gross and microscopic findings of AMI during 1 to 3 days:
|
(1) Pallor of the infarcted tissue
|
|
|
Gross and microscopic findings of AMI during 2 months:
|
Infarcted tissue replaced by white, patchy, noncontractile scar tissue
|
|
|
Gross and microscopic findings of AMI during 3 to 7 days:
|
(1) Red granulation tissue surrounds the area of infarction.
|
|
|
Gross and microscopic findings of AMI during 7 to 10 days:
|
(1) The necrotic area is bright yellow
|
|
|
Heart block occurs in 5% of ____ AMIs and 3% of _____ AMIs
|
Inferior; anterior
|
|
|
In >80% of cases Sudden cardiac death (SCD) there is absence of:
|
Occlusive vessel
|
|
|
In Acute myocardial infarction (AMI) elevated ST segment correlate with:
|
Injured myocardial cells surrounding the area of necrosis
|
|
|
In Acute myocardial infarction (AMI) inverted T waves in ECG correlate with:
|
Areas of ischemia at the periphery of the infarct
|
|
|
In Acute myocardial infarction (AMI) new Q waves correlate with:
|
Area of coagulation necrosis
|
|
|
In Autoimmune pericarditis due to Acute myocardial infarction (AMI) there are antibodies directed against:
|
Damaged pericardial antigens
|
|
|
In cardiogenic shock due to Acute myocardial infarction (AMI) _______ improves survival:
|
Revascularization
|
|
|
In Chronic (stable) angina due to aortic stenosis or hypertension with concentric LVH O2 supply:
|
Is not adequate for the thickened muscle wall
|
|
|
In Chronic (stable) angina due to fixed, atherosclerotic coronary artery disease its likely that:
|
(a) One or more vessel obstructions.
|
|
|
In Chronic ischemic heart disease there is a replacement of:
|
Myocardial tissue with noncontractile scar tissue
|
|
|
In fibrinous pericarditis (with or without effusion) due to Acute myocardial infarction (AMI) the precordial friction rub is caused by:
|
Increased vessel permeability in the pericardium; exudate of acute inflammation
|
|
|
In mural thrombus due to Acute myocardial infarction (AMI) there is the danger of:
|
Embolization
|
|
|
In Subendocardial infarction (non-Q wave infarction) Q waves are:
|
Absent
|
|
|
In Sudden cardiac death (SCD) the cause of death is:
|
Ventricular fibrillation
|
|
|
Interventricular septum rupture due to Acute myocardial infarction (AMI) is most associated with:
|
LAD coronary artery thrombosis
|
|
|
Interventricular septum rupture due to Acute myocardial infarction (AMI) produces:
|
A left-to-right shunt causing RHF (Increased O2 saturation and pressure in right ventricle)
|
|
|
Ischemic heart disease incidence peaks in man after ___ years of age and woman after ___ years of age:
|
60;70
|
|
|
Ischemic heart disease is more common in:
|
Men
|
|
|
Ischemic Heart Disease results from:
|
Imbalance between myocardial O2 demand and supply from the coronary arteries
|
|
|
Ischemic heart disease risk factors:
|
(1)Age
|
|
|
Laboratory diagnosis of AMI include:
|
(a) Serial testing for creatine kinase isoenzyme MB (CK-MB)
|
|
|
Lactate dehydrogenase (LDH)1-2 "flip" appears within __ ___; peaks at __ to ___ ___; disappears within __ ___.
|
10 hours; 2 to 3 days; 7days
|
|
|
Lactate dehydrogenase (LDH)1-2 "flip" test has been replaced by:
|
Troponins I and T
|
|
|
Left anterior descending (LAD) coronary artery distribution:
|
(1) Anterior portion of the left ventricle
|
|
|
Left circumflex coronary artery distribution:
|
Lateral wall of the left ventricle
|
|
|
Less common causes of AMI:
|
(a) Vasculitis
|
|
|
Major cause of death in the United States:
|
Ischemic heart disease
|
|
|
Mitral valve prolapse (MVP) sudden death occurs by:
|
Arrhythmias from mitral regurgitation or CHF
|
|
|
Most common cause of death in adults in the United States:
|
Acute myocardial infarction (AMI)
|
|
|
Most common site of coronary artery thrombosis:
|
Left anterior descending (LAD) coronary artery
|
|
|
Most common variant of angina pectoris:
|
Chronic (stable) angina
|
|
|
Mural thrombus due to Acute myocardial infarction (AMI) is most often associated with:
|
LAD coronary artery thrombosis
|
|
|
Mural thrombus due to Acute myocardial infarction (AMI) occurs in:
|
10% of AMI
|
|
|
Non-Q wave AMI has increased risk for:
|
(1) Increased risk of reinfarction
|
|
|
Normally, ___ is higher than ___ but in AMI, ____ in cardiac muscle is released, causing the "flip."
|
LDH2; LDH1; LDH1
|
|
|
Posteromedial papillary muscle rupture or dysfunction due to Acute myocardial infarction (AMI) is associated with:
|
(a) RCA thrombosis(most often with inferiror AMI)
|
|
|
Prinzmetal's angina pathogenesis:
|
(1) Intermittent coronary artery vasospasm at rest with or without superimposed coronary artery atherosclerotic disease
|
|
|
Prinzmetal's angina:
|
Stress test shows ST-segment elevation (transmural ischemia).
|
|
|
Q wave AMI has ______ early mortality rate compared to non-Q wave AMI:
|
Increased
|
|
|
Q wave in lead V6 is a classic ECG patterns in AMI for:
|
Posterior wall infarction due to posterior descending artery occlusion
|
|
|
Q waves in leads I, aVL is a classic ECG patterns in AMI for:
|
Lateral wall infarction due to left circumflex artery
|
|
|
Q waves in leads II, III, aVF is a classic ECG patterns in AMI for:
|
RCA inferior wall infarction
|
|
|
Q waves in leads V1-V2 is a classic ECG patterns in AMI for:
|
Anteroseptal infarction due to proximal LAD occlusion
|
|
|
Q waves in leads V1-V4 is a classic ECG patterns in AMI for:
|
LAD coronary artery anterior wall infarction
|
|
|
Q waves in leads V4-V6, I, aVL is a classic ECG patterns in AMI for:
|
Anterolateral infarction due to mid-LAD or circumflex coronary arteries
|
|
|
R wave > S wave in lead V1 is a classic ECG patterns in AMI for:
|
Posterior wall infarction due to posterior descending artery occlusion
|
|
|
Reinfarction occurs in ___% of AMIs and reapperance of CK-MB after __ days:
|
10%; 3 days
|
|
|
Removal of irreversibly damaged myocytes improves:
|
short- and long-term function and survival.
|
|
|
Reperfusion histologically alters:
|
Irreversibly damaged cells.
|
|
|
Reperfusion histologically produces contraction band necrosis by:
|
Hypercontraction of myofibrils in dying cells due to the influx of Ca2+ into the cytosol
|
|
|
Reperfusion injury follows:
|
Thrombolytic (fibrinolytic) therapy
|
|
|
Right coronary artery (RCA) distribution:
|
(1) Posteroinferior part of the left ventricle
|
|
|
Right ventricular AMI due to Acute myocardial infarction (AMI) clinical findings:
|
Hypotension, RHF, and preserved left ventricle function
|
|
|
Right ventricular AMI due to Acute myocardial infarction (AMI) is associated with ___ thrombosis:
|
RCA
|
|
|
Right ventricular AMI due to Acute myocardial infarction (AMI) occurs in one third of _____ AMIs and clinically significant in __% of cases.
|
Inferior; 30%
|
|
|
Role of thromboxane A2 in acute myocardial infarction (AMI) pathogenesis:
|
(1) Contributes to formation of the platelet thrombus
|
|
|
Serial testing for cardiac troponins I (cTnI) and T (cTnT) false positive results are usually related to:
|
Ischemia (e.g., unstable angina).
|
|
|
Site for 15% to 20% of coronary artery thromboses:
|
Left circumflex coronary artery
|
|
|
Site for 40% to 50% of coronary artery thromboses:
|
Left anterior descending (LAD) coronary artery
|
|
|
Subendocardial infarction (non-Q wave infarction) involves:
|
The inner third of the myocardium
|
|
|
Sudden cardiac death (SCD) is a diagnosis of exclusion after the following causes are ruled out:
|
Mitral valve prolapse (MVP)
|
|
|
Sudden cardiac death (SCD) is:
|
Unexpected death within 1 hour after the onset of symptoms
|
|
|
Sudden cardiac death (SCD) occurs more frequently in the morning hours when:
|
Hypercoagulability is at its peak
|
|
|
Sudden cardiac death (SCD) pathogenesis:
|
Severe atherosclerotic coronary artery disease
|
|
|
Sudden cardiac death (SCD) risk factors:
|
Obesity
|
|
|
Tachycardia (>180 bpm) _____ ____ ____, leading to ischemia
|
Decreases filling time
|
|
|
Transmural infarction (Q wave infarction) are:
|
New Q waves develop in an electrocardiogram (ECG
|
|
|
Transmural infarction (Q wave infarction) involves:
|
Full thickness of the myocardium
|
|
|
Types of ischemic heart disease:
|
(a)Angina pectoris (most common type)
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Types of myocardial infarction:
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Transmural infarction (Q wave infarction)
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Unstable angina clinical findings:
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(1) Frequent bouts of chest pain at rest or with minimal exertion
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Unstable angina pathogenesis:
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(1) Severe, fixed, multivessel atherosclerotic disease
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Ventricular aneurysm due to Acute myocardial infarction (AMI) ______ _____ occurs during systole because blood enters the aneurism causing ______ _____ _____ movement:
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Precordial bulge; anterior chest wall
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Ventricular aneurysm due to Acute myocardial infarction (AMI) complications:
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(a) CHF occurs due to the lack of contractile tissue.
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Ventricular aneurysm due to Acute myocardial infarction (AMI) is clinically recognized within __ to __ weeks but start developing in the first ___ hours:
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4;8;48
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Ventricular aneurysm due to Acute myocardial infarction (AMI) rupture is uncommon because:
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Scar tissue has good tensile strength
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Within 1 year of a diagnosis of stable angina, 10% to 20% will develop:
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An acute myocardial infarction or unstable angina.
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