PATH - 9-28 - Ischemic Heart Disease Flashcards
(28 cards)
A: What Disease is the Leading cause of death and disability ?
B: Which Gender is more affected by Acute MI?
B2: Clinical Presentation of an Acute MI (6)
C: ___% of patients have a “silent” MI
A: Ischemic Heart Disease
B: MALE
B2:
-[Crushing Substernal Chest Pain]
- lasting x>30 minutes
- radiates to [L arm or jaw]
- diaphoresis
- [dyspnea from pulmonary congestion]
- Sx are NOT relieved with NTG
C: 10-15% of Patients have “Silent” MI
A: Describe [Congestive Heart Failure]
B:
[Systolic heart failure] is the result of progressive ______ of ______. The damaged ______ contracts weakly.
C: Causes:(2)
A: [Congestive Heart Failure] = Heart unable to maintain output that’s sufficient to meet metabolic requirement of the [Organ System]
B:
[Systolic heart failure] is the result of progressive deterioration of myocardial contraction. The damaged myocardium contracts weakly.
C: Causes:
- ischemic injury
- pressure or volume overload
Causes of Diastolic Heart Failure (3)
- L ventricular hypertrophy
- Myocardial infiltrative dz
- Constrictive Pericarditis
4 Common signs of LEFT Sided heart failure
(x) Cerebral hypOperfusion
(x) Muscle Fatigue
(x) Renal hypOperfusion
(x) Pulmonary Congestion / SOB
A: Ischemic Heart Disease consist of what 4 conditions
CASA
- Angina (Stable vs. Unstable vs. [Prinzmetal Variant])
- Acute MI
- Chronic Ischemic Heart Disease / Heart Failure
- Sudden Cardiac Death
A: Describe [Stable Typical Angina] etiology
B: Clinical presentation
A: Chronic Coronary Artery stenosis from [Stable Atherosclerotic plaque]—> more than 75% reduction in lumen—> [Transient myocardial ischemia] with INC demand
B: sx:
-Substernal chest pain with INC cardiac demand, but relieved with [rest and NTG(vasodilates veins and DEC myocardial preload]
A: Unstable Angina Etiology
B: What else plays an accessory role in [Unstable Angina]?
C: Unstable Angina is also known as what 2 other names?
D: Clinical Presentation
E: ______ are the plaques that typically cause Unstable Angina. How Stenotic are they?
A: Occurs when [Unstable Vulnerable Atherosclerotic plaque] fissures in Coronary Artery leaving SubEndothelium exposed –> Thrombocyte activation and aggregation —> PARTIAL coronary occlusion
B: Vasospasms
C: AKA [Crescendo or preinfarction angina]
D: [Frequent Chest Pressure] with less or no effort and longer duration
E: Usually 50-75% Stenotic
A: [Prinzmetal Variant Angina] is a RARE _______ unrelated to _____, ____ or _____
B: Clinical Presentation
C: Tx (2)
D: What Drug can mimic this etiology if OD?
A: [Prinzmetal Variant Angina] is a RARE [Coronary Artery Spasm] unrelated to physical activity / HR / BP.
B: Chest Pain at rest relieved with NTG or [Ca+ channel blockers]
C:
NTG or [Ca+ channel blockers]
D:
-Cocaine
A: [Myocardial Infarct] is still Reversible WITHIN THE FIRST ____ MINUTES! What happens after this time period?
B: [Transmural infarct]
C: [Non-Transmural infarct] examples (3)
A: [Myocardial Infarct] is still Reversible WITHIN THE FIRST 30 MINUTES! After 30 min —> [Coagulative Ischemic Necrosis - CIN]
B: [Transmural infarct] is when CIN involves FULL Thickeness of Ventricle
C: [Non-Transmural infarct]
- [Transient or partial obstruction] —> Regional SubEndocardial infarct (EKG - ST Depression)
- Global hypOtension—> Circumferential SubEndocardial infarct
- [small intramural vessel occlusions]–>microinfarcts
POST Myocardial Infarction Morphology
[30 min - 4 hours] post MI
Gross changes
None
POST Myocardial Infarction Morphology
[30 min - 4 hours] post MI
Microscopic changes
None
POST Myocardial Infarction Morphology
[30 min - 4 hours] post MI
Potential Complications (2)
- Cardiogenic Shock from massive ventricular infarction (x>40%)
- CHF
POST Myocardial Infarction Morphology
[4 - 12 Hours] post MI
Findings
Beginning of [Coagulative Ischemic Necrosis]
POST Myocardial Infarction Morphology
[12 - 24 Hours] post MI
- A: Gross changes*
- B: Microscopic Changes (2)*
- C: Complications*
- D: Labs (2)*
A: Dark Myocardial Mottling
B: Continued [Coagulative Ischemic Necrosis] + [Nuclei Pyknosis]
C: Arrhythmia (Tachy or Brady)
D: [Troponin i] AND [CK-MB] levels BOTH ARE PEAKED at 24 hours
POST Myocardial Infarction Morphology
[1 - 3 Days] post MI
- A: Gross Changes*
- B: Microscopic Changes (2)*
- B: Complications*
A: No Gross
B:
- Loss of myocardial nuclei and myocytes
- Neutrophils Present
C: [Acute Fibrinous pericarditis] presenting as chest pain w/friction rub (only occurs with transmural infarct)
POST Myocardial Infarction Morphology
[3 - 7 Days] post MI
- A: Gross changes*
- B: Microscopic changes*
- C: Potential Complications (3)*
A: Yellow Pallor
B:
- Myocyte disintegration
- Macrophage Phagocytosis of dead cells –> Myocyte weakning
C:
*[Ventricular Free Wall Rupture]—> [Cardiac Tamponade] and Hemopericardium
*[Interventricular Septum Rupture]–> Shunt
*Papillary muscle rupture –> Mitral insufficiency
POST Myocardial Infarction Morphology
[7- 10 Days] post MI
Findings (3)
- Well Developed Phagocytosis
- Early Granulation Tissue
- [Troponin i] levels DEC and return to normal
POST Myocardial Infarction Morphology
[10 - 14 Days] post MI
- A: Gross changes*
- B: Microscopic Changes*
A: Grossly, Red Border emerges as granulation tissue enters from edge of infarct
B: Microscopically, Granulation tissue will have plump fibroblast and [blood vessels]
POST Myocardial Infarction Morphology
[2 - 8 Weeks] post MI
- A: Gross changes*
- B: Microscopic Changes*
- C: Potential Complications*
A: White Scar
B: Fibrosis, microscopically
C:
- Ventricular Aneurysm (Chronic finding)
- [Mural Thrombus]
- [Dressler Post MI Syndrome]
Name the 2 Lab markers for Myocardial Infarct and their Timing significance
A:
[Troponin i] rises 2-4 hours after infarction –> Peaks at 24 hours —> Returns to normal [7-10 days later]
B: [CK-MB] is used for detecting ReInfarction since [CK-MB] peaks at 24 hours–> Returns to normal 72 hours later
List the 6 Therapies for an Acute MI
B: Give brief description of why their used
Pts with [Acute MI] Need OBAMA!
- NTG = VasoDilates Veins and Coronary Arteries
- Oxygen = Minimizes ischemia
- Beta Blockers = DEC HR –> DEC Arrhythmia risk
- [ASA and Heparin] = limits thrombosis
- Morphine = Pain
- ACEk2 inhibitors= DEC [L Ventricle Dilation/Remodeling]
How does [Reperfusion Injury] actually cause myocardial damage? (4)
1) [O2-derived Free Radical] production
2) [Myocyte hypercontracture] = Reperfusion of irreversibly-damaged cells–> [intracellular Ca+ accumulation]—> hypercontracture and [Contraction Band Necrosis]
3) [Leukocyte Aggregation and enzyme damage] –> Even more vascular occulusion and [Leukocyte proteases–>may cause cell death]
4) Mitochondrial Dysfunction –> Cell Apoptosis
[Dressler’s Post MI Syndrome]
A: Etiology
B: When does this occur?
A: Autoimmune pericarditis
B: Occurs [2 - 8 Weeks Post MI]
A: In [Chronic Ischemic Heart Disease]: the heart’s _____ tissue after _____ progressively decompensates from _____ –> [L ventricular _____ and _____] —> _____
B: How does Atherosclerosis play a role?
C: AKA
A: In [Chronic Ischemic Heart Disease]: the heart’s UnAffected tissue after MI progressively decompensates from chronic ischemia –> [L ventricular hypertrophy and dilation] —> CHF
B: Can also be caused by Long-term Coronary Atherosclerosis
C: AKA “Ischemic Cardiomyopathy”
