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🄼💊 CARDIO PATH/RX > PATH - 9-28 - Ischemic Heart Disease > Flashcards

PATH - 9-28 - Ischemic Heart Disease Flashcards

1
Q

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

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

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2
Q

A: Describe [Congestive Heart Failure]

B:

[Systolic heart failure] is the result of progressive ______ of ______. The damaged ______ contracts weakly.

C: Causes:(2)

A

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
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3
Q

Causes of Diastolic Heart Failure (3)

A
  1. L ventricular hypertrophy
  2. Myocardial infiltrative dz
  3. Constrictive Pericarditis
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4
Q

4 Common signs of LEFT Sided heart failure

A

(x) Cerebral hypOperfusion
(x) Muscle Fatigue
(x) Renal hypOperfusion
(x) Pulmonary Congestion / SOB

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5
Q

A: Ischemic Heart Disease consist of what 4 conditions

A

CASA

  1. Angina (Stable vs. Unstable vs. [Prinzmetal Variant])
  2. Acute MI
  3. Chronic Ischemic Heart Disease / Heart Failure
  4. Sudden Cardiac Death
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6
Q

A: Describe [Stable Typical Angina] etiology

B: Clinical presentation

A

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]

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7
Q

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

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

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8
Q

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

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

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9
Q

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

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]

  1. [Transient or partial obstruction] —> Regional SubEndocardial infarct (EKG - ST Depression)
  2. Global hypOtension—> Circumferential SubEndocardial infarct
  3. [small intramural vessel occlusions]–>microinfarcts
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10
Q

POST Myocardial Infarction Morphology

[30 min - 4 hours] post MI

Gross changes

A

None

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11
Q

POST Myocardial Infarction Morphology

[30 min - 4 hours] post MI

Microscopic changes

A

None

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12
Q

POST Myocardial Infarction Morphology

[30 min - 4 hours] post MI

Potential Complications (2)

A
  • Cardiogenic Shock from massive ventricular infarction (x>40%)
  • CHF
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13
Q

POST Myocardial Infarction Morphology

[4 - 12 Hours] post MI

Findings

A

Beginning of [Coagulative Ischemic Necrosis]

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14
Q

POST Myocardial Infarction Morphology

[12 - 24 Hours] post MI

  • A: Gross changes*
  • B: Microscopic Changes (2)*
  • C: Complications*
  • D: Labs (2)*
A

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

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15
Q

POST Myocardial Infarction Morphology

[1 - 3 Days] post MI

  • A: Gross Changes*
  • B: Microscopic Changes (2)*
  • B: Complications*
A

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)

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16
Q

POST Myocardial Infarction Morphology

[3 - 7 Days] post MI

  • A: Gross changes*
  • B: Microscopic changes*
  • C: Potential Complications (3)*
A

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

17
Q

POST Myocardial Infarction Morphology

[7- 10 Days] post MI

Findings (3)

A
  • Well Developed Phagocytosis
  • Early Granulation Tissue
  • [Troponin i] levels DEC and return to normal
18
Q

POST Myocardial Infarction Morphology

[10 - 14 Days] post MI

  • A: Gross changes*
  • B: Microscopic Changes*
A

A: Grossly, Red Border emerges as granulation tissue enters from edge of infarct

B: Microscopically, Granulation tissue will have plump fibroblast and [blood vessels]

19
Q

POST Myocardial Infarction Morphology

[2 - 8 Weeks] post MI

  • A: Gross changes*
  • B: Microscopic Changes*
  • C: Potential Complications*
A

A: White Scar

B: Fibrosis, microscopically

C:

  1. Ventricular Aneurysm (Chronic finding)
  2. [Mural Thrombus]
  3. [Dressler Post MI Syndrome]
20
Q

Name the 2 Lab markers for Myocardial Infarct and their Timing significance

A

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

21
Q

List the 6 Therapies for an Acute MI

B: Give brief description of why their used

A

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]
22
Q

How does [Reperfusion Injury] actually cause myocardial damage? (4)

A

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

23
Q

[Dressler’s Post MI Syndrome]

A: Etiology

B: When does this occur?

A

A: Autoimmune pericarditis

B: Occurs [2 - 8 Weeks Post MI]

24
Q

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

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”

25
Q

Sudden Cardiac Death

A: MOST COMMON ETIOLOGY

B: Autopsy Finding

C: least common etiology (5)

D: Clinical Presentation

A

A: Severe chronic coronary atherosclerosis –> myocardium irratibility –>[lethal ventricular arrhythmia]

B:

-[NO acute plaque disruption found on autopsy]

C. Other , non-atherosclerotic, causes of sudden cardiac death

*Hereditary or acquired [cardiac conduction] or coronary abnormalities

*Mitral valve prolapse
*Dilated/Hypertrophic cardiomyopathy

*Pulmonary HTN

*Cocaine

D: Sometimes occurs without symptoms or [death is within 1 hour after sx begin]

26
Q

[LEFT Sided Heart Failure 2º to HTN] (chronic pressure overload)

A: What occurs to the heart as a result of this? (2)

B: Can lead to …. (4)

A

[LEFT Sided Heart Failure 2º to HTN] (chronic pressure overload)

A: INC heart size –> Concentric L Ventricle Wall thickness greater than 2 cm and heavier than 500 grams!

B: Can lead to

  • CHF
  • Arrhythmias (aFib)
  • Pulmonary Congestion –> [Paroxysmal nocturnal dyspnea]
  • Activation of [Renin-Angiotensin Pathway]—> Exacerbation of CHF!
27
Q

Unstable Angina

Rx (4)

A
  1. Triple drug therapy (nitrates, beta blockers, [Ca channel blockers])
  2. IV NTG
  3. Aspirin
  4. Heparin
28
Q

Acute Coronary Syndrome consist of what 3 conditions

A

“We have ACS in the USA”

  1. [Unstable vulnerable Angina]
  2. Sudden Cardiac Death
  3. Acute MI

🄼💊 CARDIO PATH/RX (22 decks)

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