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MHD block 4 > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

what is the leading cause of death and disability

A

Heart Disease

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2
Q

Heart Failure

A

Heart unable to pump blood sufficiently to meet needs of tissue
- Ventricle unable to fill with or eject blood
“Congestive Heart Failure”

Usually progressive condition with poor prognosis

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3
Q

systolic heart failure

A

deterioration of myocardial contraction leading to an inability to pump blood (thin, weakened heart muscle)

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4
Q

Diastolic heart failure

A

Inability of heart chamber to relax, expand, and adequately fill during diastole (thick hypertrophied ventricles usually due to hypertension)

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5
Q

what is the #1 cause of right sided heart failure

A

left sided heart failure

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6
Q

Cor pulmonale

A

right sided heart failure without left sided

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7
Q

right sided heart failure causes

A

Engorgement of systemic and portal venous circulation (edema)

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8
Q

left sided heart failure causes

A

Damning of blood in pulmonary circulation
Diminished peripheral blood flow

Ischemia
HTN
Aortic/mitral valve disease
Nonichemic myocardial diseases

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9
Q

Symptoms of left sided heart failure

A

shortness of breath, worse when laying down

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10
Q

risk factors for Ischemic heart disease

A

atherosclerosis risk factors

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11
Q

how does ischemic heart failure happen

A 
Decreased perfusion (coronary blood flow)
 and Increased myocardial demand lead to:

Angina Pectoris
Acute Myocardial Infarction
Chronic Ischemic Heart Disease/ Heart Failure
Sudden Cardiac Death

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12
Q

Stable (Typical) Angina Pectoris

A

Chronic stenosing coronary atherosclerosis (>75% reduction of lumen area) (happens over years)

Increased cardiac demand and workload needs unmet
Substernal chest pressure
- Physical activity, emotional excitement
- Relieved with rest (Vasodilator, nitroglycerin)

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13
Q

what are the 3 types of angina

A

stable, unstable, and Prinzmetal Variant Angina

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14
Q

Unstable Angina Pectoris

A

(aka Crescendo angina, preinfarction angina)
Atherosclerotic plaque disruption (abrupt)
• Thrombogenic plaque components, subendothelial basement membrane exposed
• Platelets activation, aggregation
• Vasospasm
• **Partially occluding thrombus

Anginal symptoms
frequent, less effort, at rest, longer duration

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15
Q

stable vs vulnerable plaques

A 
Vulnerable plaques
Lipid rich atheromas
Thin fibrous caps
Inflammation
Moderately stenotic - 50-75%

stable plaques
smaller core
thicker cap
less inflammation
may be more stenotic
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16
Q

Prinzmetal Variant Angina

A

Coronary artery spasm
Unrelated to physical activity, heart rate, blood pressure
Responds to vasodilators

  • You will usually make sure to rule out other causes of chest pain before making this diagnosis
17
Q

MI pathogenesis/mechanisms

A

Pathogenesis

  • Plaque disruption (Hemorrhage, ulceration, rupture, fissuring)
  • Platelet adhesion, aggregation, activation
  • Vasospasm
  • Coagulation
  • OCCLUSIVE THROMBUS FORMATION
18
Q

for how long is ischemia reversible

A

30minutes - irreversible, coagulative necrosis

19
Q

transmural vs. nontransmural infarcts

A

transmural affect the full thickness of the wall - due to permanent obstruction of an arterial branch

while non-transmural are often subendocardial, can be due to a transient /partial obstruction, hypotension, or microinfarcts(spasms from cocaine use)

20
Q

when a coronary artery becomes obstructed what part of the muscle is affected first

A

subendocardial (furthest from the vessel

21
Q

Myocardial Infarction Morphology: 1/2 to 4 hours

A

No gross or light microscopic changes

22
Q

Myocardial Infarction Morphology: 4 to 12 hours

A

Beginning coagulation necrosis

23
Q

Myocardial Infarction Morphology: 12 to 24 hours

A

Gross - Dark mottling
Ongoing coagulation necrosis
Pyknosis of nuclei

24
Q

Myocardial Infarction Morphology: 1-3 days

A

Gross - mottled
Loss of nuclei and myocytes
Neutrophil infiltrate

25
Myocardial Infarction Morphology: 3-7 days
Myocyte disintegration, phagocytosis of dead cells | Gross- yellow-tan softening
26
Myocardial Infarction Morphology: 7- 10 days
Well-developed phagocytosis and early granulation tissue
27
Myocardial Infarction Morphology: 10-14 days
Granulation tissue
28
Myocardial Infarction Morphology: 2-8 weeks
scar formation
29
symptoms of a MI
Crushing substernal chest pain, dyspnea, diaphoresis Tachycardia, pulmonary congestion, edema 10-15% of patients – “silent”
30
Laboratory Evaluation of an MI
troponin (peak 24hrs after) CK-MB (peaks 18hrs) Myoglobin (peak 2 hrs) - not specific to cardiac injury
31
Triphenyltetrozolium chloride stain (LDH substrate)
stains myocardium but not the infarcted myocardium due to enzyme depletion
32
MI treatment
``` Aspirin and other antiplatelet agents Heparin Thrombolytic therapy (Drug vs interventional) Beta blockers ACE inhibitors Nitrates Oxygen ```
33
Reperfusion INJURY
Restoration of blood flow leads to local myocardial damage • Free radical production • Myocyte hypercontracture, increased Ca • Leukocyte aggregation leads to proteases, elastases • Mitochondrial dysfunction leads to apoptosis (caspase release)
34
MI complications
1. Cardiogenic shock Severe pump failure 10-15% patients Large infarcts (>40% ventricle) 2. Arrhythmia Conduction disturbances Myocardial irritability ``` 3. Myocardial rupture 3-7 days Free wall (Hemopericardium, Cardiac tamponade) Ventricular septum Papillary muscle ``` 4. Acute Pericarditis 2-3 days Transmural MI 5. Ventricular aneurysm late complication mural thrombus 6. Progressive heart failure
35
describe Progressive heart failure
when part of the heart has been previously infarcted, scar tissue forms in that area and is not contractile. The function of the heart then depends on the healthy tissue, which begins to hypertrophy to compensate. The increased size, mass, and protein synthesis requires more oxygen and nutrients than the arteries can supply. As a result small ischemic areas develop and extracellular matrix formation. eventually will lead to ischemic heart failure
36
Sudden Cardiac Death mechanism
lethal arrhythmia Underlying structural heart disease Severe chronic coronary atherosclerosis with an associated lethal arrhythmia is the etiology in 80-90% of cases -At autopsy findings of acute plaque disruption are not found in most cases -Usually NOT acute infarction -Irritability of myocardium triggers arrhythmia
37
Hypertension can lead to what affects on the heart
Hypertrophy of left ventricle | Mild blood pressure elevation can induce LVH
38
“Cor Pulmonale”
Pulmonary HTN Pathology of lung and/or lung vasculature COPD, Pulmonary fibrosis, chronic pulmonary thromboembolism, primary pulmonary HTN Increased pulmonary vascular resistance leads to Right ventricular hypertrophy Dilatation
39
what commonly leads to cardiac hypertrophy
Systemic hypertension LV wall thickness > 2cm Weight > 500 gm Aortic stenosis 800 gm Normal heart 250 - 350 gm Normal LV wall thickness ~1.5cm

MHD block 4 (9 decks)

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