10 - Cardiovascular Pathology II Flashcards
1
Q
Define ischemia
A
- Reversible cellular injury
- Therapeutic salvage may be possible
- No tissue death
2
Q
Define infarction
A
- Irreversible injury
- Myofiber coagulative necrosis
- Once these fibers die, they don’t come back
3
Q
What are the presenting factors in ischemic heart disease (IHD)?
A
- Angina pectoris
- Myocardial infarction
- Chronic IHD with heart failure
- Sudden cardiac death
4
Q
How does IHD lead to heart failure?
A
Cardiac myocytes weaken, atrophy, leads to heart failure
5
Q
What is myocardial ischemia?
A
- Insufficient oxygen supply to myocardial fibers
6
Q
Is myocardial ischemia reversible?
A
Yes
7
Q
What causes myocardia ischemia?
A
Decreased myocardial blood supply and/or Increased myocardial oxygen demand
8
Q
There are three types of agina pectoris - what are they?
A
- Stable (typical) angina
- Unstable or crescendo angina
- Prinzmetal variant angina
9
Q
Describe stable (typical) angina
A
- Most common form, produced by physical activity, emotional excitement, or any other cause of increased cardiac workload resulting in an imbalance in coronary perfusion relative to myocardial demand.
- Relieved by rest or administering nitroglycerin.
10
Q
Describe unstable or crescendo angina
A
- Pattern of increasingly frequent pain, often of prolonged duration, that is precipitated by progressively lower levels of physical activity or that even occurs at rest.
- Caused by the disruption of an atherosclerotic plaque with superimposed partial thrombosis and possibly embolization or vasospasm (or both).
- Unstable angina thus serves as a warning that an acute MI may be imminent.
Example
- Sitting on the couch and you start getting chest pain
11
Q
Describe prinzmetal variant angina
A
- Uncommon, episodic myocardial ischemia that is caused by coronary artery spasm.
- The anginal attacks are unrelated to physical activity, heart rate, or blood pressure.
- Responds promptly to vasodilators, such as nitroglycerin and calcium channel blockers.
12
Q
What is the ABPI?
A
Ankle brachial pressure index
- Assesses risk of peripheral artery disease (blockage in arms/legs)
- Compares your blood pressure measured at your ankle with your blood pressure measured at your arm
13
Q
What does ABPI tell you? What does a high ABPI tell you?
A
- An ABPI number below 0.9 can indicate calcification or narrowing/blockage of the arteries in your legs, leading to circulatory problems, heart disease or stroke.
14
Q
How can ABPI be used as a predictor for mortality?
A
ABPI may be an independent predictor of mortality, as it reflects the burden of atherosclerosis
15
Q
What is the most important form of IDH?
A
Myocardial infarction
16
Q
How many people suffer from an MI annually in the US?
A
1.5 million
Nearly 10% of myocardial infarcts occur in people under age 40, and 45% occur in people under age 65. African Americans and whites are equally affected.
17
Q
Are men or women at a higher risk?
A
Men
18
Q
What contributes to the rising trend of MI in women?
A
- The decrease of estrogen following menopause is associated with rapid development of CAD, and IHD is the most common cause of death in elderly women
- Postmenopausal hormonal replacement therapy is not currently felt to protect against atherosclerosis and IHD
- Once you reach the age of 70, the rate of MI in men and women is equal
19
Q
What are the symptoms of MI?
A
- Chest pain
- Dyspnea and diaphoresis (SOB and sweating)
- Weakness, light-headedness, nausea, vomiting, palpitations
- Loss of consciousness and sudden death
20
Q
Describe the chest pain seen in MI
A
- Levine’s sign: clenching their fist over the sternum.
- Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium, where it may mimic heartburn.
- Diabetics can have “silent MI’s” due to neuropathy
= Very elderly do not usually have the typical presentation
21
Q
How does an EKG change due to MI?
A
- ST segment depression or T wave inversion (suspicious for ischemia)
- ST segment elevation (indication of MI)
- Non-diagnostic or normal ECG (need to then check enzymes)
22
Q
What are the two serum markers we look for?
A
- Troponin (from cardiac muscle)
- CK-MB (creatinine kinase)
23
Q
Which enzyme will peak first?
A
Creatinine kinase (0-1 day)
Troponin (1-2 days)
24
Q
What is the most important consideration for treating an MI?
A
TIMING TIMING TIMING
25
Why is timing so important?
- If you get to your patient in a half hour and you can reperfused the tissue, you have a chance of salvaging the myocardium and you can actually prevent any cell death
- If hours goes on and you don’t get to your patient, you will not be able to prevent an MI – cell death will occur
26
What determines the severity of an MI?
- The size of the vascular bed perfused by the obstructed vessels
- The duration of the occlusion
- The metabolic/oxygen needs of the myocardium at risk
- The extent of collateral blood vessels
- The presence, site, and severity of coronary arterial spasm
- Other factors, such as heart rate, cardiac rhythm, and blood oxygenation
27
What is the breakdown of arteries occluded in MIs?
- Left anterior descending coronary artery (40-50%)
- Right coronary artery (30-40%)
- Left circumflex (15-20%)
28
Describe a left anterior descending coronary artery MI
infarcts involving the anterior wall of left ventricle near the apex; the anterior portion of ventricular septum; and the apex circumferentially
29
Describe a right coronary artery MI
infarcts involving the inferior/posterior wall of left ventricle; posterior portion of ventricular septum; and the inferior/posterior right ventricular free wall in some cases
30
Describe a left circumflex artery MI
infarcts involving the lateral wall of left ventricle except at the apex
31
What will we see within 1/2 to 4 hours post MI?
Wavy red fibers (see slide 61 for image)
32
What will we see within 12-24 hours post MI?
Early coagulation necrosis
33
What will we see within 1-3 days post MI?
Peak neutrophil levels
34
What will we see within 3-7 days post MI?
Myocardial rupture
- All the mechanisms of wound healing have not occurred yet
- The actual site of the MI can rupture
KNOW THIS
35
What will we see after a couple months post MI?
Over a couple months, the wound healing will take over
Dense white tissue will form in the wall of the heart
36
List the possible complications following acute MI
- Contractile dysfunction
- Arrhythmias
- Myocardial rupture
- Pericarditis
- Right ventricular infarction
- Infarct extension
- Infarct expansion
- Mural thrombus
- Ventricular aneurysm
- Papillary muscle dysfunction or rupture
- Progressive late heart failure
37
What are the three types of myocardial rupture?
- Rupture of the free wall of the left ventricle
- Rupture of the papillary muscle
- Rupture of the ventricular septum
38
What does a rupture of the free wall of the left ventricle lead to?
Cardiac tamponade
Compression of the heart by an accumulation of fluid in the pericardial sac
39
What does a rupture of papillary muscle lead to?
Acute mitral valve incompetence
40
What does a rupture of the ventricular septum lead to?
Acutely acquired VSD (ventricular septal defect)
Eventually causes right heart failure
41
What is pericarditis?
Inflammation of the pericardium
- Occurs over time following an MI
- The area of the MI rubs against the pericardium causing inflammation
42
What is delayed Dressler's syndrome?
- An autoimmune inflammatory reaction to myocardial neo-antigens that form as a result of an MI
- Typically occurs 2 weeks post-myocardial infarction (up to a few months)
43
What is a ventricular aneurysm?
- A complication occurring post-MI
- Arises from a patch of weakened tissue in a ventricular wall
- Balloon or bubble filled with blood pouches out
- Usually doesn't burst, but can block blood flow out of the heart
44
What are some non-cardiac complications of MI?
- Acute pulmonary edema and congestion
- Hepatic congestion (acute and chronic)
- Splenic congestion
- Renal failure (congestive and/or ischemic)
- Systemic thrombo-embolism
- Cerebrovascular insufficiency (due to not pumping enough blood to take care of your brain)
45
What is the prognosis of a patient who has had an MI?
- 16% mortality within 30 days
- 5% mortality per year after that due to...
- 33% sudden death
- 33% re-infarction
- 33% CHF
46
Describe the etiology of coronary heart disease
Coronary heart disease is responsible for 1 in 5 deaths in the U.S.
- Massive killer
- Due to arthrosclerosis and coronary artery disease
47
What are therapeutic options for heart failure?
```
1 - Preventative measures
2 - Coronary care unit at hospital
3 - Thrombolytic therapy
4 - Stent placement
5 - CABG (coronary artery bypass graft)
```
48
What are the preventative measures?
- Diet
- Not smoking
- Blood pressure control
- Exercise
An ounce of prevention = a pound of
49
What is a thrombolytic therapy?
TPA
Give ASAP after occlusion to dissolve the clot
50
How many patients in the US have a CABG each year?
400,000
51
What do we make grafts out of?
- Reversed autologous saphenous vein
| - Left internal mammary artery (the only artery in the body that isn't affected by artherosclerosis)
52
How long does a saphenous vein graft last?
Long-term patency (openness) of saphenous vein grafts is only 50% at 10 years
53
How long a mammary artery graft last?
Greater than 90% of internal mammary artery grafts are patent (open) at 10 years.
