Ischemic Heart Disease Flashcards
What is the primary cause of ischemic heart disease/MI?
Other causes?
- atherosclerosis (>90%)
- vasospasm (due to platelet aggregation or drugs, ie. cocaine and ephedrine)
- emboli (formed in LA due to a-fib)
- vasculitis/hematologic abnormalities
How long does it take for loss of contractility and irreversible myocardial damage to occur in an MI?
- loss of contractility <2 min
- permanent, irreversible damage ~30 mins
What are the classic symptoms of an MI?
- “crushing/stabbing” substernal chest pain
- possible radiation to back, shoulder, or jaw
- diaphoresis
- N/V
- dyspnea
What serum marker can be used to detect an MI?
- troponin (T/I); most sensitive and specific
- CK-MB; sensitive, no specific
- myoglobin; not specific
What is important to note about using serum marker in diagnosing an MI?
serum marker may not be elevated in the first 3 hours of an MI
- serial draws are necessary to rule out MI
- CK-MB returns to normal within 2-3 days of infarction; can be used to assess reinfarction
- troponin remains elevated for >5 days
What are the most common coronary vessels affected by MI?
What porions of the heart are affected with each?
left anteiror descening (LAD):
- apex, anterior LV wall, and anteiror 2/3 of septum
- most common (40-50%)
right cornary artery (RCA):
- (posterior descending branch only) posterior LV wall, posterior 1/3 of septum
- (proximal, in RCA) entire RV wall, + posterior descending
- 30-40%
left circumflex:
- lateral LV wall
- 15-20%
How does damage during an MI progress?
- intial damage occurs to inner most myocardium; most distant from coronary arteiries
- damage progresses externally until it is transmural with increased duration of infarction
if reperfusion occurs, damage may be limited to a subendocardial infarct
How does the appearance of the heart and cardiac tissue change following MI?
first 30 mins -> no change
30 mins - 4 hrs -> wavy fibers
4 - 12 hrs -> edema, early necrosis
12 - 24 hrs -> dark mottling; progressive necrosis (pyknosis, hypereosinophilia), early neutrophils
1 -3 days-> yellow-tan mottling; loss of nuclei, neutrophil infiltrates
3 - 7 days -> hyperemic border; macrophages
7 - 10 days -> depressed margins; granulation tissue
10 - 14 days -> collagen deposition
2 - 8 wks -> gray-white scar; continued collagen deposition
>2 mo -> complete scar
What is the first microscopic sign of irreversible myocardial injury?
When is it seen?
wavy fibers; viabale fibers at border of infarct pull adjacent dead fibers
-seen within 30 mins - 4 hrs
What is the first gross sign of irreversible myocardial injury?
When is it seen?
staining of myocardium with triphenyltetrazolium which binds lactate dehydrogenase (only found in live myocardium) turning it bright red
- infarcted areas and scars are not stained
- 2 - 3 hours
When is dark mottling first seen following an MI?
12 hrs - 1 day, by 1 day
When is central yellow infarct seen first seen following an MI?
1 - 3 days, by day 3
When is neutrophillic infiltration first seen following an MI?
1 - 3 days, by day 3
When is loss of myocardial nuclei first seen following an MI?
1 - 3 days, by day 3
When is a macrophage infiltrate first seen following an MI?
3 - 7 days, by 1 week
When is granulation tissue first seen following an MI?
1 - 2 wks, by 2 weeks
When is scaring/repair comlete following an MI?
by 2 months
What complications are seen with an MI and when?
Early (within 24 hours):
- lethal arrhythmia
- cardiogenic shock
Intermediate (>2-4 days):
- rupture of wall, septum or papillary muscles
- acute pericarditis (during neutrophil/macrophage infiltration)
Late (>2wks):
- chronic/immune pericarditis (Dressler syndrome)
- ventricular aneurysm
- heart failure
- arrhythmia
What is the most common cause of death due to an MI?
fatal arryhthmia, V-fib, within 24 hours of onset
What arrhythmias can be seen following an MI?
How does MI cause them? (some of the explanations are my best guesses to help understand why)
caused by conduction delays or irritabililty
- sinus bradycardia (conduction delay, SA/AV node damage?)
- A-fib (conduction delays, catches post-refractroy period)
- heart block (septal involvement, LAD and RCA/PDA?)
- tachycardia (compensatory for decreased CO?)
- V-tach (can progress to V-fib)
- V-fib (lethal) (conduction delays, catches post-refractroy period)
How does MI lead to cardiogenic shock?
too large of a portion of the mycardium is damaged to sustain adequate systemic perfusion
How does MI cause rupture?
What complications can occur due to this?
necrosis following MI weakens wall
Free wall rupture:
- blood into pericardium -> cardiac tamponade
- most common rupture, common cause of intermediate death (still after arrhythmia)
Septal rupture:
-VSD formation -> L-to-R shunt
Papillary muscle rupture:
- mitral incompitanc/regurgitation
- least common rupture
What is Dressler syndrome and how does MI cause it?
chronic, immune-mediated fibrinous pericarditis
damage of myocytes releases myocardial proteins which the immune system may recognize
How does Dressler sydrome present?
- pleuritic chest pain + friction rub
- dry cough
- fever
What is angina pectoris?
transient, possibly recurrent ischemia that is insufficient to cause infarction
-usually last for seconds to 15 mins
What are the types of angina pectoris?
(compare)
Stable angina:
- predictable, induced by activity/stress
- relieved by rest and vasodilators
Prinzmetal angina:
- induced by cornary A. vasospasm
- relieved by vasodilators
- not induced by activity/stress; not relieved by rest
Unstable angina:
- unpredictable, can occur at rest
- “crescendo pattern”; progressively worse and more frequent -> can evolve into NSTEMI
- caused by ruptured or growing plaque
What conditions are associated with increased risk of ischemia but may also obscure the perception of ischemic pain?
- diabetes (neuropathy)
- age
