Ch 11: Ischemic Heart Disease Flashcards
Your Grandfather (or Pop Pop, as you like to call him) tells you he has angina, but he can’t remember which kind. Help him out. Distinguish between the three kinds of angina, and talk about their major pathophysiologic differences from MI.
Stable angina occurs during exertion, unstable occurs at rest, and Prinzmetal is episodic pain unrelated to exertion.
Stable angina is chest pain lasting less than 20 minutes that radiates to the left arm or jaw, presenting with diaphoresis and shortness of breath. More than twenty minutes, same symptoms? MI.
For each of the anginas, this is a reversible ischemia (cellular swelling) with incomplete occlusion of the coronary artery.
In MI, this is a necrosis, and a complete occlusion of the coronary artery.
Stable angina and unstable angina will both have subendocardial ischemia, represented on the EKG as ST depression. Prinzmetal (Vasospastic) angina will be an ST elevation, and is due to transmural ischemia.
Nitroglycerin relieves the pain in all three – also, rest for stable, beta blockers for unstable, and calcium channel blockers for Prinzmetal. Nitroglycerin will not relieve the pain in an MI.
Anatomy review time! What is the most commonly affected chamber of the heart for MI, and what blood vessels service this regions? What patterns of necrosis can you predict based upon the distribution of these arteries?
Left ventricle is the most common infarct, sparing the other ventricle and atria. Left anterior descending artery is the most commonly involved artery in MI, hitting the anterior wall and anterior septum of the LV.
Right coronary artery is #2 most common, and will lead to an infarct of the posterior wall, septum, and papillary muscles of the LV.
Left circumflex artery will hit the lateral wall of the LV.
You repeat an EKG on a patient having an MI, and suddenly their ST segment has gone from depressed to elevated. What’s happened?
The MI has gone from the initial phase of infarction, <50% myocardial infarct, subendothelial, to the phase of continued or severe ischemia, where the myocardial wall is now majority infarcted – now it is transmural necrosis.
Describe the ideal patient for coronary heart disease.
Obese, hypertensive, smoker, diabetic, high cholesterol.
You finally get that coronary artery back open. What can you expect in the myocardium?
Fibrinolysis or angioplasty will open the blocked vessel. DON’T forget that reperfusion will lead to Ca++ influx, leading to hypercontraction of myofibrils (contraction band necrosis), and free radicals can damage myocytes.
Hypothermia may be used to decrease reperfusion injury.
Treatment for MI – we learned MONA therapy – ignore the morphine – what do the rest of the treatments do? How about BB, Ace inhibitors?
O2 – minimize ischemia
Nitrates – vasodilate coronary arteries, increase o2 supply
Aspirin and/or heparin – limit thrombosis
Beta blockers - reduce o2 demand
ACE inhibitor – decreases LV dilation
Your patient’s CK-MB spikes a few days after leaving the hospital for an MI. What happened?
Reinfarct. Use CK-MB to detect a reinfarct following an MI – the levels rise 4-6 hours after infarction, peak at 24 hours, and return to normal in 72 hours.
Troponin I, the gold standard, will rise 2-4 hours after infarct, peak at 24, and return to normal in 7-10 days.
Within one day of a MI, what can you expect?
Symptoms: cardiogenic shock, congestive heart failure. Arrythmia
Coagulative necrosis - no nuclei– pyknosis (condensation of chromatin), karyorrhexis (Fragmentation of nucleus)– karyolysis (dissolution of the chromatin) –
dark discoloration on gross appearance.
Within 1-3 days of an MI, what can you expect?
Inflammation - think white blood cells, a yellow appearance on gross exam.
Neutrophils -
Fibrinous pericarditis – in a transmural infarct, neutrophils will run out into the pericardium – get a friction rub and chest pain. A subendocardial infarct won’t get out into periphery, and you won’t get pericarditis.
Within 4-7 days of an MI, what can you expect?
Inflammation - think white blood cells, a yellow appearance on gross exam.
Macrophages will invade. If they rupture the ventricular wall – cardiac tamponade –
If they invade Interventricular septum – shunt
If they invade the Papillary muscles after a right coronary artery infarct - mitral insufficiency
Within 1-3 weeks of an MI, what can you expect?
1 week – granulation tissue – red border from edge of infarct – plump fibroblasts, collagen, blood vessels - precursor to the developing scar tissue.
Within 1 month of an MI, what can you expect?
After 1 month, you get a scar composed of type 1 collagen.
This fibrosis is weaker, and so you can get an aneurysm.
There is also a risk of mural thrombus due to stasis.
6-8 weeks after infarct, you can get dressler syndrome – autoimmune pericarditis.
Describe the difference between a subendothelial and a transmural infarct.
Subecondardial infarcts – hypoperfusion of the heart
Transmural infarct – full thickness – coronary artery occlusion
Collateral flow can limit the damage of an infarct, especially in a chronic hypoperfusion.
Your patient comes to your office to say hello, and dies as he’s standing there talking to your receptionist. As your staff is now understandably traumatized, describe sudden cardiac death, and what predisposes a patient to it.
Sudden cardiac death – without symptoms,
What is chronic ischemic heart disease, and what can it progress to?
Poor myocardial function leading to chronic ischemic damage, with or without infarct. It often will progress to CHF.
