Ischaemic Heart Disease Flashcards
Stable Angina
• Chest pain w exertion or stress
• Due to atherosclerosis of coronary arteries with > 70% ‘stenosis
• Represents reversible injury to myocytes (20 mins only)
Symptoms-
Chest pain radiating to jaw or left arm (20mins)
Sweating
Sob
st segment depression on EKG
Due to subendocardial ischemia
Relieved by nitroglycerin (vasodilation of both veins and arteries, basically will act on vein, dilate them, decreasing the blood returning to the heart, resulting in decrease in preload causing decrease in stress and therefore better blood supply to the myocardial cells)
Unstable Angina
• Chest pain that occurs at rest
• Due to rupture of atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery
• Represents reversible injury to myocytes
• EKG shows ST-segment depression
Due to subendocardial ischemia
• Relieved by NG (same)
• High risk of progression to MI
Prinzmetal Angina
• Due to coronary artery vasospasm
Caused by almost complete occlusions
• Leads to episodic chest pain unrelated to exertion
• Represents reversible injury to myocytes
• EKG shows ST-segment elevation due to transmural ischemia
• Relieved by NG or calcium channel blockers
Ca channels relieve coronary artery vasospasm
Myocardial Infarction
• Necrosis of cardiac myocytes
• Due to rupture of atherosclerotic plaque with thrombosis and complete occlusion of coronary artery
• Other causes include coronary artery vasospasm, ( prinzmetal for more than 20mins) emboli, and vasculitis
• Severe, crushing chest pain (> 20 minutes) that radiates to left arm or jaw
• Diaphoresis
• Dyspnea
• Symptoms not relieved by NG
Infarction usually involves LV
• RV and both atria are generally spared
MI artery involved?
1- most common artery involved in MI is LAD (so ant wall of the LV and the ant portion of the inter-ventricular septum is involved)
2- RCA is second, post wall and post IV SEPTUM will be involved
3- left circumflex: lateral wall of LV
MI initial phase
• Subendocardial necrosis involving <50% of myocardial thickness
• EKG shows ST-segment depression
Lab tests for MI
1- Troponin I is most sensitive and specific marker
• Rises 2-4 hours after infarction
• Peaks at 24 hours
• Returns to normal by 7-10 days
2- CK-MB is useful for detecting
reinfarction days after MI
• Rises 4-6 hours after infarction
• Peaks at 24 hours
• Returns to normal by 72 hours
Done for reinfarction
MI Rx
• ASA/heparin (limit additional thrombosis)
• Supplemental 02 (minimise ischemia)
• Nitrates (dilatation of veins)
• B-blocker (slow heart rate; decrease o2 demand; decrease chances of arrhythmias)
• ACE inhibitor (decrease LV dilatation By blocking production of angiotensin 2.
1- That causes constriction of peripheral arterioles decreasing the afterload
2- blocks angiotensin that goes to the adrenal glands and increases release of aldosterone, causing a increase in blood volume.
• Fibrinolysis and angioplasty
Complications:
1- Contraction band necrosis ( due to Calcium acting on the contraction bands of the dead tissue)
2- Reperfusion injury (due to free radicals)
Stages of MI
1 day
Coagulative necrosis
Causes arrhythmias, congestive heart failure
1 week
Inflammation (neutrophils then macrophages)
Arrhythmias
1 month
Healing thru granulation tissue- fibrosis and scarring
Red border surrounding the necrosis
Aneurysms
Cordea tendini supplied by which artery?
RCA supplies these cords attached to the papillary muscles present on the mitral valve cusps
MI complications during inflammatory phase 1-7 days
1- neutrophils
Fibrinous pericarditis presenting as chest pain with friction rub.
This is because in transmural infarction the exudate will go out to the pericardium as well causing pericarditis
2- macrophage (eats up necrotic debris, the walls will be the weakest)
- cardiac tamponade caused by free wall rupture of LV leading to pooling of blood inside pericardium and surrounding + compressing the heart
- intravetricular septum rupture making a shunt b/w the RV and LV
- rupture of papillary muscle causing mitral insufficiency
Late complications of MI (6-8 weeks)
1- aneurysm
2- mural thrombus
3- Dressler syndrome:
Rare
Pericardial inflammation after a transmural infarct, exposing the pericardial tissue to the immune system resulting in antibody formation against the pericardium causing Autoimmune pericarditis
Sudden cardiac death
• Unexpected death due to cardiac disease
• Occurs without svmptoms or < 1 hour after symptoms arise
• Usually due, to fatal ventricular arrhythmias
•90% of patients have preexisting severe atherosclerosis
• Less common causes include mitral valve prolapse, cardiomyopathy, and cocaine abuse
Chronic ischaemic heart disease
• Poor mvocardial function
• Due to chronic ischemic damage (with or without infarction)
• Progresses to CHF
