angina pectoris Flashcards
angina pectoris is a manifestation of?
coronary artery disease but also a disorder itself
angina=
angina= pain
pectoris= chest
chest pain
what kind of pain?
ischemic pain
-inadequate perfusion to area of heart wall, not meeting demand
etiology of angina pectoris?
- d/t atherosclerosis in most cases
- thrombus
- hemorrhage
- vasospasm (vessel constricts and stays in constricted position, tissue distal is ischemic)
pathophysiology of angina pectoris?
arteries NORMALLY dilate on demand BUT if vessel has atherosclerotic change it may be already compensating by vasodilating and CANT any further!
—> inadequate perfusion —> ischemic —> chest pain
manifestations of angina pectoris?
- CHEST PAIN
-heart wall is impacted from vessels in coronary circuit not providing adequate blood and oxygen to heart cells
-“squeezing, burning” pain
-transient to severe
-radiates to UPPER ARM SHOULDER NECK JAW
typically LEFT UPPER ARM and SHOULDER
types of angina?
stable
variant/vasospastic/prinzmetals
unstable
what is stable angina?
FIXED plaque within wall of vessel
PROTRUDING into lumen
at REST, pt has enough adequate blood flow
PAIN occurs when metabolic demand of heart INCREASES
d/t:
a) exertion (physical activity)
b) emotional stress
c) cold- vessels automatically constrict to reduce BF to periphery so heat is not lost, causes systemic response and arteries, decreased BF to heart
^^ all perfusion to heart is IMPAIRED= pain
what is unstable angina?
atheroma/plaque can rupture through wall of vessel into lumen, causing bleeding
-atheroma contains necrotic and foam cells that LEAK out fibrin and cell debris and platelets
-THROMBUS forms in lumen once plaque ruptures and has potential to dislodge “unstable”
-prostaglandin released from platelet aggregation —> triggers vasospasm —> vessel constricts —> cuts off lumen even further
PAIN more SEVERE, LONGER PAIN
-cannot withdraw trigger! pain occurs ANYTIME, ECG changes
what is variant/vasospastic/prinzmetals angina?
- SPASM of artery in CORONARY circuit
- unclear etiology, could be:
a) abnormal epithelium- SM in vessel wall constricting when doesnt need to
b) calcium ions- calcium channel blocked, SM cells inadequately handling Ca
c) sympathetic ns- hyperactivity of SNS, excessive stimulation of SM cells
d) nitric oxide- chemical compound involved in vasodilation, if decreased conc, vasoconstriction - triggered at ANYTIME
- TRIGGER UNKNOWN so difficult to manage
- DIFFICULT TO ASSESS bc can not be triggered on demand when usually u would watch the ECG by triggering angina
treatment of angina?
-rest/cease activity
-nitroglycerin!! (increase nitric oxide in cells, vasodilator)
comes in aerosal spray, patch, sublingual
systemic vasodilation
-avoid trigger to prevent recurrent episodes and decrease risk of MI!