drugs for angina, MI and CVA Flashcards
what is atherossclerosis
this is when the arterial blood supply is compromised due to narrowing and the cardiovascular and cerebrovascular supply becomes impaired
what are deprived of nutrients with atherosclerosis since blood and cerebral vascular flow are impaired
heart brain and other organs
angina pectoris, acute MI and cerebral vascular accident are all results of what
atherosclerosis and poor blood supply
endothelial injury and inflammation result in what cells migrating
immune cells to the site of injury
when are tight junctions between cells loosened
when there is endothelial injury
what is going to go into the tight junstions of cells if they are loosned
LDL
what are foam cells
this is when macrophages engulf oxdized LDL
when t-lymphocytes secrete cytokines inducing smooth muscle migration, what happens to blood vessel elasticity and responsiveness
impiares bloof vessel elasticity and responsiveness to stimuli
angina pectrois is what kind of issue
it is a demand issue
what is angina pectoris
this is acute chest pain arising from inadequate oxygen supply to the myocardium
what is characterized by a steady, intense pain that is sometimes accompanies by a crushing, constricting sensation
angina pectoris
your patient comes in with pain radiating across the left shoulder, down the left arm, they are pallor, SOB, and sweating - what do you suspect is happening
the patient is experiencing angina pectoris
what might a female patient with angina pectoris experience
nausea, abdominal pain
stable angina
predicatble frquency, duration and intensity, not associated with myocardial damage
unstable angina - intensity, variable period, frequency
variable intensity, occurs during period of rest, inceased frequncy
what is associated with an increased risk of MI
unstable angina
non-pharmacological interventions for stable angina
limit alcohol, foods high in cholestoroal, control hyperlipidemia, control hypertension, regular exercise, control blood glucose
limit alcohol, foods high in cholestoroal, control hyperlipidemia, control hypertension, regular exercise, control blood glucose
non-pharmacological interventions for stable angina
what is the goal of drug therapy
slow HR, reduce force of cardiac contraction, dilate veins, dilate arterioles
what is the first line therapy for stable angina
nitrates
what do nitrates do
they facilitate the formation of nitric acid, a potent dialator for smooth muscle
nitrate; what does the dilation of smooth muscle allow for; blood flow
decreased the amount of blood returning to the heart, CO, workload, O2 demand
decreases the amount of blood returning to the heart, CO, workload, O2 demand
nitrate
nitrates; what does the dilation of arterial smooth muscle do to blood flow and oxygen supply
increases blood flow and improves oxygen supply to the myocardium
what is the protocol for taking nitrate
rest, take drug and wait 5 min, if no imporvement take another dose wait 5 min
what is the maximum dose for nitrates
3 doses in 15 minutes
how should you withdrawl a patient off of nitrate
slowly to prevent risk of MI
adverse effects for nitrates
all rt vasodilation and decrease in blood flow - headache, dizziness weakness, hypotension, relfex tachycardia
your patient recently had angina, and is experiencing a headache and hypotension. they ask why this is happening - why
because there is vasodilation and decreased blood flow
when should you be cautious when giving nitrates
wiht pt with hypotension, hypovolemia
what drug interactions are there for nitrates
treatment for ED, alcohol
why dont you want your patient to take nitrates when they are on ED medications and drinking alcohol
because they both cause vasodliation, so could lead to hypotension
beta adrenergic antagonists are first line therapy for what- angina pectoris
first like therapy for chrinic stable angina
hwo to beta adrenergic antagonists work
they work to reduce the cardiac workload, which slows the HR and reduces contractilitiy
what works to reduce cardiac workload, slows HR and contractibility
beta adrenergic antagonists
when should you be careful when usings beta adrenergeric antogonists (4)
asthma, COPD, depression and diabetes
adverse effects of beta adrenergic antagonists - think weakness
fatigue, weakness, bradycardia, hypotension, sleep distubrances
how should you take a patient off of beta adrenergic antagonist drugs
reduce the does over 1-2 weeks
why arent calcium channel blockers firts line therapy for angina?
because they can cause low bp
calcium channel blockers are used for the prevention of what angina, and in clients whom cannot tolerate what
the prevention of chronic stable angina in clients who cannot tolerate beta blockers
what causes decreased myocardial demand, relax arteriolar smooth muscle lowering BP and decreasing afterload, and decreases heart rate
calcium channel blockers
adverse effects of CCB
dizziness, lightheadedness, fatigue, bradycardia, flushing, nausea
what should you monitor for with someone taking ccb
hypotension, and reflex tachycardia
why should grapefruit juice be avoided when on ccb
because it will increase the ccb levels
what is myocardial infarction a result of what disease
result of advanced coronary artery disease
what happens when a coronary artery is occluded
MI and necrosis
what are the goals of MI therapy
reduce myocardial oxygen demand
restore blood supplt to the damaged myocardium
thrombolytics - MI
restore blood supply to the damamged myocardium
nitrates, beta blockers, ACE inhibitors - are used to prevent what demand?????
to reduce myocardial oxyegn demand and to prevent further infarction
what is used to control or prevent MI-associated dysrhythmias
beat blockers
what is used to reduce post-MI mortality
aspirin, beta-blockers, ace inhibitors, statins
how do we manage severe pain and anxiety of MI
opiates
warning signs of stroke
paralysis on one side, vision issues, dizziness, speech problems, headache
true or false
80% of strokes are thrombotic and 20% are hemorrhagic
trie
how can we pharmacologically treat thrombotic CVA
thrombolytics
