Unit 6.3 anti-anginas and peripheral vasodilation chapter 24 and pg 448

Question Answer
vasodilators act direction on arterial venous smooth muscle to cause relaxation – they do not work through adrenergic receptors
direct acting vasodilators are useful as hypertensive drugs because of their ability to cause peripheral vasodilation
diazoxine, hydraliazine, and minoxidil work primarily through arteriolar vasodilation
sodium nitroprisside has both arteriolar and venous effect
sodium notrprsside and intravenous diazoxide are reserved for hypertensive emergencies
contraindications for vasodilators includes hypotension, cerebral edema, head injury, acute MI, and coronary artery disease
ADE of vasodilators dizziness, headache, anxiety, tachycardia, edema, dyspnea, nausea, vomiting, diarrhea, hepatitis, systemic lupus
with minoxidil overdose toxicity norepinephrine and epinephrine should not be used to revers the hypotension because of the possibility of excessive cardiac stimulation
acute coronary syndrome (ACS) a spectrum of clinical presentations compatible with acute myocardial ischemia
angina pectoris chest pain that ocucse when the hearts supple of blood carrying oxygen is insufficient to meet demands of the heart
atherosclerosis common for of arteriosclerosis involving deposits of fatty cholesterol containing material within arterial walls
chronic stable angina chest pain that is primarily caused by atherosclerosis which results in long term but relatively stable levels of obstruction in one or more coronary art
coronary arteries arteries that deliver oxygen carrying blood to the heart muscle
coronary artery disease (CAD) any one of the abnormal conditions that can affect the arteries of the heartq
ischemia poor oxygen supply
ischemic heart disease poor blood supply to the heart via the coronary arteries
MI necrosis of the myocardium following interruption of blood supply. almost always caused by atherosclerosis of the coronary arteries
reflex tachycardia rapid heartbeat cause by a variety of ANS effects such as blood pressure changes, fever, or emotional stress
unstable angina clinical presentation of acute coronary syndrome with cardiac ischemia, without persistence ST segment elevation on ECG
vasospastic angina ishchemia induced myocardial chest pain cause by spasms of the coronary arteries
the pain of angina is a result of under ischemic conditions when heart is deprived of oxygen it shifts to anaerobic metabolism to meet energy demands – byproduct is lactic acid
accumulation of lactic acid and other mediators such as bradykinin and adenosine stimulate the pain receptors surrounding the heart which produces the heart pain known as angina
unstable angina is the most dangerous and clinical presentation of acute coronary syndrome (ACS)
unstable angina diagnose by meeting one or more of the following criteria 1, angina at rest 2. recent onset 3. increase of severity of angina
three types of drugs that are used to treat angina pectoris nitrites/nitrates, B-blockers, calcium channel blockers
nitrate action dilate all blood vessels – prediminantly affect venus vascular beds; however they also have dose dependent arterial vasodilation effect
nitrates have a particularly notable effect on dilating the coronary arteries, both large and small – which causes redistribution of blood and therefore oxygen to previously ischemic tissue
nitrates produce a reduced after load due to its dose dependent relaxation of arteries in addition to its decreased left ventricular tension
contraindications of nitrates severe anemia, closed angle glaucoma, hypotension, and severe head injury
tolerance to abtianginal effect of nitrates can occur surprisingly quickly in some patients, especially in those taking long acting formulations
to prevent tolerance a regular nitrate free period is arranged to allow certain enzymatic pathways to replenish themselves
nitrates interactions alcohol, B-blockers, CCBs , phenothiazines, and erectile dysfunction drugs
B-blockers are the common mainstay in treatment of cardiovascular disease – including anging, MI, hypertension, and dysrhythmias
the physiological act of systole requires energy in the form of adenosine triphosphate (ATP) and oxygen
when B-receptors are blocked by B-blockers the rate at which the pacemaker (SA node) fires decreases, and the time it takes for the node to recover increases
B-blockers also slow conduction through the AV node and reduce myocardial contractility (negative inotropic effects)
B-blockers also have many therapeutic effects after MI – they block the harmful effects of circulating catecholamines (norepinephrine, and epinephrine)
B-blockers also suppress the activity of hormone renin, which is the first step in the renin-aldosterone-angiotensin system
renin is a potent vasoconstrictor release by ht kidneys hone they are not being adequately perfused
when B-blockers inhibit the release of renin blood vessels to and in the kidney dilate causing reduced blood pressure
B-blockers are most effecting in the treatment of exertional angina – because the usual increase in heart rate and systolic BP due to exercise or stress is blunted by these drugs
ADE of B-blockers decrease HR and output, bronchoconstriction, hypoglycaemia, fatigue, insomnia, and weakness
three types of calcium channel blockers (CCBs) phenylalkylamines, benzodiazepines, and dihydropyridines
CCB's used in treatment of chronic stable angina are diltiazem, amlodipine, nifedipine, and verapamil hydrochloride
preventing calcium from entering into the process that occurs in the heart prevents muscle contraction and promotes relaxation – relaxation of the smooth muscles surround the coronary artery causes them to dilate
dilation increases blood flow to the ischemic heart, which in turn increases the oxygen supply and helps shift supply-demand ratio back to normal
dilation from calcium channel blockers also occurs in the arteries throughout the body which results in a decrease in the force against which the heart has to exert when delivering blood to the body
another effect of CCB's is depression of the automaticity of and conduction through the SA and AV nodes. (useful in treating cardiac dysrhythmia's)
CCB's are considered first line drugs for the treatment of angina, hypertension, and supra ventricular tachycardia
CCB's are not as effective as B=blockers at blunting exercise induced elevations inherit rate and BP
CCB contraindications acute MI, second or third degree AV block and hypotension
CCB's interact with grapefruit juice which can increase bioavailability of CCB's

Leave a Reply

Your email address will not be published. Required fields are marked *