Basic cardiovascular medications Flashcards
Describe the action of beta blockers
Beta-blockers are drugs that bind to beta-adrenoceptors and thereby block the binding of norepinephrine and epinephrine to these receptors. This inhibits normal sympathetic effects that act through these receptors.
Describe the action of calcium channel blockers
Calcium-channel blockers (CCBs) bind to L-type calcium channels located on the vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue (sinoatrial and atrioventricular nodes). These channels regulate influx of calcium into muscle cells, which in turn stimulates smooth muscle contraction and cardiac myocyte contraction. In cardiac nodal tissue, L-type calcium channels play an important role in pacemaker currents and in phase 0 of the action potentials. Therefore, by blocking calcium entry into the cell, CCBs cause vascular smooth muscle relaxation (vasodilation), decreased myocardial force generation (negative inotropy), decreased heart rate (negative chronotropy), and decreased conduction velocity within the heart (negative dromotropy), particularly at the atrioventricular node.
How do calcium channel blockers lower BP?
By causing vascular smooth muscle relaxation, CCBs decrease systemic vascular resistance, which lowers arterial blood pressure. These drugs primarily affect arterial resistance vessels, with only minimal effects on venous capacitance vessels.
What are the antiarrythmic properties of CCBs
CCBs are (Class IV antiarrhythmics). They decrease the firing rate of aberrant pacemaker sites within the heart AND decrease conduction velocity and prolong repolarization, especially at the atrioventricular node. This helps to block reentry mechanisms, which can cause supraventricular tachycardia.
How many classes of CCBs are there and what are they?
Dihydropyridines- usually used for hypertension
amlodipine felodipine isradipine nicardipine nifedipine nimodipine nitrendipine
Verapamil (phenylalkylamine class)- used for angina (by reducing myocardial oxygen demand and reversing coronary vasospasm) and arrhythmias.
Diltiazem (benzothiazepine class) is intermediate between verapamil and dihydropyridines in its selectivity for vascular calcium channels. By having both cardiac depressant and vasodilator actions, diltiazem is able to reduce arterial pressure without producing the same degree of reflex cardiac stimulation caused by dihydropyridines.
What type of drug is verapamil
A calcium channel blocker. Verapamil (phenylalkylamine class), is relatively selective for the myocardium, and is less effective as a systemic vasodilator drug. This drug has a very important role in treating angina (by reducing myocardial oxygen demand and reversing coronary vasospasm) and arrhythmias.
What is diltiazem
A calcium channel blocker- Diltiazem (benzothiazepine class) is intermediate between verapamil and dihydropyridines in its selectivity for vascular calcium channels. By having both cardiac depressant and vasodilator actions, diltiazem is able to reduce arterial pressure without producing the same degree of reflex cardiac stimulation caused by dihydropyridines.
What are the …..pine class of drugs?
The most smooth muscle selective class of CCBs are the dihydropyridines. Because of their high vascular selectivity, these drugs are primarily used to reduce systemic vascular resistance and arterial pressure, and therefore are used to treat hypertension. Extended release formulations or long-acting compounds are used to treat angina and are particularly effecting for vasospastic angina; however, their powerful systemic vasodilator and pressure lowering effects can lead to reflex cardiac stimulation (tachycardia and increased inotropy), which can offset the beneficial effects of afterload reduction on myocardial oxygen demand. Note that dihydropyridines are easy to recognize because the drug name ends in “pine.”
Dihydropyridines include the following specific drugs: (Go to www.rxlist.com for specific drug information)
amlodipine felodipine isradipine nicardipine nifedipine nimodipine nitrendipine
What are side effects of CCBs
Dihydropyridine CCBs (…..pine) can cause flushing, headache, excessive hypotension, edema and reflex tachycardia. Baroreceptor reflex activation of sympathetic nerves and lack of direct negative cardiac effects can make dihydropyridines a less desirable choice for stable angina than diltiazem, verapamil or beta-blockers.
What are contraindications of CCBs
The cardiac selective, non-dihydropyridine CCBs can cause excessive bradycardia, impaired electrical conduction (e.g., atrioventricular nodal block), and depressed contractility. Therefore, patients having preexistent bradycardia, conduction defects, or heart failure caused by systolic dysfunction should not be given CCBs, especially the cardiac selective, non-dihydropyridines. CCBs, especially non-dihydropyridines, should not be administered to patients being treated with a beta-blocker because beta-blockers also depress cardiac electrical and mechanical activity and therefore the addition of a CCB augments the effects of beta-blockade.
What is a partial agonist beta blocker
Some beta-blockers, when they bind to the beta-adrenoceptor, partially activate the receptor while preventing norepinephrine from binding to the receptor. These partial agonists therefore provide some “background” of sympathetic activity while preventing normal and enhanced sympathetic activity.
Describe the three generations of beta blockers
The first generation of beta-blockers were non-selective, meaning that they blocked both beta-1 (β1) and beta-2 (β2) adrenoceptors. Second generation beta-blockers are more cardioselective in that they are relatively selective for β1 adrenoceptors. Note that this relative selectivity can be lost at higher drug doses. Finally, the third generation beta-blockers are drugs that also possess vasodilator actions through blockade of vascular alpha-adrenoceptors.
Describe the effect of beta blockers on the heart
Beta-blockers bind to beta-adrenoceptors located in cardiac nodal tissue, the conducting system, and contracting myocytes. The heart has both β1 and β2 adrenoceptors, although the predominant receptor type in number and function is β1. These receptors primarily bind norepinephrine that is released from sympathetic adrenergic nerves. Additionally, they bind norepinephrine and epinephrine that circulate in the blood. Beta-blockers prevent the normal ligand (norepinephrine or epinephrine) from binding to the beta-adrenoceptor by competing for the binding site.
Because there is generally some level of sympathetic tone on the heart, beta-blockers are able to reduce sympathetic influences that normally stimulate chronotropy (heart rate), inotropy (contractility), dromotropy (electrical conduction) and lusitropy (relaxation). Therefore, beta-blockers cause decreases in heart rate, contractility, conduction velocity, and relaxation rate. These drugs have an even greater effect when there is elevated sympathetic activity.
Describe the mechanism of action of morphine
Morphine and its metabolites act as agonists of the mu and kappa opioid receptors.1 The mu-opioid receptor is integral to morphine’s effects on the ventral tegmental area of the brain. Morphine’s activation of the reward pathway is mediated by agonism of the delta-opioid receptor in the nucleus accumbens,2 while modification of the respiratory system and addiction disorder are mediated by agonism of the mu-opioid receptor.3
What is adenosine used for and why?
The major therapeutic use of adenosine is as an antiarrhythmic drug for the rapid treatment of supraventricular tachycardias. Its supression of atrioventricular conduction makes it very useful in treating paroxysmal supraventricular tachycardia in which the AV node is part of the reentry pathway (as in Wolff-Parkinson-White Syndrome). For these indications, adenosine is administered either as bolus intravenous injection or as an intravenous infusion.
For which patients is adenosine contraindicated?
adenosine may produce undesirable AV block; however, this is usually rapidly corrected by stopping adenosine administration. Therefore, adenosine is contraindicated in patients with preexisting second or third degree AV block.
Describe the mechanism of action of ACE inhibitors
ACE inhibitors produce vasodilation by inhibiting the formation of angiotensin II. This vasoconstrictor is formed by the proteolytic action of renin (released by the kidneys) acting on circulating angiotensinogen to form angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme.
ACE also breaks down bradykinin (a vasodilator substance). Therefore, ACE inhibitors, by blocking the breakdown of bradykinin, increase bradykinin levels, which can contribute to the vasodilator action of ACE inhibitors. The increase in bradykinin is also believed to be responsible for a troublesome side effect of ACE inhibitors, namely, a dry cough.
Describe action of ACE inhibitors
Dilate arteries and veins by blocking angiotensin II formation and inhibiting bradykinin metabolism. This vasodilation reduces arterial pressure, preload and afterload on the heart.
Down regulate sympathetic adrenergic activity by blocking the facilitating effects of angiotensin II on sympathetic nerve release and reuptake of norepinephrine.
Promote renal excretion of sodium and water (natriuretic and diuretic effects) by blocking the effects of angiotensin II in the kidney and by blocking angiotensin II stimulation of aldosterone secretion. This reduces blood volume, venous pressure and arterial pressure.
Inhibit cardiac and vascular remodeling associated with chronic hypertension, heart failure, and myocardial infarction.
What are the …pril drugs
ACE inhibitors benazepril captopril enalapril fosinopril lisinopril moexipril quinapril ramipril
What is the most common side effect of ACE inhibitors?
A common, annoying side effect of ACE inhibitors is a dry cough appearing in about 10% of patients. It appears to be related to the elevation in bradykinin.
What is the risk of administering ACE inhibitors to patients with bilateral renal artery stenosis?
Patients with bilateral renal artery stenosis may experience renal failure if ACE inhibitors are administered. The reason is that the elevated circulating and intrarenal angiotensin II in this condition constricts the efferent arteriole more than the afferent arteriole within the kidney, which helps to maintain glomerular capillary pressure and filtration. Removing this constriction by blocking circulating and intrarenal angiotensin II formation can cause an abrupt fall in glomerular filtration rate. This is not generally a problem with unilateral renal artery stenosis because the unaffected kidney can usually maintain sufficient filtration after ACE inhibition; however, with bilateral renal artery stenosis it is especially important to ensure that renal function is not compromised.
Describe mechanism of action of Angiotensin Receptor Blockers (ARBs)
These drugs have very similar effects to angiotensin converting enzyme (ACE) inhibitors and are used for the same indications (hypertension, heart failure, post- myocardial infarction). Their mechanism of action, however, is very different from ACE inhibitors, which inhibit the formation of angiotensin II. ARBs are receptor antagonists that block type 1 angiotensin II (AT1) receptors on blood vessels and other tissues such as the heart. These receptors are coupled to the Gq-protein and IP3 signal transduction pathway that stimulates vascular smooth muscle contraction. Because ARBs do not inhibit ACE, they do not cause an increase in bradykinin, which contributes to the vasodilation produced by ACE inhibitors and also some of the side effects of ACE inhibitors (cough and angioedema).
What are some ARBs generic and brand names?
Examples include candesartan (Adesan, Atacand), eprosartan (Teveten), irbesartan (Abisart, Avapro, Karvea), losartan (Cozaar, Cozavan), olmesartan (Olmetec), telmisartan (Micardis, Mizart) and valsartan (Diovan)..
What is the drug class ending in ….sartan
Angiotensin Receptor Blockers (ARBs)
