Beta-blockers block vasoconstriction, decrease heart rate, decrease heart rate, decrease cardiac muscle contraction and tend to increase blood flow to the kidneys leading to a decrease in the release of renin.
Alpha Agonists stimulate the alpha receptors in the central nervous system and inhibit the cardio-vascular centers, leading to a decrease in symphatetic outflow from the CNS and a resultant drop in blood pressure.
Most calcium channel blockers decrease the force of contraction of the myocardium (muscle of the heart). This is known as the negative inotropic effect of calcium channel blockers. It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with cardiomyopathy .
Many calcium channel blockers also slow down the conduction of electrical activity within the heart, by blocking the calcium channel during the plateau phase of the action potential of the heart
The class I antiarrhythmic agents interfere with the sodium channel . Class I agents are grouped by what effect they have on the Na+ channel, and what effect they have on cardiac action potentials .
Class 1 agents are called Membrane Stabilizing agents. The 'stabilizing' is the word used to describe the decrease of excitogenicity of the plasma membrane which is brought about by these agents. (Also noteworthy is that a few class 2 agents like propranolol also have a membrane stabilizing effect .)
Class I agents are divided into three groups (1a, 1b and 1c) based upon their effect on the length of the action potential.
1A lengthens the action potential (right shift)
1B shortens the action potential (left shift)
1C does not significantly affect the action potential (no shift)
Class II agents are conventional beta blockers . They act by blocking the effects of catecholamines at the β1-adrenergic receptors , thereby decreasing sympathetic activity on the heart. These agents are particularly useful in the treatment of supraventricular tachycardias . They decrease conduction through the AV node .
Class II agents include atenolol , esmolol , propranolol , and metoprolol .
Class III agents predominantly block the potassium channels , thereby prolonging repolarization. Since these agents do not affect the sodium channel, conduction velocity is not decreased. The prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias. (The re-entrant rhythm is less likely to interact with tissue that has become refractory).
Class IV agents are slow calcium channel blockers . They decrease conduction through the AV node , and shorten phase two (the plateau) of the cardiac action potential. They thus reduce the contractility of the heart, so may be inappropriate in heart failure. However, in contrast to beta blockers, they allow the body to retain adrenergic control of heart rate and contractility.
Nitrates cause vasodilation of the venous capacitance vessels by simulating the endothelium-derived relaxing factor (EDRF). Used to relieve both exertional and vasospastic angina by allowing venous pooling, reducing the pressure in the ventricles and so reducing wall tension and oxygen requirements in heart. Short-acting nitrates are used to abort angina attacks that have occurred, while longer-acting nitrates are used in the prophylactic management of the condition.
Agents include nitroglycerin (glyceryl trinitrate) or pentaerythritol tetranitrate .
Calcium ion (Ca++) antagonists ( Calcium channel blockers ) are used in the treatment of both exertional and vasospastic angina. In vitro, they dilate the coronary and peripheral arteries and have negative inotropic and chronotropic effects - decreasing afterload , improving myocardial efficiency, reducing heart rate and improving coronary blood flow. In vivo , the vasodilation and hypotension trigger the baroreceptor reflex. Therefore the net effect is the interplay of direct and reflex actions.
Class I antiarrhythmic agents have the most potent negative inotropic effect and may cause heart failure.
Class II agents do not depress conduction or contractility.
Class III agent has negligible inotropic effect and causes almost no reflex tachycardia .
Examples include Class I agents ( e.g. , verapamil ), Class II agents ( e.g. , amlodipine , nifedipine ), or the Class III agent diltiazem .
There are several classes of hypolipidemic drugs. They may differ in both their impact on the cholesterol profile and adverse effects. For example, some may lower the "bad cholesterol" low density lipoprotein (LDL) more so than others, while others may preferentially increase high density lipoprotein (HDL), "the good cholesterol". Clinically, the choice of an agent will depend on the patient's cholesterol profile , cardiovascular risk , and the liver and kidney functions of the patient, evaluated against the balancing of risks and benefits of the medications. In the United States, this is guided by the evidence-based guideline from the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATPIII).
bile acid sequestrants (resins) are particularly effective for lowering LDL-C by sequestering the cholesterol-containing bile acids released into the intestine and preventing their reabsorption from the intestine. It decreases LDL by 15-30% and raises HDL by 3-5%. It has little effect on triglycerides but can cause a slight increase. Bile acid sequestrants may cause gastrointestinal problems, and may also reduce the absorption of other drugs and vitamins from the gut.
Localizes in the brush border of the small intestine and inhibits the absorption of cholesterol from the small intestine thus less cholesterol is delivered to the liver dropping the serum cholesterol level.
An anticoagulant is a substance that prevents coagulation ; that is, it stops blood from clotting. A group of pharmaceuticals called anticoagulants can be used in vivo as a medication for thrombotic disorders.
The oral anticoagulants are a class of pharmaceuticals that act by antagonizing the effects of vitamin K . Examples include warfarin . It is important to note that it takes at least 48 to 72 hours for the anticoagulant effect to develop fully. In cases when any immediate effect is required, heparin must be given concomitantly. Generally, these anticoagulants are used to treat patients with deep-vein thrombosis (DVT), pulmonary embolism (PE), atrial fibrillation (AF), and mechanical prosthetic heart valves .
[ edit ] Adverse effects
Patients aged 80 years or more may be especially susceptible to bleeding complications with a rate of 13 bleeds per 100 person-years. 
These oral anticoagulants are used widely as poisons for mammalian pests, especially rodents .
An antiplatelet drug is a member of a class of pharmaceuticals that decreases platelet aggregation and inhibits thrombus formation. They are effective in the arterial circulation, where anticoagulants have little effect.
They are widely used in primary and secondary prevention of thrombotic cerebrovascular or cardiovascular disease.
Aspirin irreversibly inhibits the enzyme COX, resulting in reduced platelet production of TXA2 (thromboxane - powerful vasoconstrictor which lowers cyclic AMP and initiates the platelet release reaction).
Dipyridamole inhibits platelet phosphodiesterase, causing an increase in cyclic AMP with potentiation of the action of PGI2 – opposes actions of TXA2
Clopidogrel affects the ADP-dependent activation of IIb/IIIa complex
Glycoprotein IIb/IIIa receptor antagonists block a receptor on the platelet for fibrinogen and von Willebrand factor. 3 classes:
Murine-human chimeric antibodies (e.g. abciximab)
Synthetic peptides (e.g. eptifibatide)
Synthetic non-peptides (e.g. tirofiban)
Epoprostenol is a prostacyclin which is used to inhibit platelet aggregation during renal dialysis (with or without heparin) and is also used in primary pulmonary hypertension.