I've learned a ton here recently about the heart.
I'm still in the LPN year of school, so I don't get to go into major detail until this fall. What I will say is that my Human Anatomy & Physiology courses are pretty much crucial to proper understanding of how everything works.
My teacher, also a male, explained the cardiac system beautifully in terms of plumbing.. which worked out great for me since my father used to be a plumber! It also explains nicely why people are usually on more than one blood pressure medication.
Basically, there's three things the drugs affect: contractility, preload, and afterload. Basically, this means blood before the heart, blood after the heart (peripheral resistance), and how hard the heart contracts. I'll explain each in basic terms I use to understand them.
Preload mainly affects CHF patients: they got too much fluid. This fluid is trying to enter the heart during diastole (when it's not pumping) to fill the right atrium, but there's just too much in the pipes. Expect this to be treated with Lasix or HCTZ; primarily they are diurectics (removing the fluid), but the secondary effect is lowered blood pressure because it reduces the amount of fluid being pushed into the heart during diastole.
Contractility is the force of the heart's pumping. Beta adrenergic receptor antagonists (beta blockers) are what affects this. Big word: it really scared the hell out of me when i first saw it, but it's actually pretty easy concept if we break that big word apart. Adrenergic means "adrenaline". Receptors are where the chemical/hormone/enzyme lands to cause an effect of some sort. Anatagonists means "goes against". So it's an adrenaline receptor blocker... this means that all the "receptors" that adrenaline activates on the heart are reduced: for the sake of the concept let's say they are cut in half. Since the beta blocker effectively "clogs" some of the receptor sites and renders them unusable, the heart will not contract as hard, reducing workload, and reducing the amount of oxygen the heart tissue itself needs.
Afterload means after the heart. The bad thing here is peripheral resistance. Imagine a garden hose with no nozzle: the water comes out steady, but there's not a lot of force behind it. Now, stick your thumb over the nozzle: you've got a mini pressure washer on your hands. Same is true for peripheral resistance: if those arteries or veins narrow you are essentially sticking your finger over the hose. The best way to medically treat this is with any sort of vasodilator. The bigger the pipes, the easier they flow. The ones you usually see are calcium (ca+) channel blockers. Calcium is important in muscle contraction; especially smooth muscle contraction. This means that the veins and arteries dilate rather than constrict and this eases up total peripheral resistance. Of course, there is some beneficial action in the heart itself related to calcium channel blockers, but this is just my understanding of a concept and not advanced hypertensive pharmacology.
So, now when I see that patient who is on Lasix, Norvasc, and Bisoprolol, I can visualize and understand that the Lasix reduces fluid in preload, Norvasc eases the amount of force the heart contracts, and Bisoprolol dilates the periphery. In my first nursing class, seeing two or three hypertensives on a client concerned me a bit and I started wondering about polypharmacy issues; my cardiac lecture put it in perspective pretty good.