Aim for a blood pressure under 130 over 80 in adults. The real goal is not the number — it is fewer heart attacks, strokes and failing kidneys. Everyone gets lifestyle advice as well as any tablets.

The whole decision hangs on one thing: does this person have a compelling indication? That means another condition — heart failure or diabetes, for instance — where one particular family of blood-pressure drug has actually been proven to make people do better.

• No compelling indication → start a thiazide diuretic for most people. They are proven to reduce deaths, well tolerated, and cheap.
• With one → start the class proven to help that condition, and add others later if the pressure is still high.

Here is the catch worth remembering: ACE inhibitors, ARBs and calcium channel blockers bring the number down just as well as a thiazide. They may not keep people alive as well. Lowering the reading and improving the outcome are two different achievements.

Two families are deliberately not used to start with — the centrally acting sympatholytics and the direct-acting vasodilators. They cause too many side effects to be a sensible first move.

Beta blockers switch off the receptors adrenaline works through in the heart. The heart then beats more slowly and less hard, so it pushes out less blood — which is how the pressure comes down.

Note where this comes from: your textbook explains beta blockers in a chapter your course does not assign, so this card is built from your instructor's slides.

What they are for: high blood pressure, heart failure, abnormal rhythms, after a heart attack, and ordinary exertional angina — but not the variant kind. Non-selective ones are also used for migraine prevention and glaucoma.

The split that gets tested:

• Non-selective (propranolol, nadolol, timolol) hit β₁ in the heart and β₂ in the lungs. The β₂ part tightens airways, so avoid them in asthma and COPD.
• Cardioselective (metoprolol, atenolol, bisoprolol) mostly hit β₁ only, so they are safer if the lungs are mildly affected.

Side effects: tiredness, a slow pulse, and wheeze. They also worsen heart block, so avoid them in anyone who already has it.

One reversal worth knowing: until the mid-1990s heart failure was considered an absolute reason never to give a beta blocker. That is no longer true. And metoprolol appears safe for a breastfeeding baby.

ACE inhibitors do two things at once, and every effect — helpful or not — comes from one of them: they cut angiotensin II, and they raise bradykinin.

Less angiotensin II means blood vessels relax (mostly the small arteries), the kidneys hold on to less fluid, and — most importantly — the heart and blood vessels stop being remodelled into a worse shape. That last one is why these drugs help people live longer, not just show a better reading.

• Cough comes from the bradykinin side.
• High potassium and harm to a fetus come from the ACE side.

This explains ARBs. They block angiotensin II at the receptor instead, and they leave bradykinin alone — so they cause much less cough, which is the usual reason people give up on an ACE inhibitor. Lisinopril is the typical ACE inhibitor; losartan the typical ARB.

The renin–angiotensin–aldosterone system is the body's own blood-pressure control loop. It sets pressure, blood volume, and the balance of salt and water — and it is also the thing that goes wrong in high blood pressure, heart failure and after a heart attack.

It works through two chemicals: angiotensin II and aldosterone.

Angiotensin II does two obvious things, and both push pressure up: it squeezes blood vessels, and it tells the adrenal glands to release aldosterone, which holds on to salt and water.

It does a third thing that is not about pressure at all: over time it physically reshapes the heart and blood vessels for the worse. That is why blocking this system saves lives rather than just improving a reading.

• ACE inhibitors stop angiotensin II being made — lisinopril.
• ARBs let it be made but block it at the receptor — losartan.
• Direct renin inhibitors shut the pathway down at the very first step.

One more mechanism: when an ARB blocks angiotensin II receptors in the adrenal glands, less aldosterone is released, so the kidneys pass more sodium and water — and that effect is increased further because the drug widens the kidney's own blood vessels.

Nifedipine is a calcium channel blocker of the dihydropyridine kind. At normal doses it works on the small arteries and leaves the heart alone.

• Dihydropyridines — nifedipine, amlodipine — act on arteries.
• Non-dihydropyridines — verapamil, diltiazem — act on arteries and the heart.

The important catch: "it does not affect the heart" is only true at a normal dose. In overdose it can suppress the heart dangerously, just like verapamil and diltiazem do.

Note the assigned chapter covers where nifedipine acts, then moves on to verapamil as its main example — so a full list of nifedipine's own side effects is not in the material this guide has.

Four kinds of drug do the routine work: water tablets, drugs that block the renin system, SGLT-2 inhibitors, and beta blockers. Digoxin and a few others get added when needed.

Which ones you reach for depends on the stage:

• Stage A — at risk but nothing wrong yet. Control the blood pressure, cholesterol and diabetes; stop smoking and heavy drinking.
• Stage B — the heart has changed shape but there are no symptoms. Add an ACE inhibitor and a beta blocker if the pumping is weak or there has been a heart attack.
• Stage C — symptoms have appeared. Now you are aiming at four things: clear the fluid, help them function, slow the damage, and help them live longer.
• Stage D — symptoms even at rest, on the maximum of everything. Mostly about managing fluid: daily weights, loop diuretics, sometimes into a vein. A transplant is the real answer.

The catch that trips people up: the very drugs you add in stage B become risky in stage D. Beta blockers can make severe heart failure worse, and ACE inhibitors can drop the blood pressure dangerously or damage the kidneys — so if they are used at all, it is at low dose with close watching.

A few details worth carrying:

• The ACC/AHA stages sit alongside the older NYHA classification rather than replacing it.
• In stage A, an ACE inhibitor or ARB is useful for diabetes, atherosclerosis or high blood pressure, and an SGLT-2 inhibitor for type 2 diabetes at high cardiovascular risk.
• In stage B, use an ARB if the person cannot tolerate an ACE inhibitor.
• In stage D, the loop diuretic is sometimes combined with a thiazide, and intake and output are tracked strictly as well as daily weights.
• Beyond the four main classes, digoxin, dopamine and hydralazine may be added.

And an honest negative: there is no evidence that regular exercise prevents heart failure developing, or stops stage B becoming symptomatic — though exercise is good for other reasons. Routine supplements are not recommended for prevention either.

Digoxin makes the heart contract more forcefully, so it pumps more blood per beat. It also changes the heart's electrical behaviour and its hormone signalling.

It genuinely helps how people feel — fewer symptoms, more exercise tolerance, fewer hospital stays. But it does not help them live longer, and in women it may shorten life. That is why it has dropped to a second-choice drug.

It is a dangerous drug for one specific reason: the dose that causes serious rhythm problems is close to the dose that works.

• Before starting: ECG, electrolytes, kidney function.
• Aim for a blood level of 0.5 to 0.8 ng/mL.
• Keep an eye on the pulse in case it goes too slow.
• Teach them the warning signs — a change in heart rate or rhythm, disturbed vision, or nausea and vomiting — and to ring in if they appear.

Never give it to someone in ventricular fibrillation or ventricular tachycardia. Be careful in kidney impairment or low potassium, which makes toxicity more likely — so potassium supplements and potassium-sparing water tablets must be taken exactly as prescribed.

Two things easy to lose: digoxin is licensed for heart failure AND for controlling abnormal rhythms, not just heart failure. And you check the blood level at particular moments — when someone's symptoms have not budged after starting it, or when you suspect toxicity — rather than routinely.

Amiodarone works extremely well on both upper- and lower-chamber rhythm problems. It is also toxic enough to carry two black box warnings, and its side effects can carry on for months after someone stops taking it.

Lungs — the big one. It can scar and inflame the lungs. This happens to somewhere between 2 and 17 in 100 people taking it, and about 1 in 10 of those die. The catch is that breathlessness, cough and chest pain look exactly like heart failure or pneumonia, so it gets blamed on the wrong thing. Get a chest X-ray and lung function test before starting, keep checking, and stop the drug if the lungs are damaged.

Liver. Check liver blood tests at the start and regularly. If the enzymes go above three times normal, stop the drug.

• Thyroid — in either direction. It can make the thyroid underactive or overactive, so check it regularly.
• Eyes. Nearly everyone gets tiny deposits on the cornea, and those are harmless. Very rarely the optic nerve is affected, which can end in blindness.
• Skin. It makes people burn easily in sunlight — sunblock and covered arms.

Lung damage is most likely in people on a high dose for a long time.

More detail worth holding:

• It is a class III antidysrhythmic.
• It is only approved for life-threatening ventricular rhythms that safer drugs have failed to control — even though it is widely used beyond that.
• Liver injury, when it shows at all, looks like: loss of appetite, nausea, vomiting, feeling generally unwell, tiredness, itching, jaundice and dark urine.
• An underactive thyroid is treated with thyroid hormone; an overactive one with an antithyroid drug such as methimazole, or surgery.
• The link to blindness is not proven — the book says a causal relationship has not been established.

Two aims, always: help the heart pump better, and stop them having a stroke.

In atrial fibrillation, lots of little patches of the upper chambers fire off at random instead of one organised beat. The result is a chaotic rhythm upstairs, and the lower chambers beat fast or nearly normally depending on how much gets through.

The stroke risk works like this: blood sits still in the top chambers instead of flowing through, so a clot forms. When you put the rhythm back to normal, that clot can be flung out and go to the brain. So the most dangerous moment is the moment you fix it.

• Preferred: just slow the ventricles down, long term, with a beta blocker (atenolol, metoprolol) or a heart-acting calcium channel blocker (diltiazem, verapamil). Both slow conduction through the AV node.
• The alternative: actually restore normal rhythm, either with a shock or with drugs.

Preventing the stroke is a separate decision from either of those — that is what the blood thinners are for.

For scale: atrial fibrillation is the most common sustained abnormal rhythm there is, affecting around 4 million people in the United States.

Ranolazine is the unusual one. Instead of changing how hard the heart works or how much blood reaches it, it seems to help the heart muscle use its energy better, so it needs less oxygen.

Notice the hedging — "appears to", "possibly". That is how the textbook itself puts it. Nobody is fully certain of the mechanism, and that uncertainty is worth carrying rather than tidying away.

Compare it with the others: nitrates take load off the heart by widening veins, beta blockers slow it down, calcium channel blockers widen arteries. Ranolazine changes none of those — it changes what the muscle does with the oxygen it already gets.

It is not used for the variant (spasm) kind of angina.

Whatever drug is used, the rest of angina care still applies: avoid what sets an attack off — overexertion, big meals, emotional stress and cold — and fix the risk factors, above all smoking, along with high blood pressure, high cholesterol and being sedentary.

Nitroglycerin has been treating angina since 1879 and is still the first thing you reach for to stop an attack that is happening now. It works fast and costs very little.

Never combine it with sildenafil or the other drugs of that family. Both lower blood pressure, and together they can send it through the floor. Be careful too in anyone whose pressure is already low or who is on other blood-pressure drugs.

The recurring problem is tolerance — the body stops responding if the drug is there all the time:

• Take the patch off after 12 to 14 hours, so there are 10 to 12 hours a day with none on.
• The same happens with a long continuous drip.
• Slow-release capsules must be swallowed whole, never crushed or chewed.

Under the tongue, for an attack: one tablet, repeat every 5 minutes, no more than three doses. No routine blood tests are needed — instead have them keep a diary of how often attacks come and what sets them off.

The doses and the other forms:

• Under the tongue: 0.3–0.6 mg, repeated every 5 minutes, up to three doses.
• Spray onto the tongue: 1–2 sprays, up to 3 in 15 minutes — also for an attack.
• Ointment on the skin: 1–2 inches every 6 hours, for lasting protection.

Heparin does not break up a clot. It boosts something the body already has — antithrombin, which switches off two of the clotting factors: thrombin and factor Xa. Switch those off and less fibrin gets made, so clotting slows.

• Ordinary (unfractionated) heparin knocks out thrombin and factor Xa about equally.
• Low-molecular-weight heparins mostly knock out factor Xa, and are much worse at touching thrombin.
• Fondaparinux works on factor Xa.

The reason is simply size. To switch off thrombin, the heparin chain has to carry the active bit and be long enough for thrombin to grab onto as well. Low-molecular-weight chains are too short for that second part. Switching off factor Xa only needs the active bit, so they can still do that.

Warfarin probably interacts with more drugs than anything else people take. And it can go wrong in both directions — too little effect and a clot forms, too much and they bleed.

• Some drugs make warfarin stronger: they knock it off its carrier protein, or block the liver enzymes that destroy it, or reduce clotting factors. The result is bleeding.
• Some make it weaker: they speed up the liver enzymes, increase clotting factors, or stop it being absorbed. The result is a clot.
• Some do not touch warfarin at all but make bleeding likelier anyway — by stopping platelets sticking together, or by causing stomach ulcers.

Knowing an interaction exists does not mean you cannot use the two together. It means being careful. The riskiest moment is when the other drug is started or stopped — and stopping counts just as much as starting. Check the INR then.

Tell the patient plainly: nothing new without asking you first, including things off the pharmacy shelf.

There are three ways a drug can make bleeding likelier without touching warfarin at all: stopping platelets clumping, reducing clotting factors, and causing stomach ulcers.

Rivaroxaban blocks factor Xa by attaching straight onto it. No thrombin gets made, so no clot forms.

That word directly is the point. Fondaparinux also targets factor Xa, but it works through antithrombin as a go-between. Rivaroxaban does it itself.

Compared with warfarin it has five advantages, and each one fixes a specific warfarin problem:

• It starts working quickly — warfarin is slow.
• The dose is fixed — warfarin has to be tuned per person.
• Less bleeding.
• Very few drug interactions — warfarin has more than almost anything.
• No INR blood tests.

It is used after hip and knee replacements to stop clots, and to prevent stroke in atrial fibrillation, among other uses.

Its four approved uses in full: preventing clots after hip or knee replacement, preventing stroke in atrial fibrillation, treating DVT and PE, and preventing them coming back.

Cholesterol is not simply bad. Every cell membrane in your body is partly made of it, and you cannot make oestrogen, progesterone, testosterone or bile salts without it. It even sits in the outer layer of skin, keeping water in.

Some comes from food, and some your own cells make.

The guideline is the 2018 ACC/AHA one, and it works in stages: screen people and work out their risk, then change diet and exercise, then add drugs if the risk is high. Advice of this kind has been issued since 1988.

Statins are the strongest LDL-lowering drugs there are. They also nudge HDL up and triglycerides down in some people. But the reason they come first is not the cholesterol number — it is that they have been shown to reduce heart failure, heart attacks and sudden death. Improving the reading and improving the outcome are different achievements, and statins do both.

Two bits of vocabulary: cholesterol from food is exogenous, cholesterol your cells make is endogenous. And in the skin it does two jobs — holding water in, and keeping water-soluble substances from being absorbed through it.

All water tablets do the same basic thing — get rid of fluid, so there is less volume to push around and the pressure drops. The differences are how much fluid they shift, whether they still work in a failing kidney, and which way they move potassium.

• Thiazides (hydrochlorothiazide) — a moderate amount. Good for the long term when the swelling is mild. They stop working when the kidneys are struggling, so they are no use in severe heart failure. They lower potassium.
• Loop diuretics (furosemide) — a lot of fluid, and they keep working even when the kidneys are poor. That makes them the choice in severe heart failure. They also lower potassium, and can drop the blood pressure badly by taking off too much fluid.
• Potassium-sparing (spironolactone, triamterene) — barely any fluid at all. They are not there for the water; they are there to put back the potassium the other two take out. They raise potassium.

Why potassium matters so much here: low potassium makes digoxin far more likely to cause dangerous rhythms.

Two more things. Spironolactone helps people with heart failure live longer by blocking aldosterone, not by making them pass water. And because ACE inhibitors and ARBs also push potassium up, adding a potassium-sparing tablet on top needs care.

The threshold for thiazides failing is a creatinine clearance below about 40–50 mL/min.

Cardiac output is just heart rate multiplied by stroke volume — how often it beats, times how much it pushes out each time. About 5 litres a minute in an adult, which means the heart moves your entire blood volume every minute.

Typical numbers: 70 beats a minute, 70 mL per beat, giving 4.9 litres.

• The sympathetic nerves speed the heart up, through β₁ receptors in the SA node.
• The parasympathetic nerves slow it down, through muscarinic receptors in the same place, along the vagus nerve.

That β₁ receptor is precisely what a beta blocker blocks. So "beta blockers slow the heart" is not a separate fact — it is this diagram with the accelerator disconnected.

Stroke volume depends on three things: how hard the muscle squeezes, how much pressure it has to push against, and how full the heart was to begin with.

This is why so many different drugs lower blood pressure: slow the rate, empty the tank, or relax the veins — all three end up in the same equation.

Ezetimibe works in the gut wall: it stops cholesterol from food being absorbed, and stops cholesterol in bile being taken back up. Total cholesterol, LDL and triglycerides all come down, and HDL goes up a little.

Its interactions are about what you put it with:

• With a statin — a slightly higher chance of liver irritation and of muscle problems. You can still do it, but check liver blood tests before starting and whenever it seems warranted.
• With a fibrate like gemfibrozil or fenofibrate — both make bile more cholesterol-rich, so gallstones, and both raise the muscle risk. This combination is not recommended.
• With a bile acid sequestrant like cholestyramine — less ezetimibe gets absorbed, so space the doses apart.

Worth noticing the difference: with a statin you monitor, with a fibrate you do not do it at all.

Two small additions: it also lowers apolipoprotein B, and colestipol may reduce its absorption in the same way cholestyramine does.

Aspirin is used against heart attacks in four different situations, and they are not the same thing:

• During or just after a heart attack, to stop the artery blocking again.
• In an acute heart attack, to reduce deaths from blood-vessel causes.
• After a previous heart attack, to reduce the combined risk of dying or having another one.
• To prevent a first heart attack in someone who has never had one.

That last one has a qualifier the others do not: the benefit is described for men, and for women only from age 65 onwards. Once someone has already had a heart attack, that restriction does not apply.

One honest gap: nobody knows the ideal dose for preventing a first heart attack. Low doses are what get used.

In every one of these situations, preventive aspirin can reduce illness and possibly death.