Cardiovascular drugs: the classes you will prescribe every day
Learn the mechanism and the characteristic side effect follows from it.
Cardiovascular drugs make up a large share of everything most doctors prescribe, and they are unusually rewarding to learn properly. Each class has a mechanism, and the adverse effects are not an arbitrary list to be memorised — they are consequences of that mechanism appearing somewhere you did not intend. An ACE inhibitor causes cough because the enzyme it blocks also breaks down bradykinin. A dihydropyridine causes ankle swelling because it dilates arterioles. Once the mechanism is in place, the side effects stop being separate facts.
This chapter covers the renin-angiotensin blockers, calcium channel blockers, diuretics, antiplatelets and anticoagulants, statins and digoxin. Beta-blockers have their own chapter — see Autonomic Pharmacology — and are referenced here rather than repeated.
🩺 Where this lives: Cardiovascular drugs are among the most frequent causes of preventable medication harm, and the pattern is remarkably consistent: the prescription was correct when it was written, and then the patient changed. Someone becomes dehydrated with a diarrhoeal illness while taking an ACE inhibitor and a diuretic. Renal function declines with age and digoxin accumulates. A diuretic lowers potassium and a previously safe digoxin dose becomes toxic. The drugs are safe; the unreviewed prescription is not.
💡 A note on doses. This chapter gives none, and it deliberately avoids specific INR targets and exhaustive interaction lists. Doses follow national formularies, anticoagulation targets are indication-specific, and interaction lists are long and change. What is taught here is the mechanism — which is what lets you predict an interaction you have not memorised.
The renin-angiotensin system
One pathway generates three drug classes, and understanding it explains all of their shared properties. ACE inhibitors, ARBs and aldosterone antagonists all raise potassium — so combining them, or adding one to a patient with renal impairment, requires monitoring. All three are contraindicated in pregnancy because interference with the fetal renin-angiotensin system damages the developing kidneys. And the cough that characterises ACE inhibitors comes from bradykinin accumulation, which is exactly why switching to an ARB abolishes it.
WHY THESE DRUGS RAISE CREATININE — AND WHEN THAT IS ACCEPTABLE
Angiotensin II constricts the EFFERENT arteriole, which
maintains glomerular filtration pressure. Block it, and
that constriction relaxes — so filtration pressure falls
and the creatinine rises slightly.
A SMALL, STABLE RISE after starting is expected and does
not mean the drug is damaging the kidney. Guidelines
define an acceptable rise; check yours.
BUT A LARGE OR PROGRESSIVE RISE means the kidney was
depending on that efferent constriction to filter at all.
The classic setting is BILATERAL RENAL ARTERY STENOSIS,
where perfusion is already marginal.
THE PRACTICAL RULE: check renal function and potassium
before starting and after starting or increasing the dose.
AND THE "SICK DAY" PROBLEM: during vomiting, diarrhoea or
any dehydrating illness, these drugs plus a diuretic plus
an NSAID can precipitate acute kidney injury. That
combination is sometimes called the "triple whammy" —
each drug alone is tolerable, and together in a dehydrated
patient they are not.
The antihypertensive classes
💡 Exam angle: questions frequently describe a side effect and ask which drug caused it. The identifying trio is worth committing to memory: dry cough → ACE inhibitor, ankle swelling → dihydropyridine calcium channel blocker, gout or a raised glucose → thiazide. Note that dihydropyridine ankle oedema is caused by arteriolar dilatation rather than fluid overload, which is why a diuretic does not fix it — the correct action is to change the drug.
Diuretics
The single most useful thing to hold about diuretics is their opposite effects on potassium. Loop and thiazide diuretics lose potassium; aldosterone antagonists and other potassium-sparing agents retain it. That is why a patient on a loop diuretic needs the potassium checked for hypokalaemia, and a patient on spironolactone plus an ACE inhibitor needs it checked for hyperkalaemia — the same test, watching for opposite problems.
Antiplatelets and anticoagulants
WHY THE TWO ARE NOT INTERCHANGEABLE
The distinction rests on the kind of clot.
ARTERIAL clot forms in fast-flowing, high-shear vessels on
a ruptured atherosclerotic plaque. It is PLATELET-rich.
→ ANTIPLATELET drugs
→ Coronary and cerebrovascular disease
VENOUS clot forms in slow-flowing or stagnant blood. It is
FIBRIN-rich, formed through the coagulation cascade.
→ ANTICOAGULANT drugs
→ DVT, pulmonary embolism
ATRIAL FIBRILLATION is the important case that surprises
people. Although the heart is arterial, the clot forms in
a fibrillating atrium where blood is STAGNANT — so it
behaves like a venous clot and requires ANTICOAGULATION.
Aspirin is not adequate stroke prevention in AF. This is a
favourite examination point.
WARFARIN in brief:
Vitamin K antagonist, monitored by INR
SLOW onset and offset — it cannot be used for immediate
anticoagulation, which is why heparin is used to cover
the start when immediate effect is needed
Numerous drug, alcohol and dietary interactions, largely
through hepatic metabolism and vitamin K intake
TERATOGENIC — heparins do not cross the placenta and are
the anticoagulants used in pregnancy
Targets, durations and reversal protocols come from your
national guideline.
Statins and digoxin
💡 Exam angle: digoxin toxicity is potentiated by hypokalaemia, and this generates one of the most reliable question stems in pharmacology — a stable patient on digoxin is started on a diuretic, and becomes confused, nauseated and bradycardic with visual disturbance. The digoxin dose never changed. Also note that digoxin is renally excreted, so declining kidney function produces the same picture without any prescription change at all.
Clinical reasoning: four presentations
🔍 Case 1 — a cough that is not a chest infection
PresentationA woman started on an antihypertensive six weeks ago has a persistent dry cough. She is afebrile with a clear chest. She has had two courses of antibiotics and a normal chest X-ray.
Key questionWhat was started six weeks ago?
ReasoningA dry cough beginning after an ACE inhibitor is started is a class effect caused by bradykinin accumulation. It is not an infection and antibiotics will not help.
AnswerSwitch to an angiotensin receptor blocker, which blocks the receptor rather than the enzyme and therefore does not cause cough. Blood pressure control is maintained.
🔍 Case 2 — confusion after a new diuretic
PresentationAn 80-year-old on long-standing digoxin is started on a loop diuretic for oedema. Two weeks later she is nauseated, confused and bradycardic, and mentions that things look yellowish. Her digoxin dose is unchanged.
Key clueVisual disturbance with a yellow-green tinge.
ReasoningThis is digoxin toxicity, precipitated by diuretic-induced hypokalaemia. Low potassium potentiates digoxin at the sodium-potassium pump, so a previously safe dose becomes toxic. Age-related renal decline compounds it.
AnswerStop digoxin, check potassium, renal function and a digoxin level, correct the potassium, monitor the rhythm and manage per protocol.
🔍 Case 3 — aspirin for atrial fibrillation
PresentationA 72-year-old with newly diagnosed atrial fibrillation, hypertension and diabetes is given aspirin for stroke prevention because the family are worried about bleeding on warfarin.
TrapTreating an arterial-sounding problem with an antiplatelet.
ReasoningThe clot in atrial fibrillation forms in a stagnant atrium and is fibrin-rich, behaving like a venous thrombus. Antiplatelet therapy is not adequate stroke prevention here; anticoagulation is.
AnswerFormally assess stroke and bleeding risk and offer anticoagulation per guideline. Discuss the bleeding concern honestly rather than substituting an ineffective drug for it.
🔍 Case 4 — unwell on three reasonable drugs
PresentationA man on an ACE inhibitor and a diuretic takes an NSAID for back pain, then develops gastroenteritis with vomiting and diarrhoea. He presents with acute kidney injury and a high potassium.
What happenedThree drugs that are individually reasonable, combined with dehydration.
ReasoningThe NSAID constricts the afferent arteriole, the ACE inhibitor dilates the efferent, and the diuretic plus vomiting reduces circulating volume. Glomerular filtration collapses, and the ACE inhibitor also raises potassium.
AnswerStop the contributing drugs, rehydrate, treat the hyperkalaemia per protocol, and give explicit sick-day advice about temporarily stopping these drugs during dehydrating illness.
Commonly confused
Confusion
The distinction
Why it matters
ACE inhibitor vs ARB
Enzyme versus receptor; bradykinin causes the cough
Switching abolishes the cough.
Antiplatelet vs anticoagulant
Platelet-rich arterial versus fibrin-rich stasis clot
AF needs anticoagulation, not aspirin.
Loop vs potassium-sparing diuretic
Opposite effects on potassium
Same test, opposite abnormality.
Dihydropyridine vs rate-limiting CCB
Vessels versus heart
Ankle oedema versus bradycardia.
CCB ankle oedema vs fluid overload
Arteriolar dilatation, not excess fluid
A diuretic will not fix it — change the drug.
Expected vs concerning creatinine rise
Small and stable versus large or progressive
One is tolerated; the other suggests stenosis.
Statin myalgia vs myopathy
Dark urine and a raised creatine kinase
Rare but serious.
Digoxin dose vs digoxin effect
Hypokalaemia and renal decline raise the effect
Toxicity with an unchanged prescription.
Rapid revision
MUST-KNOW FACTS
1. ACE inhibitors block the enzyme; ARBs block the receptor.
2. ACE inhibitor COUGH is caused by BRADYKININ accumulation.
3. ARBs do not cause cough — switch when cough is the problem.
4. ACE inhibitors, ARBs and aldosterone antagonists all RAISE POTASSIUM.
5. All three are CONTRAINDICATED IN PREGNANCY.
6. ANGIO-OEDEMA is a serious ACE inhibitor adverse effect.
7. These drugs dilate the EFFERENT arteriole, so creatinine rises slightly.
8. A small stable creatinine rise is expected; a large or progressive one is not.
9. Suspect bilateral RENAL ARTERY STENOSIS if renal function falls sharply.
10. Check renal function and potassium before and after starting.
11. NSAID + ACE inhibitor + diuretic in dehydration → acute kidney injury.
12. Give SICK DAY advice about pausing these drugs in dehydrating illness.
13. DIHYDROPYRIDINE CCBs act on vessels: ANKLE OEDEMA, flushing, headache.
14. CCB ankle oedema is dilatation, not fluid — a diuretic will not fix it.
15. RATE-LIMITING CCBs act on the heart: bradycardia, and caution with beta-blockers.
16. THIAZIDES: low potassium and sodium, raised glucose, urate and lipids.
17. Thiazides may precipitate GOUT.
18. LOOP diuretics are the most powerful and work in poor renal function.
19. Loop and thiazide LOSE potassium; spironolactone RETAINS it.
20. Spironolactone has prognostic benefit in heart failure; causes gynaecomastia.
21. ANTIPLATELETS for arterial, platelet-rich clot.
22. ANTICOAGULANTS for venous and stasis, fibrin-rich clot.
23. ATRIAL FIBRILLATION requires ANTICOAGULATION, not aspirin.
24. Warfarin is a vitamin K antagonist monitored by INR.
25. Warfarin has slow onset and offset and many interactions.
26. Warfarin is TERATOGENIC — heparins are used in pregnancy.
27. STATINS inhibit HMG-CoA reductase and reduce cardiovascular events.
28. Statin myalgia is common; MYOPATHY and rhabdomyolysis are rare and serious.
29. Muscle pain with dark urine → check CREATINE KINASE.
30. Statins are avoided in pregnancy.
31. DIGOXIN has a narrow therapeutic index and is renally excreted.
32. HYPOKALAEMIA POTENTIATES DIGOXIN.
33. Digoxin toxicity: nausea, confusion, YELLOW-GREEN vision, arrhythmia.
34. A new diuretic can cause digoxin toxicity at an unchanged dose.
35. Beta-blockers are covered in the Autonomic Pharmacology chapter.
💡 Exam angle: two reasoning habits carry most of the marks. First, match the side effect back to the mechanism — cough, ankle swelling and gout each name their class. Second, when a stable patient becomes toxic, ask what changed about the patient rather than about the prescription: potassium, renal function, or hydration.
Syllabus points
The renin-angiotensin pathway and its three drug classes
Why ACE inhibitors cause cough
Hyperkalaemia and pregnancy contraindication
Why creatinine rises, and when it matters
The triple whammy and sick-day advice
Calcium channel blockers: vessels versus heart
Identifying the class from the side effect
Diuretics by site of action
Opposite effects on potassium
Antiplatelet versus anticoagulant
Why atrial fibrillation needs anticoagulation
Warfarin: monitoring, interactions, pregnancy
Statins and myopathy
Digoxin toxicity and hypokalaemia
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