Cardiovascular Medicines: Classes, Mechanisms, Emergency Uses and Safety

Learning outcomes

By the end of this lesson, the emergency medicine student should be able to:

• Define cardiovascular medicines and relate drug action to cardiac output, preload, afterload, contractility, heart rate and rhythm.
• Classify medicines used for hypertension, angina, acute coronary syndromes, heart failure, dysrhythmias, thrombosis, shock and cardiac arrest.
• Explain the mechanisms, indications, major contraindications, adverse effects and monitoring requirements of common cardiovascular drug groups.
• Recognise when chest pain, dyspnoea, syncope, hypotension, bradycardia, tachycardia or oedema may represent a life-threatening cardiovascular emergency.
• Apply ABCDE, ECG, vital-sign and perfusion assessment before and after cardiovascular medicine administration.
• Explain why the same medicine can be beneficial in one patient and dangerous in another.
• Describe the emergency roles of antiplatelets, anticoagulants, fibrinolytics, vasopressors, inotropes and antiarrhythmics.
• Identify high-risk interactions, dose errors, infusion hazards and situations requiring senior or specialist review.
• Document cardiovascular medicines and communicate response, adverse effects and next actions during handover.

1. Cardiovascular system and drug targets

The cardiovascular system consists of the heart, blood vessels and circulating blood. The heart generates pressure; vessels distribute and regulate flow; blood carries oxygen, nutrients, hormones and waste. Cardiovascular medicines change one or more of these functions.

2. Cardiovascular emergencies that require rapid recognition

WHO identifies cardiovascular diseases as disorders of the heart and blood vessels, including coronary heart disease, cerebrovascular disease, peripheral arterial disease, rheumatic and congenital heart disease, deep-vein thrombosis and pulmonary embolism. Heart attacks and strokes are acute events that require immediate care.

3. General safety principles before giving cardiovascular medicines

1. Assess airway, breathing, circulation, disability and exposure before focusing on a medicine.
2. Record BP in both arms when clinically relevant, pulse rate and regularity, respiratory rate, oxygen saturation, temperature, mental status, urine output and perfusion.
3. Obtain a 12-lead ECG or rhythm strip when indicated and do not give an AV-nodal blocker without considering the rhythm.
4. Ask about allergies, pregnancy, kidney/liver disease, bleeding, erectile-dysfunction medicines, anticoagulants, stimulants and recent doses.
5. Confirm the indication, product, concentration, dose, route, infusion rate, monitoring and prescriber/protocol authority.
6. Check whether hypotension, bradycardia, dehydration, right-ventricular infarction, aortic stenosis, asthma or conduction disease changes the risk.
7. Reassess after administration; the desired effect is not merely a lower number on the monitor but improved perfusion and patient condition.

4. Classification of cardiovascular medicines

5. Antihypertensive medicines

Antihypertensives lower blood pressure by reducing vascular resistance, circulating volume, cardiac output or neurohormonal activation. Long-term control prevents stroke, heart failure, kidney disease and coronary events; emergency treatment is reserved for severe pressure elevation with acute organ injury or other defined indications.

5.1 ACE inhibitors

Examples: enalapril, lisinopril, captopril and ramipril.

Mechanism: inhibit conversion of angiotensin I to angiotensin II and reduce aldosterone. This promotes vasodilation, reduces sodium/water retention and lowers afterload and preload.

5.2 Angiotensin-receptor blockers (ARBs)

Examples: losartan, valsartan and candesartan. ARBs block the angiotensin-II receptor and generally do not cause bradykinin-related cough, but can still cause hypotension, hyperkalaemia and kidney injury. Do not combine ACE inhibitors and ARBs routinely; combination increases renal and potassium risk without routine benefit.

5.3 Calcium-channel blockers

5.4 Diuretics

5.5 Beta-blockers

Examples: metoprolol, atenolol, bisoprolol, propranolol, carvedilol and labetalol. They reduce sympathetic stimulation, heart rate, contractility and renin release. Some are beta-1 selective; selectivity is dose-dependent.

• Uses: hypertension, angina, selected arrhythmias, post-MI care, chronic heart failure with specialist titration, thyrotoxicosis and some aortic conditions.
• Adverse effects: bradycardia, hypotension, fatigue, bronchospasm, cold extremities, depression of exercise response and masking of hypoglycaemia.
• Avoid or seek urgent review: cardiogenic shock, acute decompensated heart failure, severe bradycardia, high-grade AV block and active bronchospasm.
• Do not stop abruptly: withdrawal may cause rebound tachycardia, hypertension, angina or infarction.

5.6 Alpha-1 blockers and centrally acting agents

Alpha-1 blockers such as prazosin relax arterial and venous smooth muscle but can cause first-dose postural hypotension and syncope. Centrally acting medicines such as clonidine reduce sympathetic outflow; sedation, dry mouth and rebound hypertension after abrupt withdrawal are important safety concerns. These are not usually first-line emergency choices without an authorised plan.

6. Antianginal medicines

Angina occurs when myocardial oxygen demand exceeds coronary oxygen supply. Medicines either reduce demand by lowering heart rate, contractility or wall stress, or improve supply by dilating coronary/venous vessels. New, prolonged or rest pain must be treated as possible acute coronary syndrome until assessed.

6.1 Nitrates

Examples: glyceryl trinitrate (nitroglycerin) sublingual spray/tablet, transdermal patches and IV infusion; isosorbide dinitrate/mononitrate.

Mechanism: release nitric oxide, increase cyclic GMP and relax vascular smooth muscle. Venodilation reduces preload; at higher exposure arterial dilation reduces afterload and myocardial work.

6.2 Other antianginals

• Beta-blockers: lower heart rate and contractility; useful for exertional angina when not contraindicated.
• Calcium-channel blockers: reduce afterload and/or AV conduction; useful when beta-blockers are unsuitable or for vasospastic angina.
• Ranolazine: reduces late sodium current and wall tension; specialist use, with QT and interaction precautions.
• Ivabradine: slows sinus-node rate in selected patients; requires sinus rhythm and specialist criteria.
• Antiplatelet/statin therapy: does not immediately relieve pain but reduces thrombotic and long-term atherosclerotic risk when indicated.

7. Heart-failure medicines

Heart failure is a syndrome in which the heart cannot provide adequate output or can do so only at high filling pressures. Acute decompensation may present with pulmonary oedema, peripheral congestion, fatigue, hypotension, cool extremities or altered consciousness.

8. Antiplatelet medicines

Platelets are central to arterial thrombus formation after plaque rupture. Antiplatelets reduce platelet activation and aggregation; they do not dissolve an established clot and they increase bleeding risk.

8.1 Aspirin

Aspirin irreversibly inhibits platelet cyclooxygenase and reduces thromboxane A₂ formation for the life of the platelet. It is used in selected acute coronary syndromes and secondary prevention.

• Check: true allergy, active major bleeding, suspected aortic dissection, severe thrombocytopenia, recent haemorrhagic stroke, peptic-ulcer risk and concurrent anticoagulation.
• Adverse effects: dyspepsia, gastrointestinal bleeding, bronchospasm in aspirin-sensitive asthma, renal effects and hypersensitivity.
• Emergency teaching: do not give an antiplatelet for undifferentiated chest pain until contraindications and aortic/dissection features have been assessed according to protocol.

8.2 P2Y12 inhibitors

Examples: clopidogrel, prasugrel and ticagrelor. They block ADP-mediated platelet activation and are used with aspirin in selected ACS or after coronary intervention.

9. Anticoagulant medicines

Anticoagulants reduce thrombin generation or activity and limit clot extension. They are used for venous thromboembolism, atrial fibrillation, mechanical valves, ACS and other indications. Anticoagulants do not directly dissolve a clot and can cause life-threatening bleeding.

Anticoagulant emergency assessment

• Ask which anticoagulant, dose, last administration time, indication and adherence.
• Look for gastrointestinal, urinary, vaginal, respiratory, intracranial, wound or retroperitoneal bleeding.
• After trauma or a fall, consider occult intracranial bleeding even if the patient initially looks well.
• Check BP, pulse, mental state, skin, puncture sites, urine/stool and haemodynamic status.
• Bring the medication packaging or anticoagulation record to the receiving team.
• Do not give reversal agents or blood products outside authorised advanced-care protocols.

10. Fibrinolytic (thrombolytic) medicines

Fibrinolytics convert plasminogen to plasmin, which breaks down fibrin in a thrombus. They may be considered in selected STEMI, ischaemic stroke or massive pulmonary embolism pathways where eligibility, timing, imaging and specialist oversight are confirmed.

11. Lipid-lowering and vascular-protection medicines

Statins inhibit HMG-CoA reductase, lower LDL cholesterol and reduce atherosclerotic cardiovascular risk. They are preventive medicines, not immediate pain-relief drugs. Ezetimibe reduces intestinal cholesterol absorption and may be added or used when statins are not tolerated. Monitor for muscle symptoms, liver concerns and interactions according to local guidance.

12. Antiarrhythmic medicines

Antiarrhythmics alter automaticity, conduction, refractory period or AV-node activity. The ECG diagnosis and haemodynamic stability determine whether a medicine is appropriate. A drug that treats one rhythm can worsen another.

12.1 Adenosine

Adenosine produces a very brief AV-nodal block and may terminate selected regular narrow-complex supraventricular tachycardias. It does not treat ventricular fibrillation or irregular wide-complex tachycardia.

• Explain the short-lived flushing, chest discomfort or sense of impending doom before administration when the patient is conscious.
• Use rapid administration through a suitable proximal access followed by a flush only under authorised protocol.
• Continuous ECG and resuscitation equipment must be available.
• Use caution or specialist advice in asthma/bronchospasm, pre-excited atrial fibrillation, transplant patients and interacting medicines.

12.2 Amiodarone

Amiodarone has class III potassium-channel effects plus sodium-channel, calcium-channel and beta-blocking actions. It may be used for selected ventricular or supraventricular arrhythmias and refractory VF/pulseless VT under advanced life-support protocols.

• Acute adverse effects: hypotension, bradycardia, QT prolongation and infusion-related reactions.
• Long-term toxicities: thyroid, lung, liver, eye, skin and neurological effects.
• Interactions: warfarin, digoxin and other QT-prolonging medicines require careful review.
• Monitoring: ECG/QT, BP, rhythm, liver/thyroid/pulmonary review for ongoing therapy and infusion-site safety.

12.3 Lidocaine

Lidocaine blocks fast sodium channels and can suppress selected ventricular arrhythmias. It may be considered for VF/pulseless VT unresponsive to defibrillation under current resuscitation protocols. Neurological toxicity, seizures, hypotension and bradycardia are important risks.

12.4 Beta-blockers and non-dihydropyridine calcium-channel blockers

These slow AV-node conduction and can control ventricular rate in selected atrial fibrillation/flutter or supraventricular tachycardia. Do not give blindly to an unstable patient, a patient with pre-excited AF, severe heart failure, high-grade block, hypotension or a wide-complex rhythm of uncertain origin.

12.5 Magnesium

Magnesium is important in torsades de pointes due to prolonged QT and selected electrolyte-related arrhythmias. Routine magnesium is not beneficial for every cardiac arrest or every ventricular tachyarrhythmia; use the indication and protocol.

12.6 Digoxin

Digoxin increases vagal activity and has positive inotropic effects. It has a narrow therapeutic index. Toxicity may present with nausea, vomiting, confusion, visual disturbance, bradyarrhythmia, AV block or ventricular arrhythmias. Risk increases with renal impairment, hypokalaemia, hypomagnesaemia and interacting medicines.

13. Vasopressors and inotropes

Vasoactive medicines are high-alert infusions. They require a monitored environment, an infusion pump, reliable vascular access and a team able to recognise arrhythmia, extravasation and rapid changes in perfusion.

Vasoactive infusion safety

1. Confirm patient, indication, concentration, dose units, pump rate and target parameters.
2. Use standard concentrations and an independent double-check.
3. Use a dedicated line where possible and label the tubing and syringe/bag.
4. Monitor BP frequently or continuously, rhythm, peripheral perfusion, urine output, mental status and lactate/other perfusion markers as available.
5. Check the access site frequently; stop and escalate for pain, swelling, blanching or coolness suggesting extravasation.
6. Never abruptly stop a prolonged vasopressor infusion without an authorised plan; rebound hypotension may occur.

14. Cardiovascular medicines in cardiac arrest

High-quality CPR and early defibrillation remain the foundation of cardiac-arrest care. The 2025 AHA adult advanced-life-support guidance recommends epinephrine for adult cardiac arrest, with timing linked to shockable versus non-shockable rhythms, and allows amiodarone or lidocaine for VF/pulseless VT unresponsive to defibrillation. Routine calcium, sodium bicarbonate or magnesium is not recommended for undifferentiated arrest; these may be used for selected causes such as hyperkalaemia or toxic exposure.

15. Bradycardia medicines and pacing pathway

Bradycardia is dangerous when it causes hypotension, altered mental status, ischaemic chest discomfort, acute heart failure or shock. Determine whether it is sinus bradycardia, AV block, medication effect, hypoxia, hypothermia, hyperkalaemia or another reversible cause.

• Atropine: blocks muscarinic activity and may increase sinus rate and AV conduction in selected symptomatic bradycardia. It may be ineffective in infranodal high-grade block.
• Transcutaneous pacing: may be required when medication is ineffective or the patient is unstable; provide analgesia/sedation only with appropriate monitoring and authorised expertise.
• Epinephrine or dopamine infusion: may support rate and perfusion while awaiting pacing or definitive treatment under advanced protocol.
• Correct reversible causes: hypoxia, hypothermia, myocardial infarction, medication toxicity and electrolyte abnormality.

16. Tachyarrhythmia medicines and cardioversion

First decide whether the patient is unstable. Hypotension, altered mental state, shock, ongoing ischaemic chest discomfort or acute pulmonary oedema indicate an emergency pathway, often requiring synchronised cardioversion rather than repeated medication trials.

17. Acute coronary syndrome (ACS) medicine principles

ACS includes unstable angina, NSTEMI and STEMI. The emergency team must obtain ECG and urgent clinician/cardiology input; medicine choices depend on diagnosis, bleeding risk, renal function, timing and reperfusion pathway.

1. Recognise possible ACS from symptoms and atypical presentations, especially in women, older adults and people with diabetes.
2. Obtain and communicate a 12-lead ECG promptly; repeat if symptoms or the clinical picture changes.
3. Assess BP, oxygen saturation, pulmonary oedema, shock, bleeding, allergy, anticoagulant use and recent PDE-5 inhibitor use.
4. Use antiplatelet and anti-ischaemic treatment only under the authorised ACS pathway.
5. Provide oxygen when indicated by hypoxaemia or respiratory distress rather than automatically for every chest-pain patient.
6. Arrange urgent reperfusion/transfer when STEMI or high-risk ACS is suspected.
7. Document symptom onset/last known well, ECG time, medicines, doses, response and contraindications.

18. Hypertensive urgency versus emergency

Severe BP elevation without acute organ injury is managed differently from a hypertensive emergency with encephalopathy, stroke, ACS, pulmonary oedema, aortic dissection, renal injury or eclampsia. Rapid unmonitored reduction can reduce cerebral, coronary or renal perfusion.

19. Cardiovascular drug interactions and contraindication patterns

20. Special populations and cardiovascular medicines

21. Cardiovascular medicine calculations

Use the prescribed dose, actual product concentration and current protocol. Cardiovascular infusions are high-alert medicines; calculate, label and independently check them.

1. Write the order and units without abbreviations.
2. Confirm whether the prescription uses mg/min, micrograms/min, micrograms/kg/min or another unit.
3. Check the final concentration after dilution, not only the amount in the ampoule.
4. Verify pump settings, line label, target BP/rate and maximum dose.
5. Ask for independent verification for epinephrine, norepinephrine, insulin, heparin, paediatric doses and antiarrhythmic infusions.
6. Recalculate whenever the bag, syringe, patient weight or pump setting changes.

22. Monitoring and documentation

Document

• Indication, diagnosis or emergency protocol.
• Medicine, concentration, dose, route, rate, time and prescriber/authorising clinician.
• Baseline vital signs, ECG/rhythm and relevant laboratory or history findings.
• Response: pain, BP, pulse, rhythm, oxygenation, perfusion, urine output and mental status.
• Adverse effects, withheld doses, contraindications, escalation and communication.
• For infusions: concentration, pump setting, line/site checks, titration target and handover.

23. Clinical scenarios

24. Examination and revision questions

1. Define preload, afterload, contractility, chronotropy, dromotropy and cardiac output.
2. Classify cardiovascular medicines by their main physiological target.
3. Explain the mechanism and major adverse effects of ACE inhibitors.
4. Compare ACE inhibitors and ARBs.
5. Differentiate dihydropyridine and non-dihydropyridine calcium-channel blockers.
6. List the major monitoring requirements for furosemide.
7. Explain the role and contraindications of nitrates in acute chest pain.
8. Why can beta-blockers be dangerous in shock, bradycardia or acute decompensated heart failure?
9. Differentiate antiplatelets, anticoagulants and fibrinolytics.
10. What bleeding checks are needed before anticoagulant or thrombolytic therapy?
11. Explain the main emergency role of adenosine.
12. Why must an irregular wide-complex tachycardia not be treated blindly with AV-nodal blockers?
13. Describe the important toxicities and interactions of amiodarone.
14. When may magnesium be useful in arrhythmia?
15. Describe the cardiovascular arrest roles of epinephrine, amiodarone and lidocaine.
16. Why are routine calcium, sodium bicarbonate and magnesium not given in every cardiac arrest?
17. List the safety checks for a norepinephrine infusion.
18. Explain how pregnancy, renal impairment and older age alter cardiovascular medicine safety.
19. What should be documented after administering an emergency cardiovascular medicine?
20. Describe the first actions for a patient with chest pain, hypotension and suspected ACS.

25. Key takeaways

• Cardiovascular medicines act on filling, pump function, vascular tone, clotting or rhythm.
• Always assess the patient, ECG, BP, perfusion, indication and contraindications before administration.
• Nitrates, antihypertensives and diuretics can worsen hypotension or preload-dependent states.
• Antiplatelets, anticoagulants and fibrinolytics prevent or treat thrombosis but can cause major bleeding.
• Antiarrhythmics are rhythm-specific; the wrong drug can worsen conduction or cause fatal arrhythmia.
• High-quality CPR and early defibrillation take priority over medication preparation during cardiac arrest.
• Vasoactive infusions require standard concentrations, independent checks, pumps, secure access and continuous monitoring.
• Children, pregnancy, renal disease, liver disease, frailty, asthma and shock require patient-specific review.
• Document every dose, route, rate, response, adverse effect and handover concern.

References and further study

• Cardiovascular Drugs — supplied SlideShare resource
• Unit 10 Cardiovascular Drugs — supplied SlideShare resource
• WHO — Cardiovascular diseases fact sheet
• American Heart Association — 2025 resuscitation algorithms
• AHA — 2025 Adult Advanced Life Support
• NICE — Acute coronary syndromes
• NICE — Acute heart failure
• NICE — Atrial fibrillation: diagnosis and management