Antianginal drugs: nitrates, beta blockers, calcium channel blockers
Each anti-ischaemic drug turns different dials of myocardial oxygen demand. Learn which dial each one turns, and why some of them speed the heart up.
Chapters (8)
Show how nitrates, beta blockers and calcium channel blockers each lower myocardial oxygen demand, and predict their effects on heart rate, preload and afterload.
The short version
- Oxygen demand rises with heart rate, contractility and wall tension; wall tension grows with preload and afterload.
- Nitrates dilate veins most at ordinary doses, so preload and wall tension fall.
- Beta blockers lower heart rate, contractility and blood pressure, and a slower rate lengthens diastole.
- Dihydropyridines dilate arterioles and lower afterload; non-dihydropyridines (verapamil, diltiazem) slow the rate and weaken contraction.
- Nitrates and dihydropyridines can cause reflex tachycardia: the pressure drop triggers the baroreflex and neither drug slows the heart to oppose it.
Anti-ischaemic drugs: pain relieved, pulse up
A 58-year-old man gets chest pain on the stairs. One nitroglycerin tablet under his tongue ends the pain, yet his pulse climbs from 80 to 94. Why does an anti-ischaemic drug speed up the heart?
This lesson covers the anti-ischaemic drugs used in angina: nitrates, beta blockers and calcium channel blockers. For each, you should be able to say how it lowers myocardial oxygen demand and predict its effect on heart rate, preload and afterload.[1][2]
Demand and the four dials
Ischaemia is a mismatch: demand outruns supply. Myocardial oxygen demand rises with heart rate, with contractility, and with wall tension.[1]
Wall tension grows with preload, the stretch before the beat, and with afterload, the pressure the ventricle must beat. That gives four dials: heart rate, contractility, preload and afterload. Each drug turns different dials.
Nitrates: veins, preload and reflex tachycardia
Nitroglycerin gives off nitric oxide, which raises cyclic GMP inside smooth muscle and makes it relax. At ordinary doses the veins dilate most.[1]
Blood pools in the veins, less returns to the heart, and preload falls. Lower preload means a smaller ventricle and lower wall tension, so less oxygen demand.[1]
Blood pressure dips a little, the baroreceptors notice, and the heart rate rises reflexly. That answers the opening puzzle: the pulse climbs because of the pressure drop, not because the drug stimulates the heart.
Beta blockers: rate, force and diastole
Beta blockers block beta-1 receptors in the heart. Heart rate falls, contractility falls, and blood pressure falls, which also eases afterload.[1][2]
A slower rate also lengthens diastole, the time when the left ventricle receives its coronary flow. So beta blockers lower demand and help supply.[1]
Take care in vasospastic angina, asthma and severe depression.[1]
Calcium channel blockers: two families
| Family | Examples | Main target | Effect |
|---|---|---|---|
| Dihydropyridines | Amlodipine, nifedipine | Vessels | Arterioles dilate, afterload falls; barely touch the heart muscle |
| Non-dihydropyridines | Verapamil, diltiazem | Heart | Slow the rate and weaken contraction, lowering demand like a beta blocker |
As with nitrates, the pressure drop from a dihydropyridine can trigger reflex tachycardia. Ankle swelling and flushing are common.[1][2]
Verapamil and diltiazem are avoided in bradycardia and heart block.[1][2]
The rule: which dial each anti-ischaemic drug turns
| Drug class | Dial turned down | Heart rate |
|---|---|---|
| Nitrates | Preload | May rise (reflex) |
| Dihydropyridines | Afterload | May rise (reflex) |
| Beta blockers | Heart rate and contractility | Falls |
| Non-dihydropyridines | Heart rate and contractility | Falls |
Notice something: the two drug groups that cause reflex tachycardia are the ones that do not slow the heart. So a beta blocker is often added to a dihydropyridine or a nitrate, to blunt that tachycardia.[1]
Practice question
Original · USMLE styleA 61-year-old man with stable exertional angina starts a new once-daily tablet. At follow-up two weeks later he reports fewer episodes of chest pain but new ankle swelling. Lungs are clear and there are no signs of heart failure. Findings before and after starting the drug:
| Pulse | 72/min before; 88/min after |
|---|---|
| Blood pressure | 142/88 mm Hg before; 118/70 mm Hg after |
| Central venous pressure | normal before; unchanged after |
Common questions
How do nitrates relieve angina?
At ordinary doses nitrates dilate the veins most. Less blood returns to the heart, so preload falls, the ventricle is smaller, wall tension drops and oxygen demand falls.
Why do nitrates and dihydropyridines cause reflex tachycardia?
They lower blood pressure, the baroreceptors notice, and the heart rate rises reflexly. Neither group slows the heart directly.
What is the difference between dihydropyridine and non-dihydropyridine calcium channel blockers?
Dihydropyridines such as amlodipine and nifedipine work mainly on vessels and lower afterload. Non-dihydropyridines, verapamil and diltiazem, act on the heart and slow the rate and weaken contraction.
Why are nitrates not combined with PDE-5 inhibitors?
Blood pressure can collapse when a nitrate is combined with a phosphodiesterase-5 inhibitor.
Transcript
Read the full narration, by chapter604 words
0:00Pain relieved, pulse up: the puzzle
A 58-year-old man gets chest pain on the stairs. One nitroglycerin tablet under his tongue ends the pain. Yet his pulse climbs from 80 to 94. Why does an anti-ischaemic drug speed up the heart? Today: show how nitrates, beta blockers and calcium channel blockers each lower myocardial oxygen demand, and predict their effects on heart rate, preload and afterload.
0:25Demand and the four dials
Last time, we saw that ischaemia is a mismatch: demand outruns supply. Demand rises with heart rate, with contractility, and with wall tension. Wall tension grows with preload, the stretch before the beat, and with afterload, the pressure the ventricle must beat. So there are four dials: heart rate, contractility, preload and afterload. Each drug turns different dials.
0:53Nitrates: veins, preload and reflex tachycardia
Start with nitrates. Nitroglycerin gives off nitric oxide, which raises cyclic GMP inside smooth muscle and makes it relax. At ordinary doses the veins dilate most. Blood pools in the veins, less returns to the heart, and preload falls. Lower preload means a smaller ventricle and lower wall tension, so less oxygen demand. Blood pressure dips a little, the baroreceptors notice, and the heart rate reflexly rises. That is our opening puzzle. Two warnings: headache from vasodilation, and never combine nitrates with a phosphodiesterase five inhibitor, because blood pressure can collapse.
1:36Beta blockers: rate, force and diastole
Next, beta blockers. They block beta one receptors in the heart. Heart rate falls, contractility falls, and blood pressure falls. Three dials turn down. A slower rate also lengthens diastole, the time when the left ventricle receives its coronary flow. So beta blockers lower demand and help supply. Care in vasospastic angina, asthma and severe depression.
2:03Calcium channel blockers: two families
Now calcium channel blockers, which come in two families. Dihydropyridines, like amlodipine and nifedipine, work mainly on vessels. They dilate arterioles, so afterload falls. They barely touch the heart muscle. As with nitrates, the pressure drop can trigger reflex tachycardia. Ankle swelling and flushing are common. Non-dihydropyridines, verapamil and diltiazem, act on the heart. They slow the rate and weaken contraction, so they lower demand like a beta blocker does. That is why they are avoided in bradycardia and heart block.
2:42The rule: which dial each drug turns
The rule: nitrates drop preload, dihydropyridines drop afterload, and beta blockers and non-dihydropyridines drop rate and contractility. Notice something. The two drugs that cause reflex tachycardia are the ones that do not slow the heart. So a beta blocker is often added to a dihydropyridine or a nitrate, to blunt that tachycardia.
3:07Practice question
Your turn. A 61-year-old man with stable angina starts a new once-daily tablet. Two weeks later his pulse has risen from 72 to 88. Blood pressure has fallen from 142 over 88 to 118 over 70. He has new ankle swelling, and his central venous pressure is unchanged. Which drug is he most likely taking? A, metoprolol. B, verapamil. C, isosorbide mononitrate. D, amlodipine. E, diltiazem. Pause here and decide. A is out: a beta blocker slows the pulse, it does not speed it. B is out: verapamil lowers heart rate, so the pulse would fall. E is out for the same reason: diltiazem is also a rate-slowing drug. C is tempting, because nitrates also cause reflex tachycardia. But nitrates dilate veins, so venous pressure would fall, and ankle swelling is not typical of nitrates. So the answer is D: amlodipine dilates arterioles, pressure drops, the pulse reflexly rises, and ankles swell.
4:24High-yield recap and next lesson
Three things to keep. One: nitrates dilate veins, lower preload and wall tension, and can cause reflex tachycardia. Two: beta blockers and non-dihydropyridines lower rate and contractility, so they slow the pulse. Three: dihydropyridines dilate arterioles, lower afterload, and can cause reflex tachycardia and ankle swelling. Next up: complications of myocardial infarction, by timeline.
Sources
Numbers in the text, e.g. [1], point here- Contemporary Antianginal Therapy (2026). PMC12920388. pmc.ncbi.nlm.nih.gov/articles/PMC12920388
- Present and Future Options for Pharmacotherapy in Cardiovascular Disease (2026). PMC13303951. pmc.ncbi.nlm.nih.gov/articles/PMC13303951
- Calcium Channel Blockers in Critical Care (2026). PMC13214944. pmc.ncbi.nlm.nih.gov/articles/PMC13214944
Example patient values are illustrative.
The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.
Image credits. All video diagrams are original (code-drawn); no third-party artwork is used in the video. Thumbnail A: "Anatomical Human Heart" 3D model by Nexal 3D (BlenderKit, royalty-free licence).
Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-CARD-021.
For exam study only, not medical advice. Read the medical disclaimer.
In this series
Playlist on YouTube- EP 01Pressure-volume loop explained: four phases, four valve events5:00
- EP 02Preload on the pressure-volume loop: EDV, stroke volume and the EDPVR5:04
- EP 03Afterload on the pressure-volume loop4:49
- EP 04Contractility on the pressure-volume loop: the ESPVR explained5:17
- EP 05Wiggers diagram explained: the cardiac cycle step by step5:30
- EP 06The Frank-Starling curve: preload, inotropy and heart failure4:44
- EP 07Aortic stenosis vs mitral regurgitation on the pressure-volume loop5:41
- EP 08Fick principle: how to calculate cardiac output5:07
- EP 09HFrEF vs HFpEF on the pressure-volume loop5:33
- EP 10Poiseuille's law and vascular resistance: why arterioles matter5:15
- EP 11Venous return and cardiac function curves: where they cross5:11
- EP 12The baroreceptor reflex: from stretch to vagal and sympathetic output5:17
- EP 13Myocardial oxygen supply and demand: why tachycardia causes ischaemia4:50
- EP 14Unstable angina vs NSTEMI vs STEMI: from plaque to ACS4:50
- EP 15Antianginal drugs: nitrates, beta blockers, calcium channel blockers4:56
- EP 16Complications of myocardial infarction, by timeline4:59