Myocardial oxygen supply and demand: why tachycardia causes ischaemia
Heart rate, contractility and wall tension set demand; coronary flow, mostly in diastole, sets supply. Speeding up the heart raises one and shrinks the other.
Chapters (9)
Explain the determinants of myocardial oxygen demand and supply, including why left coronary flow occurs mainly in diastole and how tachycardia provokes ischaemia.
The short version
- Myocardial oxygen demand is driven by heart rate, contractility and wall tension.
- Supply is coronary blood flow times the oxygen content of blood; the heart already extracts most of the oxygen at rest, so extra demand must be met by extra flow.
- Left coronary flow happens mainly in diastole, driven by aortic diastolic pressure minus left ventricular end-diastolic pressure.
- Tachycardia raises demand and shortens diastole at the same time.
- Behind a severe fixed stenosis the small vessels are already dilated, so flow cannot rise and ischaemia appears at a particular rate.
Myocardial oxygen supply and demand: the puzzle
A 66-year-old woman walks briskly on a treadmill. At rest her heart rate is 66 and she feels fine. At 110, her chest tightens. Why would speeding up starve the heart of oxygen?
The answer lies in myocardial oxygen supply and demand. Think of the heart muscle as a shop with a demand side and a supply side. Tachycardia pushes demand up and cuts supply down in the same moment.[1]
The demand side: rate, contractility and wall tension
Myocardial oxygen demand has three drivers.[1]
- Heart rate, because every beat costs energy.
- Contractility, because a harder squeeze costs more.
- Wall tension, the force each fibre must carry.
Peak systolic wall stress is a main determinant of myocardial oxygen use.[1] Wall tension rises with ventricular pressure and radius, and falls with wall thickness. So a high afterload, or a dilated ventricle, raises demand.
The supply side: flow times oxygen content
The muscle already takes most of the oxygen at rest, so it cannot simply extract more.
Because extraction is already high at rest, extra demand has to be met by extra flow. That is why the timing of the flow matters so much.
Coronary blood flow in diastole: when does the flow happen?
In the left ventricle, systole squeezes the vessels inside the muscle, so flow is impeded. Left coronary flow happens mainly in diastole.[1][2]
Supply falls with a low aortic diastolic pressure, a high end-diastolic pressure, or a short diastole.
The inner layer, the subendocardium, is perfused only in diastole, so it is the most vulnerable, and ischaemia starts there.[1][2]
Why tachycardia shortens diastole disproportionately
| Heart rate | One cycle | Diastole |
|---|---|---|
| 75/min | about 0.8 s | roughly 0.5 s |
| 150/min | 0.4 s | roughly 0.15 s |
Systole shortens a little, but diastole collapses. The rate doubled, yet diastolic time fell to less than a third. Tachycardia shortens the relative duration of diastole.[1]
Tachycardia meets a fixed stenosis: no flow reserve
In a healthy heart, the small coronary vessels dilate and flow keeps up. Behind a severe fixed narrowing, those vessels are already dilated, so flow cannot rise.
The heart is fine at rest, then ischaemic at one particular rate, and rest relieves it. That was the woman on the treadmill: at 66 supply matched demand, at 110 it did not.
Practice question
Original · USMLE styleA 64-year-old man undergoes a treadmill exercise test for evaluation of exertional chest discomfort. At a heart rate of 142/min he develops chest pressure, and the ECG shows new ST-segment depression in leads V3-V5. Blood pressure at that time is 148/88 mm Hg. Haemoglobin is 14.2 g/dL. Symptoms and ECG changes resolve within 4 minutes of rest. Coronary angiography shows a high-grade fixed stenosis of the left anterior descending artery with no evidence of spasm.
Common questions
What are the determinants of myocardial oxygen demand?
Heart rate, contractility and wall tension. Wall tension rises with ventricular pressure and radius and falls with wall thickness, so high afterload or a dilated ventricle raises demand.
Why does left coronary blood flow occur mainly in diastole?
In systole the contracting muscle squeezes the vessels inside the left ventricular wall and impedes flow. Most flow therefore happens in diastole, driven by aortic diastolic pressure minus left ventricular end-diastolic pressure.
Why does tachycardia cause ischaemia?
It raises oxygen demand and shortens diastole, the phase in which the left ventricle is perfused. Behind a severe fixed stenosis, flow cannot rise to compensate.
Why is the subendocardium the first layer to become ischaemic?
It is perfused only in diastole, so it is the most vulnerable layer when supply and demand are mismatched.
Transcript
Read the full narration, by chapter607 words
0:00A walker, a heart rate and a puzzle
A 66-year-old woman walks briskly on a treadmill. At rest her heart rate is 66 and she feels fine. At 110, her chest tightens. Why would speeding up starve the heart of oxygen? Today: name what drives myocardial oxygen demand and supply, and explain why tachycardia provokes ischaemia.
0:22Recap, then the shop: demand and supply
Earlier, the cardiac cycle gave us two phases, systole and diastole. Keep that split in mind. Think of the heart muscle as a shop with a demand side and a supply side. Demand has three drivers. Heart rate, because every beat costs energy. Contractility, because a harder squeeze costs more. And wall tension, the force each fibre must carry.
0:48Wall tension: why afterload and dilation raise demand
Tension rises with ventricular pressure and radius, and falls with wall thickness. So high afterload, or a dilated ventricle, raises demand. Demand: rate, contractility, wall tension. Supply is coronary blood flow times the oxygen
1:04Supply: flow times oxygen content, and why extraction cannot rise
content of blood. The heart cannot simply extract more, because it already takes most of the oxygen at rest. So extra demand must be met by extra flow.
1:18When does the flow happen? Diastole and the subendocardium
Now the twist: when does that flow happen? In the left ventricle, systole squeezes the vessels inside the muscle, so flow is impeded. Left coronary flow happens mainly in diastole. The driving pressure is the aortic diastolic pressure minus the left ventricular end-diastolic pressure. So supply falls with a low aortic diastolic pressure, a high end-diastolic pressure, or a short diastole. The inner layer, the subendocardium, is perfused only in diastole and works hardest, so ischaemia starts there. Now speed the heart up.
1:56Speeding up: diastole shrinks faster than the cycle
Illustrative numbers. At 75 beats a minute, one cycle lasts about eight tenths of a second, and diastole takes roughly half a second. At 150, the cycle is four tenths of a second. Systole shortens a little, but diastole collapses to roughly 15 hundredths. The rate doubled, yet diastolic time fell to less than a third.
2:22Tachycardia meets a fixed stenosis
Tachycardia raises demand and cuts supply at the same time. In a healthy heart, the small coronary vessels dilate and flow keeps up. Behind a severe fixed narrowing, those vessels are already dilated, so flow cannot rise. The heart is fine at rest, then ischaemic at one particular rate, and rest relieves it. That was our walker.
2:46Practice question
Let's test it. A 64-year-old man has chest pressure on a treadmill test, with ST depression, at a heart rate of 142. Blood pressure is 148 over 88, and haemoglobin is normal. Angiography shows a high-grade fixed stenosis in the left anterior descending artery, with no spasm. Which best explains his symptoms at this rate? A: a fall in aortic diastolic pressure, lowering coronary perfusion. B: a larger share of the cycle spent in diastole, raising coronary flow. C: reduced oxygen extraction by the muscle at a given flow. D: higher demand with less diastolic time for flow through a fixed stenosis. E: lower wall tension from reduced afterload, lowering demand. Take a moment. A first. His pressure is normal, so diastolic perfusion pressure did not collapse. Struck. B is backwards. At a fast rate the diastolic share falls. Struck. C fails because extraction is already high at rest; it cannot fall to explain this. Struck. E is the wrong direction. Lower wall tension would reduce demand, not cause ischaemia. Struck. D is the answer: faster rate raised demand and shortened diastole, and a fixed stenosis left no flow reserve.
4:21Recap and next lesson
Recap. Demand is rate, contractility and wall tension. Left coronary flow is mainly diastolic, driven by aortic diastolic minus end-diastolic pressure. Tachycardia raises demand while shortening diastole, and a fixed stenosis cannot compensate. Next: how a plaque ruptures and turns this mismatch into a heart attack. From Plaque to Acute Coronary Syndrome.
Sources
Numbers in the text, e.g. [1], point here- The myocardial oxygen supply:demand index revisited. J Am Heart Assoc 2014. PMC3959699. pmc.ncbi.nlm.nih.gov/articles/PMC3959699
- Assessing Coronary Blood Flow Physiology in the Cardiac Catheterisation Laboratory. Curr Cardiol Rev 2017. PMC5633718. pmc.ncbi.nlm.nih.gov/articles/PMC5633718
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, charts, the balance, the strips and all handwriting are original (code-drawn); no third-party artwork is used in the video. Thumbnail plate: Servier Medical Art (smart.servier.com), "Heart vascularization", licensed under CC BY 4.0, recoloured and resized.
Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-CARD-019.
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