Cardiac MRI — vasodilator stress perfusion

Three short-axis slices at basal, mid and apical levels for perfusion, plus full cine and late enhancement coverage.

Typical, not policy

Timings, volumes and delays here are representative values drawn from published guidance. Scanner generation, injector, cardiac output and local preference all move them. Confirm against your department's own protocol before you rely on a number.

Premedication

Given to make the acquisition work, not to treat the patient. Doses are typical — confirm against your local protocol and prescribe within your own governance.

Adenosine (vasodilator stress agent)

The vasodilator IS the test. Adenosine dilates the normal microcirculation and leaves a territory subtended by a flow-limiting stenosis unable to increase flow, so the perfusion defect that appears is the finding. Without an adequate haemodynamic response there is no stress and the study answers nothing.

Dose and route: Typically a continuous intravenous infusion of 140 micrograms/kg/min through a dedicated cannula, separate from the contrast line. Some protocols escalate to 170 and occasionally 210 micrograms/kg/min for a further period where the haemodynamic response is inadequate — escalation practice varies between centres and is not universal.
When: Infuse for roughly 3-4 minutes before injecting the perfusion bolus, and continue through the first-pass acquisition. Judge the effect rather than the clock: an acceptable response is usually taken as a rise in heart rate of about 10 beats/min or more, a fall in systolic pressure, and symptoms such as flushing, chest discomfort or breathlessness. Document the response — an undocumented stress cannot be distinguished from a failed one at reporting.
Do not give if: Caffeine within roughly 12-24 hours competitively antagonises adenosine at the A2A receptor and abolishes the effect. This is the commonest reason a stress perfusion study fails, and it is entirely preventable — the abstention instruction belongs on the appointment letter, not just in the department. Some centres extend the window to 24 hours; confirm locally.
Theophylline-type drugs competitively antagonise adenosine like caffeine does, and are withheld for around 24-48 hours. DIPYRIDAMOLE DOES THE OPPOSITE and must not be filed with them: it blocks adenosine reuptake and POTENTIATES it, so the risk is not a failed test but an exaggerated and prolonged response — high-grade AV block, hypotension, bronchospasm. Withhold for at least 24 hours (it is also in Asasantin and Aggrenox, which patients rarely name as dipyridamole), and have aminophylline drawn up. Reading this interaction as blunting invites the dangerous response, which is to escalate the dose.
Second- or third-degree AV block or sinoatrial disease without a functioning pacemaker: adenosine causes transient high-grade block and is contraindicated.
Severe reactive airways disease — active bronchospasm or severe asthma — is a contraindication; adenosine can precipitate bronchospasm.
Also avoid in symptomatic hypotension, decompensated heart failure, severe aortic stenosis, and acute coronary syndrome.
Aminophylline is the reversal agent and must be immediately available in the room, drawn up and dosed in advance, alongside full resuscitation equipment and staff competent to use it. Typical reversal is around 50-250 mg intravenously, given slowly and titrated to symptoms.
Warn the patient that flushing, chest tightness and breathlessness are expected effects that stop within seconds of the infusion ending — the half-life is of the order of seconds. Unwarned patients move or abandon the scan at exactly the moment the first pass is being acquired.
If unsuitable: Regadenoson is the usual alternative where a fixed dose and a single peripheral cannula are preferred, and is often better tolerated in mild airways disease — though it is not free of bronchospasm risk. Where vasodilator stress is contraindicated altogether, dobutamine stress CMR assesses inducible wall motion abnormality instead of perfusion; it is a different test with a different endpoint, needs continuous physician presence, and has its own antidote in a short-acting beta-blocker.

Regadenoson (selective A2A agonist)

Alternative vasodilator stress. A selective A2A agonist given as a single fixed bolus, which removes weight-based infusion calculation and the need for a second dedicated cannula and an infusion pump.

Dose and route: A fixed 400 microgram intravenous bolus over about 10 seconds, followed immediately by a saline flush. Not weight-adjusted — the fixed dose is the point of the agent.
When: The contrast bolus follows roughly 45-60 seconds after the regadenoson, at peak hyperaemia. The hyperaemic window is shorter and less easily prolonged than an adenosine infusion, so bolus timing is less forgiving; where rest perfusion is also acquired, allow the usual washout interval between.
Do not give if: The same caffeine problem applies: methylxanthine intake within roughly 12-24 hours blunts the response and is the leading avoidable cause of a failed study.
High-grade AV block or sinus node disease without a pacemaker.
Severe reactive airways disease — selectivity for A2A reduces but does not remove bronchospasm risk, and bronchospasm and respiratory arrest are described.
Symptomatic hypotension and unstable coronary syndromes.
Aminophylline must be immediately available. Its longer duration of action relative to adenosine means an adverse effect does not simply stop when an infusion is switched off, which makes ready reversal more rather than less important.
Headache, flushing and dyspnoea are common and expected; seizures have been reported, and aminophylline is not recommended for treating a regadenoson-associated seizure.
If unsuitable: Adenosine infusion where the contraindication is specific to regadenoson, or dobutamine stress where any vasodilator is contraindicated.

Dobutamine (± atropine) — where vasodilator stress is contraindicated

Inotropic stress. Used when adenosine and regadenoson are both contraindicated, most often for severe reactive airways disease or high-grade conduction disease. The endpoint is a new inducible wall motion abnormality on cine imaging, not a perfusion defect, so it is a different test rather than a substitute drug in the same protocol.

Dose and route: Typically an intravenous infusion starting at 10 micrograms/kg/min and escalating in steps of 10 every 3 minutes to a usual maximum of 40 micrograms/kg/min, with incremental atropine (commonly 0.25-0.5 mg boluses to around 1-2 mg total) added where the target heart rate is not reached.
When: Escalate at roughly 3-minute stages with cine imaging at each stage, to a target of about 85% of age-predicted maximum heart rate or until an endpoint is reached.
Do not give if: Requires continuous ECG, blood pressure and in-magnet monitoring with a physician present throughout and immediate access to the patient — this is the most demanding protocol in the cardiac MRI list and should not be run by a team unfamiliar with it.
Contraindicated in significant arrhythmia, severe hypertension, severe aortic stenosis, hypertrophic obstructive cardiomyopathy, and acute coronary syndrome.
A short-acting intravenous beta-blocker is the reversal agent and must be drawn up before the infusion starts.
Serious complications including sustained ventricular arrhythmia are uncommon but more frequent than with vasodilator stress; the elevated risk is why it is the second choice rather than an equivalent option.
If unsuitable: Where neither vasodilator nor inotropic stress is safe, the ischaemia question is better answered outside the magnet — anatomical assessment by CT coronary angiography, or invasive assessment with physiology. Practice varies and this is a decision to take with the referring cardiologist rather than at the scanner.

When to use it

Stable chest pain with intermediate pre-test probability of coronary disease.
Assessment of the functional significance of a known coronary stenosis.
Ischaemia assessment where nuclear perfusion or CT is unsuitable, including younger patients in whom radiation matters.
Suspected microvascular dysfunction.
Combined ischaemia and viability assessment in one sitting before revascularisation.

Technique

Saturation-recovery gradient-echo perfusion imaging of three short-axis slices every heartbeat during the first pass of the contrast bolus.
Vasodilator infusion to a documented endpoint before contrast injection; symptoms, heart rate and blood pressure are recorded throughout.
Rest perfusion is acquired after an interval, or omitted where late enhancement and stress perfusion answer the question — practice differs between centres.
Late gadolinium enhancement completes the study and is what separates infarct from inducible ischaemia.

Where it goes wrong

Caffeine not withheld, which blunts adenosine and produces a falsely negative study.
Dark-rim endocardial artefact on first pass being read as a genuine perfusion defect.
Bolus too slow or too dilute, flattening the first-pass signal curve.
Insufficient vasodilator effect not recognised because haemodynamic response was not documented.
Bronchospastic disease not screened for before adenosine.

Clinical questions that reach this study

Suspected pulmonary hypertension and CTEPH Stable chest pain — suspected coronary artery disease Suspected myocarditis Cardiomyopathy — characterisation and assessment Suspected heart failure Valvular heart disease — assessment and intervention planning

Contrast

Gadolinium, intravenous

An extracellular macrocyclic gadolinium agent, split between the two acquisitions: typically about 0.05-0.1 mmol/kg as a rapid bolus by power injector at roughly 3-5 mL/s with a 20-30 mL saline chaser for each first pass, and a further bolus so that the cumulative dose reaches approximately 0.1-0.2 mmol/kg before late enhancement imaging. Keep the cumulative dose within the licensed limit for the agent in use.

This is a pharmacological stress test performed inside a magnet: resuscitation equipment, monitoring and staff competence are part of the protocol, not an add-on.
The perfusion bolus is deliberately smaller and faster than a routine enhanced study. A large slow bolus saturates the T1 signal in the left ventricular cavity, which flattens the arterial input function and makes quantitative or semi-quantitative analysis unusable; a small tight bolus is what the first-pass curve depends on.
Dynamic timing: the vasodilator runs first to a documented haemodynamic endpoint, the bolus is injected at peak effect, and saturation-recovery images are acquired every heartbeat from injection through roughly 40-60 s so that both the cavity input and the myocardial upslope are captured. Where rest perfusion is performed it follows after an interval of about 10-15 minutes for contrast washout, and late enhancement imaging conventionally begins around 10-15 minutes after the final bolus.

Acquisition

Breathing: Breath-hold during each first-pass acquisition; the patient must be coached beforehand because the stress agent causes breathlessness.
Preparation: Breath-hold capacity and rhythm are the two determinants of study quality: state atrial fibrillation, frequent ectopy or inability to hold breath. Cardiac devices are common in this population; establish conditionality, generator model and local device-scanning arrangements before booking rather than at the scanner. For stress perfusion, withhold caffeine for the locally specified interval and check for reactive airways disease before adenosine or regadenoson.

Phases

Each phase is authored once and shared across every protocol that uses it, so the physiology below is the same wherever you meet it.

Non-contrast (unenhanced)No injection. Acquired before any contrast is given.
Shows intrinsic tissue attenuation, and nothing else. The transferable principle is that contrast is anti-signal for anything that is already dense: calcification, acute haemorrhage, urinary and biliary calculi, iodine-containing or haemorrhagic fluid, and intrinsic fat all lose conspicuity, or become uninterpretable, once surrounding tissue enhances. It is also the only baseline against which enhancement can be measured, so any protocol that quantifies enhancement or washout (a lesion "enhances by X HU", adrenal absolute washout, renal mass characterisation) is arithmetically impossible without it. Conversely, an unenhanced series adds dose and no information whenever the question is purely about vascularity or perfusion.
Dynamic contrast-enhanced series (multiphase gadolinium)A late arterial acquisition timed to about 15–20 s after contrast reaches the target artery (fluoroscopically triggered or test-bolus timed), a portal venous/early venous acquisition roughly 15–30 s later, and a delayed or transitional acquisition at about 2–3 min. Confirm locally.
The same volume is imaged repeatedly across the passage of a gadolinium bolus, so enhancement is read as a curve rather than as a single value. The transferable principle is that MR sees T1 shortening rather than photon attenuation, which removes the dose penalty for repeating an acquisition and therefore makes the TEMPORAL PATTERN the primary datum: rapid arterial uptake followed by relative fall-off, progressive centripetal fill-in, and persistent late enhancement are three different diagnoses that can share an identical single-timepoint appearance. Because everything downstream depends on hitting the arterial peak within a few seconds, the phase is unusually sensitive to circulation time and to breath-hold failure, and a mistimed arterial acquisition cannot be recovered by post-processing.
Delayed / equilibrium (washout) phaseQuestion-dependent: ~3–5 min for hepatic equilibrium/washout, ~15 min for adrenal absolute-washout calculations. Confirm locally.
Intravascular and interstitial compartments have equilibrated and contrast is being cleared, so most normal tissue is falling in attenuation. The transferable principle is that the diagnostic information is now in the RATE OF CHANGE rather than in the absolute density: tissues with rapid capillary exchange and a small interstitium wash out quickly, whereas fibrous, myxoid or otherwise expanded interstitial spaces retain contrast and become relatively dense. That single mechanism underlies delayed enhancement of scar and fibrosis, retained enhancement in cholangiocarcinoma and haemangioma fill-in, and the arithmetic of adrenal washout — all of which require a matched earlier acquisition to be interpretable at all.

Safety checks this protocol carries

Derived from the contrast agent and phases above, not authored here — which is why they cannot drift apart from what the protocol actually does.

Prior contrast reaction and elective premedication· nurse pre scan
Kidney function and gadolinium-based contrast· radiographer at scan
Intravenous access adequate for the planned injection· radiographer at scan
Metformin and iodinated contrast· radiographer at scan
MR safety screening for implants and foreign bodies· radiographer at scan
Sedation or anaesthesia for a child· nurse pre scan
Kidney function and intravenous iodinated contrast· radiographer at scan