| Clinical question | Useful test | What still needs another method |
|---|---|---|
| Suspected obstructive CAD | CCTA or stress imaging often precedes invasive angiography. High likelihood, high event risk, or severe refractory symptoms may justify direct angiography. | Intermediate lesions need physiology when functional significance will change management. |
| Unexplained dyspnea or suspected PH | RHC when confirming and classifying hemodynamics will change the assessment. | A pressure profile does not establish the cause of pulmonary vascular disease. |
| Uncertain HF physiology | RHC for consequential uncertainty about congestion, output, or pulmonary vascular load. | A normal resting study may miss exertional disease. |
| Discordant valve assessment | Start with echo and complementary imaging; selected invasive measurements can resolve disagreement. | Flow, rhythm, blood pressure, and measurement conditions must match the clinical question. |
| Possible constriction or shunt | A planned hemodynamic study with appropriate simultaneous pressures or an oximetry run. | Routine pressure collection alone can miss the required diagnostic information. |
Record the competing diagnoses, the noninvasive findings, and the result that would change the next decision. Decide in advance whether exercise, coronary functional testing, or congenital expertise is required. A standard coronary angiogram does not automatically include these studies.
A patient referred for “RHC/LHC” because of dyspnea needs a stated question: obstructive coronary disease, occult elevation of filling pressure, pulmonary vascular disease, or several of these. Each requires different measurements.
| Before the study | Record or reconcile |
|---|---|
| Clinical state | Indication, urgency, prior imaging, volume status, baseline symptoms, rhythm, and blood pressure. |
| Risk review | Kidney function, hemoglobin and platelet count when relevant, bleeding history, prior contrast reaction, pregnancy possibility when applicable, and vascular history. |
| Medication and sedation plan | Reconcile anticoagulants, glucose-lowering therapy, fasting needs, airway risk, and planned sedation. Use patient- and procedure-specific instructions; avoid blanket medication holds. |
| Access planning | Radial-first arterial access and ultrasound guidance are promoted in SCAI best practices; route selection still depends on anatomy, diagnostic needs, and operator expertise. |
| Measurement conditions | Document oxygen, ventilation/PEEP, sedation, vasoactive drugs, and fluids because they can alter pressure and flow. |
Minimize contrast to the diagnostic requirement and individualize hydration to kidney risk and congestion. PRESERVE did not show benefit from bicarbonate over saline or acetylcysteine over placebo in high-risk angiography patients; neither substitutes for a thoughtful contrast and volume plan.
A low wedge pressure after prolonged fasting and diuresis describes that treatment state. Record the context before concluding that elevated filling pressure cannot explain symptoms.
| Check | Interpretation consequence |
|---|---|
| Reference level and zero | A height error offsets all pressures; a precise display does not correct an incorrect reference. |
| Respiration | Read at end-expiration without breath-holding. With large respiratory swings in obesity, COPD, or exercise, average across at least 3–4 respiratory cycles and document the convention. |
| RA, RV, PA | Report mean RA; RV systolic and end-diastolic; PA systolic, diastolic, and mean. Inspect damping, catheter whip, ectopy, and implausible transitions. |
| PAWP quality | Require a credible occlusion waveform and position. A wedge blood oxygen saturation approximating systemic arterial saturation supports occlusion. |
| PAWP timing | Distinguish the respiratory phase from the cardiac-cycle measure. Mean PAWP includes atrial waves; the end-diastolic value answers a different question. |
Incomplete occlusion mixes pulmonary artery pressure into the apparent wedge and can falsely elevate PAWP. Reassess waveform, position, and occlusive saturation before assigning a PH phenotype. Large V waves can be real and do not by themselves prove mitral regurgitation.
PAWP 24 mmHg with a PA-like waveform and a poorly oxygenated wedge sample needs measurement review. Calling it post-capillary PH before verifying occlusion can change the diagnostic pathway incorrectly.
| Method | Strength and main limitation |
|---|---|
| Direct Fick | CO = oxygen consumption ÷ arterial–mixed venous oxygen-content difference. Requires measured oxygen consumption, representative blood samples, and a steady state. |
| Estimated Fick | Assumed oxygen consumption can be inaccurate in clinical populations. Estimated Fick and thermodilution frequently disagree and should not be used interchangeably. |
| Thermodilution | Average at least three measurements with credible curves. Intracardiac shunts invalidate its use for the required pulmonary/systemic flow assessment. |
| Discordant outputs | Recheck sampling, oxygen consumption assumptions, curve quality, rhythm, and physiology. Show both values and identify which underlies the final calculation. |
| Quantity | Formula | Interpretation |
|---|---|---|
| CI | CO / BSA | L/min/m²; indexing does not validate the measured CO. |
| PVR | (mPAP − mean PAWP) / Qp | Wood units; Qp equals CO when there is no shunt. |
| SVR | 80 × (MAP − mean RAP) / Qs | dyn·s·cm⁻⁵; Qs is systemic flow. |
| Stroke volume | 1000 × CO / HR | mL/beat when CO is in L/min. |
These are steady-state pressure–flow calculations, not direct measurements of contractility or intravascular volume.
| Measure | What it represents | Common interpretive trap |
|---|---|---|
| Mean PAWP | The atrial/pulmonary venous pressure burden across the cardiac cycle. | Replacing it with LVEDP can erase a clinically meaningful V wave or transmitral gradient. |
| LVEDP | LV pressure at end diastole, identified on a calibrated tracing with ECG timing. | Equating one end-diastolic value with mean left atrial pressure. |
| PAWP greater than LVEDP | Consider mitral disease, large V waves, atrial dysfunction, rhythm, and measurement error. | Calling every difference an erroneous wedge. |
| LVEDP greater than PAWP | Consider a stiff ventricle with a prominent late-diastolic rise and differences in timing or respiratory averaging. | Calling every normal mean PAWP proof of normal LV diastolic mechanics. |
In a large concurrent RHC/LHC cohort, disagreement was clinically meaningful. Atrial fibrillation, rheumatic valve disease, and left atrial enlargement were associated with PAWP overestimating LVEDP; age was associated with underestimation.
Compare studies under the same loading and respiratory conditions. Verify wedge occlusion and zero levels, inspect mean versus end-diastolic timing, then reconcile with echo and the clinical phenotype. Record both values when both were measured; do not silently replace one with the other.
Mean PAWP 23 with LVEDP 14 mmHg and a large V wave can reflect genuine left atrial pressure burden. The lower LVEDP alone does not establish a purely pre-capillary process.
| Element | What to describe |
|---|---|
| Origins and dominance | Identify ostia, unusual origins, and the artery supplying the posterior descending artery. Do not assume dominance from vessel size. |
| Left system | Left main; LAD with septal and diagonal branches; circumflex with obtuse marginal branches; ramus when present. |
| Right system | RCA, acute marginal branches, and posterior descending/posterolateral distribution according to dominance. |
| Lesions | Vessel and segment, approximate severity, length/pattern, calcification, ostial or bifurcation involvement, and any ambiguity. |
| Flow and collateral filling | Describe antegrade filling, distal visualization, collateral source and recipient, and whether the distal bed was adequately seen. |
| Prior bypass surgery | Name each conduit, origin, target, and visualized course/anastomosis; distinguish an unvisualized graft from an occluded graft. |
Use consistent structured terminology and link important findings to representative images.
Foreshortening, branch overlap, eccentric disease, diffuse narrowing, poor opacification, and catheter-related ostial distortion can undermine a visual estimate. Describe uncertainty explicitly. For an intermediate stenosis, add validated physiology when its functional significance matters; do not infer it from appearance alone.
“No obstructive CAD; no coronary functional testing performed” conveys more than “normal coronaries” when a patient still has convincing exertional angina.
| Index | Measurement concept | Conventional significance threshold |
|---|---|---|
| FFR | Distal coronary pressure / aortic pressure during maximal hyperemia. | ≤0.80 |
| iFR | Distal / aortic pressure during a defined diastolic period at rest, without pharmacologic hyperemia. | ≤0.89 |
These thresholds are used for intermediate epicardial stenoses. They are decision aids on continuous scales; a value close to the boundary deserves particular attention to measurement quality and context.
| Question | Why it matters |
|---|---|
| Was the pressure system credible? | Equalization, damping, stable signals, sensor position, and drift assessment affect a small pressure difference. |
| Was hyperemia adequate for FFR? | An inadequate hyperemic response can reduce the measured pressure gradient. |
| Focal or diffuse disease? | A distal ratio combines upstream pressure loss. Pullback separates a focal drop from diffuse disease. Check for wire-induced vessel straightening or ostial catheter damping before interpreting the gradient. |
| Any microvascular or acute setting limitation? | Altered microvascular function can change flow and the pressure response; routine stable-lesion interpretation may not transfer unchanged. |
Coronary function testing integrates pressure and flow measurements; FFR alone does not exclude microvascular dysfunction or vasospasm.
For FFR 0.81 with a drifting pressure wire, first resolve the technical uncertainty. A two-decimal display does not make the classification reliable.
| Finding | Diagnostic meaning | Qualification |
|---|---|---|
| Reduced CFR | Limited increase in coronary flow from rest to hyperemia. | Depends on resting flow, epicardial disease, acquisition method, and hyperemia. |
| Increased IMR | Raised microvascular resistance during hyperemia. | IMR ≥25 is a commonly used abnormal threshold. |
| Epicardial spasm | Provoked ≥90% epicardial narrowing with familiar symptoms and ischemic ECG change. | The full clinical/ECG/angiographic triad matters. |
| Microvascular spasm | Familiar symptoms and ischemic ECG changes during provocation without ≥90% epicardial constriction. | Symptoms alone do not establish this endotype. |
The 2024 ESC guideline uses CFR <2.5 as abnormal; the earlier EAPCI INOCA framework used <2.0. State the method and framework, especially for CFR 2.0–2.4, rather than mixing thresholds.
Obstructive disease, microvascular dysfunction, and vasospasm may coexist. A normal single component does not exclude every coronary mechanism. Pharmacologic provocation requires an experienced service, monitoring, and an established protocol; this guide covers interpretation rather than drug-administration technique.
CFR 1.7 and IMR 31 with FFR 0.92 support a microvascular abnormality in the appropriate setting. They do not, by themselves, prove that vasospasm was assessed or excluded.
| Question | Required interpretation | Pitfall |
|---|---|---|
| Aortic stenosis | Assess the systolic LV–aortic pressure difference with valid simultaneous signals when needed. | Peak LV minus peak aortic pressure is a peak-to-peak gradient: the peaks occur at different times. |
| Doppler versus catheter | Compare like measures and account for pressure recovery and different measurement locations. | The Doppler peak instantaneous gradient is not the catheter peak-to-peak gradient. |
| Mitral stenosis | Evaluate the diastolic atrial–LV gradient, with heart rate and flow documented. | Using uncorrected wedge timing or averaging unlike diastolic intervals can distort the gradient. |
| Valve area | Gorlin calculations combine transvalvular flow, filling/ejection time, and the relevant mean gradient. | An inaccurate output becomes an inaccurate calculated area; mixed lesions and low flow complicate interpretation. |
| Regurgitation | Integrate pressures with echo/CMR and loading conditions. | A V wave is supportive context, not a stand-alone grade of mitral regurgitation. |
Waveform fidelity, simultaneous timing, and the effects of flow are central to invasive valve assessment.
When valve area, gradient, and symptoms disagree, review stroke volume, blood pressure, rhythm, and the validity of each calculation. Selected stress echo, CT calcium assessment, or invasive measurements can help adjudicate low-flow states; one resting gradient should not replace the integrated evaluation.
Doppler peak gradient 64 mmHg and catheter peak-to-peak gradient 38 mmHg are not measurements of the same quantity. Compare mean gradients, timing, flow, and pressure recovery before calling either study wrong.
Unexpectedly high PA oxygen saturation or suspected left-to-right shunting warrants a stepwise oximetry assessment. Collect a coherent set of systemic arterial, caval, and right-heart samples in a stable state; annotate sites, oxygen administration, and timing.
| Pattern | Possible entry level | Why confirmation matters |
|---|---|---|
| Caval to RA increase | Atrial-level or anomalous pulmonary venous contribution. | Caval streaming and incomplete atrial mixing can mimic or obscure a step-up. |
| RA to RV increase | Ventricular-level contribution. | The sample must represent the chamber and avoid jet contamination. |
| RV to PA increase | Great-artery level, such as ductal contribution. | Branch PA differences and anatomy may require targeted sampling. |
Qp/Qs >1 indicates net left-to-right flow; <1 indicates net right-to-left flow under the assumptions of the calculation. Use Qp for PVR and Qs for SVR. Do not use thermodilution as the shunt flow measurement.
A reproducible oxygen-content step-up can support shunting, but the study must still reconcile Qp/Qs, pulmonary pressure/resistance, chamber volume loading, and anatomy. Qp/Qs alone is not an intervention decision.
| Measure | Common interpretive criterion | Limitations |
|---|---|---|
| Exercise PAWP | Supine end-expiratory PAWP ≥25 mmHg in the Borlaug protocol; use a threshold validated for the recorded respiratory convention. | Do not apply this threshold interchangeably to respiratory-averaged pressures or upright testing. Position, age, workload, and flow also matter. |
| PAWP/CO slope | >2 mmHg/L/min suggests an abnormal filling-pressure response. | Requires credible paired pressure/flow observations; interpret with the clinical phenotype. |
| mPAP/CO slope | >3 mmHg/L/min defines exercise PH in the ESC/ERS framework. | Does not distinguish pre- from post-capillary mechanisms by itself. |
| Fluid challenge | Approximately 500 mL saline over 5–10 min; PAWP ≥18 mmHg suggests occult HFpEF. | Selected monitored testing only; validation and long-term implications remain limited. |
Record resting state, posture, workload and symptoms, respiratory method, oxygen, pressures, and cardiac output at matched stages. Examine the pressure–flow relationship rather than a peak pressure without its flow. A respiratory artifact or erroneous output can steepen a slope artificially.
Normal resting PAWP with a reproducible PAWP/CO slope of 3.5 during exercise supports an abnormal exertional filling-pressure response. Integrate the finding with symptoms and cardiac imaging before assigning the final diagnosis.
| Component | Include |
|---|---|
| Indication and scope | Question, important prior findings, procedures performed, and components not performed. |
| Conditions and safety | Access, oxygen/ventilation, rhythm, sedation, relevant drugs/fluids, contrast and radiation exposure, and complications. |
| Hemodynamics | RA, RV, PA, mean PAWP with relevant waves, LVEDP if obtained, CO/CI with method, saturations, and derived resistance with the flow used. |
| Coronary and valve findings | Anatomy; lesion location/uncertainty; physiology values with quality checks; gradients with timing and flow context. |
| Provocation and shunts | Protocol, sampling sites, paired measurements, symptoms, and explicit assumptions. |
| Conclusion and handoff | Integrated phenotype, unresolved discrepancies, immediate consequences, and the next diagnostic or clinical decision. |
Preserve representative waveforms and images so the interpretation can be reviewed; avoid hiding method disagreement inside a single averaged number.
ESC/ERS definitions use mPAP >20 mmHg: pre-capillary PH additionally requires PAWP ≤15 and PVR >2 WU; post-capillary PH requires PAWP >15, with PVR ≤2 for isolated and >2 for combined post- and pre-capillary PH. Hemodynamics alone do not diagnose PAH.
“Elevated right and left filling pressures with low thermodilution output; estimated Fick is higher and depends on assumed oxygen consumption” preserves more clinically useful information than an unexplained single cardiac index.