Write the question before selecting the catheterization. Coronary angiography describes the lumen; RHC characterizes pulmonary and filling pressures plus flow; LHC may add LV pressure and valve gradients. Order the components that resolve the clinical uncertainty.
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Choose the diagnostic component

anatomy · pressure · flow
Clinical questionUseful testWhat still needs another method
Suspected obstructive CADCCTA 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 PHRHC when confirming and classifying hemodynamics will change the assessment.A pressure profile does not establish the cause of pulmonary vascular disease.
Uncertain HF physiologyRHC for consequential uncertainty about congestion, output, or pulmonary vascular load.A normal resting study may miss exertional disease.
Discordant valve assessmentStart 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 shuntA planned hemodynamic study with appropriate simultaneous pressures or an oximetry run.Routine pressure collection alone can miss the required diagnostic information.
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Plan the interpretation before the procedure

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.

Companion guide: Right Heart Cath & Hemodynamics provides waveform-focused teaching. This guide connects those measurements to broader diagnostic catheterization decisions.
Apply it

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.

Preparation protects both the patient and the validity of the data. Consent should cover the intended diagnostic study, material risks, alternatives, and the agreed boundary if an important lesion is found.
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Make the diagnostic plan reproducible

Before the studyRecord or reconcile
Clinical stateIndication, urgency, prior imaging, volume status, baseline symptoms, rhythm, and blood pressure.
Risk reviewKidney function, hemoglobin and platelet count when relevant, bleeding history, prior contrast reaction, pregnancy possibility when applicable, and vascular history.
Medication and sedation planReconcile anticoagulants, glucose-lowering therapy, fasting needs, airway risk, and planned sedation. Use patient- and procedure-specific instructions; avoid blanket medication holds.
Access planningRadial-first arterial access and ultrasound guidance are promoted in SCAI best practices; route selection still depends on anatomy, diagnostic needs, and operator expertise.
Measurement conditionsDocument oxygen, ventilation/PEEP, sedation, vasoactive drugs, and fluids because they can alter pressure and flow.
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Contrast and recovery

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.

Recovery includes access-site and distal-perfusion assessment, vital signs, and review of chest pain, dyspnea, neurologic change, bleeding, or allergic symptoms. Document complications, observation needs, and follow-up instructions.
Apply it

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.

Inspect the tracing before accepting the number. Level and zero the transducer to the appropriate reference, identify the chamber waveform, and preserve representative tracings with ECG and respiration.
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A pressure is a signal, a timing choice, and a reference

CheckInterpretation consequence
Reference level and zeroA height error offsets all pressures; a precise display does not correct an incorrect reference.
RespirationRead 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, PAReport mean RA; RV systolic and end-diastolic; PA systolic, diastolic, and mean. Inspect damping, catheter whip, ectopy, and implausible transitions.
PAWP qualityRequire a credible occlusion waveform and position. A wedge blood oxygen saturation approximating systemic arterial saturation supports occlusion.
PAWP timingDistinguish the respiratory phase from the cardiac-cycle measure. Mean PAWP includes atrial waves; the end-diastolic value answers a different question.
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When the wedge does not make sense

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.

If a reliable PAWP cannot be obtained, or the value is implausible, consider LVEDP measurement in the appropriate clinical context. Preserve the uncertainty rather than substituting a guessed wedge.
Apply it

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.

Every resistance calculation inherits the output error. Direct Fick uses measured oxygen consumption; estimated Fick assumes it. These are different methods, and the report must say which was used.
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Choose and name the flow method

MethodStrength and main limitation
Direct FickCO = oxygen consumption ÷ arterial–mixed venous oxygen-content difference. Requires measured oxygen consumption, representative blood samples, and a steady state.
Estimated FickAssumed oxygen consumption can be inaccurate in clinical populations. Estimated Fick and thermodilution frequently disagree and should not be used interchangeably.
ThermodilutionAverage at least three measurements with credible curves. Intracardiac shunts invalidate its use for the required pulmonary/systemic flow assessment.
Discordant outputsRecheck sampling, oxygen consumption assumptions, curve quality, rhythm, and physiology. Show both values and identify which underlies the final calculation.
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Keep units and denominators visible

QuantityFormulaInterpretation
CICO / BSAL/min/m²; indexing does not validate the measured CO.
PVR(mPAP − mean PAWP) / QpWood units; Qp equals CO when there is no shunt.
SVR80 × (MAP − mean RAP) / Qsdyn·s·cm⁻⁵; Qs is systemic flow.
Stroke volume1000 × CO / HRmL/beat when CO is in L/min.

These are steady-state pressure–flow calculations, not direct measurements of contractility or intravascular volume.

The denominator changes the resistanceSame pressure difference: 32 − 16 = 16 mmHgCO 4 L/minPVR 4 WUCO 6 L/min2.7 WUPVR = pressure difference ÷ pulmonary flow One pressure difference, two outputsPressure difference: 16 mmHg32 − 16 = 16CO 4 L/min → PVR 4 WUCO 6 L/min → PVR 2.7 WUPVR = pressure difference÷ pulmonary flow
Apply it. Both calculations are arithmetically correct. Verify which flow measurement is credible. Bars show calculated resistance, not blood movement. Without a shunt, Qp equals CO.
Mean PAWP and LVEDP are related, but they are not synonyms. PAWP estimates left atrial pressure under valid measurement conditions; LVEDP is the LV pressure at a specific end-diastolic instant.
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Name the compartment and the time

MeasureWhat it representsCommon interpretive trap
Mean PAWPThe atrial/pulmonary venous pressure burden across the cardiac cycle.Replacing it with LVEDP can erase a clinically meaningful V wave or transmitral gradient.
LVEDPLV 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 LVEDPConsider mitral disease, large V waves, atrial dysfunction, rhythm, and measurement error.Calling every difference an erroneous wedge.
LVEDP greater than PAWPConsider 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.

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Resolve disagreement systematically

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.

PH definitions use mean PAWP and PVR. Hemodynamic classification still needs the clinical context, particularly near a threshold or when left atrial and LV pressures diverge.
Apply it

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.

Read the complete coronary tree and its limitations. Angiography is a projection of the contrast-filled lumen. It does not directly measure ischemia, total plaque burden, microvascular function, or myocardial viability.
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A consistent anatomic read

ElementWhat to describe
Origins and dominanceIdentify ostia, unusual origins, and the artery supplying the posterior descending artery. Do not assume dominance from vessel size.
Left systemLeft main; LAD with septal and diagonal branches; circumflex with obtuse marginal branches; ramus when present.
Right systemRCA, acute marginal branches, and posterior descending/posterolateral distribution according to dominance.
LesionsVessel and segment, approximate severity, length/pattern, calcification, ostial or bifurcation involvement, and any ambiguity.
Flow and collateral fillingDescribe antegrade filling, distal visualization, collateral source and recipient, and whether the distal bed was adequately seen.
Prior bypass surgeryName 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.

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When an image does not answer the question

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.

A nonobstructive angiogram leaves several possible explanations for symptoms: vasomotor disease, microvascular dysfunction, noncoronary cardiac disease, and noncardiac causes. Choose the next test from the clinical presentation.
Apply it

“No obstructive CAD; no coronary functional testing performed” conveys more than “normal coronaries” when a patient still has convincing exertional angina.

Pressure ratios assess the functional effect of epicardial disease. They complement angiography and must be interpreted with valid acquisition, lesion distribution, and the clinical setting.
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Understand the two common ratios

IndexMeasurement conceptConventional significance threshold
FFRDistal coronary pressure / aortic pressure during maximal hyperemia.≤0.80
iFRDistal / 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.

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Before accepting a positive or negative number

QuestionWhy 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.

iFR-SWEDEHEART found an iFR-guided strategy noninferior to FFR guidance for its 12-month composite outcome. This strategy trial does not imply that the two indices always agree in an individual vessel.
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For FFR 0.81 with a drifting pressure wire, first resolve the technical uncertainty. A two-decimal display does not make the classification reliable.

Persistent angina with nonobstructive arteries may require a functional diagnosis. Selected patients benefit from testing that distinguishes impaired vasodilator reserve, increased microvascular resistance, and vasospasm.
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Know what each component adds

FindingDiagnostic meaningQualification
Reduced CFRLimited increase in coronary flow from rest to hyperemia.Depends on resting flow, epicardial disease, acquisition method, and hyperemia.
Increased IMRRaised microvascular resistance during hyperemia.IMR ≥25 is a commonly used abnormal threshold.
Epicardial spasmProvoked ≥90% epicardial narrowing with familiar symptoms and ischemic ECG change.The full clinical/ECG/angiographic triad matters.
Microvascular spasmFamiliar 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.

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Interpret the test as a phenotype

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.

In CorMicA, 151 patients with angina and no obstructive CAD were randomized to disclosure-linked stratified care or usual care. Angina and quality of life improved at one year; the trial did not establish a reduction in major cardiovascular events.
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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.

Use invasive valve assessment to resolve a defined discrepancy. Echocardiography remains the starting point. Match the invasive question to symptoms, flow state, rhythm, and complementary imaging.
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The gradient must match the valve and timing

QuestionRequired interpretationPitfall
Aortic stenosisAssess 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 catheterCompare 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 stenosisEvaluate 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 areaGorlin 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.
RegurgitationIntegrate 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.

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Low gradient does not always mean mild disease

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.

Apply it

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.

A shunt study separates pulmonary from systemic flow. Plan the sampling with congenital expertise when anatomy is complex. The 2025 ACHD guideline emphasizes ACHD specialist involvement in invasive-procedure planning and care.
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Localize before quantifying

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.

PatternPossible entry levelWhy confirmation matters
Caval to RA increaseAtrial-level or anomalous pulmonary venous contribution.Caval streaming and incomplete atrial mixing can mimic or obscure a step-up.
RA to RV increaseVentricular-level contribution.The sample must represent the chamber and avoid jet contamination.
RV to PA increaseGreat-artery level, such as ductal contribution.Branch PA differences and anatomy may require targeted sampling.
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Use oxygen content and the correct flow

Qp/Qs = (systemic arterial O₂ content − mixed venous O₂ content) / (pulmonary venous O₂ content − pulmonary arterial O₂ content). Saturation-only simplification assumes comparable hemoglobin and negligible dissolved-oxygen effects. High inspired oxygen can invalidate that simplification.

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.

Apply it

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.

A normal resting study may not explain exertional symptoms. In selected patients, exercise hemodynamics reveal abnormal filling-pressure or pulmonary vascular responses that are absent at rest.
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Specify the protocol and measurement conditions

MeasureCommon interpretive criterionLimitations
Exercise PAWPSupine 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 challengeApproximately 500 mL saline over 5–10 min; PAWP ≥18 mmHg suggests occult HFpEF.Selected monitored testing only; validation and long-term implications remain limited.
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Answer the physiologic question

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.

Exercise and fluid loading are different stresses. A negative result on one does not automatically exclude an abnormal response to the other. Volume loading is not appropriate merely to obtain a more dramatic number in an already congested or unstable patient.
Apply it

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.

Lead with the question answered, then show the measurements that support it. A structured report makes findings, methods, limitations, and next decisions easier to distinguish.
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A reusable diagnostic report

ComponentInclude
Indication and scopeQuestion, important prior findings, procedures performed, and components not performed.
Conditions and safetyAccess, oxygen/ventilation, rhythm, sedation, relevant drugs/fluids, contrast and radiation exposure, and complications.
HemodynamicsRA, 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 findingsAnatomy; lesion location/uncertainty; physiology values with quality checks; gradients with timing and flow context.
Provocation and shuntsProtocol, sampling sites, paired measurements, symptoms, and explicit assumptions.
Conclusion and handoffIntegrated 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.

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Resting PH: a classification example

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.

Before signing: confirm that reference level, waveform quality, cardiac/respiratory timing, and output method support the conclusion. Equalized diastolic pressures or a dip-and-plateau alone do not establish constriction; integrate respiratory ventricular interaction and imaging.
Apply it

“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.