Connect pressure, flow, ventricular loading, valve disease, and shock to explain clinical findings and choose what to measure before changing treatment.
A patient can have a respectable blood pressure and inadequate cardiac output. Another can have a low pressure while pumping a large volume each minute. Hemodynamics becomes useful when you separate flow, the pressure gradient driving that flow, and the resistance or obstruction between two measurement sites. Before choosing a treatment, decide which part of that relationship has failed.
Pressure needs an address
Cardiac output is heart rate multiplied by stroke volume. A rate of 80 per minute and stroke volume of 60 mL produce 4.8 L/min. Cardiac index divides output by body surface area, allowing a more useful comparison between differently sized adults. An apparently normal output may still be inadequate for unusually high metabolic demand. Oxygen delivery also depends on hemoglobin and arterial oxygen saturation, so output alone cannot establish that tissues receive enough oxygen.
CO = HR × SV SV = EDV − ESV EF = SV ÷ EDV SVR = 80 × (MAP − RAP) ÷ CO
Use cardiac output in L/min and pressures in mmHg for systemic vascular resistance in dyn·s·cm⁻⁵. For example, MAP 70, right atrial pressure 10, and output 4 give SVR 1,200. The approximation MAP ≈ CO × SVR requires consistent units and neglects right atrial pressure. A resistance calculated from pressure and output is a description of the circulation, not a direct measurement of myocardial strength. [1]
Systemic veins → RA → RV RAP or CVP describes the pressure receiving systemic venous return.
RV → pulmonary arteries → lungs PVR = (mean PA pressure − PAWP) ÷ CO, expressed in Wood units.
Pulmonary veins → LA → mitral valve → LV A valid wedge pressure estimates upstream left atrial pressure. An obstructed mitral valve can separate it from LV diastolic pressure.
LV → aortic valve → arteries A stenotic aortic valve can separate LV systolic pressure from aortic systolic pressure.
Read a pressure at its actual location. A high pressure upstream of an obstruction does not establish adequate filling downstream.
Check transducer leveling, waveform quality, respiratory conditions, and whether a wedge measurement is technically valid. Positive intrathoracic pressure can raise measured filling pressures without the same increase in distending pressure. PAWP and LV end-diastolic pressure also sample different aspects of the cycle. Their relationship is particularly unreliable with mitral disease or large atrial pressure waves. [7]
Try it here · Checkpoint 1 of 3
Make your prediction before reading the choices. A first attempt is just a starting point.
Case 1
Show answer and explanations for case 1
A. 15 dyn·s·cm⁻⁵ (Why this does not fit)
Fifteen is the pressure gradient divided by output in Wood units. Conversion to dyn·s·cm⁻⁵ requires multiplication by 80.
B. 1,400 dyn·s·cm⁻⁵ (Why this does not fit)
This uses MAP alone. Subtracting the measured downstream right atrial pressure gives a gradient of 60 mmHg.
C. 1,200 dyn·s·cm⁻⁵ (Best answer)
The calculation is 80 × (70 − 10) ÷ 4.0. The measured right atrial pressure belongs in the gradient.
D. 320 dyn·s·cm⁻⁵ (Why this does not fit)
Multiplying output by 80 omits the pressure gradient and does not calculate resistance.
Takeaway: Resistance requires a pressure difference, flow, and the correct unit conversion.
Preload is myocardial stretch before contraction. End-diastolic volume is a practical surrogate, but pressure is not volume. Compliance describes how much volume changes for a pressure change, ΔV/ΔP. A stiff chamber develops a larger pressure increase for the same added volume. Diastolic elastance, ΔP/ΔV, is the local inverse of compliance. The diastolic relationship is curved, so compliance depends on the operating volume as well as the tissue. External pericardial pressure also affects distension. [5]
Afterload is the load opposing systolic shortening. Arterial resistance matters, but so do aortic pressure, arterial properties, valve obstruction, chamber radius, and wall thickness. The simplified wall-stress relationship links higher pressure or radius to greater stress and a thicker wall to lower stress. A patient with severe aortic stenosis can therefore have very high LV afterload despite an ordinary cuff pressure.
Contractility describes force generation at comparable loading conditions; EF is influenced by both loading and contraction. Preserved EF does not exclude HFpEF. The ASE approach integrates mitral inflow, tissue velocities, pulmonary pressure estimates, atrial findings, rhythm, and the clinical setting; E/A alone cannot establish a complete diastolic diagnosis. [10][3]
1 mitral opening, 2 mitral closure, 3 aortic opening, 4 aortic closure. The drawing is schematic, with no patient pressure scale. A vertical side requires constant ventricular volume.
Loop width is EDV minus ESV. Enclosed area represents external ventricular stroke work, not all myocardial energy use. In a controlled comparison, extra preload widens the loop; increased afterload leaves more end-systolic volume; increased inotropy permits a smaller end-systolic volume. The end-systolic pressure-volume relationship describes systolic chamber behavior. It must not be confused with the diastolic stiffness curve. A tall pressure loop alone does not prove higher contractility. [4]
Valves decide where the volume goes
Four lesions, four useful distinctions
Lesion
Main pressure or flow problem
LesionAortic stenosis
Main pressure or flow problemLV systolic pressure exceeds aortic pressure across the obstructed outlet. Chronic pressure loading favors concentric hypertrophy.
LesionAortic regurgitation
Main pressure or flow problemDiastolic aortic runoff returns blood to the LV. Chronic adaptation can produce a large total stroke volume and wide pulse pressure.
LesionMitral stenosis
Main pressure or flow problemLA pressure must exceed LV diastolic pressure across the narrowed inlet. Tachycardia shortens the time available for filling.
LesionMitral regurgitation
Main pressure or flow problemSystolic LV emptying includes backward flow into the LA. Total ejection can overstate effective systemic output.
A Doppler peak gradient estimates the greatest simultaneous pressure difference using 4v² when proximal velocity is negligible. The mean gradient averages instantaneous gradients over ejection. Catheter peak-to-peak subtraction compares LV and aortic maxima occurring at different times; it is not interchangeable with either Doppler value. [26]
Regurgitation also changes the loop itself. With mitral leakage, LV volume can fall before the aortic valve opens. With aortic leakage, LV volume can increase during the interval normally called isovolumetric relaxation. Do not preserve normal vertical sides on a schematic that is supposed to show substantial leakage. A wide loop does not automatically mean a large forward stroke volume. [4][2]
Timing matters. A chronically regurgitant aortic valve may be accommodated by a dilated LV. Abrupt severe regurgitation into an unadapted chamber can instead cause a sharp filling-pressure increase, pulmonary edema, and poor forward output. The classic bounding pulse and large cavity may be absent early. [38] In chronic severe primary MR, an EF around 55% is already concerning because ejection into the LA partly masks impaired LV performance.
After repair, a lower EF may reflect changed loading, and postoperative dysfunction can persist. New hypotension with a marked decline warrants urgent assessment of ventricular and valve function rather than assuming a harmless loading effect. [13][23][7]
Typical bedside findings connect the lesion to the cycle: AS can produce a systolic ejection murmur radiating toward the carotids and a delayed carotid upstroke; chronic AR can produce an early diastolic decrescendo murmur and a wide pulse pressure. MS produces a diastolic rumble, sometimes with an opening snap; MR commonly produces an apical systolic murmur. Murmur intensity and peripheral findings depend on flow, chronicity, and lesion mechanism, so their absence cannot exclude severe acute disease. [38][40]
A large wedge V wave supports a systolic LA pressure surge. It can occur with MR, but reduced atrial compliance can also generate it without important regurgitation. Confirm the valve mechanism with imaging. Conversely, the absence of an enormous V wave does not exclude severe MR. [14]
Pressure loading commonly adds sarcomeres in parallel; chronic volume loading commonly adds them in series. These describe tendencies, not permanent guarantees of geometry or compliance. Fibrosis can make a dilated chamber stiff. A significant left-to-right ASD chiefly loads the right heart with volume; a significant left-to-right VSD increases pulmonary return and LV volume loading. Hypertension and coarctation impose LV pressure load. [25] Sarcomeric hypertrophic cardiomyopathy has a different cause and may produce dynamic outflow obstruction, which often intensifies when ventricular filling falls. [5][18]
The right heart can limit the left heart
Acute pulmonary embolism raises RV afterload. A failing, distended RV may reduce blood reaching the LV and shift the septum toward it. The resulting low systemic output can coexist with a high CVP and a relatively low wedge pressure. A large RV is not an instruction to give more fluid. Consider filling, congestion, perfusion, and the cause together; additional volume can worsen septal interaction when the RV is already distended.
RV infarction also impairs right-sided output, but the primary defect is contraction rather than a new pulmonary arterial obstruction. A small primary RV-infarction study documented increased filling pressures without improved cardiac index after volume loading, supporting assessment of the actual response rather than a universal bolus rule. [37][16]
Pulmonary vascular resistance uses the gradient from mean PA pressure to wedge pressure, divided by output. Mean PA pressure 35, PAWP 10, and output 5 give PVR 5 Wood units. Current precapillary PH criteria require mean PA pressure above 20 mmHg, PAWP at most 15, and PVR above 2 Wood units. Classification matters because left-heart disease and pulmonary vascular disease need different treatment strategies.
Hypoxia and acidosis can increase pulmonary vasoconstriction; hypoxic vasoconstriction differs from the local systemic response to hypoxia. Isolated nocturnal obstructive sleep apnea generally does not cause sustained PH; associated lung disease or hypoventilation with daytime hypercapnia changes that assessment. Oxygen addresses hypoxemia, while nitric oxide, prostacyclin-pathway drugs, and PDE5 inhibitors have selected pulmonary indications. They are not interchangeable treatments for every raised PA pressure. [17]
Tamponade restricts filling through external pressure. Chamber collapse timing and respiratory variation on echocardiography support the diagnosis; pressure equalization is an approximate pattern affected by existing disease. Constriction more often permits rapid early filling before abrupt limitation, producing a prominent jugular y descent and sometimes a dip-and-plateau tracing. Restrictive myocardial disease can also produce that tracing. Respiratory discordance of LV and RV systolic pressure favors constriction over restriction. Constriction can be inflammatory and transient, so calcification is not required. [15]
A normal wedge pressure does not exclude a cardiac explanation for ascites. Severe RV failure, tricuspid disease, or constriction can cause systemic venous congestion. Identify which vascular bed is congested before calling an effusion or ascites noncardiac. [24][15]
Try it here · Checkpoint 2 of 3
Make your prediction before reading the choices. A first attempt is just a starting point.
Case 14
Show answer and explanations for case 14
A. Added volume directly raises LV systolic afterload (Why this does not fit)
The immediate concern in this RV pressure-overload setting is ventricular interaction and LV underfilling, not a direct rise in aortic loading.
B. Added volume corrects the pulmonary vascular obstruction (Why this does not fit)
Volume does not relieve the cause of RV afterload and can worsen the already distended RV.
C. Further RV distension can aggravate ventricular interaction and impede LV filling (Best answer)
The ventricles share the septum and pericardial space. Additional distension may impair left-sided filling instead of improving forward delivery.
D. The high RAP indicates that the LV is also already volume overloaded (Why this does not fit)
RAP and LV volume are not interchangeable; the stem documents poor LV filling despite right-sided congestion.
Takeaway: Treating a failing RV requires assessing both preload benefit and the cost of further distension.
Typical untreated patterns, with room for mixed disease
Mechanism
Flow and examination
Pressure pattern
MechanismHypovolemic
Flow and examinationLow output, often cool extremities
Pressure patternUsually low filling pressures and compensatory high SVR
MechanismLV cardiogenic
Flow and examinationLow output with pulmonary congestion
Pressure patternOften high PAWP and compensatory high SVR
MechanismDistributive
Flow and examinationOften warm with low vascular tone
Pressure patternLow SVR; output may be high, normal, or low
MechanismObstructive
Flow and examinationOutput limited by mechanical interference
Pressure patternDepends on the obstruction; PE and tamponade are not identical
Hemorrhage, dehydration, and major burns can reduce effective circulating volume. MI or myocarditis can impair the pump. Sepsis, anaphylaxis, and loss of sympathetic vascular tone in neurogenic shock can reduce resistance. PE, tamponade, and tension pneumothorax can mechanically limit flow. These are mechanism examples; associated pathology can create mixed patterns. [39] These patterns describe mechanisms, not mutually exclusive diagnoses.
Sepsis may include vasodilation, depleted effective circulating volume, and myocardial dysfunction simultaneously. A low output does not exclude sepsis or prove that infection has reached a particular time stage. High mixed venous oxygen saturation can reflect reduced extraction or shunting and does not guarantee sufficient tissue oxygenation. Lactate can rise through several mechanisms, including adrenergic stimulation and impaired clearance.
Reassess perfusion using examination, urine output, laboratory trends, and appropriate flow assessment. Current shock guidance favors echocardiography as an initial imaging tool. For further fluid decisions, a reversible preload test with measured stroke volume or output is more informative than a static CVP alone. An increase during passive leg raising indicates potential fluid responsiveness; pulmonary congestion or absence of hypoperfusion may still make fluid administration inappropriate. [7][9]
For adults with sepsis-induced hypoperfusion or septic shock, the 2026 sepsis guideline conditionally suggests at least 30 mL/kg crystalloid within three hours, with low-certainty evidence, individualized delivery, and frequent reassessment. Norepinephrine remains the first-line vasopressor for adult septic shock. Subsequent fluid administration should follow the patient's response and tolerance, rather than continue automatically until lactate normalizes. A guideline starting strategy does not eliminate the need to assess concurrent cardiac or renal disease. [8]
The older Forrester framework classified depressed cardiac index as at most 2.2 L/min/m² and high pulmonary capillary pressure as above 18 mmHg. Subset I has CI above 2.2 and pressure at most 18; II has CI above 2.2 and pressure above 18; III has CI at most 2.2 and pressure at most 18; IV has CI at most 2.2 and pressure above 18.
These are historical classification thresholds, not universal normal ranges or automatic drug orders. [20] Congestion and hypoperfusion need separate assessment. In decompensated HF, ESC guidance permits considering inotropes with systolic pressure below 90 mmHg and hypoperfusion despite standard treatment, with fluid assessment appropriate to the patient. A low EF or a cold extremity alone does not establish that indication. [11]
Predict what the intervention actually changes
Standing initially reduces central venous return through dependent pooling. The baroreflex then increases sympathetic activity. Exercise adds a skeletal muscle pump, respiratory effects, venoconstriction, faster heart rate, and increased contractility. State whether a question concerns the initial mechanical effect or the combined adapted circulation before assigning one mechanism.
Phenylephrine increases vascular tone through alpha-1 receptors; norepinephrine combines alpha-mediated vasoconstriction with beta-mediated cardiac effects. [31][32] Angiotensin II contracts vascular smooth muscle through AT1 receptors; vasopressin acts through vascular V1 receptors. [33][34] Nitrates often reduce venous filling at lower doses; arterial dilation becomes more relevant with greater exposure. [21] Hydralazine acts predominantly on arterioles. [35] Nitroprusside reduces arterial and venous tone and can increase forward output by reducing afterload even without direct positive inotropy. [36] An output increase after vasodilation is therefore not proof of stronger myocardium. [3]
Acute inotropy is a different target from long-term disease modification. Digoxin inhibits Na-K ATPase and increases intracellular calcium availability; milrinone inhibits PDE3 and increases cAMP, combining inotropy with vasodilation. [28][29] Beta blockers can initially reduce adrenergic inotropy. Verapamil, a nondihydropyridine calcium-channel blocker, can reduce contractility; calcium-channel blockers differ in cardiac and vascular selectivity. [30] These mechanisms do not make the drugs interchangeable treatments for low output.
Dobutamine produces rapid beta-adrenergic inotropy but can also change heart rate and vascular resistance. A higher output at an unchanged wedge pressure suggests improved performance; it does not establish unchanged end-diastolic volume. A microaxial LV-to-aorta pump directly drains the LV and supplies systemic flow. This can lower LV volume and filling pressure without proving myocardial recovery; different support configurations have different loading effects. [27] Follow actual device and native-heart performance rather than assuming a fixed resistance response. [12][2]
Finally, avoid turning a population tendency into a required finding. Preeclampsia includes differing output phenotypes; fetal growth restriction may accompany lower output. In chronic AR, exercise changes rate, diastolic duration, vascular resistance, and myocardial reserve. A small primary exercise study found less regurgitation and greater forward flow as SVR fell, while severe AR could still produce high exercise filling pressures. Shorter diastole alone cannot establish exercise safety or make every beta blocker inappropriate. The useful prediction names the variable changed, then checks what happened to perfusion and congestion. [19][22]
Try it here · Checkpoint 3 of 3
Make your prediction before reading the choices. A first attempt is just a starting point.
Case 16
Show answer and explanations for case 16
A. The improved flow quantifies the increase in native myocardial contractility (Why this does not fit)
Assisted flow can improve independently of intrinsic recovery. Native function requires separate assessment.
B. Mechanical unloading and assisted systemic flow can improve circulation together (Best answer)
The device can reduce ventricular loading while contributing to systemic delivery. Lower native ventricular volume need not mean lower total systemic flow.
C. The measured changes establish that systemic resistance fell (Why this does not fit)
Neither the arterial pressure gradient nor resistance is specified. Device flow does not impose a fixed SVR response.
D. The lower PAWP represents reduced volume delivery to the systemic circulation (Why this does not fit)
The pump delivers blood from the LV to the aorta, allowing unloading and increased systemic flow together.
Takeaway: Improved supported output does not establish recovery of the native myocardium.
A. Chronic pressure load across an obstructed outlet (Best answer)
Aortic stenosis adds a valvular load between the LV and aorta. Increased wall thickness can partially limit the resulting systolic wall stress.
B. Primary diastolic regurgitation into the LV (Why this does not fit)
Aortic regurgitation returns blood during diastole and primarily produces a volume load. It does not explain the stated obstructive gradient.
C. A required increase in intrinsic contractility (Why this does not fit)
Hypertrophy and a high intracavitary pressure do not establish stronger myocardium. Loading conditions must be considered when assessing contractility.
D. Primary systolic regurgitation into the LA (Why this does not fit)
MR primarily produces volume loading. The measured LV-to-aorta systolic gradient identifies an obstructed outlet.
Takeaway: Aortic valve obstruction can markedly increase LV afterload despite an ordinary systemic arterial pressure.
A. The wedge measurement proves a large LV end-diastolic volume (Why this does not fit)
PAWP reflects pressure upstream of the mitral valve. Mitral obstruction prevents equating it with LV filling pressure or volume.
B. An obstructed mitral inlet permits high LA pressure despite lower LV diastolic pressure (Best answer)
The pressure separation is expected across a narrowed mitral valve. Tachycardia further limits diastolic filling time.
C. The low LV pressure proves severe total-body hypovolemia (Why this does not fit)
A single intracavitary pressure cannot establish circulating volume. The valve lesion itself can explain the pressure separation.
D. Mean PAWP minus LVEDP is the Doppler mean transmitral gradient (Why this does not fit)
The two values summarize different parts of the cycle. A true mean diastolic transmitral gradient requires time-matched pressure differences or appropriate Doppler measurement.
Takeaway: Inlet obstruction separates upstream congestion from downstream filling.
A. Preserved EF can coexist with impaired filling and clinically important heart failure (Best answer)
EF is a fraction of chamber emptying. It does not measure filling pressure, relaxation, or exercise reserve.
B. An EF above 60% excludes a cardiac cause of dyspnea (Why this does not fit)
Preserved EF does not exclude HFpEF. Evidence of abnormal filling pressure is particularly relevant in this scenario.
C. Concentric geometry proves every aspect of systolic function is normal (Why this does not fit)
Global EF can remain preserved despite abnormalities of longitudinal function or contractile reserve. Geometry does not prove normal myocardial function.
D. An E/A ratio alone would be sufficient to grade all diastolic abnormalities (Why this does not fit)
Current assessment integrates several Doppler and structural measures and accounts for rhythm and clinical setting.
Takeaway: A normal ejection fraction is not a normal filling-pressure measurement.
A. Primary loss of LV contractility from diffuse myocardial injury (Why this does not fit)
Reduced myocardial contraction can cause low output, but the documented effusion and hemodynamic compromise identify external filling restriction here.
B. A fixed obstruction at the aortic valve (Why this does not fit)
No aortic lesion is described. Pericardial pressure limits chamber filling before systolic ejection.
C. A reduction in chamber filling caused primarily by intrinsic myocardial stiffness (Why this does not fit)
Tamponade restricts distension externally. Intrinsic stiffness is a different mechanism, as in restrictive myocardial disease.
D. External pericardial pressure reducing effective chamber distension (Best answer)
Tamponade reduces transmural filling pressure and available filling volume. A high intracavitary pressure can coexist with inadequate filling.
Takeaway: External pressure can impair filling despite apparently high measured intracardiac pressures.
A. Reduced LV filling and a smaller cavity favor dynamic outflow obstruction (Best answer)
Lower filling can increase interaction between the mitral apparatus and the outflow tract, increasing the dynamic gradient.
B. Increased venous return during sustained strain augments the ejection murmur (Why this does not fit)
Sustained strain generally reduces venous return. The filling reduction can intensify dynamic obstruction.
C. Increased cavity size increases systolic contact between the septum and mitral apparatus (Why this does not fit)
A smaller cavity favors the obstructive interaction in this setting; the proposed size change has the wrong direction.
D. Greater systemic arterial afterload is the principal cause of the louder dynamic murmur (Why this does not fit)
The relevant provocative effect during strain is reduced filling; increased arterial loading generally opposes rather than explains this obstruction response.
Takeaway: Dynamic obstruction depends on loading conditions as well as anatomy.
A. Constrictive pericardial physiology (Best answer)
The respiratory discordance supports enhanced ventricular interdependence from pericardial constraint. The dip-and-plateau finding alone would be less specific.
B. Restrictive myocardial disease solely because a plateau is present (Why this does not fit)
Restriction can produce a similar diastolic contour, but respiratory LV-RV concordance is more typical than the stated discordance.
C. Tamponade solely because both ventricles have high pressures (Why this does not fit)
Tamponade commonly limits early filling and attenuates the y descent. The provided respiratory and filling findings favor constriction.
D. Isolated aortic stenosis (Why this does not fit)
An aortic outflow lesion does not explain the characteristic respiratory ventricular interaction described here.
Takeaway: Use respiratory ventricular interaction to distinguish causes that share a diastolic pressure contour.
A. The low PAWP is sufficient evidence that more volume will improve LV output (Why this does not fit)
Low downstream pressure can coexist with failure of the congested RV to transfer blood. The measured adverse response argues against repeated uncritical loading.
B. The RV may be unable to transfer additional venous volume to the left heart (Best answer)
The measurements and response suggest right-sided pump limitation with congestion. Filling interventions must be reassessed rather than repeated by one pressure target.
C. The high RAP establishes simultaneous LV volume overload (Why this does not fit)
The wedge is low and the impaired RV can limit left-sided delivery. RAP alone does not measure LV volume.
D. Primary LV systolic failure best explains the isolated right-sided pressure burden (Why this does not fit)
The stated RV infarction, high RAP, and low PAWP favor impaired right-sided transfer. Associated LV injury can coexist but is not established as the main cause here.
Takeaway: A low left-sided filling pressure can result from failure of the pump upstream.
A. Observe the EF decline as an isolated loading effect before assessing the new hypotension (Why this does not fit)
Loading changes are relevant, but hypotension makes urgent assessment necessary; persistent myocardial dysfunction or a procedural complication must not be dismissed.
B. Use preoperative EF 55% as evidence against pre-existing LV dysfunction (Why this does not fit)
In severe primary MR, EF 55% is already concerning because total ejection includes regurgitant flow.
C. Attribute the hypotension to residual regurgitation based on the EF change alone (Why this does not fit)
The EF change does not establish residual MR. Imaging and assessment of loading, perfusion, and myocardial function are required.
D. Assess altered loading while urgently evaluating ventricular and valve function and ischemic causes (Best answer)
Eliminating the low-impedance regurgitant outlet changes ejection conditions. This mechanism may contribute, but does not exclude injury or a repair complication.
Takeaway: A plausible loading explanation does not justify dismissing new postoperative instability.
A. Primary LV systolic pressure overload (Why this does not fit)
An ASD does not create an LV-to-aortic systolic obstruction. Its main initial consequence is extra right-sided flow.
B. Right-sided volume loading from a left-to-right atrial shunt (Best answer)
Blood recirculating through the right heart increases RV filling and pulmonary flow, favoring right-sided enlargement.
C. Primary RV pressure loading from pulmonary arteriolar disease (Why this does not fit)
Pulmonary vascular disease can complicate a shunt, but the stem excludes it as the cause of the current enlargement.
D. Predominant LV volume loading from increased pulmonary venous return (Why this does not fit)
An atrial shunt recirculates blood through the right heart. Predominant LV volume loading better describes a significant ventricular-level left-to-right shunt.
Takeaway: Identify the chamber receiving extra flow before predicting its remodeling pattern.
