Venous dimension of shock: Integrating arterial inflow and venous back-pressure in hemodynamic assessment

Table 1 Hemodynamic phenotypes based on disturbances in arterial inflow and venous pressure

Phenotype	Arterial inflow	Venous pressure	AVPG	Typical clinical settings	Key bedside features
Normal perfusion	Adequate	Normal	Preserved	No clinically relevant mismatch between arterial inflow and venous outflow	Normal perfusion markers, preserved urine output, stable mentation, and no evolving organ dysfunction
Reduced arterial inflow	Decreased	Normal or low	Decreased mainly from the arterial side	Hypovolemia, cardiogenic shock, and distributive shock with impaired effective flow	Hypotension, low cardiac output, elevated or rising lactate, prolonged capillary refill time, oliguria
Predominant venous congestion	Preserved or relatively preserved	Increased	Decreased mainly from the venous side	Right ventricular failure, pulmonary hypertension, obstructive shock, fluid overload, and over-resuscitated septic shock	Elevated or rising CVP, systemic venous congestion, abnormal venous Doppler or VExUS, oliguria, renal or hepatic dysfunction
Combined inflow-congestion failure	Decreased	Increased	Markedly decreased from both sides	Advanced heart failure, late septic shock after fluid loading, RV failure with impaired LV filling, and complex cardiopulmonary failure	Hypotension or low forward flow with systemic venous congestion, elevated CVP, organ dysfunction, and persistent hypoperfusion

Representative evidence supporting these phenotypes is drawn from studies and guidelines on shock classification, venous congestion, right ventricular failure, fluid responsiveness, and septic/cardiogenic shock phenotyping[1-4,9,10,13,17,27-30,34]. These phenotypes represent dominant patterns rather than mutually exclusive categories. Microcirculatory dysfunction may complicate any phenotype and should be suspected when tissue hypoperfusion persists despite apparent correction of arterial pressure, forward flow, and venous congestion. AVPG: Arterial-venous perfusion gradient; CVP: Central venous pressure; RV: Right ventricle; VExUS: Venous excess ultrasound.

Table 2 Bedside variables and pragmatic reassessment triggers for integrated arterial-venous perfusion gradient-based hemodynamic assessment

Domain	Bedside variable/tool	Pragmatic reassessment trigger	Clinical implication
Arterial pressure	MAP, arterial waveform quality, vasopressor requirement	MAP < 65 mmHg, poor arterial waveform, low diastolic pressure, or escalating vasopressor dose	Confirm measurement accuracy and interpret MAP with tissue perfusion, baseline blood pressure, cardiac output, CVP, and shock phenotype. MAP alone does not confirm adequate organ perfusion
Forward flow	Cardiac output, LVOT-VTI, focused echocardiography, pulse pressure, ScvO2	Low cardiac output or low LVOT-VTI for clinical context; low ScvO2 with persistent hypoperfusion	Suggests inadequate forward flow. Reassess preload, contractility, obstruction, RV function, hemoglobin, oxygenation, and metabolic demand
Fluid responsiveness	Passive leg raise or small fluid challenge with SV/CO/LVOT-VTI measurement	SV/CO/LVOT-VTI increase of approximately 10%-15%	Suggests that additional preload can increase forward flow. A fluid bolus should be repeated only if the patient is also fluid tolerant.
Fluid tolerance	CVP trend, MAP-CVP, VExUS, RV size/function, lung ultrasound, oxygenation, fluid balance	Rising CVP, falling MAP-CVP, VExUS grade 2-3, worsening RV dilation/septal shift, new or increasing bilateral B-lines, worsening oxygenation, or large positive fluid balance	Suggests limited tolerance to further fluid. Shift from “Is the patient fluid responsive?” to “Can the patient tolerate more fluid?”
Tissue perfusion	Lactate, CRT, mottling, skin temperature, urine output, mental status	Lactate ≥ 2 mmol/L, rising or non-clearing lactate, CRT > 3 seconds, mottling, urine output < 0.5 mL/kg/hour, altered mentation, or worsening organ function	Suggests persistent hypoperfusion or metabolic stress. Reassess arterial pressure, forward flow, venous congestion, and microcirculatory coherence rather than giving fluid automatically
Flow-metabolism relationship	Pv-aCO2 gap, ScvO2, lactate trend	Pv-aCO2 gap > 6 mmHg, especially with raised lactate or low ScvO2	May suggest inadequate blood flow relative to metabolic demand. Reassess cardiac output, oxygen delivery, hemoglobin, hypoxemia, and source control
Venous pressure/AVPG surrogate	CVP and MAP-CVP trend	CVP > 12-15 mmHg or rising; low or falling MAP-CVP, especially < 50 mmHg with organ dysfunction	Suggests venous back-pressure may be contributing to organ dysfunction. Assess RV function, VExUS, intra-abdominal pressure, ventilator pressures, and fluid balance
Venous congestion ultrasound	IVC, hepatic, portal, and intrarenal venous Doppler; VExUS score	Dilated IVC with abnormal venous Doppler, portal pulsatility > 30%, discontinuous or monophasic intrarenal venous flow, or VExUS grade 2-3	Supports clinically relevant venous congestion. Avoid unnecessary fluid loading and consider venous-pressure reduction when perfusion pressure is supportable
Right ventricular assessment	Focused echocardiography: RV size/function, RV:LV ratio, septal motion, TAPSE, S′, TR	RV dilation, RV:LV ratio > 1, septal flattening/shift, TAPSE < 17 mm, S′ < 9.5 cm/seconds, significant TR, or pulmonary pressure overload	Suggests RV-mediated venous hypertension or combined inflow-congestion failure. Avoid blind fluid loading; optimize RV preload, afterload, contractility, and systemic pressure
Extrinsic contributors to venous pressure	PEEP, auto-PEEP, dynamic hyperinflation, intra-abdominal pressure, tamponade or tension physiology	High PEEP or auto-PEEP, intra-abdominal pressure ≥ 12 mmHg, tamponade physiology, tension pneumothorax, or abdominal compartment physiology	These factors can raise venous pressure and impair organ drainage despite acceptable MAP. Correcting the driver may improve the effective AVPG
Pulmonary fluid tolerance	Lung ultrasound B-lines, oxygenation, ventilatory requirement, and EVLW where transpulmonary thermodilution is available	New or increasing bilateral B-lines after fluid, worsening oxygenation, or rising EVLW or increasing ventilatory support	Suggests reduced pulmonary fluid tolerance. B-lines should not be interpreted as systemic venous congestion alone but should prompt reassessment before further fluid administration. Where transpulmonary thermodilution is available, extravascular lung water may provide additional quantitative information on pulmonary fluid accumulation and fluid tolerance, but it should be interpreted as an adjunct rather than a direct measure of systemic venous congestion
Residual microcirculatory dysfunction	Persistent CRT delay, mottling, lactate non-clearance, oliguria, altered mentation, or organ dysfunction despite corrected macrocirculation	Persistent hypoperfusion despite MAP ≥ 65 mmHg, adequate or improved forward flow, and no major venous congestion	Suggests possible loss of hemodynamic coherence. Reassess source control, oxygen delivery, hemoglobin, hypoxemia, acidosis, temperature, excessive vasoconstriction, and inflammatory or metabolic injury

Suggested reassessment triggers are based on guideline recommendations, physiological studies, observational data, and ultrasound literature; they are intended as pragmatic triggers rather than validated universal treatment thresholds[4,12,34,37,44-59]. They should be interpreted with shock etiology, baseline blood pressure, right ventricular function, venous Doppler findings, tissue perfusion, and response to intervention. AVPG: Arterial-venous perfusion gradient; CO: Cardiac output; CRT: Capillary refill time; CVP: Central venous pressure; IAP: Intra-abdominal pressure; IVC: Inferior vena cava; LVOT-VTI: Left ventricular outflow tract velocity-time integral; EVLW: Extravascular lung water; MAP: Mean arterial pressure; PEEP: Positive end-expiratory pressure; PLR: Passive leg raise; Pv-aCO₂: Veno-arterial carbon dioxide tension difference; RV: Right ventricle; ScvO₂: Central venous oxygen saturation; SV: Stroke volume; TAPSE: Tricuspid annular plane systolic excursion; TR: Tricuspid regurgitation; VExUS: Venous excess ultrasound.