By Abdolghader Pakniyat, peer-reviewed by Dr. Sabrina Berdouk.

The traditional RUSH examination gave emergency physicians a rapid way to evaluate undifferentiated hypotension. Its main strength was speed: identify major obstructive, cardiogenic, or hypovolemic causes before the patient deteriorated further.

RUSH 2.0 expands that concept.

It separates the evaluation into two distinct pathways:

• CRUSH for the actively crashing patient
• I-RUSH for the hypotensive patient who allows time for more deliberate hemodynamic assessment

The important change is not simply the addition of more ultrasound measurements. RUSH 2.0 reframes shock evaluation as an iterative process:

Clinical perfusion assessment → HIMAP ultrasound → four-interface synthesis → shock phenotype → intervention → reassessment

This approach is particularly useful because many emergency patients do not have a single, pure shock mechanism. Septic patients may be simultaneously vasodilated and hypovolemic. Patients with RV failure may be systemically congested but have inadequate LV preload. A hyperdynamic LV may still generate a critically low stroke volume.

The objective is therefore not just to identify whether shock is present. It is to understand why flow, pressure, and tissue perfusion are failing in that specific patient.

CRUSH: when the patient is actively deteriorating

When the patient is peri-arrest or rapidly spiraling, there is no time for detailed Doppler measurements or complex hemodynamic interpretation.

The Crashing RUSH—CRUSH—exam should be completed in less than 30 seconds using the familiar HIMAP sequence:

• H – Heart
• I – IVC
• M – Morison’s pouch
• A – Aorta
• P – Pulmonary

The purpose is to identify immediately reversible threats:

Heart

Use rapid parasternal long-axis and apical four-chamber views to evaluate:

• Pericardial effusion or tamponade
• Gross chamber-size abnormalities
• Severe RV enlargement
• Markedly impaired LV contraction

IVC

Perform a qualitative assessment:

• Small versus plethoric
• Collapsing versus non-collapsing

Do not delay resuscitation for precise measurements.

Morison’s pouch

Scan the hepatorenal interface down to the inferior pole of the right kidney, ideally with the patient in Trendelenburg, looking for significant intraperitoneal bleeding.

Aorta

Obtain rapid views through the abdominal aorta to identify an abdominal aortic aneurysm.

Pulmonary

Use anterior lung views to rapidly evaluate for tension pneumothorax.

CRUSH is a threat-detection examination. Once the patient has been stabilized—or if the patient was never actively crashing—the clinician can move to the more comprehensive I-RUSH framework.

I-RUSH: moving from diagnosis to physiology

The Interface-Informed RUSH examination integrates clinical examination and ultrasound to evaluate four connected hemodynamic interfaces:

1. Arterial microcirculation
2. Left ventricle
3. Venous microcirculation
4. Right ventricle

The key is not to interpret each variable independently. A plethoric IVC, low LVOT VTI, abnormal CRT, or enlarged RV only becomes meaningful when the findings are integrated.

Start with the clinical examination

Ultrasound does not independently determine whether a patient is in shock.

The I-RUSH clinical examination includes:

• SBP, DBP, MAP, and pulse pressure
• Capillary refill time
• Pulse-oximeter waveform and perfusion index
• Mottling
• Distal skin temperature
• Mentation

The framework uses:

• CRT ≤3 seconds as a normal reference
• Perfusion index >2.0 as a reassuring value

These findings assess tissue perfusion rather than pressure alone.

A patient may have an acceptable MAP but remain confused, mottled, and peripherally vasoconstricted with a prolonged CRT. This represents a failure of the microcirculation despite apparent improvement in the macrocirculation—often described as hemodynamic incoherence.

Conversely, a patient with low blood pressure, warm skin, normal CRT, and a strong perfusion index may still have relatively preserved tissue flow but inadequate vascular tone.

The HIMAP examination in I-RUSH

Heart

The core views are:

Parasternal long axis

Assess:

• Pericardial effusion and tamponade
• Global LV systolic function
• EPSS when appropriate

Apical four chamber

Assess:

• Relative RV and LV chamber size
• Gross RV dilation
• Qualitative biventricular function

Additional measurements may include:

• LVOT VTI
• TAPSE
• Tricuspid-regurgitation velocity
• Qualitative valve assessment
• Parasternal short-axis evaluation of septal shape and regional wall motion

The reference values in the framework include:

• LVOT VTI: approximately 18–22 cm
• TAPSE: >1.7 cm
• TR velocity: ≤2.8 m/s

IVC and venous system

Assess:

• End-expiratory IVC size
• Respiratory collapsibility
• Changes after treatment

The source uses an end-expiratory diameter of less than 2 cm as a normal reference.

If the IVC is plethoric, extend the examination to venous Doppler assessment, particularly the portal vein, as part of VEXUS.

A plethoric IVC does not automatically mean fluid overload. It may reflect:

• RV failure
• Pulmonary hypertension
• Severe tricuspid regurgitation
• Positive-pressure ventilation
• Excessive intravascular volume

The mechanism must be identified before choosing diuresis, inotropic support, afterload reduction, or another treatment.

Morison’s pouch and aorta

These views remain important in any patient with hypotension or suspected bleeding.

A negative Morison’s view does not exclude:

• Gastrointestinal bleeding
• Retroperitoneal bleeding
• Early or low-volume intraperitoneal hemorrhage

The abdominal aorta should be assessed through multiple levels rather than relying on one reassuring image.

Pulmonary assessment

The pulmonary component includes:

• Bilateral anterior upper-lung views for pneumothorax and interstitial edema
• Additional posterolateral lower-lung views when evaluating interstitial edema or pleural fluid

The four interfaces

1. Arterial microcirculation

Ask:

• Is CRT normal?
• Is the perfusion index reassuring?
• Are the extremities warm or cool?
• Is mottling present?
• Is mentation preserved?

This interface answers the clinically important question:

Is blood reaching the tissues effectively?

Blood pressure alone cannot answer this.

2. Left ventricle

Ask:

• Is LV contractility adequate?
• Is forward stroke volume adequate?
• Is the LV underfilled?
• Is afterload excessive?
• Is valvular regurgitation reducing effective forward flow?

LVOT VTI is useful as a surrogate for forward stroke volume, but it must be interpreted in context.

A low LVOT VTI may reflect:

• Low preload
• Reduced LV contractility
• High systemic vascular resistance
• Significant mitral regurgitation

A high LVOT VTI may reflect:

• Vasoplegia
• High-output physiology
• Aortic regurgitation

A hyperdynamic ejection fraction does not guarantee adequate cardiac output. A small LV may eject a high percentage of a very small end-diastolic volume.

3. Venous microcirculation

Ask:

• Is the venous system collapsed or congested?
• Is the IVC plethoric?
• Is portal venous flow markedly pulsatile?
• Is congestion worsening after treatment?

VEXUS evaluates venous congestion, not simply total-body fluid volume.

A patient can have severe venous congestion and low cardiac output simultaneously, particularly in RV failure.

4. Right ventricle

Ask:

• Is the RV enlarged?
• Is TAPSE reduced?
• Is pulmonary pressure elevated?
• Is the septum affecting LV filling?
• Is RV forward flow adequate?

Systolic septal flattening supports RV pressure overload. Diastolic flattening is more consistent with RV volume overload.

RV failure can reduce LV preload through two mechanisms:

• Reduced RV forward flow
• Septal shift that impairs LV filling

The result may be a low LVOT VTI despite normal intrinsic LV contractility.

Four practical cases

Case 1: mixed septic shock

A 67-year-old patient with pneumonia presents with:

• BP 82/38 mmHg
• Warm extremities
• CRT 5 seconds
• LVOT VTI 12 cm
• Small hyperdynamic LV
• Flat, collapsible IVC
• No diffuse pulmonary B-lines

Interpretation

The low DBP, wide pulse pressure, and warm skin support vasodilation.

The small LV, flat IVC, and low VTI support low preload and reduced forward stroke volume.

The prolonged CRT shows that tissue perfusion is already impaired.

This is not pure vasodilatory shock. It is a mixed phenotype:

Vasodilatory shock plus low-preload, low-flow physiology

Management implication

Both mechanisms should be addressed:

• Start norepinephrine to restore vascular tone and diastolic pressure.
• Give a cautious fluid challenge because the patient appears underfilled.
• Immediately reassess LVOT VTI, CRT, lungs, IVC, and venous congestion.

Suppose the LVOT VTI rises and CRT improves, but new diffuse B-lines appear.

The patient is fluid responsive—but no longer fluid tolerant.

Further fluid should be stopped.

This distinction is fundamental:

Fluid responsiveness does not automatically justify more fluid.

Case 2: LV cardiogenic shock

A 73-year-old patient presents with:

• Cool mottled extremities
• CRT 6 seconds
• Narrow pulse pressure
• LVEF 20%
• LVOT VTI 8 cm
• Diffuse bilateral B-lines
• Plethoric IVC

Interpretation

The patient has:

• Poor LV contractility
• Critically reduced forward flow
• Pulmonary congestion
• Elevated filling pressures
• Impaired microcirculatory perfusion

The dominant phenotype is LV cardiogenic shock.

Management implication

A routine fluid bolus is likely to worsen pulmonary edema without meaningfully increasing stroke volume.

The priorities are:

• Maintain coronary and systemic perfusion pressure
• Improve forward cardiac output
• Treat the underlying ischemic, mechanical, or myocardial cause
• Reassess LVOT VTI and CRT after treatment

A vasopressor may be required to maintain perfusion pressure. An inotrope may be necessary when low output persists.

After intervention:

• Rising VTI indicates improved forward stroke volume.
• Shortening CRT indicates improved tissue perfusion.
• Increasing B-lines or worsening venous congestion indicates reduced treatment tolerance.

Improvement in one variable should never be interpreted as proof that the entire hemodynamic state has normalized.

Case 3: acute RV failure from pulmonary embolism

A 55-year-old patient presents with sudden dyspnea, chest pain, and hypotension.

Ultrasound shows:

• Enlarged RV
• Reduced TAPSE
• Plethoric, non-collapsing IVC
• Systolic septal flattening
• Small underfilled LV
• Low LVOT VTI
• Abnormal portal-vein pulsatility

Interpretation

The dominant problem is acute RV pressure overload with RV failure.

The low LVOT VTI does not represent primary LV pump failure. It reflects reduced LV preload caused by:

• Impaired RV forward flow
• Septal shift toward the LV
• Reduced LV diastolic filling

The patient is simultaneously:

• Systemically venously congested
• Low output
• Poorly perfused

Management implication

A large fluid bolus may worsen RV dilation, septal shift, tricuspid regurgitation, and LV filling.

The priority is to treat the cause of elevated RV afterload—for example, pulmonary vascular obstruction—while supporting RV perfusion and function.

This case illustrates another central principle:

Venous congestion does not mean the circulation has adequate forward flow.

The patient may have a plethoric IVC and high VEXUS findings while still having severe systemic hypoperfusion.

Case 4: occult hemorrhage

A patient presents with hypotension and abdominal discomfort.

Findings include:

• Cool skin
• Narrow pulse pressure
• CRT 5 seconds
• Small hyperdynamic LV
• LVOT VTI 10 cm
• Flat, collapsible IVC
• Negative Morison’s pouch view

Interpretation

The hemodynamic pattern is strongly consistent with low circulating volume and reduced stroke volume.

The hyperdynamic LV does not indicate adequate cardiac output. It reflects vigorous contraction of an underfilled ventricle.

A negative Morison’s view does not exclude hemorrhage.

The clinician should continue searching for:

• Gastrointestinal bleeding
• Retroperitoneal bleeding
• Aortic pathology
• Pelvic bleeding
• Other occult blood loss

Management implication

Resuscitation must occur alongside rapid source identification and control.

The response to blood products or fluid should be evaluated by reassessing:

• LVOT VTI
• CRT
• Pulse pressure
• Lung findings
• IVC and venous congestion

Persistent low VTI despite resuscitation should prompt reconsideration of ongoing hemorrhage, inadequate source control, myocardial dysfunction, or an alternative shock mechanism.

Common interpretation errors

“The EF is normal, so cardiac output is adequate”

False.

EF is a proportion. A small underfilled LV may have a high EF and still produce a very low stroke volume.

“The IVC is flat, so the patient needs fluid”

Not necessarily.

IVC findings must be integrated with:

• LVOT VTI
• CRT and perfusion index
• Lung findings
• RV function
• Clinical context

“The patient’s VTI increased after fluid, so more fluid should be given”

Not automatically.

The patient may be fluid responsive but not fluid tolerant.

New B-lines, a plethoric IVC, or abnormal portal venous pulsatility should stop automatic fluid escalation.

“The MAP improved, so the hemodynamics improved”

Not always.

If norepinephrine raises MAP but LVOT VTI falls and CRT worsens, the patient may have better pressure but worse flow.

“A plethoric IVC means the patient should receive diuretics”

Not automatically.

A plethoric IVC may result from RV failure, PE, pulmonary hypertension, severe tricuspid regurgitation, positive-pressure ventilation, or volume overload. Treatment depends on the mechanism.

A practical bedside loop

The most useful way to apply RUSH 2.0 is as a repeated cycle:

1. Determine whether the patient is truly in shock

Assess CRT, perfusion index, skin temperature, mottling, mentation, and blood-pressure pattern.

2. Choose CRUSH or I-RUSH

• Crashing patient: CRUSH
• Stable enough for detailed assessment: I-RUSH

3. Acquire HIMAP views

Heart, IVC, Morison’s pouch, aorta, and pulmonary views.

4. Interpret the four interfaces

• Arterial microcirculation
• LV
• Venous microcirculation
• RV

5. Identify the dominant and secondary shock mechanisms

Do not force mixed physiology into a single label.

6. Treat the physiology

Choose fluids, vasopressors, inotropes, decongestion, RV support, or definitive treatment according to the dominant mechanism.

7. Reassess

Repeat:

• LVOT VTI or LV function
• CRT and perfusion index
• Pulse pressure
• Lung findings
• IVC and VEXUS
• RV size and function when relevant

RUSH 2.0 is therefore not a one-time diagnostic scan. It is a dynamic hemodynamic monitoring strategy.

Take-home messages

• Use CRUSH when the patient is actively crashing.
• Use I-RUSH when there is time to phenotype the hemodynamics.
• Do not interpret blood pressure without assessing flow and tissue perfusion.
• A normal or high EF does not guarantee adequate cardiac output.
• LVOT VTI is useful, but it is load-dependent and must be repeated after intervention.
• Fluid responsiveness and fluid tolerance are different concepts.
• Venous congestion does not exclude low cardiac output.
• A low LVOT VTI may be caused by low preload, impaired contractility, excessive afterload, or mitral regurgitation.
• Mixed shock is common.
• Reassessment is not an optional final step; it is part of the examination itself.

The practical value of RUSH 2.0 is not that it gives us more measurements. It helps us connect pressure, flow, congestion, ventricular interaction, and tissue perfusion at the bedside—and then determine whether our treatment actually improved the patient.

EMCrit 429 – RUSH 2.0 – The I-RUSH and CRUSH Exams