A Practical Step-by-Step Guide From Basic Views to Advanced Hemodynamics
Cardiac POCUS becomes useful when we stop thinking of it as “taking pictures of the heart” and start using it to answer physiological questions.
In a hypotensive or critically ill patient, I want to know:
Is there tamponade?
Is the LV failing—or hyperdynamic?
Is the RV under pressure?
Is forward flow low?
Is there a major valve catastrophe?
Will increasing preload actually increase stroke volume?
Did my intervention improve the physiology?
Current ESICM guidance suggests echocardiography as the first-line imaging modality for defining the type of shock, and recommends dynamic rather than static measures when assessing fluid responsiveness.
This guide is deliberately practical. Follow the sequence, reproduce the view, identify the anatomy, and then add interpretation.
One important limitation: reading this guide can teach the method, but reliable cardiac POCUS still requires repeated supervised scanning. Advanced interpretation should be matched to the operator’s competence. Ultrasound-guided pericardiocentesis in particular requires procedural training and an experienced operator.
This is an adult guide. Reference limits assume appropriate acquisition; they are not isolated treatment thresholds. A technically limited scan is inconclusive. Persistent concern or discordant findings require comprehensive echocardiography or other definitive assessment, without delaying resuscitation. See the ASE focused ultrasound recommendations.
The rule for the unstable patient
2D FIRST. NUMBERS SECOND.
In a crashing patient, do not begin with Simpson EF, pulmonary acceleration time, or a complicated Doppler calculation.
Start with:
1. Pericardium — effusion/tamponade?
2. LV — hyperdynamic, normal, reduced, severely reduced?
3. RV — smaller, equal to, or larger than LV?
4. Septum — round LV or D-shaped?
5. Chambers — gross enlargement or collapse?
6. Right-sided pressure context — IVC and venous findings?
7. Lungs — B-lines, pleural fluid, pneumothorax?
Then ask:
What physiology is threatening this patient right now?
Only after that should you add measurements that answer a specific clinical question.
PART 1 — BEFORE YOU PUT THE PROBE ON
Probe
Use a phased-array cardiac transducer, generally in the low-frequency range. Use 2–4 MHz phased or microconvex probes as appropriate for focused cardiac imaging.
Select the cardiac preset.
Confirm how the probe marker maps to the screen before following a tutorial’s probe directions.
Start slightly deeper than necessary.
Find the heart.
Then reduce depth so the heart fills most of the screen.
Adjust gain until blood is dark and myocardial borders are visible.
Save cine clips, not only still images. Motion is the information.
Patient position
For an unstable patient:
Scan the patient where they are.
Do not roll or reposition a hypotensive trauma patient simply to improve your PLAX.
For a stable patient, left lateral decubitus often improves parasternal and apical windows. Supine positioning may improve the subcostal view.
The four hand movements
Learn these separately:
Slide — move the whole probe to another location.
Rotate — turn it clockwise/counterclockwise.
Fan/tilt — sweep the ultrasound plane through the heart.
Rock/angle — change the beam direction without changing the footprint much.
A useful rule:
Big movement to FIND the window. Small movement to PERFECT it.
Practical echo teaching is all about taking your time to focus on each movement instead of just randomly wiggling the probe all over the place at once.
Visual: where the main cardiac windows live
Practical video course for all six views
TheICUdoc has individual acquisition videos for PLAX, PSAX, A4C, A5C, A2C and subcostal four-chamber.
Watch the step-by-step basic cardiac view course
PART 2 — BASIC FOCUSED CARDIAC POCUS
1. Subcostal four-chamber view
This is often the fastest window in trauma, hypotension and cardiac arrest.
Step 1 — start below the xiphoid
Place the probe just inferior to the xiphoid.
Find the liver first.
Step 2 — use the liver as your window
The liver conducts ultrasound well.
Do not point the probe vertically into the abdomen.
Flatten it so the ultrasound beam travels under the sternum toward the heart.
Step 3 — identify the structures
Near field:
Liver
then:
RV
then:
interventricular septum
then:
LV
You should eventually identify:
RA → tricuspid valve → RV
and
LA → mitral valve → LV
The RV is closest to the liver because it is the most anterior cardiac chamber.
Ask four questions
Is there pericardial fluid?
Is the RV markedly enlarged?
Is LV contraction obviously poor or hyperdynamic?
Is there organized cardiac activity?
Troubleshooting
If you see only liver:
flatten the probe more.
If the heart sits at the edge of the image:
rock/fan slowly.
If everything is very small:
reduce depth after finding the heart.
Practical video
Watch particularly how shallow the probe angle becomes.
2. Parasternal long axis — PLAX
This is one of the richest views in emergency echocardiography.
Step 1 — find an intercostal window
Start along the left parasternal border, commonly around the third to fifth intercostal space.
There is no need to be tied to one textbook interspace.
Patients’ hearts do not all sit in the same position.
Move from interspace to interspace until myocardium appears clearly.
Step 2 — make the LV long
Once you see the heart, rotate and fine-tune until the LV is maximally elongated, rather than short or round.
The true apex is usually outside the PLAX plane; do not try to manufacture an apex in this view.
Step 3 — identify the anatomy
From near to far:
RV/RVOT
interventricular septum
LV
Then find:
mitral valve
LVOT
aortic valve
aortic root
left atrium
and the descending thoracic aorta behind the LA.
Ask
How is LV systolic function?
Is there pericardial fluid?
Does the mitral valve look grossly abnormal?
Does the aortic valve/root look abnormal?
Can I perform EPSS?
Is there dynamic LVOT obstruction? — later, in the advanced section.
Major trap
An oblique PLAX may make the ventricle appear:
smaller
thicker
or falsely hyperdynamic.
Never measure a bad image simply because the machine gives you calipers.
Practical acquisition video
Watch Sonosite’s 3D Parasternal Long-Axis demonstration
3. Parasternal short axis — PSAX
Once PLAX is excellent, rotate approximately 90° while maintaining the same acoustic window.
Think of this as cutting the heart into slices.
Aortic valve level
You may see the three aortic cusps—the classic “Mercedes-Benz” appearance.
Around it you can see the RVOT and pulmonary valve.
This level becomes important for pulmonary acceleration time later.
Mitral valve level
The mitral valve can resemble a fish mouth.
Papillary-muscle level
This is the key ED level.
You want:
round LV
two papillary muscles
crescent-shaped RV
Ask
Is LV contraction symmetric?
Is there a regional abnormality?
Is the septum flat?
Is there a D-sign?
Does the cavity almost disappear during systole?
Normal
The LV should remain approximately round.
Sweep from base to apex and compare with long-axis views. One short-axis slice cannot establish global function or exclude regional dysfunction.
RV pressure/volume loading
When the RV pushes the septum toward the LV, the LV becomes D-shaped.
Be careful with an off-axis PSAX: an oblique slice can create a falsely flattened-looking septum.
Practical video
4. Apical four-chamber — A4C
This is the key comparison view for the right and left heart.
Step 1 — find the real apex
Do not simply place the probe at the textbook fifth intercostal space.
Find the patient’s actual apex/PMI.
Cardiomegaly, COPD and body habitus can move it substantially.
Step 2 — aim toward the cardiac base
Once you are at the apex, direct the beam toward the base.
Step 3 — optimize
The interventricular septum should be reasonably vertical.
Both ventricular cavities should be fully visualized.
The LV apex should look pointed rather than truncated.
How to recognize the RV
Do not identify it only based on which side of the monitor it occupies.
The RV is:
- more trabeculated
- thinner-walled
- may show a moderator band
- associated with a tricuspid valve that inserts slightly more apically than the mitral valve.
Foreshortening
If the LV looks short and rounded:
➡️ you probably missed the true apex.
This matters enormously.
A foreshortened A4C produces unreliable:
LV volumes
Simpson EF
chamber comparisons
and regional wall interpretation.
Practical video
Watch Sonosite’s 3D Apical Four-Chamber demonstration
5. Chamber size in A4C
Do your initial comparison at end-diastole.
Ask: RV:LV
Normal
RV < LV
Concerning
RV ≈ LV
Clearly abnormal
RV > LV
For more formal assessment, the 2026 acute PE guideline lists an RV basal end-diastolic diameter ≥41 mm as abnormal and an echo RV/LV end-diastolic ratio >0.9 as an abnormal RV finding.
But your bedside conclusion should be:
A large RV tells me there is RV loading. It does not tell me why.
Possible causes include acute PE, chronic pulmonary hypertension, severe lung disease, RV infarction, severe TR, congenital disease and chronic RV failure.
6. Apical five-chamber — A5C
Start from a good A4C.
Do not move to another part of the chest.
Fan/tilt anteriorly.
The LVOT and aortic valve should appear.
The so-called “fifth chamber” is not a chamber at all—it is the LVOT/aortic outflow coming into the imaging plane.
Basic purpose
Recognize:
LV → LVOT → aortic valve
Advanced purpose
This is one of your main windows for:
PW Doppler of the LVOT
→ VTI
→ stroke volume
→ cardiac output
→ response to passive leg raise
Practical video
The A5C section is included as a dedicated acquisition video here:
Watch A5C acquisition in theICUdoc basic course
7. Apical two-chamber — A2C
Return to A4C.
Keep the transducer at the apex.
Rotate until the right heart disappears.
You should now see:
LV
LA
mitral valve
but no RV.
Why we need A2C
It gives another plane through the LV.
It is particularly useful for:
anterior wall
inferior wall
apex
and for Simpson biplane EF together with A4C.
Practical video
TheICUdoc includes a dedicated A2C acquisition demonstration.
Watch the A2C acquisition video
There are also moving A2C examples in this open-access echo teaching paper.
7A. Apical three-chamber / apical long-axis — useful advanced extension
For more advanced critical-care echo, learn A3C as well.
Continue rotating from A2C.
You should eventually bring:
LV
mitral valve
LA
LVOT
aortic valve/root
into one long-axis plane.
It is useful for:
- LVOT obstruction
- aortic valve assessment
- mitral-aortic anatomy
- wall motion
- Doppler alignment in selected patients.
See A2C and A3C acquisition with moving examples
8. LV regions — keep this clinically usable
Learn to obtain the views before memorizing all 17 segments.
First know the major walls.
A4C
Think:
septal ↔ lateral
A2C
Think:
inferior ↔ anterior
PLAX
Think primarily:
anteroseptal ↔ inferolateral
PSAX
You can compare the LV circumferentially.
ACEP provides a practical ED-oriented wall map and emphasizes confirming an apparent regional abnormality in an orthogonal imaging plane.
9. Regional wall motion abnormalities
A normally contracting myocardial segment does two things:
It moves inward AND it thickens.
Do not look only at motion.
A damaged segment may be passively pulled inward by neighboring healthy myocardium.
Describe the segment
Normal
Good systolic inward movement and thickening.
Hypokinetic
Reduced movement/thickening.
Akinetic
Essentially absent systolic movement/thickening.
Dyskinetic
Paradoxical outward movement during systole.
ED rule
If you identify one abnormal segment:
Confirm it in another view.
Apparent wall-motion abnormalities can result from:
- poor imaging plane
- ventricular pacing
- bundle-branch block
- previous infarction/scar
- cardiomyopathy
- RV pressure overload.
Do not diagnose an acute coronary occlusion from one questionable segment.
For clinicians who want to develop this skill further, this ED-focused wall-motion resource includes moving examples of hypokinesis, akinesis and dyskinesis.
Watch a practical coronary wall-motion teaching session
10. LV systolic function — eyeballing
This remains one of the highest-yield Emergency Medicine skills.
Do not immediately try to assign an EF of 38%.
Ask:
Does this ventricle squeeze vigorously, normally, poorly, or barely at all?
Look in at least two views.
Assess:
1. Endocardial excursion
2. Systolic wall thickening
3. Change in cavity size
Then classify:
Hyperdynamic
Normal
Reduced
Severely reduced
Hyperdynamic LV
The LV cavity becomes very small during systole.
You may even see near cavity obliteration.
But:
Hyperdynamic LV ≠ “give fluid.”
It may occur with:
- true hypovolemia
- vasodilatory shock
- high catecholamine state
- sepsis
- dynamic LVOT obstruction.
Always integrate the heart with:
lungs + RV + perfusion + venous congestion + response to intervention.
EF is an emptying fraction, influenced by preload, afterload and heart rate. A small LV can eject a large fraction yet deliver little blood. Preserved EF does not establish adequate forward flow or exclude heart failure. Interpret it alongside flow and perfusion. Acute-care ultrasound consensus.
Practical LV-function assessment
Watch the Emergency Medicine LV-function workshop with Dr Thomas Cook
11. Basic RV assessment: S + S + S
Keep RV POCUS simple initially.
SIZE
Use A4C.
Is RV:
< LV
≈ LV
or
> LV?
SEPTUM
Use PSAX.
Round LV?
or
D-shaped LV?
SQUEEZE
Does the RV free wall contract convincingly?
Later you can quantify with TAPSE, S′ and FAC.
12. Septal motion and the D-sign
This is ventricular interdependence made visible.
Normally LV pressure exceeds RV pressure and the LV stays round in PSAX.
When RV pressure becomes very high:
RV pressure rises
→ septum shifts left
→ LV becomes D-shaped
→ LV filling may fall
→ stroke volume falls.
Timing matters
Septal flattening predominantly in systole supports RV pressure loading.
More prominent diastolic flattening can occur with RV volume overload.
Severe loading may affect both.
A D-sign is therefore:
evidence of altered RV loading—not a PE diagnosis.
13. Acute versus chronic RV strain
A large RV can be acute or chronic.
Look for adaptation.
More acute-looking pattern
Dilated RV
relatively thin RV wall
acute compatible presentation
More chronic-looking pattern
RV hypertrophy
RA enlargement
chronic pulmonary-pressure phenotype
The 2025 ASE guideline defines RV wall thickness ≥0.5 cm as abnormal.
But:
Thin RV ≠ acute PE.
It is only one piece of the phenotype.
14. IVC — useful, but easy to misuse
Find the IVC in long axis.
Prove it is the IVC by following it into the right atrium and identifying hepatic veins entering it.
Where to measure
Current ASE guidance describes measuring at end-expiration approximately 0.5–3 cm proximal to the RA ostium, distal to the hepatic-vein insertion.
For formal RAP estimation in spontaneously breathing adults:
- IVC ≤2.1 cm with ≥50% inspiratory/sniff collapse is compatible with normal RAP.
- A dilated IVC with reduced collapse supports increased RAP.
But positive-pressure ventilation, pregnancy, athletic physiology and other circumstances change interpretation.
The key ED interpretation point
IVC is not an intravascular-volume meter.
It is influenced by:
- right atrial pressure
- inspiratory effort
- mechanical ventilation
- RV failure
- pulmonary hypertension
- severe TR
- tamponade
- intra-abdominal pressure
- patient position.
Therefore:
Do not ask
“Is this patient dry?”
Ask
“What does the IVC add to my understanding of right-sided pressure and the rest of the hemodynamic picture?”
And never assume:
Small/collapsible IVC = automatically give fluid.
Practical video
Watch POCUS of the IVC — practical acquisition video
Use the video for acquisition technique; apply the more nuanced interpretation above at the bedside.
15. Pericardial effusion
Fluid is usually dark/anechoic.
But first prove that the fluid really lies inside the pericardial sac.
PLAX trick
Find the descending thoracic aorta behind the LA.
Pericardial fluid
Tracks anterior to the descending aorta.
Left pleural fluid
Can extend posterior to the descending aorta.
Epicardial fat
Usually:
- more anterior
- heterogeneous
- contains internal echoes
- moves differently from simple fluid.
Scan more than one window
Loculated postoperative, inflammatory or traumatic collections can easily be missed if you depend on a single view.
ACEP’s basic cardiac page includes normal and pathological moving clips for comparison.
Open ACEP’s cardiac POCUS clips
16. Tamponade
Memorize this distinction:
Pericardial effusion is anatomy. Tamponade is physiology.
A large effusion does not automatically equal tamponade.
A small rapidly accumulating haemopericardium can be catastrophic.
Physiological sequence
Pericardial pressure rises.
Low-pressure right-sided chambers become compressed.
Venous return becomes impaired.
Stroke volume falls.
Compensatory tachycardia/vasoconstriction develops.
Eventually output and perfusion fall.
Echo findings
Look for:
RA collapse/inversion
RV diastolic collapse
plethoric IVC
marked respiratory interaction
and Doppler inflow variation when performing advanced assessment.
The 2025 ESC guideline lists RA collapse, RV diastolic collapse, respiratory Doppler variation and IVC plethora among the important echocardiographic features.
How do I know RV collapse occurs in diastole?
Use the mitral valve as a clock.
Mitral valve open = diastole.
If the RV free wall collapses inward during that period, the finding is concerning.
Important exception
High baseline right-heart pressure can make textbook RA/RV collapse less obvious.
Think about:
- pulmonary hypertension
- positive-pressure ventilation
- markedly elevated RV pressure.
So a single absent sign does not independently rule out tamponade.
Airway warning
Positive-pressure ventilation can reduce venous return and worsen tamponade physiology. The 2025 ESC guideline advises avoiding positive airway pressure when possible in tamponade while urgent drainage is being arranged.
17. POCUS during cardiac arrest
Cardiac ultrasound can help identify:
tamponade
severe hypovolemia
massive RV-loading patterns
and organized myocardial activity.
But ultrasound becomes harmful if it prolongs the compression pause.
Practical workflow
Before the rhythm check:
probe positioned and ready
During the scheduled pause:
acquire a short clip
Then:
restart compressions immediately
Interpret the clip after CPR resumes.
Avoid spending the pause trying to perfect the image; resume compressions promptly.
ACEP’s current advanced cardiac-arrest Sonoguide emphasizes integrating ultrasound without disrupting resuscitation.
Watch ACEP’s ultrasound-guided ACLS examples
And remember:
RV dilation during cardiac arrest does not independently diagnose PE.
PART 3 — ADVANCED FOCUSED CARDIAC POCUS
Before adding advanced measurements, start with one rule:
Only measure something if the answer can change your understanding or management.
Do not collect numbers because the machine has buttons.
18. Doppler before measurements
Color Doppler
Use color to answer:
Where is abnormal or accelerated flow occurring?
Practical uses:
- find MR
- find TR
- identify AR
- identify VSD flow
- find LVOT turbulence.
Remember that color appearance depends heavily on machine settings and flow conditions.
Do not grade severe regurgitation from “how colorful” the image looks.
Pulsed-wave Doppler — PW
PW answers:
What is the velocity at this exact sample location?
Use it for:
- LVOT VTI
- RVOT VTI
- pulmonary acceleration time
- mitral inflow.
The limitation is aliasing at high velocities.
Continuous-wave Doppler — CW
CW measures high velocities along the whole beam.
Use it for:
- TRV
- aortic stenosis
- dynamic LVOT obstruction.
You lose precise depth localization.
Tissue Doppler — TDI
Instead of measuring blood velocity, TDI measures myocardial/annular movement.
Useful for:
- RV S′
- mitral e′
- diastolic assessment.
Doppler rule
Alignment matters.
Velocity is underestimated when the Doppler beam is not parallel to flow.
19. EPSS — E-point septal separation
A quick objective adjunct for LV function.
Step 1
Obtain a good PLAX.
Step 2
Activate M-mode.
Step 3
Place the cursor through the tip of the anterior mitral leaflet.
Step 4
Freeze a good tracing.
You will see the classic mitral leaflet motion.
The first large diastolic excursion is the E point.
Step 5
Measure: E point → interventricular septum
An EPSS >7 mm is an adjunctive clue to reduced LV systolic function, not a stand-alone diagnosis or a precise EF estimate. Diagnostic performance varies with the population and technique. Original ED study.
Why?
With good LV function, the anterior leaflet opens close to the septum.
A dilated, poorly contracting LV often has:
large cavity
less leaflet-to-septum approximation
→ larger EPSS.
Pitfalls
EPSS becomes unreliable with:
- mitral stenosis/abnormal leaflet motion
- important aortic regurgitation
- hypertrophic cardiomyopathy
- abnormal rhythms
- distorted geometry.
EPSS supports the eyeball. It does not replace it.
Practical video
Watch Dr Thomas Cook demonstrate EPSS step by step
20. MAPSE
MAPSE = mitral annular plane systolic excursion.
It looks at longitudinal LV contraction.
Step 1
Obtain A4C.
Step 2
Identify the lateral mitral annulus.
Step 3
Place M-mode through the annulus.
Keep the line as parallel to its movement as possible.
Step 4
Measure its systolic excursion toward the apex.
Meaning
Less excursion generally means worse longitudinal LV systolic function.
Why useful in acute care?
Sometimes endocardial definition is too poor for precise Simpson tracing but annular movement remains visible.
Important limitation
MAPSE is an adjunct, not a universal stand-alone substitute for EF.
Regional disease, annular calcification, mitral surgery/prosthesis and angle problems can alter it.
Interpret MAPSE in clinical context rather than relying on one hard “failure cutoff” on an ED pocket card.
Practical video
Watch MAPSE measurement step by step
21. Fractional shortening and Teichholz
These methods help you understand how early quantitative LV measurements were constructed.
From PLAX/M-mode, measure the LV diameter at:
end-diastole
and
end-systole.
Fractional shortening is: FS = [(LVEDD − LVESD) / LVEDD] × 100
Teichholz then uses linear LV measurements and assumed ventricular geometry to estimate volumes and EF.
Why this is limited
The LV is not always a symmetrical geometric object.
Accuracy deteriorates when there is:
- regional infarction
- ventricular aneurysm
- asymmetric remodeling
- distorted geometry.
Modern chamber-quantification guidance recommends biplane Simpson as the standard conventional 2-D method for LV volumes and does not recommend linear Teichholz-style calculations for routine clinical LV volume determination.
So:
Learn Teichholz to understand the method. Do not make it your preferred ED EF measurement.
Practical LV measurement resource
Watch linear LV measurements, fractional shortening, EPSS and MAPSE
22. Simpson biplane EF
This is the main conventional quantitative 2-D EF method.
You need
A4C
A2C
Both should show the true apex.
Step 1
Identify end-diastole.
Trace the LV endocardial border.
Step 2
Identify end-systole.
Trace again.
Step 3
Repeat in A2C.
The machine calculates:
EDV
ESV
and EF. EF = [(EDV − ESV) / EDV] × 100
The biplane method of disks—modified Simpson—is the recommended conventional 2-D method.
Biggest error
A major acquisition error is:
beautifully tracing a foreshortened ventricle.
Bad acquisition → precise-looking bad number.
Practical video
23. Advanced RV assessment — TAPSE
TAPSE = tricuspid annular plane systolic excursion.
Step 1
Obtain a good A4C, ideally an RV-focused view.
Step 2
Put M-mode through the lateral tricuspid annulus.
Step 3
Align the cursor with the base-to-apex movement.
Step 4
Measure maximal systolic excursion.
The 2025 ASE right-heart guideline defines normal M-mode TAPSE as >1.70 cm.
But:
TAPSE measures longitudinal basal RV motion, not the entire RV.
It should not be interpreted alone.
It can be misleading:
- after cardiac surgery
- with altered RV geometry
- with major TR
- when alignment is poor.
Practical video
Watch TAPSE measurement step by step
24. RV S′ — useful advanced adjunct
From an RV-focused A4C:
place TDI at the lateral tricuspid annulus.
Measure the peak systolic tissue velocity: S′
The 2025 ASE guideline considers S′ >9.5 cm/s normal.
Like TAPSE, S′ is angle-dependent and predominantly reflects basal longitudinal RV movement.
Both also vary with loading conditions.
Use it to support an integrated RV assessment—not replace it.
25. RV fractional area change — FAC
FAC gives you a more global two-dimensional measure of RV systolic function.
Step 1
Obtain an RV-focused A4C.
Step 2
Trace RV endocardial area at end-diastole in an RV-focused view, including trabeculations and the moderator band within the cavity area. Use the same border convention at end-systole.
Step 3
Trace again at end-systole.
Calculate: FAC = [(RVEDA − RVESA) / RVEDA] × 100
The 2025 ASE guideline considers FAC >35% normal.
This is useful because it incorporates more of the RV than TAPSE alone, though it still excludes the RVOT.
26. TR velocity and estimated RV systolic pressure
Step 1 — find TR
Use color Doppler.
Step 2 — align CW Doppler
Put CW through the TR jet.
Use the best complete, dense envelope and seek the highest well-aligned velocity.
Step 3 — measure peak TRV
Then use simplified Bernoulli: ΔP = 4V²
Example:
TRV = 3 m/s. 4 × (3)² = 36 mmHg
Then: RVSP ≈ 4 × (TRV)² + RAP
Current ASE guidance recommends using the highest-quality TR velocity and integrating RAP; RVSP is approximately equivalent to PASP only when there is no relevant RV outflow, pulmonary-valve, or proximal pulmonary-artery obstruction. Incomplete or poorly aligned TR envelopes and severe TR can make pressure estimates unreliable. An unmeasurable TR jet does not exclude pulmonary hypertension.
PE warning
TRV is not a PE test.
A peak TR velocity around ≥2.9 m/s supports increased pulmonary pressure, but it does not identify the cause.
27. Pulmonary acceleration time — PAT / RVOT AccT
Get PSAX at the aortic/pulmonary level.
Identify:
RVOT
pulmonary valve
main pulmonary artery
Step 1
Activate PW Doppler.
Step 2
Place a small PW sample volume within the RVOT just proximal to the pulmonary valve, align with flow, and obtain a complete systolic envelope before measuring acceleration time.
Step 3
Obtain the systolic flow envelope.
Step 4
Measure: onset of systolic flow → peak velocity
That interval is acceleration time.
Physiology
As pulmonary vascular resistance increases:
the RV encounters resistance earlier
→ peak flow occurs sooner
→ acceleration time shortens.
The 2025 ASE right-heart guideline considers RVOT acceleration time >105 ms generally normal, while emphasizing that heart-rate extremes affect the measurement and it should not be used in isolation.
PE warning again
Use PAT as part of:
RV size
septum
TAPSE/S′/FAC
TRV
clinical context
—not as “PAT short = PE.”
28. Pulmonary embolism: what echo can and cannot do
This is worth stating explicitly.
The 2026 multisociety acute PE guideline says:
Echocardiography is not recommended to confirm or refute suspected acute PE.
Most acute PE does not produce enough RV dysfunction for echo to be diagnostic, and RV abnormalities are not specific to PE.
Echo becomes especially valuable for:
RV functional assessment
hemodynamic phenotype
risk stratification
and the unstable patient where immediate physiology matters.
The guideline recommends assessing, when possible:
- RV/LV end-diastolic ratio
- RV dimensions
- TAPSE
- RVSP
- free-wall motion
- TR velocity
- septal motion
- IVC variation.
So the correct bedside language is:
“This patient has acute RV pressure-overload physiology compatible with PE in the right clinical context.”
Not:
“The echo proves PE.”
29. LVOT VTI — the advanced skill every acute-care clinician should understand
This is one of the most useful quantitative tools in critical-care echocardiography.
VTI means velocity-time integral.
Think of it as:
How far the column of blood travels through the LVOT during one systole.
Step 1 — obtain A5C or apical long-axis
You need the LVOT aligned as parallel as possible to the ultrasound beam.
Step 2 — activate PW Doppler
Step 3 — place the sample volume
Place the PW sample volume in the LVOT proximal to the aortic valve. If flow acceleration broadens the spectrum, move the gate slightly toward the apex until a clean, narrow systolic envelope is obtained. Do not sample the valve jet.
Step 4 — obtain a clean systolic envelope
Step 5 — trace the waveform
The machine gives VTI in cm.
Practical video
A practical video resource for this section:
Stroke volume
Measure LVOT diameter inner-edge to inner-edge in a zoomed PLAX view during systole, perpendicular to the outflow tract. Match the anatomic level to the Doppler sampling convention. LVOT area = π × (LVOT diameter / 2)²; diameter error is amplified because it is squared.
Then: SV = LVOT area × LVOT VTI
And: CO = SV × HR. If SV is in mL and HR in beats/min, divide by 1,000 to report CO in L/min.
The 2025 European emergency/critical-care cardiac-ultrasound consensus describes an adult LVOT VTI reference range of approximately 18–22 cm. This is not a universal shock cutoff: stroke volume also depends on LVOT area, and cardiac output on heart rate.
Why trends are often more useful
LVOT diameter should not change from minute to minute.
Therefore over a short interval:
Percentage change in VTI approximates percentage change in stroke volume.
That is why VTI works so well for serial hemodynamic assessment.
30. VTI pitfalls — extremely important
Do not treat VTI as a magical cardiac-output number.
Sources of error include:
Incorrect sample-gate location
Poor Doppler angle
LVOT diameter measurement error
Arrhythmia
Respiratory pressure changes
Significant aortic regurgitation
intracardiac shunt
dynamic LVOT obstruction
and operator technique.
The 2025 European consensus specifically notes that in atrial fibrillation, multiple cycles are required and recommends averaging 10 beats. It also warns that significant AR and dynamic LVOTO can make LVOT VTI misleading for estimating forward stroke volume.
With significant AR, systolic LVOT flow includes blood that subsequently regurgitates; it can exceed effective systemic flow.
So:
Bad waveform = no useful VTI.
Do not trace noise.
31. Passive leg raise + VTI
Now we move from:
“Does the IVC look empty?”
to the physiologically better question:
“Will stroke volume actually increase if I increase preload?”
Baseline
Place the patient semi-recumbent if feasible.
Obtain a clean LVOT VTI.
Example: VTI₁ = 15 cm
Passive leg raise
If repositioning is safe, use the bed to lower the trunk from about 45° to horizontal and raise the legs to about 45°. Avoid active leg lifting, pain and coughing; these can change flow independently of preload.
The maneuver transfers venous blood toward the thorax—a reversible endogenous preload challenge.
Repeat quickly
Use:
same view
same gate
same Doppler alignment
Measure: VTI₂
Capture the maximal response promptly, usually within the first minute. Then restore the starting position and check that flow returns toward baseline. A delayed measurement can miss the transient response. If the signal or baseline is unstable, call the test indeterminate. PLR technique.
Example: VTI₂ = 18 cm
Calculate: %ΔVTI = [(18 − 15) / 15] × 100 = 20%
The arithmetic gives a 20% VTI increase. With a consistent acquisition and suitable physiology, that supports an increase in stroke volume. Keep the same operator and gate, average appropriate beats, record heart rate, and do not interpret small changes that could reflect measurement variation as a definite response. TTE reproducibility study.
Current shock guidance recommends assessing fluid responsiveness before continuing fluid in persistent shock and favors dynamic variables over static preload markers.
But memorize this
Fluid responsive ≠ fluid required.
A patient can be preload responsive but still have:
pulmonary edema
venous congestion
ARDS
RV failure
or another reason that additional fluid could be harmful.
You have answered:
“Can more preload increase stroke volume?”
You have not yet answered:
“Should I give fluid?”
Give further fluid only when improved perfusion is needed and the likely benefit outweighs congestion risk. If fluid is given, reassess actual flow, tissue perfusion, lungs and venous congestion; a predicted response does not prove benefit. ESICM shock guidance.
32. Mitral regurgitation — especially acute severe MR
Always start in 2D.
Do not switch on color before looking at anatomy.
Look for
- flail leaflet
- prolapse
- poor coaptation
- torn chordae
- papillary-muscle abnormality.
Then add color Doppler.
Look for systolic flow: LV → LA. In the video below, the color shortcut is oversimplified: check the displayed color map, jet origin and systolic timing. Blue within the LA alone does not establish MR, and color-jet appearance alone does not grade severity.
Practical video
Major trap
Big color jet ≠ automatically severe MR.
Jet appearance changes with:
- machine settings
- LA pressure
- LV-LA driving pressure
- eccentricity
- wall impingement.
ASE guidance recommends integrated assessment. Findings strongly supporting severe primary MR include a major structural lesion such as a flail leaflet or ruptured papillary muscle, vena contracta width ≥0.7 cm, and systolic flow reversal in more than one pulmonary vein.
ED catastrophe: acute MR
After MI, papillary-muscle rupture can produce:
sudden pulmonary edema
hypotension/shock
± a new murmur.
The LA may not be enlarged because there has been no time for remodeling.
In a very hypotensive patient, the color jet may also look less impressive than expected because the driving pressure is lower.
Think anatomy + physiology, not jet area alone.
Suspected acute severe MR with shock needs urgent comprehensive TTE/TEE and cardiology/surgical assessment. A small jet or limited TTE is not reassuring.
33. Diastolic function and filling pressure — advanced, not a one-number diagnosis
For ICU/ED clinicians, the practical question is usually:
Does this patient appear to have elevated left-sided filling pressure?
You may use:
mitral E/A
mitral annular e′
E/e′
TR velocity/pulmonary pressures
LA structure
and other findings.
But diastology is a multiparametric assessment.
Do not assume:
“E/e′ above X = pulmonary edema.”
The 2025 ASE update explicitly uses an integrated approach and includes dedicated algorithms for special populations where standard interpretation changes.
This becomes particularly challenging with:
- atrial fibrillation
- tachycardia
- significant valve disease
- pacing
- mechanical ventilation
- severe mitral annular disease
- critical illness.
For focused ED echo, it is better to say:
“Findings support elevated LV filling pressure”
than to pretend one Doppler number directly equals the wedge pressure.
34. Dynamic LVOT obstruction — a critical-care trap worth actively looking for
Recognizing dynamic LVOT obstruction is an important part of advanced ED/ICU echocardiography.
Dynamic LVOTO is not restricted to classic hypertrophic cardiomyopathy.
It may appear with:
- marked hypovolemia
- catecholamines/inotropes
- sepsis
- small hyperdynamic LV
- Takotsubo
- hypertrophic anatomy.
The 2025 European acute-care consensus specifically recognizes dynamic LVOTO in severe hypovolemia, structural disease and Takotsubo.
What do you see?
2D PLAX/A3C
Small hyperdynamic LV.
Possible systolic anterior motion—SAM—of the mitral valve.
Color
Turbulence/aliasing in the LVOT.
MR
Often a posteriorly directed SAM-associated MR jet.
CW Doppler
A classic late-peaking, dagger-shaped systolic envelope.
Why it matters
The usual reflex in shock—more inotropy—may make dynamic obstruction worse.
More contractility:
→ higher ejection velocity
→ more SAM/LVOT narrowing
→ greater obstruction
→ lower forward output.
Likewise, severe preload reduction may worsen it.
The presence of dynamic obstruction therefore changes the entire hemodynamic interpretation.
35. Gross aortic-valve emergencies
This is beyond very basic POCUS, but critical-care clinicians should recognize the phenotype.
Severe aortic stenosis — clues
Look for:
heavily calcified valve
markedly restricted cusp opening
LV hypertrophy
and, when competent with Doppler, high transaortic velocities/gradients.
Do not attempt to formally grade AS from one poor apical window.
Also remember:
A patient with low cardiac output may have severe AS without a spectacularly high Doppler gradient.
If critical AS is suspected, obtain comprehensive echocardiography/cardiology input.
Acute aortic regurgitation
Look for:
abnormal aortic valve anatomy
diastolic color flow from aorta → LV
In the ED, acute significant AR should make you think about dangerous etiologies including:
acute aortic syndrome
infective endocarditis
valve disruption.
Acute severe AR may cause pulmonary edema and shock before there has been time for major LV dilation.
36. Post-MI mechanical complications — know these patterns
A patient deteriorating after acute MI deserves another echo.
Do not assume every episode of shock is simply “poor EF.”
Papillary-muscle rupture
Think:
acute severe MR
→ pulmonary edema
→ rapidly falling output.
Look for flail leaflet, ruptured apparatus and severe MR.
Ventricular septal rupture
Look for a new septal defect.
Use color Doppler.
You may see high-velocity left-to-right systolic flow across the septum.
TTE with color Doppler is central to the rapid diagnosis of post-MI VSR.
LV free-wall rupture
Think:
sudden collapse
new haemopericardium
tamponade physiology.
This is a surgical catastrophe.
37. Acute aortic syndrome — use POCUS to find danger, not to “rule it out”
Focused TTE can sometimes reveal:
- dilated aortic root/ascending aorta
- visible intimal flap
- new aortic regurgitation
- pericardial effusion
- tamponade
- regional wall-motion abnormalities from coronary involvement.
But TTE does not visualize the entire thoracic aorta well.
Its sensitivity is substantially lower for descending/type-B disease; therefore a normal focused echo does not rule out aortic dissection.
There are published POCUS cases where the flap is visible from multiple transthoracic windows, which is useful for visual learning.
Your bedside conclusion should be:
Positive POCUS finding can accelerate diagnosis. Negative POCUS cannot safely exclude acute aortic syndrome.
Definitive imaging—commonly CTA or, in selected unstable circumstances, TEE—depends on the clinical situation and local resources.
38. Echo-guided pericardiocentesis
Do not memorize:
“Tamponade = subxiphoid needle.”
That is no longer the correct ultrasound-guided mental model.
Step 1 — confirm the problem
Effusion + hemodynamic tamponade physiology.
Step 2 — scan the entire effusion
Look at:
subcostal
parasternal
apical
and other useful windows.
Step 3 — choose the safest route
Find:
largest accessible fluid pocket
shortest safe skin-to-fluid path
no lung, liver, major vessel or other critical structure in the trajectory.
The best approach may be:
parasternal
apical
or
subcostal.
Step 4 — ultrasound guidance
ACEP’s procedure guide includes videos showing:
- subxiphoid effusion
- parasternal approach
- apical approach
- skin-to-fluid assessment
- needle visualization
- agitated-saline confirmation
- pericardial clot.
Watch the complete ACEP ultrasound-guided pericardiocentesis guide and procedural clips
Safety
Unstable tamponade requires urgent drainage by an appropriately trained team. Suspected aortic dissection or myocardial free-wall rupture needs immediate specialist surgical assessment: decompression can worsen bleeding, and any rescue drainage should follow an expert-led plan. Surgical drainage may also be needed when percutaneous access is unsuitable, including purulent or clotted collections.
Traumatic haemopericardium can also clot, making simple needle aspiration ineffective.
39. Putting everything together in shock
This is where cardiac POCUS becomes clinically powerful.
Do not force every patient into one textbook category. Mixed shock is common.
Think in phenotypes.
Phenotype 1 — low preload / vasodilatory physiology
Possible echo:
small or normal RV
small hyperdynamic LV
low forward flow if preload is inadequate
IVC may be small, but do not stop there.
Ask:
Does PLR increase VTI?
Check lungs and venous congestion before giving more fluid.
Phenotype 2 — LV pump failure
Possible echo:
reduced LV systolic function
low VTI
elevated left-sided filling-pressure/congestion pattern
B-lines
Possible acute MR or mechanical complication.
Now ask:
Is shock actually because of LV failure?
Or does the patient happen to have a chronic low EF while another process is causing the shock?
Phenotype 3 — RV failure/obstruction
Possible findings:
large RV
D-shaped LV
poor RV systolic function
low LV filling
high right-sided pressure phenotype
Causes include:
- acute PE
- severe pulmonary hypertension
- RV infarction
- severe hypoxic pulmonary vasoconstriction
- positive-pressure/ventilator-related RV loading
- other RV pathology.
Again:
Large RV ≠ PE.
Phenotype 4 — tamponade
Effusion
impaired right-sided filling
congested systemic venous circulation
falling output/perfusion.
Treat the pressure problem.
Phenotype 5 — dynamic LVOT obstruction
small hyperdynamic LV
SAM
LVOT turbulence
late-peaking CW Doppler
possibly with posterior MR.
This is exactly the situation where blindly escalating inotropy can be counterproductive.
Phenotype 6 — mixed shock
Probably more common than we admit.
Examples:
septic vasodilation + septic cardiomyopathy
PE + sepsis
MI + hemorrhage
LV dysfunction + RV pressure overload
chronic HFrEF + acute distributive shock.
This is why you must repeat the scan.
The 2025 ESICM shock guideline supports sequential echocardiographic assessment and monitoring of stroke volume/cardiac output when initial treatment fails.
40. Reassessment is part of the examination
The first echo is a snapshot.
Critical illness changes.
After:
fluid
vasopressor change
inotrope
ventilator change
pericardial drainage
reperfusion
or another major intervention:
scan again.
Ask:
Did LV filling change?
Did VTI rise?
Did RV size/function improve or worsen?
Did septal position normalize?
Did congestion increase?
Did LVOT obstruction appear?
Did the intervention actually improve forward flow?
That is much more valuable than collecting twenty static measurements at one point in time.
A practical two-pass scan for the ED/ICU
FIRST PASS — unstable patient
2D FIRST. NUMBERS LATER.
Pericardium
Effusion/tamponade?
LV
Hyperdynamic / normal / reduced / severely reduced?
RV
Smaller / equal / larger than LV?
Septum
Round or D-shaped?
Major structural catastrophe
Acute MR? VSD? obvious aortic/root abnormality?
IVC/right-sided pressure context
Lungs
Then:
What physiology is threatening perfusion?
SECOND PASS — when the patient allows it
LV
Eyeball
→ EPSS / MAPSE
→ Simpson if clinically useful
Teichholz = learn the concept, not your preferred routine quantitative method.
RV
Size
→ septum
→ TAPSE
→ S′ / FAC
→ TRV / PAT if the question requires them
Forward flow
LVOT VTI
→ treatment or PLR
→ repeat VTI
Valve problem
2D anatomy first
→ color
→ spectral Doppler where appropriate
→ comprehensive echo/escalation when necessary.
Pericardium
Effusion
→ filling physiology
→ clinical tamponade?
→ image-guided intervention when indicated.
The five sentences every emergency physician should remember
1. A big RV does not equal PE.
2. A collapsible IVC does not equal “give fluid.”
3. A hyperdynamic LV does not equal “give fluid.”
4. Pericardial effusion does not equal tamponade.
5. Fluid responsiveness does not equal fluid requirement.
I would add a sixth for advanced users:
A low blood pressure does not automatically mean the heart needs more inotropy—look for dynamic LVOT obstruction first.
The fastest way to learn this hands-on
Do not spend four hours watching videos before touching a probe.
Use this cycle:
Watch 2–5 minutes → take the probe → reproduce the view → name every structure → optimize it → repeat without the video.
Then:
normal volunteer → abnormal saved clips → supervised sick patient → repeat measurements → clinical integration.
Recommended video sequence – basic cardiac POCUS practice
1. All six views
theICUdoc basic cardiac echo course
2. Subcostal
3. PLAX
Sonosite — Parasternal Long Axis
4. PSAX
5. A4C
Sonosite — Apical Four-Chamber
6. Regional wall motion
Practical wall-motion teaching for non-cardiologists
7. LV function
Cardiac POCUS — LV function workshop
8. IVC acquisition
9. Effusion/tamponade
ACEP basic cardiac POCUS clips
Recommended video sequence – advanced cardiac POCUS practice
1. EPSS
EPSS step-by-step — Dr Thomas Cook
2. MAPSE
3. Simpson EF
Watch Simpson biplane EF on YouTube
4. TAPSE
5. MR
Mitral Regurgitation with Color Doppler
6. LVOT VTI + cardiac output + PLR
LVOT VTI in the management of shock — complete practical tutorial
7. Post-MI VSD
Watch post-MI ventricular septal rupture on YouTube
8. Pericardiocentesis
ACEP Ultrasound-Guided Pericardiocentesis
9. Cardiac arrest
ACEP Ultrasound-Guided Advanced Cardiac Life Support
Core evidence behind this guide
For readers who want to go beyond the practical article, these are the documents I would keep bookmarked:
2025 European consensus: cardiac ultrasound in cardiovascular emergency and critical care
2025 ESICM guideline: circulatory shock and hemodynamic monitoring
2025 ASE guideline: right-heart assessment and pulmonary hypertension
2025 ASE guideline: LV diastolic function
ASE chamber quantification guideline: Simpson and LV measurement
ASE guideline: native valvular regurgitation
2025 ESC guideline: pericardial disease and tamponade
2026 multisociety acute pulmonary embolism guideline
ACEP Emergency Physician Cardiac Sonoguide
Final bedside message
Focused cardiac ultrasound is not about producing a cardiology report in the resuscitation bay.
It is about recognizing physiology quickly.
Get the image right.
Look at the whole heart before measuring one number.
Use Doppler when it answers a question.
Integrate heart, lungs and perfusion.
Treat the patient, then scan again.
That is the point where cardiac POCUS stops being a collection of ultrasound views and becomes hemodynamic bedside medicine.
