top of page
Search

POCUS in Acute Pulmonary Embolism







Juan V. Resendez MD

Clinical Ultrasound Fellow

LA General Medical Center/USC

POCUS IN ACUTE

PULMONARY EMBOLISM


OVERVIEW

Pulmonary Embolism Review

Pathophysiology of Right Heart Strain

POCUS findings in Acute PE

Advanced Echocardiography in Acute PE


SAVE YOUR SCANS

Patient’s MRN under Patient ID (not under MRN)

Your E Number under Operator

US Faculty or Fellow E/C Number under Referring Physician


WHAT IS A PE?

What is a PE?

Risk factors of PE?

Clinical Presentation?

Physiologic changes in submassive/massive PE?


RISK FACTORS?




HYPERCOAGULABILITY

ENDOTHELIAL

INJURY

VENOUS

STASIS


CLINICAL PRESENTATION?




PATHOPHYSIOLOGY OF RIGHT HEART STRAIN




Proximal Arterial Obstruction


Acute Increase in Pulmonary Vascular Resistance


Acute Decrease in Pulmonary Vascular Compliance


Increased RV Afterload




RV sustains higher systolic pressure to maintain output


Thin compliant RV immediately dilates


RV ischemia from increased O2 demand


RV falls off the Starling Curve due to pressure overload


=


RV failure > Decreased LV output > Obstructive Shock



POCUS FINDINGS


RV:LV SIZE RATIO

A4C / PLAX


RV:LV SIZE RATIO

Normal RV:LV size is 0.6:1


> 0.6:1 is considered RV dilation

Mild 0.6 - 1.0 : 1.0

Moderate 1.1 - 1.5 : 1.0

Severe > 1.5 : 1.0


RV:LV Ratio

RV:LV SIZE RATIO


RV:LV SIZE RATIO


RV Wall Thickness

Measure RV free wall (SX)

Can help determine chronicity of RV dilation

>5 mm suggests hypertrophy, chronic process


ABNORMAL SEPTAL MOTION

PSAX


Normal PSAX view of RV and LV

ABNORMAL SEPTAL MOTION


Septal Bowing, D-Sign

ABNORMAL SEPTAL MOTION


ABNORMAL SEPTAL MOTION


McCONNELL’S SIGN

RV Focused A4C


RV free wall hypokinesis w/ apical sparing

Apex tethered to LV

Ballooning of RV free wall

RV ischemia > RWMA

RV (RCA)

Apex (RCA + LAD)


McCONNELL'S SIGN


McCONNELL'S SIGN


TAPSE

RV Focused A4C



** stress importance of obtaining this


TAPSE




Tricuspid Annular Plane Systolic Excursion

Vertical displacement of lateral TV annulus

Measure of RV systolic function

TAPSE <1.7 cm suggests RV dysfunciton

Muscle fibers that contribute to longitudinal contraction of the RV comprise ~80% of RV EF


IVC VIEW

SX



IVC diameter and respirophasic variation used to estimate CVP/RAP

Thin IVC + >50% collapse (3 mmHg)

Equivocal IVC evaluation (8 mmHg)

Plethoric IVC + <50% collapse (15 mmHg)




ADVANCED

ECHO FINDINGS


What is a PE?

Risk factors of PE?

Clinical Presentation?


TRICUSPID REGURGITATION

A4C, PSAX, RV Inflow View


TRICUSPID REGURGITATION

Regurgitant jets seen on color doppler

TR occurs due to dilation of the RV. As the thin, compliant right ventricular free wall balloons outward in the setting of increased PVR, the TV annulus dilates > decreased coaptation of the tricuspid leaflet > results in regurgitation of flow through the TV.


TRICUSPID REGURGITATION

TRVmax = maximum TR velocity

Used as an indicator for severity of RV strain

Measured using continuous wave doppler through the TR jet

TRVmax > 2.8–2.9 m/s indicates elevated RV systolic and pulmonary artery pressures


Pulmonary Artery Systolic Pressure (PASP) /

Right Ventricular Systolic Pressure (RVSP)



PASP is used as marker of increased pulmonary vascular resistance

PASP > 35 mmHg in absence of chronic pHTN suggests RV strain and dysfunction

Estimated using simplified Bernoulli Equation:

PASP = ΔPRV-RA + RAP

ΔPRV-RA  =  4 x TRVmax2

This value then added to RAP (derived from IVC assessment: ~3, 8, 15 mmHg)

PASP = 4 x TRVmax2 + RAP

*assumes no significant RVOT obstruction or pressure gradient across the pulmonic valve

*with the above assumption, PASP = RVSP

Pulmonary Artery Systolic Pressure (PASP) /

Right Ventricular Systolic Pressure (RVSP)



60/60 SIGN


Mention Early Systolic Notching here


60/60 SIGN


Tricuspid Regurgitation Pressure Gradient (TRPG) ≤ 60 mmHg (corresponding to a TRVmax < 3.9 m/s)

TRPG  =  4 x TRVmax2


Pulmonary Artery Acceleration Time (PAAT) < 60 ms


If both TRPG and PAAT are < 60 → acute obstructive process (proximal thrombus)


In the setting of chronic pulmonary hypertension, the TRPG can reach > 60 mmHg due to free wall hypertrophy until there is eventual RV failure


60/60 SIGN

Pulmonary Artery Acceleration Time (PAAT)


Time interval from onset of PA ejection to the peak flow velocity across the PV


PAAT shortens with increasing degrees of pulmonary pressures


In acute proximal PE, will see earlier velocity peak due to earlier return of reflected pressure waves in non-compliant pulmonary vasculature


**fix image to first highlight the view we are wanting to obtain


60/60 SIGN

Pulmonary Artery Acceleration Time (PAAT)


Time interval from onset of PA ejection to the peak flow velocity across the PV


PAAT shortens with increasing degrees of pulmonary pressures


In acute proximal PE, will see earlier velocity peak due to earlier return of reflected pressure waves in non-compliant pulmonary vasculature


**fix image to first highlight the view we are wanting to obtain


EARLY SYSTOLIC NOTCHING



RIGHT VENTRICULAR BUBBLE TIME


10cc of agitated NS given as IVP while performing echo

“Bubble Time” = measured amount of time agitated saline was seen in the RV

“Bubble Time” of > 40 sec (Sn 97%, Sp 87%) was predictive of RV dysfunction


RIGHT HEART CLOT IN TRANSIT

A4C, SX4C, PSAX

3 Types of Clot in Transit

Type A: Serpentine, from DVT and highest risk of causing massive PE

Type B: Mural, ovoid and adherent to the right heart walls, less mobile

Type C: Amorphous or ball-shaped, resemble myxomas, less common, freely mobile


THANK YOU

 
 
 
bottom of page