Pulmonary embolus (PE)

Images by Genevieve Carbonatto  Subcostal view. Large right ventricle, small left ventricle, intraventricular septum flattened

Subcostal 4-chamber view demonstrating severely dilated right heart with significantly reduced right ventricular contractility.  The interventricular septum is flattened more during diastole.  Small cavity left ventricle.  (RV is the “preload” of the LV). There is the appearance of a small amount of free fluid anterior to the RV wall.

Subcostal 4-chamber view demonstrating severely dilated right heart with colour across the tricuspid valve. Again the small amount of free fluid is seen.

Subcostal short axis view at the level of the papillary muscles showing severely dilated right ventricle and small cavity left ventricle with significant flattening of the interventricular septum, (IVS) mainly during diastole due to RV volume overload. Note again the free fluid adjacent to the RV wall.

Subcostal view demonstrating long axis of the dilated inferior vena cava, (IVC) with no collapse on inspiration consistent with elevated right heart pressures.

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Maximum diameter of the IVC is ~ 22mm. Dilated IVC.  IVC measurement taken between 0.5cm and 3.0cm from the junction with the right atrium, (RA) and measured inner edge to inner edge.

Transverse view of the right common femoral vein, (CFV) and common femoral artery, (CFA) at the level of the groin with colour over the CFV.  There is organised thrombus visualised within the CFV and some flow in a reduced lumen, shown with the colour.  Note the colour scale has been reduced to display the flow.

Transverse view of the right  femoral vein and profunda femoris vein, (FV and PFV) at the level of the bifurcation of the superficial femoral artery and profunda femoris artery distal to the groin using compression.  The profunda femoris vein is seen to compress but there is only partial compression of the  femoral vein. Conclusion is that the PE originates from the right lower limb deep vein thrombosis, (DVT).

Discussion

How, in this patient would  you differentiate chronic obstructive pulmonary  disease and pulmonary hypertension from an acute PE ?

The major difference between an acute condition (such as PE) and chronic pulmonary hypertension is that, in PE, the right ventricle is subjected to an acute increase in pressure after load and dilates, (no time for compensatory RV wall hypertrophy).  The RV walls will therefore, remain  thin compared to the LV.   In chronic pulmonary hypertension, the RV has had time to adjust to the increased pressures and the walls of the RV will hypertophy.  Over time the RV  pressures will increase sufficiently to cause  IVS  flattening towards the LV throughout the entire cardiac cycle (due to this RV pressure overload). So we would have a dilated RV with thick (hypertrophied) walls and an IVS flattened throughout the cardiac cycle.

RV pressures generated may become significant. To calculate RV systolic pressure you need to look at tricuspid regurgitation pressure and add the estimated right atrial pressures using the IVC size and collapsibility. (NB: RVSP only equals PASP in the absence of RVOT obstruction or Pulmonary stenosis).  The bottom line is that RV pressures in chronic pulmonary hypertension will be much greater than RV pressures from an acute cause such as a pulmonary embolism.

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When pulmonary pressures are normal, the RV is crescent shaped, the RV  thin walled and the LV is round. Normal LV pressures are around 120mmHg and RV pressures are approximately, 20 -25mmHg.

In chronic pulmonary hypertension,  the LV becomes D shaped in the PSAX (parasternal or subcostal short axis view). Right ventricular systolic pressures may exceed 100mmHg.

On the other hand with a PE, there is rapid acute pressure increase in the pulmonary resistance with rapid RV dilatation and the RV walls are thin. Because the RV has dilated and has poor systolic function, it cannot generate high pressures across the TV. RV pressures in acute PE are typically between 30 and 60 mmHg. In fact in PE, RV pressures rarely exceed 45mmHg.

Other signs of pulmonary embolism include:   McConnell’s sign (akinesis of the RV free mid wall, whilst the  apical motion is preserved) and  visualisation of a thrombus in the pulmonary artery.

Signs of RV strain such as poor RV wall contraction, decreased TAPSE (tricuspid annular plane systolic excursion) occurs with both chronic and acute pulmonary hypertension.

The IVC size and collapsibility helps in diagnosing high right atrial pressures. A non-collapsing, plethotic IVC indicates high right atrial pressures in this clinical setting.

This patient does not show evidence of  RV hypertrophy on his subcostal 4 chamber view.

References

  1. Pulsatile Lower Limb Venous Doppler Flow: Prevalence and value in cardiac Disease Diagnosis – Journal of Ultrasound  www.jultrasoundmed.org/content/suppl/2015/03/24/15.11.747…/15.11.747.pdf
  2. Pulsatile venous Doppler flow in lower limbs: Highly indicative of elevated right atrium pressure : American Journal of Roentgenology 167(4):977-80 · November 1996
  3. Whole body ultrasonography : Dr Daniel A Lichtenstein

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