Images and text Genevieve Carbonatto and Tina Cullen.
A 72 year old man presents to the Emergency Department with shortness of breath (SOB). He is severely SOB on minimal effort and has been unable to get out of bed for 2 days. He gives a story of 6 months of increasing SOB. This is corroborated by his carer who also confirms that he has become more SOB over 6 months. He has become progressively more house bound. He is a heavy life long smoker. He has had a mild cough but no fevers. His cough has become worse over the last 2 days. He has never been investigated for COPD and is not on any bronchodilators.
Cachexic, equal air entry, poor air entry to bases, mild scattered wheeze. Sats of 75 % on RA, 93% on 3l of oxygen, BP 101/60, RR 30/min HR 91/min, temperature 35.4 He does not appear to be in significant respiratory distress and is communicating easily.
His ECG is shows right axis deviation, low voltage QRS precordial leads, incomplete right bundle branch block.
His Chest Xray
The chest Xray shows a big heart and increased vascular markings. Is this pulmonary oedema?
His right anterior upper chest ultrasound using Lichtenstein’s BLUE points
One fixed B line and occasionally a second is seen. This is an A profile – lung sliding and A lines ( + less than 3 B lines between 2 consecutive ribs)
Right anterior lower chest:
A profile – no B lines.
Left anterior upper chest
Here we have 2 broad B lines and an irregular pleural line, on balance this may be due to the ultrasound position on the chest (it is not at complete right angles to the chest wall) and this looks like an A profile.
Lung ultrasound shows therefore bilateral A lines. The second BLUE point on the left was not possible because of the heart.
We put all this in the clinical context. Bi-basal scattered wheeze, poor saturations, lowish blood pressure, life long smoker, cough for 2 days, hypothermic, A profile bilaterally anteriorly. We have excluded heart failure. We are thinking this may be an acute infective exacerbation of COPD.
We start bronchodilators and give antibiotics to cover for infection. His BP is 101 systolic. We start iv fluids.
We go away and see another patient.
One hour later the nurse comes to find us, “doctor could you review your patient please, his BP has dropped to 75 systolic”
We go back and see him. He does not appear more breathless. His BP is 75/40, his HR 98/min
No widespread anterior B lines. We decide to do an ECHO to look for a cardiac cause for his hypotension as his heart is enlarged. He may have a cardiomyopathy, a pericardial effusion, significant pulmonary hypertension.
We are unable to get any parasternal or apical views. We get a beautiful subcostal view.
Note the large RV which is hardly moving and the small, under-filled squashed looking LV. The RV wall does not appear hypertrophied. The IVS moves towards the LV in diastole. As the tricuspid valves open, the IVS moves towards the LV and in systole the IVS does move towards the RV but the LV never reverts to its completely rounded normal shape. If the IVS is flattened throughout the cardiac cycle it is caused by RV pressure overloaded. If the IVS is flattened during diastole only and reverts to a normal rounded LV in systole, that is due to volume overload.
The tricuspid regurgitation appears to be mild on this view but the angle of incidence is poor and the RA is large. The RA pressure may be elevated and hence the colour TR may appear insignificant due to rapid equalisation of RV/ RA pressure gradient.
We get a subcostal short axis view
The D shaped ventricle has IVS flattening during the entire cardiac cycle and is due to RV pressure overload.
This is his IVC
The IVC is fixed and dilated suggesting high right sided pressures.
We think we have the diagnosis – This man has a PE, but he may also have co-existing pulmonary hypertension from COPD.
We go down to his right CFV.
There is clearly a non obstructive thrombus in the right CFV
The FV is also partially coapting on pressure indicating a partial thrombus in his right FV
We have made the diagnosis. This man has had a PE which is the cause of both his hypotension and SOB.
There are 2 points for discussion here
- How do you differentiate a man who possibly has chronic obstructive pulmonary disease and pulmonary hypertension from someone who has an acute PE ?
- How do we explain this man’s deteriorating respiratory function over the past 6 months with a rapid deterioration over 2 days associated with a cough but no fever.
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.
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.
Our patient does not show evidence of RV hypertrophy on his subcostal 4 chamber view.
He has significant apical trabeculations, but otherwise his RV walls are quite thin.
So in this case, we have a patient who may well have underlying pulmonary hypertension but on balance appears to have a thin walled RV suggesting an acute cause for increased RV pressures.
How do we explain this man’s deteriorating respiratory function over the past 6 months with a rapid deterioration over 2 days associated with a cough but no fever?
This man’s respiratory function had been deteriorating over 6 months. Could he have been showering pulmonary emboli during that time?
He had formal vascular studies done in the Emergency department, which showed that he had evidence of old thrombi from his right external iliac vein to his popliteal vein. Synechiae, or old fibrosed thrombi were visible in his external iliac vein.
From this study it appears that he had had a DVT along the length of his right leg for a while which may have been throwing off emboli over the previous 6 months.
We would have come to the diagnosis of pulmonary embolism earlier by examining his heart immediately after we examined his lungs. The clue was in the Xray, the diagnosis was in his ultrasound.
Teaching point: It goes without saying that the clinical context dictates the interpretation of the different imaging modalities. The standard imaging modalities such as Xray complement the ultrasound findings and vice versa. Having ultrasound as a skill gives an added invaluable tool to the critical care physician.
- 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
- Pulsatile venous Doppler flow in lower limbs: Highly indicative of elevated right atrium pressure : American Journal of Roentgenology 167(4):977-80 · November 1996
- Whole body ultrasonography : Dr Daniel A Lichtenstein