Cardiology Case #4

Primary Author: Dr Alastair Robertson;    Co-Authors: Dr Hywel James and David Law


Background:


A male in his 60s presents to ED with an episode of central, sharp, non-pleuritic chest pain, with associated breathlessness.

Of note he has a background of OSA, high cholesterol, and previous DVT which was treated with 6 months of rivaroxaban (since ceased).

He is stable but dyspneic.

RR 24, Sats 95% on air, HR 113, BP 173/75, temp 36.0


Here is his initial ECG

    • the most common ECG finding in PE is sinus tachycardia.

    • RV strain pattern is important as it suggests sub/massive PE - TWI typically in anterior leads. TWI in V1 is most specific. TWI in >/= 7 leads diagnoses RV strain

    • ST elevation in aVR

    • S1Q3T3 pattern is suggestive but not that common

    • RBBB and/or p-pulmonale

    • Atrial arrythmias (new AF, SVT).

    This ECG shows sinus tachycardia with a normal axis, but does have some T-wave inversion in V1, Q wave and S wave in III, and some borderline ST elevation in aVR.

    • Pulmonary; pneumothorax, pneumonia

    • Cardiac - acute MI, pericarditis, pericardial effusion

    • Vascular - acute aortic dissection

    • Abdominal - PUD, gastritis, biliary, pancreatitis

    • MSK - costochondritis

The CT scanner is busy, troponins have been sent to the lab.

How could POCUS narrow down your differential?

How could POCUS alter your management?


 

Below is the initial POCUS

What do you think now?

Parasternal Long axis (top), Parasternal Short-axis (middle) and Apical 4-chamber (bottom)

    • Parasternal Long-axis shows an RV that appears large (PLAX should show RV, Aortic Root, LA all roughly equal widths. The interventicular septum also appears to have dysynchronous movement

    • In PLAX the LV is not distended. Mitral and aortic valves appear to be working normally, aortic root is not dilated. There does not appear to be any pericardial effusion.

    • The Short-axis view should show a circular LV in cross section. Here the interventricular septum (from 10-12 o’clock) is being pushed into the LV. This is a “D-shaped'“ septum which is suggestive of elevated RV pressures. The RV also also appears very large on this view too (larger than the LV which is abnormal).

    • In the apical view you can see the RV in the centre, and the vertical line of the interventricualr septum. The RV is enlarged, and extends to control the apex.

    • “McConnell’s sign” is present - if you look at the RV movement, the apex is being displaced inwards/outwards, whilst the lateral wall is not moving in, but moving longitudinally.

    • All of these features are suggestive of RV strain, most likely from acute PE.

 

The patient was stable, proceeded to CTPA, of which some slices are shown below.

A saddle PE can be seen at the pulmonary artery bifurcation, with further clots extending into the L and R pulmonary arteries.

This slice shows a large, distended RV compared to the LV with distortion of the septum into the LV.

 

POCUS Pearls

In this case POCUS can narrow your differentials for breathlessness (e.g exclude tamponade and pneumothorax) and facilitate early recognition with other clinical information of a life-threatening PE.

It assists in anticipating deterioration or arrest if the patient became unstable prior to confirmation through a CTPA. The above ultrasound images would allow you to confidently treat this as massive PE.

Basic POCUS

Again, a good parasternal long- and short-axis views can tell you a lot about the cardiac status. Start at the left sternal edge, in 3rd/4th ICS with the marker pointed towards the patient’s right shoulder for a long axis. Assess the ratio RV / Aorta / LA size (Normal ~1:1:1). Note LV size and function and look for pericardial effusion.

Turn the probe 90 degrees clockwise (marker to patients left shoulder) to get a SAX-view. The LV should appear circular. In this case the large RV size was pressing in to create a “D-shaped septum” which is a sign of acute PE.

Familiarise yourself with McConnell’s sign, watch the video below several times on loop. Identify the apex bouncing up and down, whilst the lateral free wall is hypokinetic, only contracting longtitudinally (towards apex) rather than inwards. You can imagine a “tiny person on a trampoline” bouncing up and down on the apex.


Intermediate POCUS

In suspected PE, progress to assess the RV outflow tract and pulmonary arteries.

From a parasternal short axis, tilt up to get the Aortic Valve in cross-section (see below, normal tri-leaflet valve). The RV outflow tract and Pulmonary valve sits just up and right of the AV, and the pulmonary trunk extends down the right side of the aortic valve. In this video the RV again appears large, and clot can probably be seen sitting at the bifurcation of the pulmonary trunk (saddle PE as seen on CT).

Putting PW doppler in the RVOT will give you a doppler trace. Assess the trace for notching on the downslope, and you can measure a ‘time-to-peak’. Downslope notching and acceleration times of under ~80ms are both suggestive of raised pulmonary pressures.

 

Intermediate/Advanced POCUS

In Acute PE another important measure is the stroke volume. Measure this by calculating the LVOT diameter (on PLAX) and then the LVOT VTI trace.

SV = LVOT area x LVOT VTI

Given that the RV stroke volume must equal the LV stroke volume, a decreased LV stroke volume is indicative of reduced cardiac output = obstructive shock.

This would be a reason to consider thrombolysis or thrombectomy in such a patient with Submassive PE.


Case Conclusion

The patient remained stable, and once the diagnosis was confirmed on CT he was initiated on therapeutic LWMH and admitted to ICU. Troponin peaked at around 200. He was subsequently discharged on a DOAC.


Extra Tips: 

POCUS can be useful in assessing undifferentiated chest pain/breathlessness. Here the suspicion for PE was high and multiple POCUS features of PE could affirm clinical suspicion.

This patient had PE with markers of RV strain, thus reflecting a Submassive PE. The evidence regarding thrombolysis is not clear in Submassive PE, but he was haemodynamically stable and was managed with simple anticoagulation.

Massive PE is classically defined as any of:

  • Cardiac Arrest

  • SBP <90mmHg for >15mins

  • SBP fall of >40mmHg from usual for >15mins

  • Vasopressor/Inotrope requirement

  • Persistent bradycardia

In which case Thrombolysis would be indicated.

Usual dose is Alteplase 100mg IV (1.5mg/kg if <65kg)

—> 10mg bolus

—> rest over 2 hours

In cardiac arrest give 50mg bolus, repeated in 15mins if no ROSC.

Alternative; Tenecteplase IV

  • <60kg: 30mg

  • 60-70kg: 35mg

  • 70-80kg: 40mg

  • 80-90kg: 45mg

  • >90kg: 50mg

    Refer to your local departmental guidelines.


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Cardiology Case #3