Special thanks to Dr Ben Clarke (EM Consultant) for this excellent case.
A 47 year old female presented with one week’s history of lethargy, left sided chest pain, progressively worsening dyspnoea and general malaise following her first dose of chemotherapy for metastatic Lung Ca. She presented looking pale, unwell, in discomfort and tachypnoeic, albeit SpO2 were approx 95% on room air. Clinical examination was largely unremarkable with mildly decreased AE to her R base.
She had an ECG which is shown below – what does this show? What ought to happen next?
What does the echo show?
This shows a very large pericardial effusion with a ‘swinging heart’, producing the electrical alternans on ECG. It is difficult to be certain from this image whether there is clear echocardiographic evidence of tamponade but it appears very suggestive – see below.
The patient was transferred to the local cardiology centre and had a pericardial drain inserted, draining over 1L initially. This effusion is thought to be secondary to metastatic lung cancer for which she is on chemo. Chest XR from 2 months before showed no obvious cardiomegaly.
Cardiac tamponade is defined as “an abnormal increase in fluid accumulation in the pericardial sac, which, by raising intracardiac pressures, impedes normal cardiac filling and reduces cardiac output.” Cardiac Tamponade is a medical emergency and an important cause of obstructive shock. The textbook findings of Beck’s Triad (hypotension, engorged neck veins and muffled heart sounds) are only observed in a minority of patients and we now have more sensitive tools to approach this diagnosis.
Whilst POCUS may allow visualisation of pericardial fluid, care must be taken not to over-diagnose tamponade and put patients through risky invasive procedures unless necessary. The presence of pericardial fluid is an “anatomical diagnosis” whilst cardiac tamponade is a “physiological diagnosis”. This can only really be proven retrospectively after an observed improvement in physiological parameters following pericardial decompression.
However, there are echocardiographic signs indicating the physiological derangements of tamponade that may be seen before the development of overt shock.
Understanding the Pathophysiology:
The heart is surrounded by the pericardium, comprising of the outer fibrous pericardium and the serous pericardium (in turn divided into parietal and visceral pericardia). Under normal conditions there is a small amount of lubricating serous fluid in the pericardial cavity, between the parietal and visceral pericardia.
The effect of increased pericardial fluid (effusion, blood, pus etc) depends on the rate of accumulation and capability of the pericardium to stretch. If this accumulation is gradual, the pericardium can stretch to accommodate this, sometimes extensively (as in this case). If fluid accumulates rapidly, the capability of the pericardium to stretch is overcome and pericardial pressure rises steeply.
As pericardial pressure increases, it encroaches and eventually exceeds cardiac chamber filling pressures. Since the RA has the lowest filling pressure of all cardiac chambers, this is the first to be exceeded by pericardial pressure, and venous return (VR) is reduced.
PRA – Right Atrial Pressure
RV – Venous vascular resistance
MSFP – Mean systemic filling pressure
The echocardiographic signs of tamponade reflect the physiological changes:
RA systolic collapse*: When pericardial pressure exceeds PRA, the RA free wall will collapse. This is first seen during ventricular systole/atrial diastole and is highly sensitive for pericardial tamponade.
RV diastolic collapse: As pericardial pressure rises further, it exceeds PRV during ventricular diastole, and RV free wall diastolic collapseis seen. This is highly specific but less sensitive than RA systolic collapse.
Plethoric IVC: The IVC should be plethoric with little respiratory variation, reflecting the raised PRA. The absence of a plethoric IVC virtually excludes tamponade.
Mitral & Tricuspid peak inflow velocity variation: this is a more advanced technique that involves assessing peak inflow velocity variation across the MV/TV during the respiratory cycle. It reflects a greatly exaggerated stroke volume variation (SVV) and is in essence the echocardiographic proof of ‘pulsus paradoxus’.
There are other methods and a lot more physiology to consider but that is beyond the scope of today’s case.
*This is confusingly denoted as both ’RA systolic collapse’ and ‘RA diastolic collapse’ in the literature but refers to ventricular systole which is atrial diastole, when RA pressures are lowest.
- Appleton C, Gillam L, Koulogiannis K. Cardiac Tamponade. Cardiol Clin. 2017 Nov;35(4):525-537. doi: 10.1016/j.ccl.2017.07.006. PMID: 29025544.
- Alerhand S, Carter JM. What echocardiographic findings suggest a pericardial effusion is causing tamponade? Am J Emerg Med. 2019 Feb;37(2):321-326. doi: 10.1016/j.ajem.2018.11.004. Epub 2018 Nov 17. PMID: 30471929.
- Sternbach G. Claude Beck: cardiac compression triads. J Emerg Med. 1988 Sep-Oct;6(5):417-9. doi: 10.1016/0736-4679(88)90017-0. PMID: 3066820.
- Verhoeff K, Mitchell JR. ‘Cardiopulmonary physiology: why the heart and lungs are inextricably linked’. Adv Physiol Educ 2017; 41:348-353.