Cardiology Case #9
Primary Author: Dr Alastair Robertson; Co-Authors: Dr Hywel James and David Law
Background:
A 72 year old man presented to ED with 10 days of malaise, lack of energy and breathlessness. A set of blood tests performed in the community a week prior showed elevated inflammatory markers and he had been commenced on a course of antibiotics for a possible pneumonia.
He was otherwise well and vitals were within normal limits.
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ECG shows a sinus rhythm with normal axis and normal intervals. There are small Q waves in lead III, and non-specific T wave flattening. The QRS voltages are relatively small. Bifid p-waves, more noticeable in inferior leads suggests p mitre which can indicate left atrial enlargement or mitral valve disease.
CXR shows cardiomegaly, with addition collapse/consolidation and possible pleural effusion in the left lower zone.
Blood tests showed inflammatory markers remained elevated, but the diagnosis was still unclear so cardiac ultrasound was used to assess his heart.
Cardiac POCUS
Video 1 - parasternal long-axis
Video 2 - Apical 4-chamber
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These clips show a very large pericardial effusion.
In the first video, the heart can be seen in the centre, with the large effusion (anechoic, black fluid) running circumferentially from anterior to posterior. The largest depth of effusion appears to be anteriorly or around the apex, with a smaller depth on the posterior aspect.
The LV function appears okay. There is some abnormal wall movement, particularly around the posterior aspect of the left atrium.
The second video again shows the large pericardial effusion. Both Right and Left atria appear to be falling in on themselves during diastole but not systole.
This shows the importance of echo, as without putting a probe on the chest, it could be easy to put this presentation simply down to a left lower zone pneumonia given the x-ray appearance.
Pericardial Tamponade?
Given the large pericardial effusion the immediate concern was whether the patient was showing signs of pericardial tamponade.
Pericardial tamponade is ultimately a clinical diagnosis, remember Beck’s triad:
Hypotension/Shock
Distended Neck Veins
Muffled Heart Sounds
However, these features are not always present or obvious, and technology, tools and skills have advanced since the 1930s. Echo can be crucial in assessing the amount of haemodynamic compromise to guide urgency of intervention.
Echo Features of Pericardial Tamponade
The following are features consistent with pericardial tamponade, and in the unstable or shocked patient constitute a medical emergency which may require immediate pericardial decompression.
Large pericardial effusion
Large effusion is >3cm. Beware - smaller effusions can still cause tamponade, when they rapidly accumulate or in conditions causing a stiff pericardium. Effusion size is usually measured at end-diastole.
Right Atrial systolic collapse
Right Ventricular diastolic collapse
The right sided chambers have lower pressures, so are likely to show signs of extrinsic compression before the left sided chambers. These features suggest that the pressure in the pericardial space is overcoming that of cardiac pressures, and thus obstructive shock is impending. In systole, atrial pressures should be rising thus collapse is concerning. Likewise in diastole ventricular pressures should be rising thus collapse is concerning.
Dilated IVC with no, or minimal respiratory variation
Other features suggestive of pericardial effusion are:
Cardiomegaly on CXR, especially a large ‘bulbous’ heart
Low voltage QRS complexes on ECG
“Electrical Alternans” - beat-to-beat variation in QRS voltages due to the heart swinging back and forth in the pericardium.
“Pulsus paradoxus” - accurately seen during invasive blood pressure monitoring (via arterial line)
Basic POCUS
The first video shows a PSAX of the aortic valve. To get this view, from a PLAX, centre the aortic valve in the middle of the screen and rotate the probe 90 degrees clockwise (marker now towards patient’s left shoulder, 1-2 o’clock).
We see the aortic valve opening in the centre of the image, with the Right Atrium, Right ventricle and RVOT/pulmonary artery wrapping around the top the valve (from left to right). The left atrium is sitting at the bottom of the image.
As seen in the apical images, there is some abnormal motion of the right side of the heart, but the right atrium is not collapsing in systole, and the right ventricle is not collapsing in diastole.
The bottom video shows the IVC which is dilated, and with only slight respiratory variation suggesting an element of haemodynamic compromise.
Progress:
The patient was haemodynamically stable, with no hard echo findings of tamponade or impending obstructive shock. The next step was to assess for early signs of haemodynamic compromise.
Intermediate POCUS - Ventricular Interdependence
Ventricular Interdependence describes the physiological effects of how the filling of one ventricle affects the other given that they share a wall (the interventricular septum). As one ventricle fills, expansion of the septum influences the other ventricle. Ventricular filling is also affected by the respiratory cycle. During inspiration negative thoracic pressure pulls blood into the right atrium, thus filling of the right heart is slightly favoured, whilst during expiration left heart filling is favoured.
Remember: Right sided valvular murmur accentuated by INSPIRATION, Left sided murmurs louder in EXPIRATION
Ventricular interdependence is usually very minor, but in certain conditions it is exaggerated and is a marker of haemodynamic compromise. Essentially the ventricles are fighting each other for volume due to a constrictive pathology.
Ventricular Interdependence can be exaggerated (and identified on echo) in:
Pericardial Tamponade
Constrictive Pericarditis
Pulmonary Hypertension/Cor Pulmonale
May be seen with ASDs
Echo Features of Ventricular Interdependence:
Dilated IVC with reduced respiratory variation
Retrograde flow into hepatic veins on Expiration
Mitral Inflow Variations: an E-wave variability of >25% with the respiratory cycle.
This can also be represented by tricuspid inflow E wave variability of >50% with respiratory cycle.
Stroke volume variability with respiratory cycle: LVOT VTI variability of >10% with respiration. This is echogenic “Pulsus Paradoxus”.
Septal shift towards the RV during expiration
Mitral Inflow Variations:
This shows PW doppler signal over the mitral inflow. The two peaks represent LV filling during diastole; the E wave (here the smaller peak, early diastolic filling), then the A wave (larger peak, atrial kick).
The E wave amplitude is measured in inspiration (+) and then expiration (x). There is greater than 25% difference here (14/34 = 41%) indicating that during inspiration the LV is being ‘starved’ of inflow as it is fighting with the RV for volume.
The same can be done for tricuspid inflows, but a variation of up to 50% can be normal here.
LVOT variability
This shows PW doppler signal in the LV outflow tract (just proximal to the aortic valve). VTI is the area under the triangular curve (can be calculated by the machine after tracing around a curve) and shows blood flow out through the LVOT. Stroke volume can be calculated by multiplying the VTI by the LVOT diameter.
You can see even by eye the variability in volume of these curves with respiration. The VTI area falls during inspiration (as the RV is favoured for filling) and a difference in VTI of >10% indicates “Pulsus Paradoxus”, or haemodynamic compromise.
Note in atrial fibrillation the stroke volume varies beat-to-beat due to the variable diastolic filling time, so these methods are not as reliable in identifying ventricular interdependence.
Case Conclusion:
The echo showed features of ventricular interdependence suggesting early haemodynamic compromise but not tamponade/obstructive shock (yet).
He was closely observed in CCU and IV antibiotics continued. A pericardial drain was inserted the following day which drained over 1000ml of pericardial fluid.
Final diagnosis was thought to be likely pericarditis and he was discharged home on anti-inflammatories with close follow-up.
