Move to the beat

What do you think?



Have a closer look at V4. I. Keep. Dancing. On. My. Own. Could it be?

And one and two, and one and two. Pericardial effusion and electric alterans! Surely the heart seems to have found a beat within the beat. Cardiac depolarization hasn’t changed, just the angle at which the ECG machine records it. But is this an emergency cardiac tamponade? They say that cardiac tamponade is a clinical diagnosis. Let’s look at the tachycardic patient. Presenting with acute onset dyspnea and palpitations. Distended neck veins, hypotension and muffled heart-sound together form Beck’s triad. It is in fact cardiac tamponade! But remember the differential: tension pneumothorax, pulmonary embolism, cardiogenic shock, constrictive pericarditis. Even the astute clinician may feel obliged to reach for the ultrasound probe.

An overanxious subcostal view. As for treatment? In the non-traumatic tamponade, 500-1000mL IV bolus crystalloid would facilitate right heart filling and temporarily improve hemodynamics. Pericardiocentesis next. But the game isn’t always that easy. What if the patient gestalt and vital parameters were not past the threshold of an emergency? Let’s look at a similar patient who is less affected and with a blood pressure of 100/60. Large amounts of pleural fluid are present on the right. There is a high suspicion of malignancy per history.

Is this tamponade? Clinically the patient is not quite there. Recall that pericardial effusion volume is second to pericardial effusion rate in cardiac tamponade. As little as 150ml of pericardial effusion may cause tamponade if very rapid, while as much as 1000ml may not if produced over a long period of time. When the pressure in the pericardial sack exceeds the normal filling pressure of the right ventricle, the result is restricted filling of the RV and decreased cardiac output. When effusion volumes aren’t extensive and clinically we’re in doubt, fret not, Mr. Ultrasound will untangle the knot. As the pericardial pressure rises to the diastolic pressures of the heart, space becomes a rare commodity and the chambers become diastolically dependent on each other. This leads to a cascade of logically predictable events ominously ending in right ventricular diastolic collapse.

Systems seem up and running. Diastolic collapse of RA, LA, and some trampoline bouncing on the RV in systole. How about left ventricular output variation? A systolic BP drop of >10mmHg upon inspiration known as pulsus paradoxus can be estimated more exactly by measuring the mitral valve flow.

There is a variation of about 20% on the mitral ”double-mountain” flow chart (>25% is significant for tamponade). All in all one could refer to this as pre-tamponade. The BP soon dropped a bit more, and a subacute parasternal pericardiocentesis was performed.

Parsternal left view with a linear transducer. Apologies for the picture, but the elbows aren’t the best tools for hitting small buttons. At the 3 cm line we can see a ”black” anechoic horizontal layer representing the pericardial fluid. The moving shadow deeper past that line is part of the right ventricular free wall. The needle can be seen moving diagonally from the upper right torward the center and pericardial effusion. 320ml of dark-red fluid was removed, and patient symptoms and vitals improved significantly.

Until next time, keep on dancing.

P.S. Head on over to, check out Niklas Jonsson’s case on traumatic cardiac tamponade and be sure to read the discussion.

1. Triage strategy for urgent management of cardiac tamponade: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Ristić et al. Eur Heart J. 2014 Sep 7 (pdf)
2. Pericardial effusion. Introduction to Bedside Ultrasound: Volume 1 by Matthew Dawson och Mike Mallin (free at Itunes)
3. Pericardiocentesis. Introduction to Bedside Ultrasound: Volume 2 by Matthew Dawson och Mike Mallin (free at Itunes)
4. Ultrasound Guided Pericardiocentesis Microcast! @

Ultrasound saves lives! # 1

6-year-old previously healthy girl arrives by ambulance. Initially somnolent, tachycardic, hypoxic and hypotensive. In the ambulance a peripheral venous line was placed and Ringer acetate set for infusion. During transport, five minutes from the hospital, she suddenly lost consciousness and stopped breathing. Assessed as cardiac arrest CPR was started. Upon arrival there was no palpable pulses or meassurable BP. CPR was continued. ECG showed a narrow complex SVT with a rate of 130 BPM. Hence PEA until echo. Adrenaline was administered, CPR continued. A bolus of 800cc fluid ex-juvantibus was administered without effect. Bedside echo during CPR seen below.

 The heart looks hyperdynamic. The inferior vena cava is completely collapsed.

Taking the clinical scenario and echo into account, it was considered reasonable to suspect septic shock and the patient was immediately treated with 1L bolus of fluid due to grave hypovolemia. Furthermore, rapid overview ultrasound shows the following findings in the lateral lung quadrant.

A normal lung ought to beyond the superficial pleura have a black and grey appearance without any organized structures, so called artifacts since the air level can’t reflect the sound waves. In this case we can see organized echogenic consolidations in the lung. Most frequently these changes represent severe pneumonia with empyema or a tumor. Overall assessment was severe hypovolemia secondary to pneumosepsis with shock. The patient responed to the fluid bolus, regained pulse and blood pressure, and was admitted to the intensive care unite for further treatment. She was discharged home 10 days later without any complications.