Move to the beat

What do you think?

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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 ultrasoundsweden.com, check out Niklas Jonsson’s case on traumatic cardiac tamponade and be sure to read the discussion.

References
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! @ http://www.ultrasoundpodcast.com

Ill weed grows fast

Just when I thought the sun would set behind the mountain, it rose and made yet another run across the valley. Time to step out of the twilight zone and get back on the donkey. Three hours away from the closest hospital and with an ultrasound probe in hand, I made another run for it.

A peculiar case this middle aged man was, bearing a captivating odor of fermented fish. Priorly morbidly obese with OSAS and CPAP night-time, he’d undergone laparoscopic gastric bypass a year previously, lost massive amounts of weight and was now carrying his skin like a half-empty sack of potatoes. His main complaint was tiredness and impaired life-lust. Family and friends had noticed his indifference. For the past months he’d slept most of the days, experienced muscle- and joint aches and some dizziness. I wasn’t immediately alarmed. Might as well have prescribed him antidepressants. I persisted and he answered question after question.

His apathy had almost rubbed off on me when I heard “visual disturbance, night-sweats” and snapped back. Two days ago he had suddenly gone blind on one eye. Five minutes later he regained vision only to be followed by another similar episode. This was a clear-cut case of…
Vitals were fine and he was afebrile. CRP 110. No cutaneous changes. But upon cardiac auscultation a pan-systolic and diastolic murmur was discovered! And wouldn’t you know, he’d had periodontitis for the past 20 years and root canal fixed three months ago. So what was in the Chinese fortune cookie?

Infective endocarditis. A dancing vegetation is present on the aortic valve non-coronary cusp and anterior mitral leaflet. There is an aortic regurgitation. And the crown jewel? Fistula between the aortic root and left atrium. Anatomically the aortic- and mitral annuli are fused at the fibrous trigone predisposing any vegetation to travel between one another sometimes producing an apparent abscess or fistula.

He was immediately admitted to the hospital. Antibiotics were prescribed and the patient planned for subacute surgery due to high risk of embolization. Blood cultures grew Streptococcus mitis, an inhabitant of the oral cavity. The cause of amaurosis fugax proved to be what we expected unfortunately. MR brain showed two small infarcts caused by septic embolization. Neurologic function remained intact however. And like any other success story, christmas didn’t arrive a day too early. The diseased valves were replaced by two intracardiac Philippe Pateks working around the clock keeping his life ticking.

Ultrasound saves lives! #2

A 55 yo woman lost consciousness at home. When the ambulance arrived she was pale, BP 70/40 with an irregular heart rhythm and ventricular frequency varying between 20 and 40 BPM. The ECG was sent through the “cloud” and the cardiologist on call ordered fluids and atropine. Upon arrival in the ED the patient was very ill, giving the impression of imminent cardiac failure. Diaphoretic, somnolent, BP 100/60 with an unchanged heart rate and frequency. The past medical history was significant for chronic kidney disease, pre-dialysis. Priority number one was to attach the defibrillator plates. Number two – an ECG.

Regular rhythm? P-waves present? QRS width? QTc? ST-segments and T-waves?

It seems to be some kind of a nodal escape rhythm. What about the ultrasound? UnFortunately you’ll have to use your fantasy on this one. I’ll be faster with the trigger finger next time. Imagine a gorgeous ejection fraction, the best one you’ve seen. The problem was that the ventricular rhythm was irregular, frequency low and successively getting lower by the minute. The impressions was that there was a failure of the SA-node, AV-node and other escape foci. Last swan dance.

Any electrolyte disorder that springs to mind?

The blodgas rightfully showed a potassium of 8, pH 7, creatinine 640 (6.8mg/dL), lactate 5.5, Base excess -20, pCO2 10.4, sodium 132. Not completely unexpected. Full measures were taken. Membrane-stabilizing calcium IV without any ECG improvements. Sodium bicarbonate, insulin/glucose and salbutamol nebulization followed. An isoprenalin-drip was started. The result?

Rising potassium and lactate. Dropping heart rate.

Lactic acidosis leads to rising extracellular potassium and vice versa. Like a dead fish turns its belly up, drifting away in loneliness, the mitral valve made a grand final agonal motion whereupon the gracious magic vanished. Seconds felt like minutes. A swirl of spontaneous contrast began making its presence. True ultrasound-witnessed asystole. What do the guidelines say? Compressions/ventilations/Adrenalin?

Based on the ultrasound and the appreciation of the hearts capabilities, the decision was made to try an alternative treatment modality. With continuous ultrasound observation, the external pacing function was started on the defibrillator. Note that part of the pacing-electricity was transmitted to the operator 🙂 (Don’t try this at home kids)

Eureka! Time to pacing was of utmost importance. Any further delays and the race would have been lost. Followup blodgas showed improvement on all values. But why now? Most probably the cardiac output, previously deranged, now managed to deliver the drugs to the systemic circulation. The patient was dialyzed and had a temporary transvenous pacemaker implanted. She was discharged from the ICU after three days without any further complications. Neurological sequela? Nada.

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.

Misleading chest pain #1

30 year old man with acute onset chest pain two hours earlier. Radiation to the neck and left arm.

ECG shows ST-elevation V4-V6 with a hint of ST-elevation V2-V3. The morphology leans towards the convex, valley, side. Reciprocal ST depression might be suspected in limb lead III. The patient informs of a fever and diarrhea for the past three days.

Ultrasound of course:

Can you see the regional wall motion abnormality? The inferolateral part of the apex is affected. So how do we proceed? The history and age raises a suspicion of perimyocarditis, but STEMI must be excluded. An emergency percutaneous coronary angiography was performed and showed absolutely fine coronary artery. The first highly sensitive Troponin T 650. In conclusion myocarditis with localized inferolateral RWMA was diagnosed.

See also Amal Mattu’s approach on how to differ myocardial infarction from pericarditis by ECG.

http://ekgumem.tumblr.com/post/30868011279/ecg-findings-in-pericarditis-vs-stemi-episode

Creeping NSTEMI

35-year-old woman seeking due to exercise-induced chest pain for three days which has now transitioned into constant pain.

ECG on arrival shows ST depression v4-v6.

Repeat ECG after 15 minutes shows regression of the ST-depressions.

The patient has just performed a stress-ECG!

Can you see the regional wall motion abnormality (RWMA)?

In a stepwise fashion, evaluate each region. As a novice it might be difficult to distinguish RWMA from normal myocardium when looking at the heart as a whole. Feel free placing the mouse pointer over the endocardium to look for dynamic changes in the wall thickness. This is referred to as radial contraction.

Systematic review shows RWMA in the apex and the entire lateral wall.

NSTEMI treatment was instituted. Because of persistent chestpain PCI was performed two hours later showing total occlusion of the LCx.

The Whistleblower

It was a sunny July afternoon and time to wrap up for the day. A quick glance at the patient list however, and before you knew it I was taking a history.
Intermittent lower leg edema the last couple of months in a 40-or so woman. Physically active every day. No other complaints. No past medical history and no medication. A pinch of short stature and a pinch of overweight. Vital signs were ok. Lower extremities slender. All in all currently asymptomatic and seemingly well. This was a clear-cut case of thoracic aortic aneurysm involving the roots of the coronary arteries. Now all I had to do was convince the surgeon to perform a composite graft implantation.
A quick physical revealed a diastolic decrescendo murmur 2/6 at IC2-3 left parasternal. No rumbling, anterior mitral leaflet Austin-Flynt murmur over the apex, but it was good enough to justify a bedside echo. Lo and behold, a 6cm wide ascending thoracic aortic aneurysm with a mild aortic insufficiency.

But let’s drop the cool. Was this simply an ad-hoc finding? What was I looking for with the ultrasound? To make things clear, a diastolic murmur always warrants further diagnostics. But was the absent lower extremity edema related to the TAA? Perhaps it was, perhaps it wasn’t, perhaps it was hormones. Her neck was a bit short. Webbing of the neck springs to mind, and as such Noonan and Turner syndromes. Just as in Marfan-, Ehler-Danlos- and Loeys-Dietz syndromes, diseases effecting connective tissue, there is a relation to pathology of the aorta. Did I think of this? No. Upon focused history regarding chest pain, burried beneath a thick layer of anxiety, in the trunk of an old caaar, much was revealed. Onset, location, duration, character, alleviating- & aggravating factors, accessory symptom and radiating pain. First onset one year ago, 1-4 times a week, increasing in frequency lately. Episodes described as sudden in onset, retro sternal, stabbing chest pain radiating to the right arm and back. Aggravate by lifting boxes at work or while straining upon defecation, 5-10 minutes of duration, alleviated by rest.  Accessory symptom of dispnea while lying supine, alleviated by lying in lateralt decubitus. Compression of adjacent organs? She admitted to rationalizing the pain because there was no radiation to the left arm.

Boy oh boy was I worried. A young, vital woman in her prime with an intermittently symptomatic TAA and open heart surgery around the corner. I’ll leave you suspended in mid-air to appreciate the emotional limbo. Goal systolic BP < 120 until then.