Medical Image of the Week: Pulsus Alternans

Figure 1. Telemetry display including arterial pressure waveform, which demonstrates alternating beats of large (large arrows) and small (small arrows) pulse pressure. Concurrent pulse oximetry could not be performed at the time of the image due to poor peripheral perfusion.

A 52 year old man with a known past medical history of morbid obesity (BMI, 54.6 kg/m²), heart failure with preserved ejection fraction, hypertension, untreated obstructive sleep apnea, and obesity hypoventilation syndrome presented with increasing dyspnea over several months accompanied by orthopnea and weight gain that the patient had treated at home with a borrowed oxygen concentrator. On arrival to the Emergency Department, the patient was in moderate respiratory distress and hypoxic to SpO2 70% on room air. Physical examination was pertinent for pitting edema to the level of the chest. Assessment of jugular venous pressure and heart and lung auscultation were limited by body habitus, but chest radiography suggested pulmonary edema. The patient refused aggressive medical care beyond supplemental oxygen and diuretic therapy. Initial transthoracic echocardiography was limited due to poor acoustic windows but suggested a newly depressed left ventricular ejection fraction (LVEF) of <25%. The cause, though uncertain, may have been reported recent amphetamine use. The patient deteriorated, developing shock and respiratory failure; after agreeing to maximal measures, ventilatory and inotropic/vasopressor support was initiated.

Shortly after placement of the arterial catheter, the ICU team was called to the bedside for a change in the arterial pressure waveform (Figure 1), which then demonstrated alternating strong (arrow) and weak beats (arrow head) independent of the respiratory cycle. The waveform was recognized as pulsus alternans. Repeat bedside echocardiography suggested severe biventricular systolic impairment and LVEF of approximately 5-10%, later confirmed by formal transesophageal ehocardiography performed prior to a cardioversion for atrial flutter.

Pulsus alternans was first formally described in 1872 and associated with severe left ventricular systolic dysfunction (1). The pattern of pulsus alternans is detectable by palpation, arterial pressure waveform analysis, and Doppler echocardiography. Competing theories in the early 20^th century attempted to explain this finding. Wenkebach and Straub, using the Starling relationship, suggested that the alternating force of the pulse is due to alternating filling volumes: greater diastolic volumes accommodated by increased fiber length caused forceful contraction/greater stroke volume with subsequently reduced end systolic and therefore end diastolic volumes for the next (weaker) beat; the consequently reduced force left again greater end systolic and end diastolic volumes for the next (more powerful) beat thereafter. Gaskell, Hering, and Wiggers alternatively proposed the phenomenon was rooted in myocardial contractility fluctuations independent of volumes. Laboratory and animal data supported both theories, but seminal clinical work in the 1960s using concurrent ventriculography and ventricular pressure measurements demonstrated that both mechanisms, in fact, occur in different human subjects (2). The second, Starling-independent mechanism is now thought to be due at least in part to delayed intracellular calcium cycling leading to rhythmic fluctuations in excitation-contraction coupling (3).

Regardless of the underlying physiology, the significance of pulsus alternans as a harbinger of severe ventricular dysfunction and poor prognosis has been recognized and unquestioned since its description. This was unfortunately true in the case of our patient, who developed multiorgan failure despite resuscitative efforts and died three days after admission.

Luke M. Gabe, MD

University of Arizona College of Medicine

Department of Internal Medicine

Division of Pulmonary, Allergy, Critical Care and Sleep Medicine

1501 N. Campbell Ave.

Tucson, AZ USA

References

1. Traube L. Ein fall von pulsus bigeminus nebst bemerkungen tiber die lebershwellungen bei Klappenfehlern und über acute leberatrophic. Ber Klin Wschr. 1872;9:185.
2. Cohn KE, Sandler H, Hancock EW. Mechanisms of pulsus alternans. Circulation. 1967 Sep;36(3):372-80. [CrossRef] [PubMed]
3. Euler DE. Cardiac alternans: mechanisms and pathophysiological significance. Cardiovasc Res. 1999 Jun;42(3):583-90. [CrossRef] [PubMed]

Cite as: Gabe LM. Medical image of the week: pulsus alternans. Southwest J Pulm Crit Care. 2016;13(5):266-7. doi: https://doi.org/10.13175/swjpcc123-16 PDF 

Medical Image of the Week: Bronchial Clot Removal via Cryotherapy

Figure 1. Chest x-ray showing complete opacification of the left hemithorax.

Figure 2. Flexible bronchoscopy with cryotherapy was used to remove clot that formed casts of the bronchial tree. Black arrow: depicts segmental branch of the left upper lobe.

A 38-year-old man with a history of non-ischemic dilated cardiomyopathy presented with decompensated heart failure, acute renal failure, and possible sepsis. He underwent right cardiac catheterization but developed hemoptysis with concern for pulmonary artery rupture. Subsequently, the patient suffered a cardiac arrest but was resuscitated. Emergent bronchoscopy revealed copious amounts of blood and clot that could not be cleared at the time. The patient was then taken to the operating room and placed on A-A ECMO (left ventricle to aorta). The following morning chest x-ray (Figure 1) revealed a completely opacified left lung. Flexible bronchoscopy showed blood clot along the entire left bronchial tree. Initial attempts to remove the clot with suction and endobronchial graspers was unsuccessful. Ultimately, cryotherapy was used to remove the majority of the clot in fragments (Figure 2).

The use of cryotherapies and specifically, in this case, a cryoprobe, has been shown to safely and effectively remove thrombus from the bronchial tree. The basis behind this technique is the use of pressurized nitrous oxide or carbon dioxide to cool a metal probe tip. The probe then freezes any substance it comes in direct contact with, such as a blood clot. Thus, cryoadherence of the probe to the clot allows for effective removal via flexible endoscopy.  Sriratanaviriyakul et al. (1) reported success rates for cryoextraction of blood clots to be >90%.

Cathy V. Ho MD, Ryan Matika MD, and Mimi Amberger MD

¹Division of Trauma, Critical Care, Burn and Emergency Surgery. Department of Surgery

²The Department of Anesthesia

University of Arizona

Tucson, AZ USA

Reference

1. Sriratanaviriyakul N, Lam F, Morrissey BM, Stollenwerk N, Schivo M, Yoneda KY.Safety and clinical utility of flexible bronchoscopic cryoextraction in patients with non-neoplasm tracheobronchial obstruction: a retrospective chart review. J Bronchology Interv Pulmonol. 2015 Oct;22(4):288-93. [CrossRef] [PubMed] 

Cite as: Ho CV, Matika R, Amberger M. Medical image of the week: bronchial clot removal via cryotherapy. Southwest J Pulm Crit Care. 2016;13(5):253-4. doi: https://doi.org/10.13175/swjpcc109-16 PDF