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: Tumor-Induced Hypoglycemia

 

Figure 1. CT of the abdomen with IV contrast (axial image) demonstrating numerous large enhancing liver metastases (red oval) and tumor thrombus in the anterior segment branch of the right portal vein (arrow).

A 39 year-old man with a history of widely metastatic (brain, liver and lung) nonseminomatous germ cell tumor was admitted to the hospital with severe abdominal pain and altered mental status. A CT of the abdomen and pelvis with IV contrast revealed a marked increase in the size of the liver metastases, portal vein tumor thrombus and changes of pseudocirrhosis. There were numerous large heterogeneously enhancing masses within the liver parenchyma with central necrosis (Figure 1).

The patient had significant and sustained hypoglycemia, with the lowest glucose recorded of 30 mg/dl. He required multiple IV doses of 50% dextrose and an infusion of 10% dextrose to maintain a serum glucose level greater than 55 mg/dl. His mental status improved with treatment of the hypoglycemia. The patient decided to pursue a palliative approach to care and was discharged with home hospice services.

Tumor-induced hypoglycemia (TIH) is a paraneoplastic syndrome that is uncommon in clinical practice (1). The more common cause of TIH is insulin hypersecretion in the setting of pancreatic beta-cell tumors. Mechanisms that may lead to TIH without insulin hypersecretion include the hypersecretion by tumors of insulin-like growth factor 2 (IGF2) and it’s precursors, insulin-like growth factor 1 (IGF1), somatostatin, and glucagon-like peptide 1. Other pathogenic causes of hypoglycemia include tumor autoimmune hypoglycemia, massive tumor burden, massive tumor liver infiltration, and pituitary or adrenal gland destruction by the tumor. TIH unrelated to pancreatic tumors is called non-islet-cell tumor hypoglycemia (NICTH). The most common cause of NICTH is the hypersecretion of IGF2 and IGF2 precursors by the tumor. This results in increased glucose consumption peripherally and decreased production of glucose in the liver. We did not measure levels of IGF2 in our patient. It was felt the most likely cause of his hypoglycemia was extensive tumor invasion and destruction of the liver due to his advanced disease.

Pavan Parashar MD¹, Meghan Bullock BSN, RN, OCN, Linda Snyder MD²

¹Department of Medicine, Geriatrics, Palliative and General Medicine, Banner University Medical Center-Tucson

²Department of Medicine, Pulmonary, Critical Care and Palliative Medicine, Banner University Medical Center-Tucson

Reference

1. Iglesias P, Díez JJ. Management of endocrine disease: a clinical update on tumor-induced hypoglycemia. Eur J Endocrinol. 2014;170(4):R147-57. [CrossRef] [PubMed] 

Reference as: Parashar P, Bullock M, Snyder L. Medical image of the week: tumor-induced hypoglycemia. Southwest J Pulm Crit Care. 2015;10(5):300-1. doi: http://dx.doi.org/10.13175/swjpcc049-15 PDF