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British Journal of Anaesthesia 2006 96(2):268-269; doi:10.1093/bja/aei636
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


CORRESPONDENCE

Acute intracardiac right-to-left shunt in a patient with acute respiratory distress syndrome and shock successfully treated with nitric oxide

* E-mail: Greet.Hermans{at}uz.kuleuven.ac.be

Editor—In patients with acute respiratory distress syndrome (ARDS) hypoxia can be aggravated by intracardiac right-to-left shunt through a patent foramen ovale.1 Positive pressure ventilation and PEEP may increase shunting.1 We report a patient in whom high dose norepinephrine seemingly triggered an acute right-to-left shunt, successfully treated with inhaled nitric oxide (NO).

A 57-yr-old female was admitted to another hospital with a 1-week history of fever and dyspnoea. Previous medical history included a breast tumour treated with surgery, radiotherapy and chemotherapy 3 yr earlier. She was in respiratory distress with tachypnoea (35 breaths per minute), cyanosis and peripheral oxygen saturation of 88% breathing ambient air. Blood pressure was 87/55 mm Hg and heart rate 113 bpm. Blood analysis demonstrated 87x109 leucocytes per litre, with 74% promonocytes. Acute myeloid leukaemia was later confirmed. Chest X-ray showed bilateral pulmonary infiltrates. Fluid resuscitation, antibiotics and hydroxycarbamide were started. The patient required tracheal intubation and ventilation 24 h after admission. Over the next day her condition worsened with rapid increase in oxygen need and progressive hypotension despite therapy with fluid and norepinephrine. She was transferred to our centre. She remained hypotensive with norepinephrine at 1 µg kg–1 min–1, and hypoxic (Formula ratio of 59 mm Hg) despite ventilation with 100% Formula at 10 cm H2O PEEP and plateau-pressure of 32 cm H2O. Hydrocortisone was started (100 mg bolus followed by 200 mg/24 h). Transpulmonary thermodilution curve (PiCCO-monitor, Pulsion Medical Systems, Munich, Germany) revealed a double-hump suggesting intracardiac right-to-left shunt (Fig. 1A). This was confirmed by trans-oesophageal echocardiography, showing a patent foramen ovale with major shunt and moderately dilated right ventricle. Inhaled NO was started. This immediately improved oxygenation (Formula 78 mm Hg) and the thermodilution curve (Fig. 1B) despite persistent and unchanged norepinephrine dose of 1 µg kg–1min–1 and same ventilatory settings. NO was titrated to 20 ppm. Twelve hours later norepinephrine was reduced to 0.3 µg kg–1min–1 and NO was reduced to 3 ppm as the double hump had completely disappeared (Fig. 1C). In the next 48 h norepinephrine and NO were discontinued and the trachea was successfully extubated 1 week later.


Figure 1
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Fig 1 Transpulmonary thermodilution curve before and during NO treatment. (A) Double hump sign characteristic of right-to-left intarcardiac shunt before start of NO therapy. (B) Reduction of double hump sign by adding NO. (C) Disappearance of the double hump sign during recovery. Doses of NO and norepinephrine (norepi) and PEEP values are shown.

 
Norepinephrine can cause a significant increase in pulmonary artery pressures in ARDS and sepsis.2 In this case, pulmonary pressures apparently were sufficient to cause right-to-left intracardiac shunt through a patent foramen ovale. The shunt presented as profound hypoxia exacerbated by increasing norepinephrine and the double hump on the transpulmonary thermodilution curve, suggested a short pass of the indicator.

Besides reducing ventilation–perfusion mismatch,3 4 inhaled NO can also improve oxygenation by resolving intracardiac shunt.5 6 Here, the shunt was likely triggered by the high dose of norepinephrine as reduction allowed weaning from NO. This quick improvement was unlikely to be regression of ARDS.

In patients with ARDS and worsening hypoxemia receiving high dose norepinephrine, right-to-left shunt should be suspected. Visual analysis of the transpulmonary thermodilution curve may suggest the diagnosis. Therapy with NO should be considered. The effect can be assessed by the shape of the thermodilution curve.

G. M. Hermans*, A. Wilmer, D. C. Knockaert and H. Bobbaers

Leuven, Belgium

References

1 Cujec B, Polasek P, Mayers I, Johnson D. Positive end-expiratory pressure increases the right-to-left shunt in mechanically ventilated patients with patent foramen ovale. Ann Intern Med 1993; 119: 887–94[Abstract/Free Full Text]

2 Papazian L, Bregeon F, Gaillat F, et al. Does norepinephrine modify the effects of inhaled nitric oxide in septic patients with acute respiratory distress syndrome? Anesthesiology 1998; 89: 1089–98[CrossRef][Medline]

3 Rossaint R, Pison U, Gerlach H, Falke KJ. Inhaled nitric oxide: its effects on pulmonary circulation and airway smooth muscle cells. Eur Heart J 1993; 14 Suppl I: 133–40

4 Papazian L, Roch A, Bregeon F, et al. Inhaled nitric oxide and vasoconstrictors in acute respiratory distress syndrome. Am J Respir Crit Care Med 1999; 160: 473–9[Abstract/Free Full Text]

5 Michard F, Alaya S, Medkour F. Monitoring right-to-left intracardiac shunt in acute respiratory distress syndrome. Crit Care Med 2004; 32: 308–9[Medline]

6 De Backer D, Moures JM, Vachiery JL, et al. Oxygenation improvement with nitric oxide in right-to-left shunt without significant effects on pulmonary arterial pressure. Chest 1996; 110: 1361–3[Abstract/Free Full Text]


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