Blowing Soap Bubbles: Teaching Pursed-Lip Breathing

Blowing Soap Bubbles: Teaching Pursed-Lip Breathing

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Blowing Soap Bubbles: Teaching Pursed-Lip Breathing To the Editor: A number of different techniques have been used t o teach patients pursed-lip breathing. These te chniques emphasize a prolonged expiration through pursed lips. This provides an external resistance to expiration that increases airway pressure. 1 Pursed-lip breathing has been shown to decrease dyspnea when it is utilized with activities that produce tachypnea, which leads to progressive air trapping 2 Frequently, a candle analogy i s sed; u that is, one should "bend the flam e of the candle." However, this metaphor is cumbe rsome in teaching pati ents pursed-lip breath ing. Using a child's soap bubble wand and blowing one big soap bubble, patients will experience a p erfect pursed-lip exhalation. Other benefits of blowing soap bubbles are: (1) measurable means of visualizing a pursed-lip exhalation; (2) immediate patient feedback; ( 3) noticeable relaxation of patients' upper bodies and decreased use of accessory breathing muscles; and (4) an enjoyable group activity. Patients should practice blowing soap bubbles at home wh en they are clinically well and in control of their breathing so that they \viii be comf01table utilizing the bubble-blowing, pursed-lip exhalation technique when they need t ocontrol dyspnea. Patients report that they experience better control of their dyspnea and fewer p anic attacks when practicing this te chnique.

Lisa M. Custodio, BA Pulmonary Rehabilitation John Muir Rehabilitation Services Walnut Creek, CA REFERENCES 1 Hodgkin JE , Connors GL, Bell CW. Pulmonmy rehabilitation: guidelines to success. Philadelphia: JB Lippincott Co, 1993 2 Casaburi R, Petty TL. Principles and practice of pulmonary rehabilitation. Philadelphia: WB Saunders Co, 1993 1224

Primary Pulmonary Hypertension or Portopulmonary Hypertension? To t he Editor: Rossoff and coworke rs (August 1997)1 present a fascinating case of a patient with CDS!f-cell large granulocyte leuke mia who showed r egression of primaty pulmonaty hyperte nsion (PPH ) following treatment with cladribine. The authors a sl o present an inte resting and carefully thought-out hypothesis concerning possible interaction between the endothelial cell and the CDS!f-cell in the pathogenesis of pulmonaty hypertension in this patient, and perhaps also in HIV-infected patients. Although the authors stated that "our patient de monstrated severe pulmonaty hypertension \vith all diagnostic studies highly charactetistic of PPH ," the cardiac output and pulmonary vascular resistance in their patient were uncharacteristic o f PPH . The PPH registry2 reported h emodynamic data on 187 patients \vith PPH and found a mean pulmonaty artety pressure of 60 mm Hg. pulmonaty vascular r esistance of 2,080 dyne · sec · em- s, and a cardiac index of 2.3 Umin/m 2 . Although the authors' patient had a comparable pulmonaty artery pressure of 59 mm Hg, his pulmonaty vascular resistance was only 369 dyne · sec· em - ·5, and his cardiac output was a whopping 10.6 L /min. These values are much more consistent \vith th e hemodynamic findings in portopulmonary hypertension (which may also show plexogenic pathology) and raise the question of whether the patient had leuke mic infiltration of his liver and portal hyp ertension. 3 Although a liver biopsy 15 years prior to the development of le ukemia was repmted to be normal, I wonder whether the authors have any data concerning liver function at the tim e of diagnosis of pulmonaty hypertension. If leukemia i nvolved the liver, it is possible that treatm ent with cladribine may have resulted in regression of portopulmonary hypertension. This possibility is fmih er supported b y aconcomitant fall in thei r patient's cardiac output-a pattern that wou ld b e typical for improve ment in portopulmonary hypertension. In contrast, improve ment in PPH is typically associated \vith an increase in cardiac output.4 The s ustain ed r egression of pulmona1y hypertension is certainly impressive re gardless of its etiology. A lthough cladribine treatment may have caused r egression of pulmonary hypertension, I b leieve it is equally possible (from the data presented ) that long-term treatment with nifedipine may have been at least partially responsible . Sustained r egression of pulmonary arte1y pressure in PPH has been documented with calcium channel blockers and with continuous infusion of prostacyclin 4 ·5 At the time of the initial diagnosis of pulmonary hypertension in the authors' patient, nifedipine resulted in a 31 % decrease in mean pulmonary artery pressure and a 42% decrease in pulmonary vascular resistance. These decreases are similar to those reported by Rich and coworkers,6 who showed that patients with PPH who respond quickly to calcium channel blockers may have sustained hemodynamic benefit and regression of right ventricular hypertrophy.-5 The authors' patient may have had a response to calcium channel blockers that persisted d espite discontinuation of these agents. If so, it may b e possible to wean long-term vasodilator therapy in selected patients with PPH who show complete or Communications to the Editor