Nursing Care of Dyspnea: The 6th Vital Sign in Individuals with ...

Nursing Best Practice GuidelinePractice RecommendationsAssessmentRecommendation 1.0:Nurses will acknowledge and accept the patients’ self-report of dyspnea. (Level of Evidence =IV)Discussion of Evidence:Dyspnea is a subjective symptom of difficult or uncomfortable breathing that cannot be measuredobjectively (Heinzer, Bish & Detwiler, 2003; Killian, 1985; Killian & Gandevia, 1996). It is the disabling symptom ofCOPD and must not be confused with observed changes in either rate or depth of respiration that may notproduce a subjective experience of breathlessness (Altose, 1985; Gift, 1990; 1993; Janson-Bjerklie, Carrieri-Kohlman& Hudes, 1986; Tobin, 1990).In general, there is consensus in the literature concerning the physiological research that suggests that thedegree of perceived breathlessness is proportional to respiratory effort. That is, the greater the unsuccessfulrespiratory effort exerted by an individual, the greater the sensation of breathlessness experienced (Campbell& Howell, 1963; El-Manshawi et al., 1986; Jones, 1992; Jones & Wilson, 1996). Although cognizant of its significantcontribution to the understanding of the phenomena, investigation of this mechanically inappropriateposition is not, however, supported as the complete explanation of reported breathlessness in all clinicalsituations (Adams, 1996; Adams, Lane, Shea, Cockcroft & Guz, 1985; Demediuk, Manning, Lilly, Fencl, Weinberger, Weiss et al., 1992).Other factors related to biochemical and mechanical stimulation have also been offered as partialexplanations of the phenomena. Research into the role of chemoreceptors as co-collaborators in theprecipitation of dyspnea has also proven controversial and inconclusive (Burki, 1987; Tobin, 1990). This debatehas centred on the independent and combined effect of hypercapnea, hypoxia, and muscle contraction.Earlier work contended that elevations in arterial carbon dioxide did not contribute to sensations ofdyspnea (Noble, Eisele, Trenchard & Guz, 1970). Current research asserts, however, that hypercapnea doescontribute to the sensation of uncomfortable breathing both independently and in the presence ofrespiratory effort (Adams et al., 1985; Chonan, Mulholland, Leitner, Altose & Cherniak, 1990; Freedman, Lane & Guz, 1987).It is believed that the mechanoreceptors in the upper and lower airways, lung parenchyma, and chest walllikewise contribute to the genesis of uncomfortable breathing. A plethora of respiratory research hasdemonstrated that afferent information from these peripheral sensors does moderate ventilatory patternsand is essential to the perception of dyspnea (Breslin, 1992a; 1992b). Stimulation of the trigeminal nerve forexample, can either reduce or promote the sensation of difficult breathing (Schwartzstein, Lahive, Pope,Weinberger & Weiss, 1987; Simon, Basner, Weinberger, Fencl, Weiss & Schwartzstein, 1991). Pursed-lip breathing,hypothesized to alter the transmural pressure gradients and generate afferent sensory messages, alsoameliorates the feeling of breathlessness (Breslin, 1992b; O’Donnell, Sanii, Anthonisen & Younes, 1988; O’Donnell, Sanii,Giesbrecht & Younes, 1987; Sitzman, Kamiya & Johnston, 1983; Thoman, Stoker & Ross, 1966). The research done withheart-lung transplant individuals who possess denervated lungs illustrates the as yet little understoodcontribution of vagal input in modifying the sensation of breathlessness (Sciurba, Owens, Sanders, Griffith,Hardesty, Paradis et al., 1988). Finally, chest wall receptors also appear to affect the perception of dyspnea. Insome research the greater the chest wall movement, the larger the perceived reduction in difficultbreathing (Breslin, 1992b; Schwartzstein et al., 1987).21