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Journal articles on the topic 'Dyspnea'

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Author: Grafiati

Published: 4 June 2021

Last updated: 7 September 2024

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1

Campbell, Margaret L. "Dyspnea." AACN Advanced Critical Care 22, no. 3 (July 1, 2011): 257–64. http://dx.doi.org/10.4037/nci.0b013e318220bc4d.

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Patients experiencing a dyspnea exacerbation will often report feeling smothered or suffocated. This highly distressing, prevalent, multidimensional symptom is the chief complaint signifying pulmonary dysregulation. Increasing dyspnea intensity heralds the onset of respiratory failure, leading to hospitalization and/or admission to the intensive care unit (ICU). Dyspnea can only be known from the patient’s report about the personal experience. However, many ICU patients experience temporary or permanent cognitive impairment precluding a symptom report; thus, a behavioral assessment is indicated. Comprehensive dyspnea assessment informs subsequent treatment. Conventional treatment of dyspnea includes reducing or eliminating the underlying cause, mechanical ventilation, supplemental oxygen, balancing rest with activity, and positioning. Opioids and benzodiazepines reduce dyspnea and the associated fear or anxiety and are most often used to maintain ventilator–patient synchrony, in terminal illness or during the withdrawal of mechanical ventilation. Inhaled furosemide is under investigation as an alternative to opioids. The focus of this article is to provide an evidence-based approach to nursing assessment and management of dyspnea.

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2

Horie, Takashi. "Dyspnea." Nihon Kikan Shokudoka Gakkai Kaiho 48, no. 2 (1997): 145–46. http://dx.doi.org/10.2468/jbes.48.145.

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3

Gift, Audrey G. "Dyspnea." Nursing Clinics of North America 25, no. 4 (December 1990): 955–65. http://dx.doi.org/10.1016/s0029-6465(22)02993-0.

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4

Arena, Sara. "Dyspnea." Home Healthcare Now 39, no. 4 (July 2021): 221–22. http://dx.doi.org/10.1097/nhh.0000000000000991.

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5

Dryden, Jefferson. "Dyspnea." Anesthesiology 136, no. 5 (October 5, 2021): 861. http://dx.doi.org/10.1097/aln.0000000000004014.

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6

Lee, Byung Jae, and You Young Kim. "Dyspnea." Journal of the Korean Medical Association 40, no. 2 (1997): 236. http://dx.doi.org/10.5124/jkma.1997.40.2.236.

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7

Chang, Jung Hyun. "Dyspnea." Journal of the Korean Medical Association 48, no. 3 (2005): 254. http://dx.doi.org/10.5124/jkma.2005.48.3.254.

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8

Spector, Nancy, Maria A. Connolly, and Karen K. Carlson. "Dyspnea." AACN Advanced Critical Care 18, no. 1 (January 1, 2007): 45–60. http://dx.doi.org/10.4037/15597768-2007-1006.

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Dyspnea is a common symptom in patients with acute and chronic critical illness as well as in patients receiving palliative care. While dyspnea can be found in a variety of clinical arenas and across many specialties, the mechanisms that cause dyspnea are similar. Although not often the cause for admission to critical care, it may complicate and extend length of stay. This article defines and describes dyspnea and its pathophysiology. Critical care nurses should strive to implement interventions supported by evidence whenever possible. An evidence-based plan of care for the assessment, planning, intervention, and evaluation of the patient with dyspnea is outlined, using levels of recommendation based on the strength of available evidence. Two case studies are presented to illustrate its application to clinical practice.

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9

Mahler, Donald. "Dyspnea." Medicine & Science in Sports & Exercise 23, no. 11 (November 1991): 1322. http://dx.doi.org/10.1249/00005768-199111000-00027.

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10

Moorehead, Paul. "Dyspnea." Canadian Medical Association Journal 173, no. 6 (September 12, 2005): 639. http://dx.doi.org/10.1503/cmaj.050909.

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11

Medarov, Boris I. "Dyspnea." Public Health and Emergency 1 (June 29, 2016): 7. http://dx.doi.org/10.21037/phe.2016.06.06.

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12

Mahler, D. A. "Dyspnea." Critical Care Medicine 20, no. 1 (January 1992): 155. http://dx.doi.org/10.1097/00003246-199201000-00037.

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13

Killian, Kieran. "Dyspnea." Journal of Applied Physiology 101, no. 4 (October 2006): 1013–14. http://dx.doi.org/10.1152/japplphysiol.00635.2006.

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14

GOLDEN, WILLIAM E., and ROBERT H. HOPKINS. "Dyspnea." Internal Medicine News 43, no. 8 (May 2010): 29. http://dx.doi.org/10.1016/s1097-8690(10)70431-5.

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15

Spector, Nancy, Maria A. Connolly, and Karen K. Carlson. "Dyspnea." AACN Advanced Critical Care 18, no. 1 (January 2007): 45–58. http://dx.doi.org/10.1097/01256961-200701000-00006.

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16

&NA;. "Dyspnea." AACN Advanced Critical Care 18, no. 1 (January 2007): 59–60. http://dx.doi.org/10.1097/01256961-200701000-00007.

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17

Burke, Catherine C., and Mary Pat Lynch. "Dyspnea." Clinical Journal of Oncology Nursing 10, no. 3 (June 1, 2006): 323–26. http://dx.doi.org/10.1188/06.cjon.323-326.

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18

Shiber, Joseph R., and Jose Santana. "Dyspnea." Medical Clinics of North America 90, no. 3 (May 2006): 453–79. http://dx.doi.org/10.1016/j.mcna.2005.11.006.

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19

Williams, Cynthia M. "Dyspnea." Cancer Journal 12, no. 5 (September 2006): 365–73. http://dx.doi.org/10.1097/00130404-200609000-00006.

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20

Campbell, Margaret L. "Dyspnea." AACN Advanced Critical Care 22, no. 3 (2011): 257–64. http://dx.doi.org/10.1097/nci.0b013e318220bc4d.

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21

Campbell, Margaret L. "Dyspnea." Critical Care Nursing Clinics of North America 29, no. 4 (December 2017): 461–70. http://dx.doi.org/10.1016/j.cnc.2017.08.006.

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22

Tobin, Martin J. "Dyspnea." Archives of Internal Medicine 150, no. 8 (August 1, 1990): 1604. http://dx.doi.org/10.1001/archinte.1990.00040031604007.

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23

Burki, N. K. "Dyspnea." Lung 165, no. 1 (December 1987): 269–77. http://dx.doi.org/10.1007/bf02714443.

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24

Morris, Deborah, and Marissa Galicia-Castillo. "Dying With Dyspnea in the Hospital." American Journal of Hospice and Palliative Medicine® 34, no. 2 (July 11, 2016): 132–34. http://dx.doi.org/10.1177/1049909115604140.

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Background: While many patients hope to die at home, many die in hospitals. Patients die with unrecognized and untreated symptoms including dyspnea. Objective: We sought to determine prevalence of dyspnea at end of life in patients dying in acute hospital care and examine treatment patterns. Design/Participants: A retrospective chart review of deaths at tertiary care hospital over a 3-month period evaluated dyspnea in last 24 hours of life, opioid orders and administration as well as presence of palliative care consultation. Results: Of 106 decedents, 88 experienced dyspnea or tachypnea in last 24 hours of life. Health care providers noted only 50% as dyspneic, even those undergoing terminal comfort extubation. Almost all patients with dyspnea documented by staff had orders and received opioids; however, few orders described treatment specifically for dyspnea. Patients with palliative care consultations more often received opioids ( P = .0007), and opioid orders more often specified treatment of dyspnea ( P = .013). Conclusion: These findings support that previous work noting many patients experience dyspnea at end of life. Despite national guidelines, health care providers may still be underrecognizing and likely not optimally treating dyspnea at the end of life in the hospital. Collaboration with palliative medicine providers may improve assessments and treatments for quality end-of-life care for hospitalized patients.

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25

Kopjar, Tomislav, Bojan Biocina, and Hrvoje Gasparovic. "Less Dyspnea Is Better Than More Dyspnea." Journal of the American College of Cardiology 66, no. 8 (August 2015): 979–80. http://dx.doi.org/10.1016/j.jacc.2015.04.084.

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26

Burki, Nausherwan K., Wheeler J. Dale, and Lu-Yuan Lee. "Intravenous adenosine and dyspnea in humans." Journal of Applied Physiology 98, no. 1 (January 2005): 180–85. http://dx.doi.org/10.1152/japplphysiol.00913.2004.

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Intravenous adenosine for the treatment of supraventricular tachycardia is reported to cause bronchospasm and dyspnea and to increase ventilation in humans, but these effects have not been systematically studied. We therefore compared the effects of 10 mg of intravenous adenosine with placebo in 21 normal subjects under normoxic conditions and evaluated the temporal sequence of the effects of adenosine on ventilation, dyspnea, and heart rate. The study was repeated in 11 of these subjects during hyperoxia. In all subjects, adenosine resulted in the development of dyspnea, assessed by handgrip dynamometry, without any significant change ( P > 0.1) in lung resistance as measured by the interrupter technique. There were significant increases ( P < 0.05) in ventilation and heart rate in response to adenosine. The dyspneic response occurred slightly before the ventilatory or heart rate responses in every subject, but the timing of the dyspneic, ventilatory, and heart rate responses was not significantly different when the group data were analyzed (18.9 ± 5.8, 20.3 ± 5.5, and 19.7 ± 4.5 s, respectively). During hyperoxia, adenosine resulted in similar effects, with no significant differences in the magnitude of the ventilatory response; however, compared with the normoxic state, the intensity of the dyspneic response was significantly ( P < 0.05) reduced, whereas the heart rate response increased significantly ( P < 0.05). These data indicate that intravenous adenosine-induced dyspnea is not associated with bronchospasm in normal subjects. The time latency of the response indicates that the dyspnea is probably not a consequence of peripheral chemoreceptor or brain stem respiratory center stimulation, suggesting that it is most likely secondary to stimulation of receptors in the lungs, most likely vagal C fibers.

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27

Sahasrabudhe, TusharR. "Psychogenic dyspnea." Medical Journal of Dr. D.Y. Patil University 6, no. 1 (2013): 14. http://dx.doi.org/10.4103/0975-2870.108627.

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28

Hoffmann, S. J., and T. Blok. "DYSPNEA - VOLLEYBALL." Medicine & Science in Sports & Exercise 27, Supplement (May 1995): S222. http://dx.doi.org/10.1249/00005768-199505001-01248.

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29

McGinley, Mark J., Jonathan B. Orens, and Dhruv Kumar. "Cryptogenic Dyspnea." Clinical Pulmonary Medicine 4, no. 5 (September 1997): 295–301. http://dx.doi.org/10.1097/00045413-199709000-00007.

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30

Ferrin, Marianne S., and Gregory Tino. "Acute Dyspnea." AACN Clinical Issues: Advanced Practice in Acute and Critical Care 8, no. 3 (August 1997): 398–410. http://dx.doi.org/10.1097/00044067-199708000-00009.

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31

Fischer, Anastasia N. "Dyspnea - Running." Medicine & Science in Sports & Exercise 37, Supplement (May 2005): S132. http://dx.doi.org/10.1249/00005768-200505001-00686.

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32

Fischer, Anastasia N. "Dyspnea - Running." Medicine & Science in Sports & Exercise 37, Supplement (May 2005): S132. http://dx.doi.org/10.1097/00005768-200505001-00686.

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33

Bascom, Paul B. "Subjective Dyspnea." Journal of Palliative Medicine 18, no. 9 (September 2015): 805–6. http://dx.doi.org/10.1089/jpm.2015.0109.

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34

Krüger, S., D. Frechen, M. Das, R. Dembinski, and E. Noll. "Dyspnea lusoria." Pneumologie 63, no. 04 (March 16, 2009): 205–6. http://dx.doi.org/10.1055/s-0028-1119677.

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35

Baldwin, Jennifer, and Jaclyn Cox. "Treating Dyspnea." Medical Clinics of North America 100, no. 5 (September 2016): 1123–30. http://dx.doi.org/10.1016/j.mcna.2016.04.018.

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36

Lepley, S., and S. M. Simons. "DYSPNEA - SWIMMING." Medicine & Science in Sports & Exercise 30, Supplement (May 1998): 303. http://dx.doi.org/10.1097/00005768-199805001-01720.

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37

GILLESPIE, DELMAR J., and BRUCE A. STAATS. "Unexplained Dyspnea." Mayo Clinic Proceedings 69, no. 7 (July 1994): 657–63. http://dx.doi.org/10.1016/s0025-6196(12)61344-5.

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38

Govindaraj, Madathil. "Defining Dyspnea." Chest 121, no. 2 (February 2002): 662. http://dx.doi.org/10.1378/chest.121.2.662.

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39

Ramirez-Icaza, Carlos, Helen T. Winer-Muram, Cristopher A. Meyer, and S. Gregory Jennings. "Seasonal Dyspnea." Chest 121, no. 6 (June 2002): 2040–43. http://dx.doi.org/10.1378/chest.121.6.2040.

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40

Yusen, Roger D. "Defining Dyspnea." Chest 121, no. 2 (February 2002): 662–63. http://dx.doi.org/10.1016/s0012-3692(16)35484-8.

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41

AMBROSE, MARGUERITE S. "Chronic dyspnea." Nursing 28, no. 5 (May 1998): 41–47. http://dx.doi.org/10.1097/00152193-199805000-00019.

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42

O'Doherty, C. J., and J. A. Savin. "Dermatologic Dyspnea." International Journal of Dermatology 25, no. 1 (January 1986): 58–59. http://dx.doi.org/10.1111/j.1365-4362.1986.tb03407.x.

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43

Tay, Melvin, Tow Keang Lim, and Pyng Lee. "Puzzling Dyspnea." Chest 142, no. 4 (October 2012): 997A. http://dx.doi.org/10.1378/chest.1389478.

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44

Nishino, Takashi, Naohito Shimoyama, Tohru Ide, and Shiroh Isono. "Experimental Pain Augments Experimental Dyspnea, but Not Vice Versa in Human Volunteers." Anesthesiology 91, no. 6 (December 1, 1999): 1633. http://dx.doi.org/10.1097/00000542-199912000-00014.

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Background Pain and dyspnea frequently coexist in many clinical situations. However, whether the two different symptoms interact with each other has not been elucidated. To elucidate the interaction between pain and dyspneic sensations, the authors investigated separately the effects of pain on dyspnea and the effects of dyspnea on pain in 15 healthy subjects. Methods Subjects were asked to rate their sensation of pain or dyspnea using a visual analog scale (VAS) during pain stimulation produced by tourniquet inflation (inflation cuff pressure: 350 mmHg) around the calf, and/or the respiratory loading consisted of a combination of resistive load (77 cm H2O x l(-1) x s(-1)) and hypercapnia induced by extra mechanical dead space (255 ml). In addition to changes in VAS scores, changes in ventilatory airflow and airway pressure were continuously measured. Results Pain stimulation and loaded breathing increased VAS scores, ventilation, and occlusion pressure (P0.1). The addition of a pain stimulus during loaded breathing increased the dyspneic VAS score (median 56 [interquartile range 50-62] vs. 64 [55-77]: before vs. after addition of pain stimulus, P < 0.05) with concomitant increases in minute ventilation (10.8 [10.1-13.3] vs. 12.4 [11.0-14.8] l/min, P < 0.05) and P0.1 (5.5 [4.9-7.2] vs. 6.8 [5.8-9.0] cm H2O, P < 0.05). The addition of respiratory loading during pain stimulation did not cause a significant change in pain VAS score (40 [33-55] vs. 31 [30-44]: before vs. after addition of respiratory loading), although both additional burdens increased further minute ventilation (10.0 [8.8-10.9] vs. 12.0 [10.6-13.2] l/min, P < 0.05) and P0.1 (2.5 [2.0-3.0] vs. 6.2 [4.9-7.0] cm H2O, P < 0.05). Conclusion The authors' findings suggest that pain intensifies the dyspneic sensation, presumably by increasing the respiratory drive, whereas dyspnea may not intensify the pain sensation.

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45

Inui, Shohei, Soon Ho Yoon, Ozkan Doganay, Fergus V. Gleeson, and Minsuok Kim. "Impaired pulmonary ventilation beyond pneumonia in COVID-19: A preliminary observation." PLOS ONE 17, no. 1 (January 25, 2022): e0263158. http://dx.doi.org/10.1371/journal.pone.0263158.

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Background Coronavirus disease 2019 (COVID-19) may severely impair pulmonary function and cause hypoxia. However, the association of COVID-19 pneumonia on CT with impaired ventilation remains unexplained. This pilot study aims to demonstrate the relationship between the radiological findings on COVID-19 CT images and ventilation abnormalities simulated in a computational model linked to the patients’ symptoms. Methods Twenty-five patients with COVID-19 and four test-negative healthy controls who underwent a baseline non-enhanced CT scan: 7 dyspneic patients, 9 symptomatic patients without dyspnea, and 9 asymptomatic patients were included. A 2D U-Net-based CT segmentation software was used to quantify radiological futures of COVID-19 pneumonia. The CT image-based full-scale airway network (FAN) flow model was employed to assess regional lung ventilation. Functional and radiological features were compared across groups and correlated with the clinical symptoms. Heterogeneity in ventilation distribution and ventilation defects associated with the pneumonia and the patients’ symptoms were assessed. Results Median percentage ventilation defects were 0.2% for healthy controls, 0.7% for asymptomatic patients, 1.2% for symptomatic patients without dyspnea, and 11.3% for dyspneic patients. The median of percentage pneumonia was 13.2% for dyspneic patients and 0% for the other groups. Ventilation defects preferentially affected the posterior lung and worsened with increasing pneumonia linearly (y = 0.91x + 0.99, R2 = 0.73) except for one of the nine dyspneic patients who had disproportionally large ventilation defects (7.8% of the entire lung) despite mild pneumonia (1.2%). The symptomatic and dyspneic patients showed significantly right-skewed ventilation distributions (symptomatic without dyspnea: 0.86 ± 0.61, dyspnea 0.91 ± 0.79) compared to the patients without symptom (0.45 ± 0.35). The ventilation defect analysis with the FAN model provided a comparable diagnostic accuracy to the percentage pneumonia in identifying dyspneic patients (area under the receiver operating characteristic curve, 0.94 versus 0.96). Conclusions COVID-19 pneumonia segmentations from CT scans are accompanied by impaired pulmonary ventilation preferentially in dyspneic patients. Ventilation analysis with CT image-based computational modelling shows it is able to assess functional impairment in COVID-19 and potentially identify one of the aetiologies of hypoxia in patients with COVID-19 pneumonia.

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46

Hui, David, Farley Hernandez, Saji Thomas, Zhanni Lu, Ahmed F. Elsayem, Dave Balachandran, Lara Bashoura, and Eduardo Bruera. "High flow oxygen for dyspnea in hospitalized patients with cancer: A 4x4 crossover randomized clinical trial." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): 12077. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.12077.

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12077 Background: Dyspnea is common in hospitalized cancer patients and highly distressing. High flow oxygen (HFOx) is administered for oxygenation in this setting; however, its effect on dyspnea has not been well examined, particularly among non-hypoxemic patients. In this phase II trial, we assessed the effect of HFOx, high flow air (HFAir), low flow oxygen (LFOx) and low flow air (LFAir) on dyspnea. We hypothesized that HFO and HFA can alleviate dyspnea. Methods: This double-blind, 4x4 crossover clinical trial enrolled hospitalized patients with cancer who were dyspneic (NRS ≥3 at rest) and non-hypoxemic (SpO2>90% on room air). Patients were randomized to 10 minutes of HFOx, HFAir, LFOx and LFAir in different orders. The flow rate was titrated between 20-60 L/min in the high flow groups and 2 L/min in the low flow groups. The primary outcome was dyspnea 0-10 numeric rating scale (NRS) “now”, where 0=none and 10=worst. Secondary outcomes included modified Borg scale dyspnea intensity and unpleasantness, adverse effects, and overall preference. We compared among the interventions with a linear mixed model adjusting for time, treatment effect, period effect and carryover effect. Results: 17 patients completed 55 interventions in a random order. Mean age 51, 58% female, mean baseline dyspnea NRS 6.3 (SD 1.7). The absolute change of dyspnea NRS between 0 and 10 minutes was -1.8 (SD 1.7) for HFOx, -1.8 (2.0) for HFAir, -0.5 (0.8) for LFOx and -0.6 (1.2) for LFAir. In mixed model analysis, HFOx group provided greater dyspnea relief than LFOx (mean difference [95% CI] -0.80 [-1.45, -0.15], P=0.02) and LFAir (-1.24 [-1.90, -0.57], P<0.001). HFAir also provided a significantly greater dyspnea relief than LFOx (-0.95 [-1.61, -0.30], P=0.005) and LFAir (-1.39 [-2.05, -0.73], P<0.001). No difference was found between HFOx and HFAir nor between LFOx and LFAir. There was no significant carryover effect. Dyspnea Borg scale intensity and unpleasantness showed similar changes. Oxygen saturation increased in the HFOx group (97.2% to 99.7%) and LFOx group (95.5% to 98.2%) but not HFAir nor LFAir groups. HFOx was well tolerated. At the end of the study, 7 (54%), 4 (31%), 1 (8%) and 1 (8%) patients blindly preferred HFOx, HFAir, LFOx and LFAir, respectively. Conclusions: For the first time, we found that HFOx and HFAir provided a rapid and clinically significant reduction of dyspnea at rest in hospitalized cancer patients even when they were non-hypoxemic, supporting a role for high flow devices to provide palliation beyond oxygenation. Larger studies are needed to confirm these findings. Clinical trial information: NCT02932332 .

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47

NISHINO, Takashi. "Physiology of Dyspnea." JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA 29, no. 4 (2009): 341–50. http://dx.doi.org/10.2199/jjsca.29.341.

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48

Branson, R. D., T. C. Blakeman, and B. R. Robinson. "Asynchrony and Dyspnea." Respiratory Care 58, no. 6 (May 25, 2013): 973–89. http://dx.doi.org/10.4187/respcare.02507.

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49

Terasaki, H. "Dyspnea in Anesthesia." Nihon Kikan Shokudoka Gakkai Kaiho 45, no. 2 (1994): 143. http://dx.doi.org/10.2468/jbes.45.143.

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50

Gift, Audrey G., and Linda C. Pugh. "DYSPNEA AND FATIGUE." Nursing Clinics of North America 28, no. 2 (June 1993): 373–84. http://dx.doi.org/10.1016/s0029-6465(22)02868-7.

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