Breathwork Interventions for Adults with Clinically Diagnosed Anxiety Disorders: A Scoping Review.

Anxiety disorders are the most common group of mental disorders, but they are often underrecognized and undertreated in primary care. Dysfunctional breathing is a hallmark of anxiety disorders; however, mainstays of treatments do not tackle breathing in patients suffering anxiety. This scoping review aims to identify the nature and extent of the available research literature on the efficacy of breathwork interventions for adults with clinically diagnosed anxiety disorders using the DSM-5 classification system. Using the PRISMA extension for scoping reviews, a search of PubMed, Embase, and Scopus was conducted using terms related to anxiety disorders and breathwork interventions. Only clinical studies using breathwork (without the combination of other interventions) and performed on adult patients diagnosed with an anxiety disorder using the DSM-5 classification system were included. From 1081 articles identified across three databases, sixteen were included for the review. A range of breathwork interventions yielded significant improvements in anxiety symptoms in patients clinically diagnosed with anxiety disorders. The results around the role of hyperventilation in treatment of anxiety were contradictory in few of the examined studies. This evidence-based review supports the clinical utility of breathwork interventions and discusses effective treatment options and protocols that are feasible and accessible to patients suffering anxiety. Current gaps in knowledge for future research directions have also been identified.

End-tidal carbon monoxide measurements in infant respiratory distress syndrome.

BACKGROUND: RDS involving inflammatory and oxidative processes may lead to increased production of carbon monoxide (CO). AIM: The relationship between end-tidal CO, corrected for inhaled CO (ETCOc), and RDS severity was investigated in preterm infants as well as the value of early ETCOc measurements to predict chronic lung disease. METHODS: 78 infants (30 no RDS, 32 moderate RDS, 16 severe RDS) were included. ETCOc was measured using the CO-Stat End Tidal Breath Analyzer. RESULTS: ETCOc was significantly higher in RDS compared to no RDS during the first week (p<0.05). Severity of RDS was the most significant independent variable in a stepwise regression model related to ETCOc (F-test: 18.17). Negative predictive value of early (within first 12 h of life) ETCOc measurement (<2.5 ppm) for development of chronic lung disease was excellent (100%). CONCLUSION: During severe RDS, inflammation may contribute to increased lipid peroxidation leading to increased local CO production in the lung, indicated by increased ETCOc. Early ETCOc determinations may be helpful to exclude occurrence of chronic lung disease.

Is carbon monoxide-mediated cyclic guanosine monophosphate production responsible for low blood pressure in neonatal respiratory distress syndrome?

Infant respiratory distress syndrome (RDS) involves inflammatory processes, causing an increased expression of inducible heme oxygenase with subsequent production of carbon monoxide (CO). We hypothesized that increased production of CO during RDS might be responsible for increased plasma levels of vasodilatory cGMP and, consequently, low blood pressure observed in infants with RDS. Fifty-two infants (no-RDS, n = 21; RDS, n = 31), consecutively admitted to the neonatal intensive care unit (NICU) between January and October 2003 were included. Hemoglobin-bound carbon monoxide (COHb), plasma cGMP, plasma nitric oxide (NOx), and bilirubin were determined at 0-12, 48-72, and at 168 h postnatally, with simultaneous registration of arterial blood pressure. Infants with RDS had higher levels of cGMP and COHb compared with no-RDS infants (RDS vs. no-RDS: cGMP ranging from 76 to 101 vs. 58 to 82 nmol/l; COHb ranging from 1.2 to 1.4 vs. 0.9 to 1.0%). Highest values were reached at 48-72 h [RDS vs. no-RDS mean (SD): cGMP 100 (39) vs. 82 (25) nmol/l (P < 0.001); COHb 1.38 (0.46) vs. 0.91 (0.26)% (P < 0.0001)]. Arterial blood pressure was lower and more blood pressure support was needed in RDS infants at that point of time [RDS vs. no-RDS mean (SD): mean arterial blood pressure 33 (6) vs. 42 (5) mmHg (P < 0.05)]. NOx was not different between groups and did not vary with time. Multiple linear regression analysis showed a significant correlation between cGMP and COHb, suggesting a causal relationship. Mean arterial blood pressure appeared to be primarily correlated to cGMP levels (P < 0.001). We conclude that a CO-mediated increase in cGMP causes systemic vasodilation with a consequent lower blood pressure and increased need for blood pressure support in preterm infants with RDS.

Antioxidant protection against free radicals is reduced in fetal plasma after intrauterine red blood cell transfusion.

After intrauterine transfusion for red cell alloimmunization, a 2- to 20-fold increase of plasma Hb, a strong pro-oxidant, was observed. The increase of fetal plasma Hb after transfusion leads to a highly significant reduction of plasma antioxidant capacity, measured as the peroxyl radical trapping capacity. Consequently, the posttransfusion reduced antioxidant protection may enhance the peroxidation of lipids in e.g. donor erythrocyte membranes, leading to the shortened life span of these cells in the fetus.

Early neonatal antioxidant capacity after preexisting impaired placental function.

Plasma antioxidant capacity in very preterm infants (n=17), measured as the ferric-reducing ability of plasma (FRAP), increased significantly until day 2 postpartum and decreased thereafter until day 7. Within this period, the FRAP values in matched infants, born after impaired placental function (IPF, n=17), did not change. Their FRAP values were lower and the incidence of oxidative stress-related diseases was significantly higher in these infants.

Nitric oxide production and plasma cyclic guanosine monophosphate in premature infants with respiratory distress syndrome.

A low blood pressure is common in preterm infants with respiratory distress syndrome (RDS). A diminished vascular resistance appears to be an important cause. The endogenous production of nitric oxide (NO), a mediator of vascular smooth muscle relaxation, has been shown to be higher in infants with RDS than in those without. Infants with persistent pulmonary hypertension showed decreased endogenous NO levels as compared with controls. Severe RDS in preterm infants may be accompanied by persistent pulmonary hypertension. To elucidate the role of NO in RDS and low blood pressure, we determined the endogenous NO production in infants with and without RDS by measuring urinary nitrite and nitrate excretions and plasma cGMP levels. In consecutively admitted preterm infants (gestational age <32 weeks), urine samples for measurement of NO(2) and NO(3) and plasma samples for the determination of the cGMP concentrations were serially collected during the 1st week of life. Arterial blood pressure, therapy to support blood pressure, and additional relevant clinical data were registered simultaneously. 27 infants with and 39 without RDS were included. The urinary NO(x) levels increased in all patients and were not different between both groups. The plasma cGMP concentrations were higher in the RDS group on days 2, 3, 4, and 7 (p < 0.05). The severity of RDS was positively correlated with plasma cGMP (r = 0.50, p = 0.0001). Although the arterial blood pressure did not differ between the groups, more blood pressure support was needed in the RDS infants during the first 4 days (p < 0.05). A positive correlation was found between blood pressure support and plasma cGMP (r = 0.34, p < 0.0001). The endogenous NO production was not different in infants with and without RDS. Increased plasma cGMP levels in the RDS infants were associated with the severity of RDS and the intensity of antihypotensive treatment. The origin of cGMP in infants with RDS requires further research.

Prophylactic administration of porcine-derived lung surfactant is a significant factor in reducing the odds for peri-intraventricular haemorrhage in premature infants.

We hypothesized that prophylactic treatment with a porcine-modified lung surfactant (PLS) reduces the rate of peri-intraventricular haemorrhage (PIVH) more than rescue treatment. We performed a meta-analysis of three prophylactic versus rescue trials conducted with PLS in four countries using individual data. Overall (grades 1-4) or severe (grades 3 and 4) PIVH of 671 newborns was the outcome. A logistic regression analysis was performed. Prophylactic exposure to PLS was a significant independent factor in reducing the incidence of overall (OR 0.65; 95% CI 0.47-0.90) and severe (OR 0.56; 95% CI 0.35-0.89) PIVH. Moreover, for severe PIVH, the adjusted OR for outborn babies exposed to prophylactic treatment with PLS was highly significant (OR 0.11; 95% CI 0.02-to 0.49). The results we obtained show that prophylactic treatment with PLS reduces the rate of PIVH more than rescue treatment.