Heart rate variability is reduced in COVID-19 survivors and associated with physical activity and fatigue.

Reduced heart rate variability (HRV) and fatigue are common after COVID-19 infection and both are potentially influenced by physical activity (PA). We compared resting HRV, PA from accelerometers and questionnaires, and self-reported fatigue in 41 COVID-19 survivors (~8 months postinfection, 38 ± 17 years) with 41 matched controls. Differences in HRV were observed on acceleration capacity (p = 0.041), deceleration capacity (p = 0.032), high-frequency peak frequency (p = 0.019), absolute low-frequency power (p = 0.042), relative very low-frequency power (p = 0.012), SD2 (from Poincare plot; p = 0.047), and DFA2 (slope of long-term detrended fluctuation analysis; p = 0.004). Fatigue was greater in COVID-19 survivors (p < 0.001) with no differences in PA. Moderate-vigorous physical activity (MVPA) (Standardized Beta = -0.427, p = 0.003) and steps per day (Standardized Beta = -0.402, p = 0.007) were associated with DFA2 in COVID-19 survivors after controlling for age, sex, and body fat percentage. Fatigue was correlated to less MVPA (Spearman's rho = 0.342, p = 0.031) and fewer steps per day (rho = 0.329, p = 0.038) in COVID-19 survivors, and was indirectly linked to HRV through these PA mediators (Estimate = -0.20; p = 0.040). We present a model showing the complex relations between HRV, PA, and fatigue that provides the foundation for strategies to improve outcomes and rehabilitation after COVID-19 infection.

Quantification of Tissue Oxygen Saturation in the Vastus Lateralis Muscle of Chronic Stroke Survivors during a Graded Exercise Test.

Purpose: This study examined tissue oxygen saturation (StO2) of the vastus lateralis (VL) muscles of chronic stroke survivors during a graded exercise test (GXT). We hypothesized the reduction in StO2 will be blunted in the paretic vs. non-paretic VL during a maximum-effort GXT. Methods: Chronic stroke survivors performed a GXT and StO2 of the VL in each leg was measured using near infrared spectroscopy. Twenty-six stroke survivors performed a GXT. Results: At rest, there was no difference in StO2 between the paretic and non-paretic VL (65±9% vs. 68±7%, respectively, p=0.32). The maximum change in StO2 from rest during the GXT was greater in the non-paretic vs. the paretic VL (-16±14% vs. -9±10%, respectively, p<0.001). The magnitude of the oxygen resaturation response was also greater in the non-paretic vs. the paretic VL (29±23% vs. 18±15%, respectively, p<0.001). VO2 Peak was associated with the magnitude of the VL StO2 change during (r2=0.54, p<0.0001) and after (r2=0.56, p<0.001) the GXT. Conclusions: During a GXT there is a blunted oxygen desaturation response in the paretic vs. the non-paretic VL of chronic stroke survivors. In the paretic VL there was a positive correlation between the oxygen desaturation response during the GXT and VO2 Peak.

Who is wearing a mask? Gender-, age-, and location-related differences during the COVID-19 pandemic.

Masks are an effective tool in combatting the spread of COVID-19, but some people still resist wearing them and mask-wearing behavior has not been experimentally studied in the United States. To understand the demographics of mask wearers and resistors, and the impact of mandates on mask-wearing behavior, we observed shoppers (n = 9935) entering retail stores during periods of June, July, and August 2020. Approximately 41% of the June sample wore a mask. At that time, the odds of an individual wearing a mask increased significantly with age and was also 1.5x greater for females than males. Additionally, the odds of observing a mask on an urban or suburban shopper were ~4x that for rural areas. Mask mandates enacted in late July and August increased mask-wearing compliance to over 90% in all groups, but a small percentage of resistors remained. Thus, gender, age, and location factor into whether shoppers in the United States wear a mask or face covering voluntarily. Additionally, mask mandates are necessary to increase mask wearing among the public to a level required to mitigate the spread of COVID-19.

Moderate, Short-Term, Local Hyperglycemia Attenuates Forearm Endothelium-Dependent Vasodilation After Transient Ischemia-Reperfusion in Human Volunteers.

OBJECTIVE: Acute hyperglycemia causes endothelial dysfunction in diabetic patients, abolishes ischemic pre- and postconditioning, and is an independent predictor of adverse outcome after myocardial infarction in nondiabetic patients. Its effects on endothelial-dependent vasodilation are controversial in healthy subjects. The authors studied the effect of moderate short-term local hyperglycemia on forearm endothelium-dependent vasodilation in healthy volunteers. DESIGN: Randomized, crossover, blinded, 2-visit, pilot design. SETTING: Veterans Affairs Medical Center. PARTICIPANTS: Five male and 3 female healthy adult volunteers (23±4 years; height 171±13 cm; weight 66±9 kg; [mean±standard error of the mean]). INTERVENTIONS: At each visit, volunteers received an infusion through a brachial artery catheter of either 0.9% saline or dextrose in the experimental, non-dominant arm, to establish mild forearm hyperglycemia. Hemodynamics and forearm blood flow (FBF; plethysmography) were measured at baseline, during brachial artery infusions of acetylcholine in consecutive increments (5, 10, and 15 µg/min), before ischemia (20 min, blood pressure cuff at 200 mmHg), and after 15 minutes of reperfusion. Blood glucose and insulin concentrations were determined from venous samples. The effect of duration of intra-arterial dextrose on FBF was examined. MEASUREMENTS AND MAIN RESULTS: Dextrose increased steady-state blood glucose concentration in the experimental but not the control arm (dominant arm). Dextrose increased FBF compared with saline (4.5±0.5 v 2.6±0.4 mL/min/100 g of tissue, respectively). Acetylcholine caused similar increases in FBF in the absence and presence of dextrose (+239±90% v+203±75%, respectively, during 15 µg/min). The duration of dextrose did not affect this acetylcholine-induced vasodilation. Acetylcholine-stimulated increases in FBF were attenuated in dextrose-treated versus saline after reperfusion (+180±18% v+257±53%, respectively, during 10 µg/min). Interventions in the experimental arm did not affect FBF in the control arm. CONCLUSION: These results indicated that moderate, short-term, local hyperglycemia induced by intra-arterial administration of dextrose attenuated forearm endothelial-dependent vasodilation after ischemia-reperfusion injury in healthy volunteers.

The effectiveness of oxygen delivery and reliability of carbon dioxide waveforms: a crossover comparison of 4 nasal cannulae.

BACKGROUND: Effective O2 delivery and accurate end-tidal CO2 (ETCO2) sampling are essential features of nasal cannulae (NCs) in patients with compromised respiratory status. We studied 4 NC designs: bifurcated nasal prongs (NPs) with O2 delivery and CO2 sensing in both NPs (Hudson), separate O2/CO2 NPs (Salter), and CO2 sensing in NPs with cloud O2 delivery outside the NPs via multi vents (Oridion) and dual vents (Medline). We hypothesized that design differences between NCs would influence O2 delivery and ETCO2 detection. METHODS: Forty-five healthy volunteers, 18 to 35 years, participated in an unrestricted, randomized block design, each subject serving as their own control in a 4-period crossover study design of 4 NCs during one session. Monitoring included electrocardiogram, posterior pharynx O2 sampling from a Hauge Airway (Sharn Anesthesia Products, Tampa, FL), and NC ETCO2. In 11 volunteers, radial artery blood was sampled from a catheter for partial pressures of O2 and carbon dioxide (PaO2 and PaCO2) determination. Per randomization, each NC was positioned, and data were collected over 2 minutes (ETCO2, pharyngeal O2, PaO2, and PaCO2) during room air and during O2 fresh gas flows (FGFs) of 2, 4, and 6 Lpm. Statistical analyses were performed with SAS Analytics Pro, Version 9.3, and JMP Statistical Software, Version 11 (SAS Institute Inc., Cary, NC), significance at P < 0.05. RESULTS: Blood gas analyses indicated PaCO2 during steady state at each experimental time period remained unchanged from physiologic baseline. PaO2 did not differ between NC devices at baseline or 2 Lpm O2. The PaO2 at 4 Lpm from the separate NPs and bifurcated NCs was significantly higher than the multi-vented NC. Pharyngeal O2 with the NC with separate NPs was significantly higher than multivented and dual-vented cloud delivery NCs at 2, 4, and 6 Lpm FGF. Pharyngeal O2 with the NC with bifurcated NPs was significantly higher than the multi-vented NC at 2 Lpm, and higher than cloud delivery NCs at 4 and 6 Lpm FGF. ETCO2 was significantly lower with the NC with bifurcated NPs compared to the other 3 NCs, consistent with errant CO2 tracings at higher FGF. CONCLUSIONS: NCs provide supplemental inspired O2 concentrations for patients with impaired pulmonary function. Accurate measures of ETCO2 are helpful in assessing respiratory rate and determining whether CO2 retention is occurring from hypoventilation. These findings suggest the NC with separate NPs was the most effective in delivering O2 and the most consistent at providing reliable CO2 waveforms at higher FGFs.

The efficacy of dexmedetomidine versus morphine for postoperative analgesia after major inpatient surgery.

UNLABELLED: Thirty-four patients scheduled for elective inpatient surgery were randomized equally to receive either dexmedetomidine (initial loading dose of 1- microg/kg over 10 min followed by 0.4 microg. kg(-1). h(-1) for 4 h) or morphine sulfate (0.08 mg/kg) 30 min before the end of surgery. We determined heart rate (HR), mean arterial blood pressure (MAP), respiratory rate (RR), sedation and analgesia (visual analog scale), and use of additional morphine in the postanesthesia care unit (PACU) and up to 24 h after surgery. Groups were similar for patient demographics, ASA physical status, surgical procedure, baseline hemodynamics, and intraoperative use of drugs and fluids. Dexmedetomidine-treated patients had slower HR in the PACU (by an average of 16 bpm), whereas MAP, RR, and level of sedation were similar between groups. During Phase I recovery, dexmedetomidine-treated patients required significantly less morphine to achieve equivalent analgesia (PACU dexmedetomidine group, 4.5 +/- 6.8 mg; morphine group, 9.2 +/- 5.2 mg). Sixty minutes into recovery only 6 of 17 dexmedetomidine patients required morphine in contrast to 15 of 17 in the morphine group. The administration of dexmedetomidine before the completion of major inpatient surgical procedures significantly reduced, by 66%, the early postoperative need for morphine and was associated with a slower HR in the PACU. IMPLICATIONS: The use of dexmedetomidine for postoperative analgesia resulted in significantly less additional pain medication (morphine) and slower heart rates than a control group receiving only morphine. These outcomes may prove advantageous for patients who might be placed at higher risk by tachycardia or large doses of morphine.

Vascular responsiveness to brachial artery infusions of phenylephrine during isoflurane and desflurane anesthesia.

UNLABELLED: Compared with equi-minimum alveolar anesthetic concentration (MAC) isoflurane, desflurane is associated with greater levels of sympathetic nerve activity in humans but similar reductions in blood pressure. To explore these divergent effects, we evaluated vascular alpha(1)-adrenoceptor responses in the human forearm during isoflurane and desflurane anesthesia to determine if alpha(1)-adrenoceptor responses were more substantially attenuated during desflurane administration. Bilateral forearm venous occlusion plethysmography was used to examine arterial blood flow and to determine changes in forearm vascular resistance during brachial artery infusions of saline and phenylephrine (0.2, 0.4, 0.8, and 1.6 microg/min) in 22 conscious subjects and during anesthesia with 0.65 and 1.3 MAC isoflurane or desflurane. Infusion of phenylephrine into the brachial artery increased the forearm vascular resistance in a dose-dependent manner. The arterial response to phenylephrine was significantly attenuated by 0.65 and 1.3 MAC desflurane and similarly attenuated during 1.3 MAC isoflurane (P < 0.05). Impaired arterial alpha(1)-adrenoceptor responsiveness occurred during desflurane. However, this effect was statistically similar (P > 0.05) to the impaired responses during isoflurane. Blood pressure decreases during volatile anesthesia may be, in part, caused by decreased alpha(1)-adrenoceptor responsiveness. IMPLICATIONS: alpha-receptors on blood vessels regulate constriction and dilation and therefore modulate blood pressure. This research indicates that vasoconstriction via the alpha(1)-receptor vascular response is impaired during isoflurane and desflurane anesthesia.