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Intercostal and forearm muscle deoxygenation during respiratory fatigue in patients with heart failure: potential role of a respiratory muscle metaboreflex.

Moreno AM, Castro RR, Silva BM, Villacorta H, Sant'Anna Junior M, Nóbrega AC - Braz. J. Med. Biol. Res. (2014)

Bottom Line: Intercostal and forearm muscle blood volume and oxygenation were continuously monitored by near-infrared spectroscopy with transducers placed on the seventh left intercostal space and the left forearm.Data were compared by two-way ANOVA and Bonferroni correction.These results suggest that respiratory fatigue in patients with heart failure causes an oxygen demand/delivery mismatch in respiratory muscles, probably leading to a reflex reduction in peripheral limb muscle perfusion, featuring a respiratory metaboreflex.

View Article: PubMed Central - PubMed

Affiliation: Procordis Hospital Cardiológico, Niterói, RJ, Brasil.

ABSTRACT
The purpose of this study was to determine the effect of respiratory muscle fatigue on intercostal and forearm muscle perfusion and oxygenation in patients with heart failure. Five clinically stable heart failure patients with respiratory muscle weakness (age, 66 ± 12 years; left ventricle ejection fraction, 34 ± 3%) and nine matched healthy controls underwent a respiratory muscle fatigue protocol, breathing against a fixed resistance at 60% of their maximal inspiratory pressure for as long as they could sustain the predetermined inspiratory pressure. Intercostal and forearm muscle blood volume and oxygenation were continuously monitored by near-infrared spectroscopy with transducers placed on the seventh left intercostal space and the left forearm. Data were compared by two-way ANOVA and Bonferroni correction. Respiratory fatigue occurred at 5.1 ± 1.3 min in heart failure patients and at 9.3 ± 1.4 min in controls (P<0.05), but perceived effort, changes in heart rate, and in systolic blood pressure were similar between groups (P>0.05). Respiratory fatigue in heart failure reduced intercostal and forearm muscle blood volume (P<0.05) along with decreased tissue oxygenation both in intercostal (heart failure, -2.6 ± 1.6%; controls, +1.6 ± 0.5%; P<0.05) and in forearm muscles (heart failure, -4.5 ± 0.5%; controls, +0.5 ± 0.8%; P<0.05). These results suggest that respiratory fatigue in patients with heart failure causes an oxygen demand/delivery mismatch in respiratory muscles, probably leading to a reflex reduction in peripheral limb muscle perfusion, featuring a respiratory metaboreflex.

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Changes in heart rate (A), perceived effort(B), systolic blood pressure (SBP) (C), anddiastolic blood pressure (DBP) (D) during the respiratory fatigueprotocol in patients with heart failure and in healthy controls. Data are reportedas means±SD. Fatigue: average of the last 3 s before fatigue occurred; REC:recovery. *P<0.05 fatigue vs baseline (two-way ANOVA followedby the Bonferroni post hoc test).
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f01: Changes in heart rate (A), perceived effort(B), systolic blood pressure (SBP) (C), anddiastolic blood pressure (DBP) (D) during the respiratory fatigueprotocol in patients with heart failure and in healthy controls. Data are reportedas means±SD. Fatigue: average of the last 3 s before fatigue occurred; REC:recovery. *P<0.05 fatigue vs baseline (two-way ANOVA followedby the Bonferroni post hoc test).

Mentions: Patients with HF developed respiratory fatigue earlier (5.1±1.3 min) in the respiratoryprotocol than controls (9.3±1.4 min; P<0.05). Figure1 shows that during respiratory fatigue, changes in heart rate (HF, 22±5 bpm;controls, 24±4 bpm), perceived effort (HF, 8±1 units; controls, 8±1 units), and systolicblood pressure (HF, 22±2 mmHg; controls, 23±1 mmHg) were similar between groups(P>0.05). SpO2 was lower (P<0.05) in patients with HF [pre, 96%(94-97%); fatigue, 95% (95-96%)] than in healthy controls [pre, 97% (96-98%); fatigue,97% (96-98%)], but did not change during the protocol (P>0.05). Figure 2 shows that at respiratory fatigue, blood volume (leftpanels) and tissue oxygenation (right panels) decreased in both intercostal (upperpanels) and forearm muscles (lower panels) only in patients with HF (P<0.05).


Intercostal and forearm muscle deoxygenation during respiratory fatigue in patients with heart failure: potential role of a respiratory muscle metaboreflex.

Moreno AM, Castro RR, Silva BM, Villacorta H, Sant'Anna Junior M, Nóbrega AC - Braz. J. Med. Biol. Res. (2014)

Changes in heart rate (A), perceived effort(B), systolic blood pressure (SBP) (C), anddiastolic blood pressure (DBP) (D) during the respiratory fatigueprotocol in patients with heart failure and in healthy controls. Data are reportedas means±SD. Fatigue: average of the last 3 s before fatigue occurred; REC:recovery. *P<0.05 fatigue vs baseline (two-way ANOVA followedby the Bonferroni post hoc test).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4230287&req=5

f01: Changes in heart rate (A), perceived effort(B), systolic blood pressure (SBP) (C), anddiastolic blood pressure (DBP) (D) during the respiratory fatigueprotocol in patients with heart failure and in healthy controls. Data are reportedas means±SD. Fatigue: average of the last 3 s before fatigue occurred; REC:recovery. *P<0.05 fatigue vs baseline (two-way ANOVA followedby the Bonferroni post hoc test).
Mentions: Patients with HF developed respiratory fatigue earlier (5.1±1.3 min) in the respiratoryprotocol than controls (9.3±1.4 min; P<0.05). Figure1 shows that during respiratory fatigue, changes in heart rate (HF, 22±5 bpm;controls, 24±4 bpm), perceived effort (HF, 8±1 units; controls, 8±1 units), and systolicblood pressure (HF, 22±2 mmHg; controls, 23±1 mmHg) were similar between groups(P>0.05). SpO2 was lower (P<0.05) in patients with HF [pre, 96%(94-97%); fatigue, 95% (95-96%)] than in healthy controls [pre, 97% (96-98%); fatigue,97% (96-98%)], but did not change during the protocol (P>0.05). Figure 2 shows that at respiratory fatigue, blood volume (leftpanels) and tissue oxygenation (right panels) decreased in both intercostal (upperpanels) and forearm muscles (lower panels) only in patients with HF (P<0.05).

Bottom Line: Intercostal and forearm muscle blood volume and oxygenation were continuously monitored by near-infrared spectroscopy with transducers placed on the seventh left intercostal space and the left forearm.Data were compared by two-way ANOVA and Bonferroni correction.These results suggest that respiratory fatigue in patients with heart failure causes an oxygen demand/delivery mismatch in respiratory muscles, probably leading to a reflex reduction in peripheral limb muscle perfusion, featuring a respiratory metaboreflex.

View Article: PubMed Central - PubMed

Affiliation: Procordis Hospital Cardiológico, Niterói, RJ, Brasil.

ABSTRACT
The purpose of this study was to determine the effect of respiratory muscle fatigue on intercostal and forearm muscle perfusion and oxygenation in patients with heart failure. Five clinically stable heart failure patients with respiratory muscle weakness (age, 66 ± 12 years; left ventricle ejection fraction, 34 ± 3%) and nine matched healthy controls underwent a respiratory muscle fatigue protocol, breathing against a fixed resistance at 60% of their maximal inspiratory pressure for as long as they could sustain the predetermined inspiratory pressure. Intercostal and forearm muscle blood volume and oxygenation were continuously monitored by near-infrared spectroscopy with transducers placed on the seventh left intercostal space and the left forearm. Data were compared by two-way ANOVA and Bonferroni correction. Respiratory fatigue occurred at 5.1 ± 1.3 min in heart failure patients and at 9.3 ± 1.4 min in controls (P<0.05), but perceived effort, changes in heart rate, and in systolic blood pressure were similar between groups (P>0.05). Respiratory fatigue in heart failure reduced intercostal and forearm muscle blood volume (P<0.05) along with decreased tissue oxygenation both in intercostal (heart failure, -2.6 ± 1.6%; controls, +1.6 ± 0.5%; P<0.05) and in forearm muscles (heart failure, -4.5 ± 0.5%; controls, +0.5 ± 0.8%; P<0.05). These results suggest that respiratory fatigue in patients with heart failure causes an oxygen demand/delivery mismatch in respiratory muscles, probably leading to a reflex reduction in peripheral limb muscle perfusion, featuring a respiratory metaboreflex.

Show MeSH
Related in: MedlinePlus