Respiratory sinus arrhythmia (RSA) may improve the efficiency of pulmonary gas exchange by matching the pulmonary blood flow to lung volume during each respiratory cycle. If so, an increased demand for pulmonary gas exchange may enhance RSA magnitude. We therefore tested the hypothesis that CO2 directly affects RSA in conscious humans even when changes in tidal volume (V(T)) and breathing frequency (F(B)), which indirectly affect RSA, are prevented. In seven healthy subjects, we adjusted end-tidal PCO2 (PET(CO2)) to 30, 40, or 50 mmHg in random order at constant V(T) and F(B). The mean amplitude of the high-frequency component of R-R interval variation was used as a quantitative assessment of RSA magnitude. RSA magnitude increased progressively with PET(CO2) (P < 0.001). Mean R-R interval did not differ at PET(CO2) of 40 and 50 mmHg but was less at 30 mmHg (P < 0.05). Because V(T) and F(B) were constant, these results support our hypothesis that increased CO2 directly increases RSA magnitude, probably via a direct effect on medullary mechanisms generating RSA.
Isocapnic hyperpnoea at the end of surgery results in shorter and less variable time to removal of the airway after anaesthesia with isoflurane and nitrous oxide.
A 53-year-old man with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) underwent a gastrectomy. We administered bicarbonated Ringer's solution, which has a physiological concentration of bicarbonate. The level of serum lactate did not increase significantly, and metabolic acidosis did not occur throughout surgery or for 3 h after surgery. Aggressive warming was needed to maintain normothermia, presumably because the mitochondrial respiratory chain, which is responsible for thermogenesis, is impaired in MELAS patients. It is important to maintain normothermia in MELAS patients in order to avoid further mitochondrial metabolic depression.
The aim of this study was to test our hypothesis that both phasic cardiac vagal activity and tonic pulmonary vagal activity, estimated as respiratory sinus arrhythmia (RSA) and anatomical dead space volume, respectively, contribute to improve the efficiency of pulmonary gas exchange in humans. We examined the effect of blocking vagal nerve activity with atropine on pulmonary gas exchange. Ten healthy volunteers inhaled hypoxic gas with constant tidal volume and respiratory frequency through a respiratory circuit with a respiratory analyser. Arterial partial pressure of O 2 (P aO 2 ) and arterial oxygen saturation (S pO 2 ) were measured, and alveolar-toarterial P O 2 difference (D A−aO 2 ) was calculated. Anatomical dead space (V D,an ), alveolar dead space (V D,alv ) and the ratio of physiological dead space to tidal volume (V D,phys /V T ) were measured. Electrocardiogram was recorded, and the amplitude of R-R interval variability in the high-frequency component (RRIHF) was utilized as an index of RSA magnitude. These parameters of pulmonary function were measured before and after administration of atropine (0.02 mg kg −1 ). Decreased RRIHF (P < 0.01) was accompanied by decreases in P aO 2 and S pO 2 (P < 0.05 and P < 0.01, respectively) and an increase in D A−aO 2 (P < 0.05). Anatomical dead space, V D,alv and V D,phys /V T increased (P < 0.01, P < 0.05 and P < 0.01, respectively) after atropine administration. The blockade of the vagal nerve with atropine resulted in an increase in V D,an and V D,alv and a deterioration of pulmonary oxygenation, accompanied by attenuation of RSA. Our findings suggest that both phasic cardiac and tonic pulmonary vagal nerve activity contribute to improve the efficiency of pulmonary gas exchange in hypoxic conscious humans. The cardiovascular system mediates the interchange of oxygen and carbon dioxide between the lungs and the tissues (Richter et al. 1991;Coleridge et al. 1997). A high degree of co-ordination between the cardiovascular and respiratory system has been required from the earliest stages of vertebrate evolution (Taylor et al. 1999). The vagal nervous system is involved in the function of both systems and may play a role in co-ordinating their activity. Phasic activity of the cardiac vagal outflow is closely linked to respiration and produces respiratory sinus arrhythmia (RSA), which causes increases in heart rate during inspiration and decreases during expiration. It may improve pulmonary gas exchange by matching pulmonary capillary perfusion to alveolar ventilation during each respiratory cycle (Hayano et al. 1996;Hayano & Yasuma, 2003). Hayano et al. (1996) demonstrated that in vagotomized dogs whose heart rates were controlled with a pacemaker, artificially generated RSA improved the efficiency of gas exchange as a result of decreasing the ratio of physiological dead space to tidal volume (V D,phys /V T ) and the fraction of intrapulmonary shunt. Giardino et al. (2003) also reported that the magnitude of RSA was associated with efficiency of pulmonary gas exch...
An N95 mask can be modified to administer a clinically equivalent FiO2 to a nonrebreathing mask while maintaining its filtration and isolation capabilities.
The transradial approach for coronary catheterization is now a routine technique without serious complications at the puncture site. We report a case of complex regional pain syndrome type II (CRPS type II) in the hand after the transradial coronary intervention, which may alert medical personnel that the technique may cause serious regional pain with disability. A 61-year-old woman underwent coronary intervention via the right radial artery for the treatment of unstable angina. After the operation she complained of severe pain in the right hand, consistently felt along the median nerve distribution. The nerve conduction study suggested carpal tunnel syndrome. We made a diagnosis of CRPS type II, and the patient received stellate ganglion blockade, cervical epidural blockade, and administration of amitriptyline and loxoprofen. The symptoms gradually improved and her activities of daily living markedly improved. The median nerve appeared to be damaged by local compression and potential ischemia. Careful attention should be paid to avoid CRPS type II, associated with excess compression.
When fat embolism is suspected, serial MRI scans of the brain should be performed to diagnose the etiology of cerebral embolism as well as to evaluate the severity of brain damage.
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