Peripheral chemoreceptors determine the respiratory sensitivity of central chemoreceptors to CO2 : role of carotid body CO2.

We asked if the type of carotid body (CB) chemoreceptor stimulus influenced the ventilatory gain of the central chemoreceptors to CO2 . The effect of CB normoxic hypocapnia, normocapnia and hypercapnia (carotid body PCO2 ≈ 22, 41 and 68 mmHg, respectively) on the ventilatory CO2 sensitivity of central chemoreceptors was studied in seven awake dogs with vascularly-isolated and extracorporeally-perfused CBs. Chemosensitivity with one CB was similar to that in intact dogs. In four CB-denervated dogs, absence of hyper-/hypoventilatory responses to CB perfusion with PCO2 of 19-75 mmHg confirmed separation of the perfused CB circulation from the brain. The group mean central CO2 response slopes were increased 303% for minute ventilation (V̇I)(P ≤ 0.01) and 251% for mean inspiratory flow rate (VT /TI ) (P ≤ 0.05) when the CB was hypercapnic vs. hypocapnic; central CO2 response slopes for tidal volume (VT ), breathing frequency (fb ) and rate of rise of the diaphragm EMG increased in 6 of 7 animals but the group mean changes did not reach statistical significance. Group mean central CO2 response slopes were also increased 237% for V̇I(P ≤ 0.01) and 249% for VT /TI (P ≤ 0.05) when the CB was normocapnic vs. hypocapnic, but no significant differences in any of the central ventilatory response indices were found between CB normocapnia and hypercapnia. These hyperadditive effects of CB hyper-/hypocapnia agree with previous findings using CB hyper-/hypoxia.We propose that hyperaddition is the dominant form of chemoreceptor interaction in quiet wakefulness when the chemosensory control system is intact, response gains physiological, and carotid body chemoreceptors are driven by a wide range of O2 and/or CO2 .

Efficacy of peripheral interventional radiologists performing endovascular stroke therapy guided by CT perfusion triage of patients.

PURPOSE: To assess safety and efficacy of intraarterial mechanical thrombectomy for treatment of ischemic stroke in a community hospital by peripheral interventional radiologists employing computed tomography (CT) perfusion imaging for patient selection. MATERIALS AND METHODS: Forty patients, 11 men (27.5%) and 29 women (72.5%), were treated between February 2008 and October 2011. Eligible patients had a National Institutes of Health Stroke Scale (NIHSS) score greater than 8 and diagnosis of large-vessel ischemic stroke by head CT angiogram, and met previously reported CT perfusion imaging triage criteria. RESULTS: The baseline NIHSS score was 18.0 ± 7.9 (range, 8-35). Sixteen patients (40%) had a baseline NIHSS score greater than 20. Symptom onset was unknown in five patients. Symptom onset to device time in the remaining 35 patients was 254.8 minutes ± 150.9 (range, 75-775 min). A total of 65% of patients showed thrombolysis in cerebral infarction (TICI) 2a, 2b, or 3 flow following the procedure. Symptomatic intracranial hemorrhage was seen in four patients (10.0%). At 90 days, 32 patients (80%) were alive and eight (20%) had died. The modified Rankin scale (mRS) score at 90 days was no more than 2 in 20 patients (50.0%). The mean mRS score at 90 days was 2.9 ± 2.0 (range, 0-6). NIHSS score at 90 days was 5.1 ± 6.1 (range, 0-24). In patients with successful recanalization (ie, TICI 2 or 3 flow), a good clinical outcome (ie, mRS score ≤ 2) was achieved in 65.3% of patients (mean, 2.4 ± 1.9; range, 0-6), and 90-day mortality rate was 15.4%, compared with 28.6% in patients with TICI 0/1 flow. CONCLUSIONS: Peripheral interventional radiologists who use CT perfusion imaging for patient triage can have good neurologic outcomes and provide sustainable, safe, and complete around-the-clock coverage for endovascular stroke treatment.

An Unusual Case of Postpartum Empyema.

We present the case of a 32-year-old woman with a left empyema and T12 osteomyelitis resulting from group B Streptococcus infection occurring 3 weeks after instrumental delivery of a healthy boy. Empyema is a rare complication of instrumental delivery, and this patient highlights the maternal risk resulting from group B Streptococcus bacteremia.

Peripheral chemoreceptors determine the respiratory sensitivity of central chemoreceptors to CO(2).

We assessed the contribution of carotid body chemoreceptors to the ventilatory response to specific CNS hypercapnia in eight unanaesthetized, awake dogs. We denervated one carotid body (CB) and used extracorporeal blood perfusion of the reversibly isolated remaining CB to maintain normal CB blood gases (normoxic, normocapnic perfusate), to inhibit (hyperoxic, hypocapnic perfusate) or to stimulate (hypoxic, normocapnic perfusate) the CB chemoreflex, while the systemic circulation, and therefore the CNS and central chemoreceptors, were exposed consecutively to four progressive levels of systemic arterial hypercapnia via increased fractional inspired CO(2) for 7 min at each level. Neither unilateral CB denervation nor CB perfusion, per se, affected breathing. Relative to CB control conditions (normoxic, normocapnic perfusion), we found that CB chemoreflex inhibition decreased the slope of the ventilatory response to CNS hypercapnia in all dogs to an average of 19% of control values (range 0-38%; n = 6), whereas CB chemoreflex stimulation increased the slope of the ventilatory response to CNS hypercapnia in all dogs to an average of 223% of control values (range 204-235%; n = 4). We conclude that the gain of the CNS CO(2)/H(+) chemoreceptors in dogs is critically dependent on CB afferent activity and that CNS-CB interaction results in hyperadditive ventilatory responses to central hypercapnia.

Contribution of the carotid body chemoreceptors to eupneic ventilation in the intact, unanesthetized dog.

We used extracorporeal perfusion of the reversibly isolated carotid sinus region to determine the effects of specific carotid body (CB) chemoreceptor inhibition on eupneic ventilation (Vi) in the resting, awake, intact dog. Four female spayed dogs were studied during wakefulness when CB was perfused with 1) normoxic, normocapnic blood; and 2) hyperoxic (>500 mmHg), hypocapnic ( approximately 20 mmHg) blood to maximally inhibit the CB tonic activity. We found that CB perfusion per se (normoxic-normocapnic) had no effect on Vi. CB inhibition caused marked reductions in Vi (-60%, range 49-80%) and inspiratory flow rate (-58%, range 44-87%) 24-41 s following the onset of CB perfusion. Thereafter, a partial compensatory response was observed, and a steady state in Vi was reached after 50-76 s following the onset of CB perfusion. This steady-state tidal volume-mediated hypoventilation ( approximately 31%) coincided with a significant reduction in mean diaphragm electromyogram (-24%) and increase in mean arterial pressure (+12 mmHg), which persisted for 7-25 min until CB perfusion was stopped, despite a substantial increase in CO(2) retention (+9 Torr, arterial Pco(2)) and systemic respiratory acidosis. We interpret these data to mean that CB chemoreceptors contribute more than one-half to the total eupneic drive to breathe in the normoxic, intact, awake animal. We speculate that this CB contribution consists of both the normal tonic sensory input from the CB chemoreceptors to medullary respiratory controllers, as well as a strong modulatory effect on central chemoreceptor responsiveness to CO(2).

Achieving Disease-Specific Care Joint Commission Certification: The Impact of Clinical Nurse Specialist Practice.

PURPOSE: The aims of this study are to describe a program to achieve disease-specific care (DSC) certification from The Joint Commission and highlight the value of the advanced practice nurse in the certification outcome. DESCRIPTION OF PROGRAM: The expertise in clinical practice, performance improvement, and leadership skills demonstrated by the clinical nurse specialist (CNS) can be instrumental in building a strong foundation for a DSC certification program. As an organization prepares for a DSC on-site review, the CNS can guide the program stakeholders in identifying gaps in care, developing action plans to meet certification standards, and preparing team members for the DSC on-site review. OUTCOME: At this Midwestern, 504-bed facility, The Joint Commission DSC certifications were achieved in 5 separate categories: diabetes, stroke, sepsis, total hip replacement, and total knee replacement. CONCLUSION: By influencing a certain patient population throughout the organization, population-focused CNSs are in a unique role to lead an interprofessional team or serve as an expert consultant in pursuing DSC certification from The Joint Commission.

Chronic intermittent hypoxia increases the CO2 reserve in sleeping dogs.

We hypothesized that chronic intermittent hypoxia (CIH) would induce a predisposition to apnea in response to induced hypocapnia. To test this, we used pressure support ventilation to quantify the difference in end-tidal partial pressure of CO(2) (Pet(CO(2))) between eupnea and the apneic threshold ("CO(2) reserve") as an index of the propensity for apnea and unstable breathing during sleep, both before and following up to 3-wk exposure to chronic intermittent hypoxia in dogs. CIH consisted of 25 s of Pet(O(2)) = 35-40 Torr followed by 35 s of normoxia, and this pattern was repeated 60 times/h, 7-8 h/day for 3 wk. The CO(2) reserve was determined during non-rapid eye movement sleep in normoxia 14-16 h after the most recent hypoxic exposure. Contrary to our hypothesis, the slope of the ventilatory response to CO(2) below eupnea progressively decreased during CIH (control, 1.36 +/- 0.18; week 2, 0.94 +/- 0.12; week 3, 0.73 +/- 0.05 l.min(-1).Torr(-1), P < 0.05). This resulted in a significant increase in the CO(2) reserve relative to control (P < 0.05) following both 2 and 3 wk of CIH (control, 2.6 +/- 0.6; week 2, 3.7 +/- 0.8; week 3, 4.5 +/- 0.9 Torr). CIH also 1) caused no change in eupneic, air breathing Pa(CO(2)); 2) increased the slope of the ventilatory response to hypercapnia after 2 wk but not after 3 wk compared with control; and 3) had no effect on the ventilatory response to hypoxia. We conclude that 3-wk CIH reduced the sensitivity of the ventilatory response to transient hypocapnia and thereby increased the CO(2) reserve, i.e., the propensity for apnea was reduced.

Increased propensity for apnea in response to acute elevations in left atrial pressure during sleep in the dog.

Periodic breathing is commonly observed in chronic heart failure (CHF) when pulmonary capillary wedge pressure is abnormally high and there is usually concomitant tachypneic hyperventilation. We hypothesized that acute pulmonary hypertension at pressures encountered in CHF and involving all of the lungs and pulmonary vessels would predispose to apnea/unstable breathing during sleep. We tested this in a chronically instrumented, unanesthetized dog model during non-rapid eye movement (NREM) sleep. Pulmonary hypertension was created by partial occlusion of the left atrium by means of an implanted balloon catheter in the atrial lumen. Raising mean left atrial pressure by 5.7 +/- 1.1 Torr resulted immediately in tachypneic hyperventilation [breathing frequency increased significantly from 13.8 to 19.9 breaths/min; end-tidal P(CO2) (P(ET(CO2))) fell significantly from 38.5 to 35.9 Torr]. This tachypneic hyperventilation was present during wakefulness, NREM sleep, and rapid eye movement sleep. In NREM sleep, this increase in left atrial pressure increased the gain of the ventilatory response to CO2 below eupnea (1.3 to 2.2 l.min(-1).Torr(-1)) and thereby narrowed the CO2 reserve [P(ET(CO2)) (apneic threshold) - P(ET(CO2)) (eupnea)], despite the decreased plant gain resulting from the hyperventilation. We conclude that acute pulmonary hypertension during sleep results in a narrowed CO2 reserve and thus predisposes toward apnea/unstable breathing and may, therefore, contribute to the breathing instability observed in CHF.

Increased propensity for apnea via dopamine-induced carotid body inhibition in sleeping dogs.

We determined the effects of specific carotid body chemoreceptor inhibition on the propensity for apnea during sleep. We reduced the responsiveness of the carotid body chemoreceptors using intravenous dopamine infusions during non-rapid eye movement sleep in six dogs. Then we quantified the difference in end-tidal Pco(2) (Pet(CO(2))) between eupnea and the apneic threshold, the "CO(2) reserve," by gradually reducing Pet(CO(2)) transiently with pressure support ventilation at progressively increased tidal volume until apnea occurred. Dopamine infusions decreased steady-state eupneic ventilation by 15 +/- 6%, causing a mean CO(2) retention of 3.9 +/- 1.9 mmHg and a brief period of ventilatory instability. The apneic threshold Pet(CO(2)) rose 5.1 +/- 1.9 Torr; thus the CO(2) reserve was narrowed from -3.9 +/- 0.62 Torr in control to -2.7 +/- 0.78 Torr with dopamine. This decrease in the CO(2) reserve with dopamine resulted solely from the 20.5 +/- 11.3% increase in plant gain; the slope of the ventilatory response to CO(2) below eupnea was unchanged from normal. We conclude that specific carotid chemoreceptor inhibition with dopamine increases the propensity for apnea during sleep by narrowing the CO(2) reserve below eupnea. This narrowing is due solely to an increase in plant gain as the slope of the ventilatory response to CO(2) below eupnea was unchanged from normal control. These findings have implications for the role of chemoreceptor inhibition/stimulation in the genesis of apnea and breathing periodicity during sleep.

Cardiovascular effects of the respiratory muscle metaboreflexes in dogs: rest and exercise.

In awake dogs, lactic acid was injected into the phrenic and deep circumflex iliac arteries to elicit the diaphragm and abdominal muscle metaboreflexes, respectively. At rest, injections into the phrenic or deep circumflex iliac arteries significantly increased mean arterial blood pressure 21 +/- 7% and reduced cardiac output 6 +/- 2% and blood flow to the hindlimbs 20 +/- 9%. Simultaneously, total systemic, hindlimb, and abdominal expiratory muscle vascular conductances were reduced. These cardiovascular responses were not accompanied by significant changes in the amplitude or timing of the diaphragm electromyogram. During treadmill exercise that increased cardiac output, hindlimb blood flow, and vascular conductance 159 +/- 106, 276 +/- 309, and 299 +/- 90% above resting values, lactic acid injected into the phrenic or deep circumflex iliac arteries also elicited pressor responses and reduced hindlimb blood flow and vascular conductance. Adrenergic receptor blockade at rest eliminated the cardiovascular effects of the respiratory muscle metaboreflex. We conclude that the cardiovascular effects of respiratory muscle metaboreflex activation are similar to those previously reported for limb muscles. When activated via metabolite production, the respiratory muscle metaboreflex may contribute to the increased sympathetic tone and redistribution of blood flow during exercise.

Welfare to work: the effect of a health-care program in child-care centers.

OBJECTIVE: Welfare reform has increased pressure on welfare recipients to enter the labor force. When they become employed, former recipients often do not have paid leave that can be used to care for their young children when they are sick. We wished to determine whether an on-site health-care program in child-care centers serving low-income families affected the amount of time parents took off of work to care for mildly ill children. METHODS: We surveyed parents in 6 child-care centers with an on-site health-care program and in 2 comparison centers without such a program. To analyze survey results, a regression model including demographic and other variables was used to determine which, if any, variables were associated with time taken by parents from work to care for sick children. RESULTS: Analyzing the variables of employer leave policy, poverty level, age of child, and enrollment in the health-care program, only the variable of health-care program enrollment was associated with taking less time from work to care for sick children. CONCLUSION: Health-care programs in child-care settings can help parents meet the health needs of their children while reducing absenteeism from work, thereby contributing to job stability.

Chemotherapy for bone sarcoma does not affect fertility rates or childbirth.

There have been unprecedented improvements in the survival of patients with bone sarcomas because of advances in chemotherapy during the past two decades. However, along with improved survival, there have been concerns of gonadal toxicity and fertility. These problems with chemotherapy are well documented for conditions like lymphomas and testicular cancers. There are few reports on fertility outcomes with chemotherapy for bone sarcomas. The purpose of this study was to review the rate of successful conceptions, pregnancy outcomes, incidence of birth defects, and fertility rates in young adults who had chemotherapy for high-grade bone sarcomas. A retrospective chart review of all eligible patients was done. No laboratory assessment of fertility was done. Fifteen of the 36 patients attempted conceptions, and all were successful [corrected] One miscarriage occurred and one medical termination of pregnancy was done because of a spinal metastasis. There were 13 successful full-term pregnancies with no birth defects. The conception rate was 1.6. Despite the common misconception of probable infertility, these patients can have high expectations to conceive, with uneventful childbirth and no birth defects in the newborns. Although counseling should include the possibility of infertility, patients also should be reminded of the high rate of success of having a normal conception and childbirth.