News - Part 9

The Effect of Successful Heart Transplant Treatment of Heart Failure on Central Sleep Apnea

The Effect of Successful Heart Transplant Treatment of Heart Failure on Central Sleep ApneaCentral sleep apnea (CSA) associated with Cheyne-Stokes respiration is observed during stages 1 and 2 sleep in approximately 30% of patients with congestive heart failure (CHF), and is characterized by typical waxing and waning hyperventilation interspersed with central apneas or hypopneas. It has been shown that hyperventilation results from acquired changes in ventilatory responses to hyper-capnia and hypoxia within a few weeks in experimentally induced CHF, and probably relates to changes in carotid body nitric oxide or elevated catecholamines. Moreover CSA severity can be attenuated in humans by the introduction of anti-heart failure therapy and improvement in heart function over several weeks. The responsible mechanisms for altered respiratory control are thought to relate to sympathoexcitation, circulatory delay, and possibly pulmonary congestion with vagal afferent stimulation. http://cheap-asthma-inhalers.com/
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The Changing Face of Organ Failure in ARDS: Conclusion

The Changing Face of Organ Failure in ARDS: ConclusionAPACHE II scores between the 1984-to-1990 and 1994-to-1999 patient groups were equivalent, so it is unlikely that group severity of illness was substantially different. The risk factors for the development of ARDS were not statistically different between the groups, but there was a nonstatistically greater percentage of pneumonia and sepsis (without significant changes in the contribution from trauma) in the earlier ARDS group. We recognize that the number of patients in this study may preclude finding a statistical difference in risk factors between the two groups that might be present, but this reinforces the necessity of reporting organ failure specifically in large future trials. itat on

Unidentified cointerventions may have altered organ failure distribution and therefore have affected mortality. Therapy for critically ill patients has evolved. Examples of cointerventions that may have impacted ARDS are numerous, and include permissive hypercapnea, lowered airway pressure, and reduced tidal volume during mechanical ventilation, All of these could have reduced intrathoracic pressure and led to higher cardiac output. CNS blood flow might have increased and thereby preserved neurologic function. We recognize that animal and human evidence indicate that ventilatory strategies can be important in the genesis of cytokines that cause lung damage. However, we do not have adequate ventilatory data available to assess whether more recent ventilatory strategies are responsible for the changes we observed in organ failure distributions.

Furthermore, our available data do not allow us to draw inferences regarding potential mechanisms of injury or repair. Until definitive data become available, any conclusions remain speculative.
We recognize that changes in care over time at our single center may not have reflected changes in care over time nationwide. However, many research centers have noted increased survival among ARDS patients, and the evidence suggests that mortality may have decreased since the 1970s. In addition, patients identified in the 1980s were identified using different criteria than those applied to patients in the 1990s. We accounted for this difference by comparing patients with similar oxygenation inefficiency criteria (ie, P/F).
Changes in organ failure distribution are a contributor in our environment to changes in mortality among ARDS patients. This observation may extend to the community at large. These observations of different organ failure distributions associated with different mortality rates among ARDS patients from 1987 to 1990 and from 1994 to 1999 emphasize the need for rigorous experimental design and reporting in future ARDS clinical investigations.

The Changing Face of Organ Failure in ARDS: Discussion

Fewer total nonpulmonary organ failures were noted in 1994-to-1999 patients (Fig 3, with more patients having no and one organ failure, and fewer patients having two and three organ failures in 1994 to 1999 (p < 0.05). Cardiovascular and CNS failure, and sepsis were significantly lower prior to ARDS onset (Fig 4) and after ARDS onset (Fig 5) among 1994-to-1999 patients. Hepatic failure was lower in the 1994-to-1999 patients only after ARDS onset (Fig 5). Patients with higher arterial oxygenation efficiency (P/F, > 105) and those with lower arterial oxygenation efficiency (P/F, < 105) in the 1994-to-1999 group had similar total nonpulmonary organ failure at ARDS onset (Fig 6) and similar distributions of organ failures both prior to ARDS onset (Fig 7) and after ARDS onset (Fig 8). In contrast, the 1987-to-1990 patients had a lower incidence of hepatic failure after ARDS onset, as ARDS evolved.
We found an inverse association between higher initial arterial oxygenation efficiency (ie, P/F) and lower mortality (Fig 2, Table 3). This association of mortality with P/F was notably absent in the report of Zilberberg and Epstein.2 Their reported mortality rate was 58% both for patients with ALI and those with ARDS. However, their overall patient numbers were small, and they did not investigate mortality as a function of arterial oxygenation efficiency within the ARDS patient group. In addition, they studied only medical ICU patients, whereas we studied both medical and surgical patients. http://birthcontroltab.com/

We found an association between higher initial arterial oxygenation efficiency (ie, P/F) and specific organ failure before and after ARDS onset (Figs 3-5, Table 3). The association of a greater incidence of organ failure in ARDS patients with a higher mortality is well-described and was observed in our 1994-to-1999 patients. However, the change in organ failure distribution that we observed has not been reported previously. A review of the literature (Table 4) demonstrated the paucity of reports of specific organ failures at or after the onset of ARDS. Bell et al reported that increased organ failure occurring during ARDS was associated with increased mortality. They found CNS, GI, renal, endocrine, and coagulation failure to be associated adversely with survival. Subsequent publications rarely have reported specific organ failures. Zilberberg and Epstein2 and the ARDS Network reported specific organ failures or the relation of mortality to specific organ failures. The evolution of organ failure following ARDS onset, and as a function of year of onset of ARDS, has not been reported systematically. In particular, longitudinal studies are lacking.
Fig3
Figure 3. Nonpulmonary organ failure for a P/F of < 105 at ARDS onset for 1987-to-1990 and 1994-to-1999 patients. The horizontal axis represents the number of nonpulmonary organ failures. The numbers on the bar graphs are the total number of patients for that group.
Fig4
Figure 4. Organ failure distribution for a P/F of < 105 at ARDS onset for 1987-to-1990 and 1994-to-1999 patients. CV = cardiovascular; Coag = coagulation. Numbers on the bar graphs are the total number of patients for that group.
Fig5
Figure 5. Organ failure distribution for a P/F of < 105 after ARDS onset for 1987-to-1990 and 1994-to-1999 patients. See the legend of Figure 4 for abbreviations not used in the text. Numbers on the bar graphs are the total number of patients for that group.
Fig6
Figure 6. Nonpulmonary organ failure at ARDS onset for 1994-to-1999 Patients vs P/F. The horizontal axis represents the number of nonpulmonary organ failures, and the numbers on the bar graphs are the total number of patients for that group.
Fig7
Figure 7. Organ failure distribution at ARDS onset for 1994-to-1999 patients vs P/F. See the legend of Figure 4 for abbreviations not used in the text. Numbers on the bar graphs are the total number of patients for that group.
Fig8
Figure 8. Organ failure distribution after ARDS onset for 1994 to 1999 patients vs P/F. See the legend of Figure 4 for abbreviations not used in the text. Numbers on the bar graphs are the total number of patients for that group.

Table 4 —Previous ARDS Reports With Organ Failure

Study/Year Patients,No. ICUType APACHE II Score Organ Failure Reported Organ Failure Distribution Reported
Before ARDS Onset After ARDS Onset
Bell/1983 141 Mixed NA Yes Yes Yes
Montgomery/1985 207 Mixed NA No No Cause of death
Millberg/1995 918 Mixed NA No No No
Doyle/1995 57 Mixed NA No Multiple linear regression No
Stewart/1998 120 Mixed 22 Yes No No
Zilberberg and Epstein2/1998 81 Med 19 Yes No Yes
Abel/1998 129 Mixed 14 Yes No No
ARDS Network/2000 1832 Mixed 811 No Yes Yes
ARDS Network/2000 861 Mixed 821 No Yes No

The Changing Face of Organ Failure in ARDS: ARDS onset

The Changing Face of Organ Failure in ARDSAll data for scoring were collected prospectively and daily for all time points, and were stored in the database. APACHE (acute physiology and chronic health evaluation) II score was calculated prospectively, using the data from the first 24 h after the onset of ARDS. We used the lowest recorded Glasgow coma scale prior to intubation and/or after the patient was extubated to determine CNS failure.
We divided patients into the following two groups by year of ARDS onset: 1987 to 1990; and 1994 to 1999. We did not have complete data sets for 1990 to 1994 due to a temporary change in our research support. We therefore did not include the 1990 to 1994 patients. The oxygenation criterion for selecting ARDS patients in 1987 to 1990 used P(A-a)O2 ratio. The subsequent publication of the North American-European Consensus Criteria led to the widespread adoption of a different and less severe set of criteria using a P/F criterion. In order to compare 1994-to-1999 patients with 1987-to-1990 patients, we established a correspondence between P(A-a)O2 ratio and P/F (Fig 1). A P/F of < 105 corresponded to a P(A-a)O2 of < 0.2. In addition, for the 1994 to 1999 patients only, we compared patients identified with a P/F of 106 to 173 to those identified with P/F < 105. in detail

We used death at the time of hospital discharge as the end point. We analyzed data by independent t test and Pearson \2 analysis, and expressed the results as the mean ± SEM.
Results
We identified a total of 516 ARDS patients with a P/F of < 105 at ARDS onset (1987 to 1990, 256 patients; 1994 to 1999, 260 patients). We identified 288 patients (1994 to 1999) with a P/F range of 106 to 173.
A total of 548 ARDS patients (260 + 288) were identified between 1994 and 1999. Mortality was lower in 1994-to-1999 patients when compared to 1987-to-1990 patients (p < 0.011) [Fig 2]. Fewer deaths occurred in the 1994-to-1999 group for P/F values of both < 105 and 106 to 173. Mortality was lower for those with higher arterial oxygenation efficiency (P/F, 106 to 173) than for those with lower arterial oxygenation efficiency (P/F, < 105) [Table 3]. Between-group differences for age, gender, or risk factor for ARDS were not significant (Table 3).

Fig1
Figure 1. The Lines originating at the origin encompass the calculations for an Fio2 of 0.4 to 1.0. For all calculations Pao2 = (barometric pressure —47) Fio2 — Paco2 (Fio2 + [1 — Fio2]/R), where barometric pressure = 647 mm Hg (the Salt Lake City altitude), Paco2 = 45 mm Hg, and respiratory quotient = 0.8. The thick, black horizontal arrow indicates a P(A-a)O2 ratio of 0.20, the value used for ARDS screening from 1987 to 1990. The thick, black vertical arrow indicates aP/F of 173, the value used for ARDS screening from 1994 to 1999. When the P(A-a)O2 ratio is < 0.20 at an Fio2 of approximately 0.8, the P/F is 105 (thin vertical arrow). Therefore, we chose this value as the common oxygenation inefficiency selection criterion for the two time periods.
Fig2
Figure 2. ARDS mortality by year of onset.

Table 3—Patient Characteristics

P/F 1987-1990 P/F < 105 (n = 256) 1994-1999
P/F < 105 (n = 260) P/F 106-173 (n = 288) P/F < 173 (n = 548)
Dead 54 44 ft 27ft 35 f
Age, yr 54 ± 10 50 ± 11 52 ± 10 51 ± 10
Male gender, % 48 55 57 56
APACHE II score 20 ± 7 20 ± 8 19 ± 8 20 ± 8
Pneumonia 42 35 31 33
Sepsis 31 26 26 26
Trauma 9 15 18* 17
Other 18 23 25 24

The Changing Face of Organ Failure in ARDS: ARDS identification

From February 1994 to March 1996, we identified ARDS patients by the presence of all of the following: (1) acute onset of lung injury requiring endotracheal intubation and mechanical ventilation; (2) Pao2/fraction of inspired oxygen (Fio2) ratio (P/F) £ 150 mm Hg; (2) Pw of £ 18 mm Hg or no clinical evidence of left atrial hypertension; (3) diffuse chest radiograph infiltrates in three of four quadrants; and (4) appropriate risk for ARDS (Table 1).
From March 1996 to March 1999, we identified ARDS patients by the presence of all of the following: (1) acute onset of lung injury requiring endotracheal intubation and mechanical ventilation; (2) P/F of £ 173 mm Hg (equivalent to 200 mm Hg at sea level); (3) bilateral chest radiograph infiltrates; (4) Pw of £ 18 mm Hg or no clinical evidence of left atrial hypertension; and (5) appropriate risk for ARDS (Table 1).
We assigned one primary risk factor for ARDS to each patient at ARDS identification (ie, pneumonia, trauma, sepsis, and “other”). Other causes included massive transfusion, aspiration, shock, pancreatitis, drug overdose, and unknown. The electronic, hospital-wide database for these identified patients was extensive and comprehensive, allowing us to probe the database in detail.

We used the onset of ARDS as the temporal reference point for organ failure. We determined organ failure using the moderate dysfunction criteria from the Brussels organ failure scoring system for each patient for each day prior to the onset of ARDS and each day after its onset. We scored each organ failure daily as present or absent. An organ failure on any day prior to or after the onset of ARDS established organ failure as being present for the period prior to or after the onset of ARDS (Table 2). We evaluated sepsis using the severe dysfunction criteria of Montgomery et al for each day prior to the onset of ARDS and each day after its onset. The definition for sepsis was identical for both time periods.

Table 2—Brussels Organ Failure: Moderate Organ Dysfunction

Organ Definition of Failure
Cardiovascular Systolic BP < 90 mm Hg and unresponsive to fluids or receiving vasopressors
CNS, Glasgow coma score < 12
Coagulation, 103 platelets/^L < 80
Kidney, creatinine mg/dL > 2.0
Liver, mg bilirubin/dL) > 2.0

The Changing Face of Organ Failure in ARDS

The Changing Face of Organ Failure in ARDSReported mortality in ARDS patients varies from 30 to 50%. These values are lower than those previously reported. Zilberberg and Epstein2 reported that the lower mortality in ARDS was independent of the initial level of arterial oxygenation. The North American-European Consensus Conference redefined the criteria for ARDS. These new criteria require less severe arterial hypoxemia and may identify less severely injured patients than did previous criteria, This may explain some of the recently observed reductions in mortality from ARDS.
Longitudinal studies of ARDS at the same institution, using constant selection criteria are infrequent. During the 1990s, Milberg et al noted decreased mortality over an 11-year period using a constant definition of ARDS at a single institution. Abel et al also described a marked reduction in mortality for a small group of patients over a 7-year period during the 1990s in the United Kingdom. While these two studies reported decreased mortality, the paucity of longitudinal studies compromises conclusions about why ARDS mortality is changing. add comment

There are other reasons for the uncertainty regarding ARDS mortality. Included among these are changes in risk factor distribution for the development of ARDS, changes in physician reporting of ARDS patients or secular changes in care. In addition, patient host factors may be different due to changes in health care (ie, new drugs). All of the above changes might influence the development of organ failure during ARDS, with an effect on mortality. Noting a gap in the literature, we tested the hypotheses that organ failure during ARDS has changed, and that this change is associated with decreased mortality.
Materials and Methods
We prospectively identified ARDS patients at the LDS Hospital in Salt Lake City, UT (Table 1). From May 1987 to December 1990, we identified ARDS patients by the presence of all of the following conditions: (1) acute onset of lung injury requiring endotracheal intubation and mechanical ventilation; (2) alveolar-arterial oxygen pressure difference (P(A0a)O2) of £ 0.2; (3) pulmonary capillary wedge pressure (Pw) of £ 15 mm Hg or no evidence of left atrial hypertension; (4) total static thoracic compliance of £ 50 mol/cm H2O; (5) the presence of bilateral chest radiograph infiltrates; and (6) appropriate risk for ARDS (Table 1).

Table 1—ARDS Definition Used at LDS Hospital

1987-1990 1994-1996 1996-1999
P/F £ 105 f £ 150 £ 173
Pw, mm Hg £ 15 £ 18 £ 18
Cth, mL/cm H2O £ 50 Not used Not used
Chest radiograph Bilateral infiltrates Bilateral infiltrates Bilateral infiltrates
Presence of risk factors Required Required Required

Clinical Spectrum of Mediastinal Cysts: Summary

Ribet and colleagues followed up two patients with bronchogenic cysts who refused surgery for 15 years and found that one patient remained free of symptoms and the other died of a malignancy of unknown origin. As for thymic and mesothelial cysts, watchful observation data were not available in our experience. An accurate imaging diagnosis may allow these lesions to leave alone. Many patients with mediastinal cysts were initially asymptomatic, later with occasional severe outcomes. Read more »

Clinical Spectrum of Mediastinal Cysts: Surgery and Outcome

Clinical Spectrum of Mediastinal Cysts: Surgery and OutcomeThe two patients with meningoceles appeared without respiratory symptoms. Recurrent chest pain was associated with the thoracic duct cyst similar to the previous report.
As for the diagnostic modality, chest radiograph was once the most cost- and time-efficient method of diagnosing surgical lesions, and was the only diagnostic tool in our early series. Before the introduction of CT scan, pneumomediastinum used to be a diagnostic tool for mediastinal mass. Currently, mediastinal cysts can be accurately diagnosed with imaging modalities such as CT, MRI, and ultrasonography. Read more »

Clinical Spectrum of Mediastinal Cysts: Mediastinum

St-Georges et al reviewed 86 bronchogenic cysts and found major complications such as fistulization with airway, and ulcerations or hemorrhage in mediastinal cysts that were observed with parenchymal cysts. In addition, other potential complications including arrhythmia or superior vena cava syndrome may occur. Another important issue is that malignancy is associated with bronchogenic cysts. Read more »

Clinical Spectrum of Mediastinal Cysts: Patients with bronchogenic cysts

Clinical Spectrum of Mediastinal Cysts: Patients with bronchogenic cystsSymptomatic patients were seen in 39.2% with bronchogenic/ esophageal cysts, 40% with thymic cysts, and 15.8% with pericardial/pleural cysts, respectively. Asymptomatic patients were most common in patients with mesothelial cysts compared to type of cysts (p = 0.06). Read more »

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