Ventilatory Response to Carbon Dioxide Inhalation in Depression

Shershow, John C.; Kanarek, David J.; Kazemi, Homayoun

doi:10.1097/00006842-197607000-00007

Cited by 30 publications

(8 citation statements)

References 12 publications

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“…To normalize the results across individuals, each graph portrays the degree of change in minute volume, at 1-min intervals, relative to the subject's baseline respiration (i.e., the mean minute volume while breathing air). Several individuals with bipolar I, all with bipolar II, and some with major depression had an inhibited response, as seen elsewhere with depression, 48,49 and many of the bipolar I cases displayed a striking deviation from the classic rise-plateau pattern described earlier and apparent in each of the subjects who did not have a major mood disorder.…”

Section: Respiratory Behavior As An Experimental Modelsupporting

confidence: 74%

“…The plateau effect is consistent with the natural tendency to optimize the balance of respiratory effort versus need (as signaled by elevated arterial CO 2 ) 47 . Individuals with major depression have been shown to mount an inhibited response to CO 2 48,49 . Individuals with a history of panic attacks tend to experience panic attacks on CO 2 and in the process, to hyperventilate 50,51 …”

Section: Respiratory Behavior As An Experimental Modelsupporting

confidence: 60%

“…47 Individuals with major depression have been shown to mount an inhibited response to CO 2 . 48,49 Individuals with a history of panic attacks tend to experience panic attacks on CO 2 and in the process, to hyperventilate. 50,51 Prior analysis of the respiratory response to 5% CO 2 among euthymic individuals with bipolar disorder revealed a widely varied response, and dramatic shifts in respiration for some individuals across the 15-min trial.…”

Section: Respiratory Behavior As An Experimental Modelmentioning

confidence: 99%

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Bipolar Disorder as Maladaptive Arousal

MacKinnon

2008

Annals of the New York Academy of Sciences

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Bipolar disorder can be understood as a disorder of behavioral regulation. Manic and depressed individuals are impaired in the titration of appetitive arousal, possibly at the level of neuronal plasticity. An experiment in which fixed 5% CO2 stimulates respiration and blocks satiety tests the regulation of appetitive arousal. In preliminary analysis of data from 35 individuals (24 with bipolar disorder) individuals with bipolar disorder were more likely to fail to find a stable state of respiratory adjustment to CO2. If confirmed, the unstable respiratory response to CO2 may prove useful as a bipolar-disorder endophenotype.

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Section: Respiratory Behavior As An Experimental Modelsupporting

confidence: 74%

Section: Respiratory Behavior As An Experimental Modelsupporting

confidence: 60%

Section: Respiratory Behavior As An Experimental Modelmentioning

confidence: 99%

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Bipolar Disorder as Maladaptive Arousal

MacKinnon

2008

Annals of the New York Academy of Sciences

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“…There is evidence that depression is associated with a diminished hypercapnic ventilatory response (31-33) and reduced cerebral vasomotor reactivity to hypercapnia (34). These factors could prolong apnea/hypopnea episodes, leading to even greater sympathetic activation and cardiovascular strain during sleep.…”

Section: Discussionmentioning

confidence: 99%

Interactive Associations of Depression and Sleep Apnea With Adverse Clinical Outcomes After Acute Myocardial Infarction

Hayano

Carney²,

Watanabe³

et al. 2012

Psychosomatic Medicine

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Objective Depression and sleep apnea (SA) are common among patients after acute myocardial infarction (AMI), and both are associated with increased risk for adverse outcomes. We tested the hypothesis that there is an interaction between depression and SA in relation to prognosis in post-AMI patients. Methods Participants were 337 depressed and 379 nondepressed post-AMI patients who participated in a substudy of the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial. SA was identified from Holter ECG at the entry by an algorithm that detects cyclic variation of heart rate. Results During a median follow-up of 25 months, 43 (6.0%) of patients died and 83 (11.6%) either died or experienced a recurrent AMI. Among 94 patients with both depression and SA, these endpoints occurred in 20 (21.3%) and 25 (26.6%), the prevalence that was 6.9 and 3.9 times higher than predicted probabilities by ENRICHD clinical risk scores (P <.001 for both). In the patients with depression alone, SA alone, or neither, the frequencies did not differ significantly from the predicted probability. Although both depression and SA predicted death and the combined endpoint, we observed depression by SA interactions (P = .03 and .02). SA independently predicted these endpoints in depressed (P <.001 and P = .001), but not in nondepressed patients (P = .73 and .84). Similarly, depression independently predicted these endpoints in SA (P <.001 for both), but not in non-SA patients (P = .61 and .12). Conclusion The combination of depression and SA estimated by CVHR is associated with long-term adverse clinical outcomes after AMI.

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“…Obstructive events terminate when chemoreceptors detect rising arterial CO 2 (hypercapnia) and signal respiratory centers in the brain to clear the airway and resume inspiration. There is evidence that depression in medically well psychiatric patients may blunt the respiratory response and delay the cortical arousal response to hypercapnia (5–8). A recent fMRI study of depressed patients with documented OSA found more lesions in the frontal cortex, insula, cingulate, and areas proximal to the amygdala and hippocampus in depressed compared to ND patients (9).…”

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confidence: 99%