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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this article, we describe a case of a subarachnoid hemorrhage (SAH) in an acute severe asthma patient following mechanical hypoventilation. A 49-year-old man was admitted to an Intensive Care Unit with an acute exacerbation of asthma. After 3 days of mechanical ventilation (hypercapnia and normoxaemia), it was noted that his right pupil was fixed, dilated, and unreactive to light. Computed tomography (CT) scan showed localized SAH within the basilar cisterns and diffuse cerebral swelling. On the fourth day, a new CT scan showed hemorrhage resorption and a cerebral swelling decrease. In the following days, the patient's condition continued improving with no detectable neurological deficits. A review of similar published reports showed that all patients performed respiratory acidosis, normoxaemia, and hypercapnia. The most frequent neurological sign was mydriasis, and all subjects showed cerebral edema. Since normoxaemic hypercapnia has been associated with absence, or less cerebral edema, we considered additional factors to explain cerebral edema and intracranial hypertension causes. Thus, intrathoracic pressures due to patient's efforts by forcibly exhaling, or during mechanical ventilation, would further increase intracranial pressure by limiting cerebral venous drainage. This case emphasizes the fact that patients with acute severe asthma who have developed profoundly hypercarbic without hypoxia before or during mechanical ventilation, may have raised critical intracranial pressure.
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PMID:Subarachnoid hemorrhage following permissive hypercapnia in a patient with severe acute asthma. 1059 94

All patients with bronchial asthma are at risk of developing severe episodes of airway narrowing that do not respond to the usual medical treatment, a life-threatening situation referred to as status asthmaticus. In some cases, ventilatory failure occurs, necessitating mechanical ventilation to support gas exchange and to unload the respiratory muscles, giving time for other therapeutic interventions to improve the functional status of the patient. Mechanical ventilatory support poses additional risks to the patients, due to interaction between the pathophysiology of the disease and the process of mechanical ventilation. Dynamic hyperinflation, a cardinal feature of the pathophysiology, may cause serious complications during mechanical ventilation. Setting the ventilator, such as to minimize the dynamic hyperinflation, is a key point in the management of mechanically ventilated patients with status asthmaticus. Strategies to reduce dynamic hyperinflation, such as hypoventilation (permissive hypercapnia), increase of expiratory time and promotion of patient-ventilator synchrony are mandatory and significantly decrease the morbidity and mortality of the disease. Continuous monitoring of the effectiveness of these strategies, as well as the functional status of the patient, is crucial in order to limit complications associated with mechanical ventilation and to identify the time that weaning can start.
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PMID:How to set the ventilator in asthma. 1078 31

From a pathophysiologic perspective, the changes that occur in asthma are multiple, diverse, and complex. Assessment of the mechanical properties of the ventilatory apparatus provides several different types of information, depending on the gravity of the bronchial obstruction. During asthma, or induced bronchial obstruction, the function of the muscles is altered, causing changes in respiratory timing. Expiratory duration decreases more than inspiratory duration, and the functional residual capacity (FRC) increases, due to mechanical changes within the airways that lead to air trapping. The related hypoventilation is responsible for hypoxemia and hypercapnia, but it does not severely affect the diffusion capacity of the alveolocapillary membrane. We describe the pathophysiology of the bronchial obstruction in asthmatic patients, underlining the critical function of the respiratory muscles. Moreover, we clarify the relations between the ventilatory changes and gas-exchange alteration.
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PMID:Asthma: pathophysiology of the bronchial obstruction. 1091 7

We present a 2.5-year-old girl in severe asthma crisis who clinically deteriorated on conventional mechanical ventilation, but was successfully ventilated with high-frequency oscillatory ventilation (HFOV). Although HFOV is accepted as a technique for managing pediatric respiratory failure, its use in obstructive airway disease is generally thought to be contraindicated because of the risk of dynamic air-trapping. However, we suggest that obstructive airway disease can safely be managed with HFOV, provided certain conditions are met. These include the application of sufficiently high mean airway pressures to open and stent the airways ("an open airway strategy"), lower frequencies to overcome the greater attenuation of the oscillatory waves in the narrowed airways, permissive hypercapnia to enable reducing pressure swings as much as possible, longer expiratory times, and muscle paralysis to avoid spontaneous breathing.
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PMID:Status asthmaticus treated by high-frequency oscillatory ventilation. 1101 38

Respiratory acidosis, or primary hypercapnia, is the acid-base disorder that results from an increase in arterial partial pressure of carbon dioxide. Acute respiratory acidosis occurs with acute (Type II) respiratory failure, which can result from any sudden respiratory parenchymal (eg, pulmonary edema), airways (eg, chronic obstructive pulmonary disease or asthma), pleural, chest wall, neuromuscular (eg, spinal cord injury), or central nervous system event (eg, drug overdose). Chronic respiratory acidosis can result from numerous processes and is typified by a sustained increase in arterial partial pressure of carbon dioxide, resulting in renal adaptation, and a more marked increase in plasma bicarbonate. Mechanisms of respiratory acidosis include increased carbon dioxide production, alveolar hypoventilation, abnormal respiratory drive, abnormalities of the chest wall and respiratory muscles, and increased dead space. Although the symptoms, signs, and physiologic consequences of respiratory acidosis are numerous, the principal effects are on the central nervous and cardiovascular systems. Treatment for respiratory acidosis may include invasive or noninvasive ventilatory support and specific medical therapies directed at the underlying pathophysiology.
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PMID:Respiratory acidosis. 1126 56

Asthma and chronic obstructive pulmonary diseases (COPD) lead to functional obstruction of airways, identified by increased inspiratory and expiratory resistances. Increased expiratory resistances cause, in turn, a reduction in expiratory flow. The analysis of flow-volume loops shows that, as the disease progresses, the flow generated during expiration of a tidal volume becomes very close to the flow generated during forced maximal expiration. In such condition, where there is little or no reserve of expiratory flow, higher tidal volumes need to be reached in order to increase the expiratory flow, and hyperinflation inevitably occurs. Hyperinflation, a key feature in COPD pathophysiology, is generated by two mechanisms: reduction of elastic recoil of the lung (static hyperinflation) and interruption of expiration at lung volumes still higher than FRC, due to reduction of expiratory flow (dynamic hyperinflation). When dynamic hyperinflation occurs, a residual positive pressure remains in the alveoli, which is defined as intrinsic positive end-expiratory pressure (PEEPi). Hyperinflation carries several consequences: 1) Respiratory mechanics: at lung volumes close to total lung capacity, lung compliance is physiologically reduced, and elastic work required to generate the same inspiratory volume is therefore increased; 2) Respiratory muscles: contractile properties of diaphragm deteriorate when the dome is pushed downward by an increased lung volume, inspiration is mainly performed by inspiratory muscles, and expiration becomes active; 3) Circulation: pulmonary vascular resistances increase due to compression exerted by hyperinflation on alveolar vessels and to hypoxic vasoconstriction; right ventricle afterload increases and right sided hypertrophy and dilation ensue; left ventricular afterload may increase due to increased negative intrapleural pressure which translates into an increased transmural pressure which needs to be overcome by ventricular contraction. Ventilatory support of COPD patients should decrease work of breathing and improve gas exchange without increasing hyperinflation. This target can be achieved during assisted ventilation by applying a positive pressure both during inspiration and expiration; the level of PEEP should equal PEEPi. During mechanical ventilation in sedated paralyzed patients hyperinflation should be limited by decreasing minute volume and by increasing expiratory time, eventually choosing controlled hypercapnia.
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PMID:[Physiopathology of acute respiratory failure in COPD and asthma]. 1137 10

The authors describe the application of NIV as a useful tool to correct hypercarbia, gas exchanges and to reduce the complications caused by mechanical ventilation with ETT in patients with acute exacerbation of COPD and acute asthma attack.
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PMID:[NIV in the treatment of acute exacerbation of COPD and status asthmaticus]. 1137 14

Obstructive sleep apnoea may be accompanied by various cardiovascular consequences resulting from alteration of the activity of the autonomous nervous system. These changes are mediated by: a--hypoxemia developing during the apnoea, b--severe hypoxemia, hypercapnia and acidosis in postapnoea, c--powerful but ineffective ventilatory efforts causing arousal and stimulation of the cardioexcitatory and vasomotor centres. There are four main pathogenetic mechanisms implementing the cardiovascular changes: 1--Functional alteration in the conduction system and the myocardium resulting in nocturnal cardiac dysrhythmias. 2--Vasoconstriction manifesting as angina pectoris, myocardial infarction, brain attacks and pulmonary or systemic hypertension. 3--Pulmonary congestion leading to cardiac or bronchial asthma or even lung oedema. 4--Neuroendocrine activation, including the sympathetic nervous system, renin-angiotensin-aldosterone system, atrial natriuretic peptide and erythropoietin, which may result in nycturia, nocturnal hypotension and diurnal hypertension.
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PMID:[Mechanisms in the development of cardiovascular complications in obstructive sleep apnea]. 1170 79

Severe asthma, although difficult to define, includes all cases of difficult/therapy-resistant disease of all age groups and bears the largest part of morbidity and mortality from asthma. Acute, severe asthma, status asthmaticus, is the more or less rapid but severe asthmatic exacerbation that may not respond to the usual medical treatment. The narrowing of airways causes ventilation perfusion imbalance, lung hyperinflation, and increased work of breathing that may lead to ventilatory muscle fatigue and life-threatening respiratory failure. Treatment for acute, severe asthma includes the administration of oxygen, beta2-agonists (by continuous or repetitive nebulisation), and systemic corticosteroids. Subcutaneous administration of epinephrine or terbutaline should be considered in patients not responding adequately to continuous nebulisation, in those unable to cooperate, and in intubated patients not responding to inhaled therapy. The exact time to intubate a patient in status asthmaticus is based mainly on clinical judgment, but intubation should not be delayed once it is deemed necessary. Mechanical ventilation in status asthmaticus supports gas-exchange and unloads ventilatory muscles until aggressive medical treatment improves the functional status of the patient. Patients intubated and mechanically ventilated should be appropriately sedated, but paralytic agents should be avoided. Permissive hypercapnia, increase in expiratory time, and promotion of patient-ventilator synchronism are the mainstay in mechanical ventilation of status asthmaticus. Close monitoring of the patient's condition is necessary to obviate complications and to identify the appropriate time for weaning. Finally, after successful treatment and prior to discharge, a careful strategy for prevention of subsequent asthma attacks is imperative.
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PMID:Clinical review: severe asthma. 1194 Feb 64

There has been increasing recognition that mechanical ventilation can cause acute parenchymal lung injury (ventilator-induced lung injury, or VILI) in addition to the more widely recognized forms of barotrauma. Furthermore, in patients with acute lung injury, this type of injury may cause considerable morbidity and mortality. Subsequently, the goals of mechanical ventilation have been altered to avoid this outcome. In patients with relatively normal lungs who are receiving mechanical ventilation because of neuromuscular dysfunction or impaired conscious level or for short-term postoperative support, maintaining normal blood-gas tensions without risk of VILI is usually easy. In patients with acute asthma, chronic obstructive pulmonary disease, or acute lung injury, however, accepting abnormal blood-gas tensions, particularly an elevated PaCO2 (permissive hypercapnia), to improve survival and reduce complications is frequently necessary. Extensive experience has shown that ventilated patients usually tolerate moderate hypercapnia and frequently some degree of hypoxemia in the absence of shock, anemia, severe cardiac disease, or other contraindications.
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PMID:Permissive hypercapnia. 1248 13


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