Case study 21 copd with respiratory failure answers
The fact that most hypercapnic COPD patients can achieve normocapnia by voluntarily increasing their ventilation 55 makes the two hypotheses above untenable. The problem with maintaining V ' E above normal levels is that this is associated with significant mechanical impediments to breathing. Since COPD patients are characterised by increased airflow resistance and reduced dynamic compliance, the resistive and elastic loads are increased and hence the inspiratory muscles have to generate higher forces to inflate the lung.
The emphysematous changes in the lung cause hyperinflation, which forces the inspiratory muscles to operate at shorter than normal lengths and reduces their ability to lower the intrathoracic pressure. More importantly, the dynamic hyperinflation that develops in these patients due to limitation of expiratory flow imposes a severe strain on the respiratory muscles because of the additional load that is placed on them intrinsic positive end-expiratory pressure PEEP i and because of impairment of their operating length and geometry.
A subnormal respiratory output has long been postulated as a mechanism of hypercapnia in patients with COPD. However, neural drive assessed by mouth occlusion pressure has been found to be higher in COPD patients than in normal subjects 56 , although no significant differences were found between normocapnic and hypercapnic patients.
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In addition, neural drive assessed by surface electromyographic activity of the diaphragm was also found to be increased in both normocapnic and hypercapnic COPD patients Furthermore, the voluntary drive to breathe has been shown not to be decreased in hypercapnic COPD patients Consequently, although, in these patients, the respiratory drive to breathe is increased, they are better off shortening the t I , a process that results in a lower V T.
The reduction in V T is largely offset by an increase in the f R , such that V ' E is well preserved. However, rapid shallow breathing has undesirable consequences. The pattern of breathing in COPD patients has been examined in several studies. These data were confirmed by Gorini et al.
The mechanisms leading to alterations in respiratory timing in patients with COPD have not yet been clearly defined. Changes in the pattern of breathing may represent a behavioral response in order to minimise the sense of dyspnoea. The sense of dyspnoea is a complex perceptual construct, probably multifactorial Studies indicate that the sense of breathlessness increases with increases in the intrathoracic pressure required to maintain airflow and V T , t I relative to t tot and f R.
Thus, at a given V ' E and set of respiratory mechanics, the pattern of breathing determines the intensity of breathlessness. Thus it could be suggested that, as the disease progresses, the critical level of power output for muscle fatigue is exceeded in order to permit the patient to maintain adequate V ' A. Thus it seems evident that, when the muscles become unable to develop enough force, the activation system comes into play and may alter the pattern of breathing in an attempt to optimise the performance of the muscles and possibly postpone or prevent severe fatigue.
Case study patient with copd
Although the underling mechanisms are not known, it is speculated that afferents from the small fibres stimulated by the heavy work ergoreceptors, type III or noxious substances nociceptors, type IV modify CNS output. Acute deterioration in a patient with chronic respiratory failure is termed acute-on-chronic respiratory failure.
Patients may present with worsening dyspnoea, deteriorating mental status or respiratory arrest after relatively minor, although often multiple, insults. Acute-on-chronic respiratory failure is usually seen in patients known to have severe COPD. Patients with severe but stable COPD exist in a very critical balance between increased demands and limited reserves. Any factor that potentially interferes with this balance either increase in demands or decrease in reserves leads to respiratory muscle fatigue and acute respiratory failure.
Patients with COPD experience an increased respiratory system load due to abnormal airway resistance and respiratory system elastance. The increased resistance is caused by bronchospasm, airway inflammation or physical obstruction by mucus and scarring. The most significant contributor to the elastic load is dynamic hyperinflation that develops whenever the t E is insufficient to allow the lungs to deflate to V r prior to the next inspiration.
This tends to occur under conditions in which expiratory flow is impeded increased airway resistance or when the t E is shortened increased f R 39 , Expiratory flow may also be retarded by other mechanisms such as persistent constriction of the respiratory muscles during expiration. Most commonly, however, dynamic pulmonary hyperinflation is observed in COPD patients who exhibit expiratory flow limitation during resting breathing and plays a paramount role in causing respiratory failure. When breathing takes place at lung volumes greater than V r , a positive elastic recoil pressure called PEEP i remains at end-expiration.
When PEEP i is present, the inspiratory muscles have to generate greater effort to overcome an equal amount of pressure before airflow starts. In this respect, PEEP i acts as an inspiratory threshold load which increases the static elastic work of breathing. Apart from increasing elastic loads, dynamic hyperinflation is accompanied by a concomitant decrease in the effectiveness of the inspiratory muscles as pressure generators, because the inspiratory muscle fibres become shorter and their geometric arrangement changes see Pulmonary hyperinflation section.
Schematic representation of the sequence of responsible mechanisms that lead to acute-on-chronic respiratory failure in patients with chronic obstructive pulmonary disease. Acute ventilatory failure in these patients is usually triggered by airway infection. The increased f R , which is invariably present in acutely ill COPD patients 39 , 63 due to shortened t E , further exacerbates dynamic hyperinflation, which promotes an increase in the static elastic work of breathing due to both PEEP i and decreased lung compliance.
At the same time, an acute increase in airway resistance bronchoconstriction and copious secretions causes an increase in the resistive work of breathing. The increased work of breathing associated with this impaired muscle effectiveness leads to an increase in energy requirements, which, at a critical point, exceeds the diminished energy available hypoxaemia and impaired diaphragmatic blood flow due to forceful contractions and respiratory muscle fatigue ensues with a further increase in P a,CO 2.
Although the processes leading to acute hypercapnic respiratory failure have been thoroughly elucidated, the pathophysiological mechanisms responsible for chronic carbon dioxide retention are not yet clear. Although no indisputable evidence exists to prove the mechanisms involved in chronic carbon dioxide retention, there are sufficient data to permit speculation concerning the way in which peripheral mechanical or chemical stimuli are transferred and modify the pattern of breathing 36 , Until the early s, the respiratory central nervous discharge had been considered to be affected predominantly by central and peripheral chemoreceptors and vagal afferents, and to a lesser extent by muscular afferents, with a role that seemed of minor importance.
The effects of sensory information traveling via the phrenic nerves on the central respiratory centres were not very well elucidated, although it was known that nonmyelinated fibres constituted a large proportion of the entire phrenic nerve 64 , Under states of severe thoracic stress muscle tension, local ischaemia and accumulation of toxic metabolites , afferents from the respiratory muscles may play a predominant role in the genesis of the particular breathing pattern.
As has been shown, the characteristic response to breathing against a fatiguing load or in a state of reduced respiratory blood flow is tachypnoea, initially followed by bradypnoea and respiratory arrest 14 , Since this response is not affected in animals, by either vagotomy, eliminating vagal afferents, or cross-perfusion of the head, eliminating chemoreceptor afferents, it seems reasonable to suggest that afferent information from type III and IV receptors would potentially increase their effect on the central respiratory controllers and alter ventilatory timing 36 , The influence of afferent phrenic fibres on breathing pattern, as well as possible stimuli triggering them, has been studied in anaesthetised animals during eupnoea or fatigue trials 38 , In conscious goats, strenuous resistive breathing was associated with a biphasic electromyographic response in the diaphragm 67 , consisting of an initial and immediate increase facilitation followed by a partial decrease inhibition.
A direct link between stimulation of group III and IV afferents and the central elaboration of endogenous opioids has also been suggested by Kumazawa et al. Other investigators have confirmed these results in cats and demonstrated that the phenomenon involved a supraspinal mechanism 69 which could be prevented by pretreatment with naloxone 32 , thus strongly indicating involvement of endogenous opioid pathways. The role of exogenous or endogenously generated opioids as neurotransmitters or neuromodulators of a complex inhibitory system of respiration has been extensively studied.
When injected into the cisternal cerebrospinal fluid, heroin caused a reduction in V T 33 , indicating a direct inhibitory effect of this opioid on respiration. In COPD patients whose respiratory responses to flow resistive loading were absent, the responses could be immediately restored by administration of naloxone 34 , suggesting that the chronic increase in airway resistance in these patients generated endogenous opioids as an adaptive response, which served to lessen the stress of prolonged dyspnoea.
Both V T and mean inspiratory flow rate could be transiently increased by naloxone administration, demonstrating that a proportion of these effects could have been meditated by elaboration of endogenous opioids. These data imply that endogenous opioids caused a progressive decline in the discharge rate of the respiratory centres that allow a reduction in inspiratory activity per breath in order to minimise the work of the respiratory muscles, since a reduced V T requires less pressure development, and delay or prevent the onset of overt muscle fatigue.
Reproduced with permission from Although the stimuli for the production of the cytokines are not known, reactive oxygen species produced within the respiratory muscles during fatiguing resistive breathing 76 , 77 could probably be responsible. Thus it is possible that plasma cytokine induction during resistive breathing is differentially regulated by various stimuli, some of them being common reactive oxygen species , whose relative importance varies with each respective cytokine. Even though the present authors acknowledge that the time profile brief and intensity much greater of the increased resistance in the above mentioned models are different from those in patients with chronic carbon dioxide retention, given that strenuous breathing causes diaphragm muscle fibre injury consisting of membrane damage, sarcomere disruption 44 , 45 and lactic acid production 38 , the following hypothesis could be arrived at fig.
The ensuing stimulation of the hypothalamic-pituitary-adrenal axis by the cytokines might have a dual purpose: the ACTH response may represent an attempt of the organism to reduce the injury occurring in the respiratory muscles through the production of glucocorticoids by the adrenals POMC: pro-opiomelanocortin.
The respiratory system consists essentially of two parts: a gas exchanging organ, the lungs, and a pump that ventilates the lungs. The pump consists of the chest wall, the respiratory muscles that displace the chest wall, the respiratory centres of the CNS that control the muscles and the nerves connecting the centres to the muscles.
Both parts of the system are vital. In general, failure of the gas exchanging function due to lung disease i. ARDS, pneumonia and pulmonary emboli results mainly in hypoxaemia with normocapnia or hypocapnia type I respiratory failure. Failure of the pump i.
CNS depression, weakness and trauma , which also causes hypoxaemia, leads to hypoventilation and hypercapnia which is the hallmark of ventilatory failure type II respiratory failure. In all these conditions, pathophysiologically, the common denominator is reduced V ' A for a given V ' CO 2. Mechanical disorders are often a cause of alveolar hypoventilation.
Disorders with hypoventilation can easily be seen in chest wall trauma flail chest , excessive hyperinflation in hyperinflated patients with obstructive lung disease and kyphoscoliosis. Neuromuscular disorders in which the patients present with a weakness, as, for example, in overdose, CNS lesions and neuromuscular diseases, lead to alveolar hypoventilation either acutely or chronically. Imbalance of energy demand and supply may eventually lead to respiratory muscle fatigue i.
Extensive discussion over many years has not provided an answer as to why some patients develop chronic hypercapnia as in chronic obstructive pulmonary disease, kyphoscoliosis and neuromyopathies. Patients facing a load have two options: either to push hard in order to maintain normal arterial oxygen and carbon dioxide tensions at the cost of eventually becoming fatigued and exhausted or breathe at a lower minute ventilation, avoiding dyspnoea, fatigue and exhaustion but at the expense of reduced alveolar ventilation.
Credence is lent to this latter option, which the present authors favour, by most recent work. This, however, culminates in alveolar hypoventilation and carbon dioxide retention. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail.uqitojacelic.tk
BEEM Cases 3 – Acute Respiratory Failure: NIPPV & POCUS
We do not capture any email address. Skip to main content. Respiratory failure C. Roussos , A. Abstract Respiratory failure occurs due mainly either to lung failure resulting in hypoxaemia or pump failure resulting in alveolar hypoventilation and hypercapnia. This study was supported by the Thorax Foundation, Athens, Greece. Pathophysiology of ventilatory pump failure There are three major causes of pump failure leading to hypercapnia 6. Pulmonary hyperinflation In normal subjects at rest, the end-expiratory lung volume FRC corresponds to the relaxation volume V r of the respiratory system, i.
Ventilatory failure in clinical conditions Hypercapnic respiratory failure may occur either acutely, insidiously or acutely upon chronic carbon dioxide retention. View this table: View inline View popup.
Table 1 Causes of alveolar hypoventilation, acute onset. Table 2 Causes of alveolar hypoventilation, insidious onset. Acute-on-chronic respiratory failure Acute deterioration in a patient with chronic respiratory failure is termed acute-on-chronic respiratory failure. Perspectives: hypothalamic-pituitary-adrenal axis and ventilatory failure Although the processes leading to acute hypercapnic respiratory failure have been thoroughly elucidated, the pathophysiological mechanisms responsible for chronic carbon dioxide retention are not yet clear.
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Conclusions The respiratory system consists essentially of two parts: a gas exchanging organ, the lungs, and a pump that ventilates the lungs. Roussos C. The failing ventilatory pump. Lung ; : 59 — OpenUrl CrossRef. Function and fatigue of respiratory muscles. Chest ; 88 : S —S. OpenUrl PubMed. Macklem PT. Respiratory muscles: the vital pump.
Chest ; 78 : — Roussos C, Macklem PR. The respiratory muscles. N Engl J Med ; : — Respiratory muscles and weaning failure. Eur Respir J ; 9 : — OpenUrl Abstract.
Chronic Obstructive Pulmonary Disease (COPD) Treatment & Management
Fatigue of the respiratory muscles and their synergistic behavior. J Appl Physiol ; 46 : — Bellemare F, Grassino A. Effects of pressure and timing of contraction on human diaphragm fatigue.