Assisted Ventilation in Status Asthmaticus Paper
Assisted Ventilation in Status Asthmaticus
When a patient is admitted in the Intensive Care Unit (ICU) with a diagnosis of status asthmaticus, it means that the asthma attack is extremely severe and critical. In this situation, the patient does not respond to high doses of steroids and inhaled bronchodilators. According to Groth, this resistance to medication is most likely the consequence of three things that make it extremely hard to get air in and lout of the lungs. These three factors are as follows:
· Bronchospasm, which is a condition of an extreme spasm of the airways.
· Edema, which is a condition when the lining of the airways is swelling.
· Thick mucus secretions in the airways.
Normally, when an individual breathe in, the airways are pulled open when the chest wall becomes larger; however, when the individual breathe out, the airways have a tendency to collapse, locking in air in the chest. However, when a person is an asthmatic, emptying the lungs takes a long time for the reason that the airways are restricted. An asthmatic person cannot totally empty the lungs prior to having to take one more breath. When a person is severely asthmatic, he/she experiences shorter breathing so he/she tries to breathe faster and he/she has little time to exhale. When this happens, the lungs keep hold of, or “trap,” lots of air, which is called hyperinflation or air-trapping. Moreover, this procedure makes it more difficult to take another breath in, and the breathing muscles have to try harder and make more effort to take in any air. Groth said that a young or if not a healthy asthmatic can more often than not surmount this complexity, but at the expense of a considerable strain on the breathing muscles. Then, when this demand is continued for too long, for instance due to resistance to medicine, the asthmatic person’s breathing muscles can get exhausted and he/she will acquire respiratory failure.
Furthermore, according to Corbridge and Hall (1995), status asthmaticus is a life threatening type of asthma described as a situation in which an increasingly worsening attack is impassive or not responsive to the customary proper treatment with adrenergic drugs and that causes pulmonary insufficiency. The most important mechanical occurrence in status asthmaticus is a progressive rise in airflow resistance. In addition, mucosal edema or inflammation and mucous plugging are the primary causes for the late recovery in status asthmaticus. Ibsen added that the combination of acidosis, hypercapia, and hypoxia together with the mechanical consequences of increased lung volumes might bring about or cardiovascular arrest or cardiovascular depression.
Indications for ICU Admission
Schwarz and Lubinsky (1997) asserts that a person with status asthmaticus should be admitted to ICU when he/she feels the following:
· Altered sensorium
· Presence of high-risk factors
· Use of continuous inhaled beta-agonist therapy
· Failure to improve in spite of adequate therapy
· Increasing PCO2 ins spite of treatment
· Markedly decreased air entry
Due to difficulty in breathing, a person with status asthmaticus admitted in then ICU is ventilated through assisted or mechanical ventilation. Groth said that a mechanical ventilator takes over the function of breathing in the course of status asthmaticus; however, it does nothing to overturn airway inflammation or bronchospasm. The main function of a mechanical ventilator is to sustain breathing for the exhausted muscles until such a time when a variety of medications become helpful and effective. For a patient in the ICU to obtain mechanical ventilation, he/she needs an endotracheal tube, which is a plastic tube that is inserted by means of the nose or mouth into the windpipe or trachea and is linked to the ventilator. Moreover, the patient must likewise be sedated with an opioid-like morphine called fentanyl and medically paralyzed so as to let the ventilator function effectively and to make the patient comfortable.
If the patient has already undergone rapid extubation but still suffers difficulty of breathing, there is probably a failure in extubation. Werner (2001) says that extubation is a major complication of translaryngeal intubation, but its impact on mortality, duration of mechanical ventilation (MV), length of intensive care unit (ICU) and hospital stay, and need for ongoing hospital care has not been adequately defined.
Hence, in the case of extubation failure, the patient in the ICU should be intubated. Epstein et al., (2000) said that as many as 20% of extubated patients require reintubation (specifically extubation failure) within 72 hours of extubation, with the exact prevalence depending on numerous factors. The pathophysiologic basis of extubation failure is often different from the cause of weaning failure. Extubation failure substantially prolongs the duration of mechanical ventilation, intensive care unit stay, and hospital stay, and substantially increases hospital mortality. Therefore, prediction of extubation outcome and prevention of extubation failure may be critically important. Unfortunately, standard weaning tests have not proven sufficiently accurate in predicting extubation outcome. New semi-objective measurements of cough strength and secretion volume can help recognize patients at increased danger for extubation failure. It is significant to observe that mortality increases with reintubation delay, which illustrates that clinical worsening might occur during the period without ventilatory support. As a result, better result possibly will come from rapid detection of patients at increased danger, followed by quick reinstitution of ventilatory support when extubation failure happens.
Schwarz and Lubinsky (1997) also said that the patient in the ICU should be intubated and mechanically ventilated he/she suffers the following:
· Diminishing level of consciousness
· Significant hypoxemia that is poorly responsive or unresponsive to supplemental oxygen therapy alone
· Apnea or respiratory arrest
· Impending respiratory failure marked by significantly rising PCO2 with fatigue, decreased air movement, and altered level of consciousness
The choice to intubate an asthmatic should be done with tremendous concern. According to Cox, Barker and Bohn (1991), positive pressure ventilation in an asthmatic person is made difficult by acute air trapping and airway obstruction that causes hyperinflated lungs, which might refuse to accept further inflation and puts the patient at high danger of barotrauma. As a result, mechanical ventilation must be carried out just in the face of constant deterioration regardless of maximal bronchodilatory therapy.
Moreover, Werner (2001) agrees that the assessment and choice to intubate an asthmatic should not be taken without due consideration, and intubation must be prevented if possible. Tracheal intubation may aggravate bronchospasm (O’Rourke & Crone, 1982) and positive pressure ventilation will significantly boost the danger of circulatory depression and barotraumas (Williams et al., 1992).
According to Corbridge and Hall (1995), ventilator management can be challenging to a certain extent. For this reason, the following principles should be applied in taking care of a patient with status asthmaticus in the ICU:
1.Do not attempt to regulate or normalize the pCO2. Tolerate hypercapnia, and make use of pharmacologic buffering agents if needed to raise the pH to >7.2. How high a pCO2 you could do with to endure is determined by the pressures required to ventilate the patient.
2.Make an effort to keep plateau (alveolar) pressures <30-35 cm H20. Peak pressures might be higher than this because of increased airways resistance.
3.Small tidal volumes are typically required because of propensity and high resistance for air trapping. 5-7 cc/kg is a logical and practical place to begin.
4.Rate must be low and expiratory time long, inspiratory time somewhat short. The plan is to leave as much time as possible for expiration, without causing the inspiratory pressure to be extremely high since you are attempting to get the gas in over too short a period. Rates of 10-14 and I:E ratios of 1:4 to 1:6 are usual.
5. Pressure cycled or volume cycled ventilation can be employed. If employing volume-cycled ventilation, be certain to look at the pressures generated cautiously. If employing pressure cycled, the ventilator will typically not arrive at “plateau” or no flow, and you have to look at the volumes delivered. Regular reassessment is vital.
6.If you come across problem with oxygenation or just cannot move the chest, manually bag the patient and re-examine therapy and ventilator strategy.
7.Case series and some anecdotes show that there has been certain success with the use of pressure support ventilation in the sedated, but not paralysed, intubated asthmatic. Its regular use has not been subjected to controlled trials.
8.The patient should be well sedated and generally paralyzed during mechanical ventilation. Constant infusions or doses scheduled on a regular basis must be used.
9.Premedicate with lidocaine and extra sedation prior to suctioning to lessen the bronchoconstriction in reaction to stimulation.
10.Go on with insistent bronchodilator therapy-aerosols or MDIs, atrovent, intravenous terbutaline, and steroids. Take into account “kitchen sink” therapies like ketamine, magnesium, isoflurane, and helium.
Respiratory Acidosis, Metabolic Acidosis and Permissive Hypercapnea as a Lung Protective Strategy
According to (Rebuck and Read, 1971), the customary regulation that respiratory acidosis determines or affects intubation has become outdated. With the start of more insistent utilization of inhaled b-agonist therapy, 1% of asthmatic children confined in the hospital (Cox, Barker and Bohn, 1991) and around 5 to 10% of asthmatic patients confined in pediatric intensive care (Pirie et al., 1998) need intubation.
Rebuck and Read (1971) maintains that asthma is a sickness of airway obstruction, specifically, increased airway resistance, causing persistence of the time constant or the time required for lung units to fill and empty. Hence, slow ventilator rates are typically required.
Tuxen and Lane (1987) also claims that during high peak airway pressures, the rule of mechanical ventilation of patients with status asthmaticus is controlled hypoventilation, putting up with higher levels of PCO2 so as to peak inspiratory pressures and reduce tidal volume.
The incidence of respiratory acidosis goes after that of hypercarbia (Nowak, 1983). In addition to acute airflow limitation, metabolic acidosis might also happen (McFadden and Lyons, 1968). Numerous instruments are possibly included. Then, according to Roncoroni et al. (1976), if cardiac output is compromised, hypoxia of the peripheral tissues might trigger lactic acidosis to build up or worsen. Furthermore, increased oxygen consumption by the respiratory muscles might be a factor as well. Also, it might likewise be generated with the aggressive administration of nonselective sympathomimetics (Appel et al, 1983).
Darioli and Perret (1984) established the idea of controlled hypoventilation with lower-than-traditional respiratory rates and tidal volumes in asthmatic adult patients, and discovered a significantly reduced frequency of barotrauma and death measured up to to historical control subjects. Meanwhile, this idea has been broadly accepted and realized to develop outcomes in asthmatic adult patients. Moreover, this concept, which is called permissive hypercapnia has also been reported in asthmatic children patients. Dworkin and Kattan (1989) dispensed mechanical ventilation to 10 children with the purpose of keeping peak inspiratory pressure , 60 cm H2O and arterial pH . 7.10; Paco2 ranged from 40 to 90 mm Hg; then, they did not detect air leak following intubation, and all of the 10 children survived. In addition, Cox et al (1991) said that when asthmatic children being given mechanical ventilation with initial tidal volumes of 10 to 12 mL/kg at rates of 8 to 12 breaths/min, inspiratory time was set at 1 to 1.5 s (considering an expiratory time of approximately 5 s), and tidal volumes were modified to keep peak inspiratory pressures at 45 cm H2O, just two postintubation pneumothoraces were observed, and all children survived without sequelae in spite of considerable hypercarbia throughout mechanical ventilation.
Werner (2001) said that permissive hypercapnia could be endured provided that the patient continues to be sufficiently oxygenated. A longer I:E ratio, frequently more than 1:3-4, helps tolerate slow but total emptying of the lungs during exhalation, helping and assisting ventilation and preventing unnecessary further air-trapping (auto-PEEP).
The utilization of positive end-expiratory pressure (PEEP) is contentious (Werner, 2001). A person with status asthmaticus in respiratory failure on mechanical ventilation frequently has a considerable amount of air trapping that causes intrinsic PEEP, which possibly will be worsened by means of continuing PEEP during exhalation. Nevertheless, a number of patients may perhaps gain by the addition of PEEP, maybe by way of preserving airway patency during exhalation. Therefore, in a patient in the ICU who continues to be refractory to the initial ventilatory settings with no or very low PEEP, carefully escalating the PEEP may possibly demonstrate to be beneficial.
Werner (2001) added that customarily, slow controlled ventilation with heavy sedation and with or without muscle relaxation is the strategy employed to ventilate patients with status asthmaticus. However, warning is necessitated, because the use of muscle relaxants with high-dose steroids has been linked with the growth of prolonged paralysis. On the other hand, a number of practitioners give an account of ventilating children with status asthmaticus with pressure support alone, enabling the patient to set his or her own respiratory rate as identified by his or her own physiologic time stable at the same time helping ventilation by means of relieving the fatigue caused by considerable work of breathing.
Noninvasive positive pressure ventilation (NPPV), for instance, continuous positive airway pressure (CPAP) or bimodal positive airway pressure (BiPAP) delivered by way of a facemask, has been utilized for support of status asthmaticus. NPPV has been demonstrated to “splint” the airways, letting better exhalation and emptying (Werner 2001).
Tuxen and Lane (1987) asserted that patients necessitate monitoring and supportive measures during mechanical ventilation. They also said that patients might be uneasy and air hungry while ventilated with low respiratory rates, and hypercapnia as a result of an approach of controlled hypoventilation.
Preferably, flow-volume loops should be monitored to determine if sufficient time is given for exhalation to evade breath stacking, which happens if the next breath is delivered prior to exhalation is finished. Moreover, monitoring auto–positive end-expiratory pressure (auto-PEEP) and exhaled tidal volume is vital as well.
Pirie et al. (1998) said that electrolytes and fluids must be monitored. Prior to arrival in the hospital, children with status asthmaticus have frequently had reduced oral intake and might have been vomiting as a consequence of respiratory difficulty or adversative effects from their medications. This causes decreased intravascular volume status that might be potentiated by the outcomes of positive pressure ventilation.
Furthermore, cardiac output might be reduced as a consequence of lessened preload that are caused by auto-PEEP and air trapping. This decreased cardiac output and intravascular volume might perhaps be complemented by metabolic acidosis. Intravascular fluid expansion is necessary to cure hypotension, hypoperfusion, or metabolic acidosis. Moreover, diastolic hypotension might irregularly develop from high doses of beta-agonists. A vasoconstrictor (specifically, phenylephrine or norepinephrine,) might be taken into account if considerable diastolic hypotension in the face of sufficient intravascular volume persists. Monitor serum electrolyte levels, as medications used to treat asthma can result in significant kaliuresis (Tuxen and Lane, 1987).
Meanwhile, Nowak et al. (19833) said that placement of indwelling arterial catheters offers nonstop blood pressure monitoring in addition to arterial blood gas sampling. They also maintained that blood gases must be monitored to evaluate response or reaction to therapy in mechanically ventilated patients.
Meanwhile, mechanical ventilation utilizing unsuitable settings can generate acute inflammatory response in the lund and acute parenchymal lung injury. The related release of cytokines into alveoli and the systemic circulation (Ranieri et al., 1999) might be a factor to multiple organ dysfunction (Slutsky and Tremblay, 1998) and mortality in acute respiratory distress syndrome (ARDS). “Lung-protective” ventilation strategies try to evade these outcomes by means of restraining peak lung distension and evading end-expiratory collapse, tolerating the hypercapnia that frequently results; such strategies decreased mortality rate in ARDS in two randomized trials (Slutsky and Tremblay, 1998).
Hypercapnia is normally considered as an adverse result of limiting alveolar stress, but in a series of studies, Laffey, Engelberts and Kavanagh (2000) have asked whether hypercapnic acidosis per se might be a factor to the advantages of lung-protective ventilation. They demonstrated that in isolated perfused rabbit lungs, respiratory acidosis protected the lung from ischemia–reperfusion injury, while respiratory alkalosis potentiated the damage. The protective result of respiratory acidosis was linked with inhibition of xanthine oxidase, and was prohibited by means of buffering the acidosis; specifically, the protection was because of the acidosis instead of hypercapnia.
Acidosis restrains the cytokine expression and respiratory burst in macrophages (Roncoroni et al., 1976). Then, Laffey, Engelberts and Kavanagh (2000) have talked about other studies recommending cytoprotection by hypercapnic acidosis. Hence, even though it appears that it is impossible that all of the evident advantage of lung protective ventilation is a direct result of hypercapnia, the hypothesis tackled by Laffey, Engelberts and Kavanagh (2000) is a significant and sensible one. If “lung-protective ventilation” in ARDS does decrease pulmonary and systemic inflammation, and possibly multiple organ dysfunction, hypercapnic acidosis as such could possibly be somewhat responsible, maybe by downregulating inflammatory cells, and perhaps other mechanisms in addition to inhibition of xanthine oxidase.
Therapy and Care in the ICU
ICU therapy begins in step-wise fashion and escalates to a “kitchen sink” approach. This is because there is fairly little data which points to one combination of therapies being superior to others, and because an asthmatic deteriorating despite “usual” therapy is in significant danger.
Standard therapy includes steroids (solumedrol) and beta-agonists (intermittent aerosols, continuous aerosols, or intravenous terbutaline). “Adjunctive” therapy includes anticholinergic agents (Atrovent). Chest physiotherapy and/or IPV (intermittent percussive ventilation) may be helpful and/or necessary for some patients.“Kitchen sink” therapies include magnesium, helium, ketamine, antibiotics, inhalational anesthetics, aerosolized lasix.
Based on the literature of Groth, the patient in the ICU must be prescribed continuous nebulization of albuterol for the first eighteen hours after the patient’s admission to the Intensive Care Unit and then switch to intermittent albuterol every two hours. Inhaled ipratropium could also be added every 6 hours. Ipratropium is an anticholinergic bronchodilator, and reduces bronchoconstriction through a different means. Then the patient will continue to be treated with a high dose of intravenous corticosteroids. He/she will also be given antibiotics if he/she has a fever, a high white blood cell count, and increased cough and mucus indicating that he/she has an infection.
Groth also asserted that several of the treatments of last resort employed in status asthmaticus consist of giving general anesthesia with inhalational anesthetics, which are very effective and powerful bronchodilators. Nevertheless, the help of an anesthesiologist will be needed to give this kind of treatment. Intravenous anesthetics like ketamin, can be useful as well.
Sin Fai Lam, Mow and Chew (1992) said that a more open-minded use of the ICU for patients with severe asthma has formerly been promoted. Procrastination might bring about a respiratory arrest. The result is at all times worse following a respiratory arrest; Lee, Tan and Lim (1997) gave an account of a merely 50% survival from hypoxic brain damage following a respiratory arrest despite good intensive care treatment. It is not advantageous to wait until the patient is almost dilapidated from CO narcosis to take control of the airway. If active airway intervention is unavoidable, it is preferable to come up with this decision early instead of late. This means that it is better to be pro-active instead of procrastinating. Early endotracheal intubation and mechanical ventilation in the patient with life threatening asthma might be practical procedures that can save life and bring about good clinical outcome. Complete signs for intubation are cardiac and respiratory arrest or considerable alteration in mental state. At other instances, the decision made in the face of increasing exhaustion and progressive deterioration. Based on the various literature discussed in this paper, would like to see more patients who need ventilation be intubated electively instead of as a consequence of a cardiorespiratory arrest. Blood gas abnormalities by itself are not a sign to intubate the patient. Several patients with respiratory acidosis and hypercapnia will respond and react to treatment with bronchodilators and do not need mechanical ventilation. More significant is the development in clinical findings and in the arterial blood gases.
Furthermore, procrastination in the instigation of mechanical ventilation when it is certainly necessary is connected to the fear of complications. Definitely, contemplation and reflection should at all times be provided to the possible dangers. Intubation in a dyspnoeic, relentless and anxious patient must be carried out by the most knowledgeable and skilled clinician available. A large endotracheal tube must be chosen because it helps suction and lessens airways resistance. Based on the literature, there are advantages of both oral and nasotracheal intubation, and sedative options in the preparation of the patient differ among people. When endotracheal intubation has been performed, the physician’s priority should be to take control with positive pressure ventilation. This will necessitate the utilization of sufficient sedation and typically paralysis with a muscle relaxant. Paralysis might regularly merely be necessary in the first stages of ventilation, and must be weaned off as soon as possible to lessen the danger of acute myopathy. Ventilation must primarily be in the CMV manner. Ventilatory settings should also be selected to evade extreme lung inflation. This approach will lessen the danger of systemic hypotension or pneumothorax. Lung inflation is lessened by means of permitting a sufficient time for exhalation (TE). Meanwhile, expiratory time may perhaps be prolonged by means of reducing minute ventilation (VE) by either minimizing inspiratory time (TI) or lowering respiratory rate RR or tidal volume (VT). Inspiratory time is lessened through increasing inspiratory flow rate and by means of employing a square flow wave form. Tidal volumes of 8-10 mls/kg with a respiratory rate of 10-14 and inspiratory flow rates of 60 L/min or higher are frequently appropriate (Sin Fai Lam, Mow and Chew, 1992). A suitable peak airway pressure of < 50 mm H20 should be aimed for.
Furthermore, controlled hypoventilation is a method employed to lessen the danger of hypotension and barotrauma. The goal is to guarantee sufficient oxygenation, stay away from extreme dynamic hyperinflation (DHI) and tolerate a degree of hypoventilation. It is completely tolerable to let the PCO 2to increase so as to evade DHI. One must not try to normalize the PCO2 to the detriment of DHI (Lee, Tan and Lim, 1997). Hypotension might be attributed to too much DHI. A short experiment of apnoea (30-45 seconds) is indicative, as blood pressure rises and venous return increases during the period of apnoea. If this does not occur, other causes of hypotension like fluid depletion, tension pneumothorax, unnecessary sedation or myocardial depression should be taken into account.
Lastly, A number of studies have evidently revealed that mechanical ventilation saves lives in life-threatening asthma (Sin Fai Lam, Mow and Chew, 1992). With good ICU management, the period of required ventilation is short, complications can be kept to a minimum, and there is more often than not no problem in weaning the patient off the ventilator. Nevertheless, we should remember that ultimately, the therapy and remedy of acute life-threatening asthma does not merely begin 3 days prior to the attack, but much earlier, as most acute attacks are avoidable with the appropriate use of standard and regular prophylactic medication, the proper education of patients, the avoidance of trigger factors, the appropriate implementation of a co-management plan between the patient and his doctor, the objective measurement of the PEFR, and the accessibility to medical care in times of crisis.#
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