Resuscitation and treatment of a critically ill asthmatic patient?
Basic medical history.
Female, 25 years old, has had “severe” asthma since birth and has been on intermittent prednisone since the age of 12. She has been on intermittent prednisone since she was 12 years old. She has been on mechanical ventilation for 2 weeks in another hospital a year ago for pneumonia and “severe asthma”, and has had progressive worsening of cough and dyspnea at rest for the past 72 hours. He has used up 2 bottles of medication in the last 5 days, has no fever, no chills, and no travel history.
Initial laboratory tests
CBC: WBC 12 Neut 8.2 Hgb 155 Plt 455
CXR: Hyperinflation but no infiltrative shadow.? Moderately severe osteoporosis
Medications
Salbutamol (ventolin) 2 sprays qid; ipratropium bromide (atrovent) 2 sprays qid; clobodimethasone dipropionate (becloforte) 2 sprays bid prn; theophylline SR 1 tablet qd
Allergy history
Multiple environmental factors; morphine (morphine) and hydromorphone (acute hypersensitivity reaction) fish (acute hypersensitivity reaction)
Patient has facial congestion, light dark complexion, moderate respiratory distress, she can only utter 2-3 words at a time, as you approach the bedside you notice a thin bead of sweat between the patient’s eyebrows and a flushed face. bp:188/95 rr:35 p:135 t:37.6 sao2:95%. Physical examination: distress and sweating; HEENT: full moon face, congestion, airway assessment Mallampati class I (laryngoscopy easier); CVS: hyperdynamic, no murmur; Resp: auxiliary respiratory muscle movement ++, prolonged expiratory phase, bilateral diffuse polyphonic croup; pulsus paradoxus = 15 mmHg; peak flow 150 L/min (moderate exertion); ABD: no abnormality; Neuro: awake, anxious
What should be done next? (choose 1 of the following 5 options)
A: salbutamol (MDI/Neb) 2.5 mg q20 min x 3 times, reassessed after 1 hr
B: salbutamol (MDI/Neb) 2.5 mg q20 min x 3 doses with immediate addition of methylprednisolone 125 mg IV
C: aminophylline 5 mg/kg IV for 30 min and add salbutamol (MDI/Neb) 2.5 mg q20 min x 3 times, reassessed after 1 hr
D: prescription of MgSO4 1 gm (8 mmol) IV 20 min x 2 times with helium-oxygen mixture (Heliox) 60:40
E: Isoproterenol (Buscopan 10 mg p.o. q6h prn) infusion 0-10 ug/min, dose adjusted according to clinical response
Ans: Early failure to use corticosteroids and conventional Beta-2 agonists in severe asthma (i.e., peak expiratory flow < 250 L/min) may be an important cause of death in asthmatic patients. A meta-analysis of more than 700 articles (including 30 RCTs) showed that intravenous or oral corticosteroids (prednisone ≥30 mg or equivalent other hormone q6h) clearly reduced hospitalization and relapse rates. There is evidence that corticosteroids can enhance the efficacy of Beta-2 agonists and reduce acute hypersensitivity reactions. According to the National Asthma Education Program Expert Committee, aminophylline alone is only 1/4 as effective as a potent Beta agonist, and when combined with Beta agonists, aminophylline may increase side effects (tachyarrhythmias, seizures, nausea, diarrhea, etc.) without enhancing bronchodilation. Methylxanthine does not relieve airflow obstruction in adults or children on repeated Beta agonist bronchodilators. Theophylline has the narrowest therapeutic index of all commonly used drugs, and MgSO4 and heliox are unproven therapeutic measures. Although some experts believe that these treatments can be effective adjuncts, there is a lack of evidence to support their use. The current view of acute asthma is that bronchospasm is only the initial manifestation, lasting approximately 1 hour, followed by 3-8 hours of airway inflammation. The history shows that this patient had a clear diagnosis of inflammatory response and therefore responded poorly to bronchodilator medication. Indeed, aggressive bronchodilator therapy may result in a decrease in PaO2, possibly related to the suppression of the hypoxic pulmonary vasospastic response localized to poor ventilation. There is evidence that untimely anti-inflammatory therapy in early asthma can lead to an increased risk of death. This female patient was not an exception. Due to the lack of data confirming its efficacy and multiple reports of lethal arrhythmias, myocardial ischemia and lethal myocardial necrosis due to isoproterenol. Therefore it has been discontinued in almost all cases. More seriously, isoprenaline has a strong vasodilating effect and can exacerbate hypotension in patients already in relative hypovolemia (reduced intake, increased nondescript loss, endogenous PEEP, etc.). The effect of any parenteral bronchodilator is questionable except in cardiac arrest, and Bloomfield et al. found a similar improvement in peak expiratory flow rate (PEFR) with 0.5 mg salbutamol IV compared with 0.5 mg nebulized inhalation in a double-blind poorer trial (22 patients). However, it significantly reduced the odd pulse (pulsus paradoxus) and reduced tachyarrhythmias due to nebulized medication.
It’s obviously not your day (it’s 4:00 am, isn’t it?) The patient gradually quieted down with strong bronchodilators and hormones.
Physical examination: unconscious; odd pulse 8 mmHg; absent croup, breath sounds difficult to hear; marked thoracoabdominal paradoxical breathing. bp:166/80 rr:44 p:155 t:37.6 sao2:89%
What should be done now?
A: Determine arterial blood gas analysis and start IV infusion of salbutamol (500 ug IV for 3 min)
B: Determine peak flow – if below 100 l/min, prepare for tracheal intubation/invasive mechanical ventilation
C: Observe for another hour – hormone takes several hours to take effect
D: Immediately prepare for endotracheal intubation
E: Start non-invasive positive pressure ventilation (BiPAP) to avoid tracheal intubation
A: The patient’s clinical manifestations undoubtedly suggest respiratory failure and the need for immediate tracheal intubation. These manifestations include: special position, sweating, inability to speak, gradual “silent chest” suggesting little airflow; other clinical manifestations suggesting fatigue with a sudden decrease in the odd pulse, which suggests that the patient’s intrathoracic pressure is insufficient for airflow; deterioration in the level of consciousness without sedation. Thoraco-abdominal paradoxical breathing and paramedian respiratory muscles are involved. Other manifestations: inability to remain in a flat position despite treatment, profuse sweating, inability to speak, progressive tachycardia and increased odd pulse; the patient also needs to be checked for signs of pneumatic injury/leakage leading to sudden deterioration.
Physical examination
No response except for painful irritation; oropharynx Mallampati class I
A reasonable protocol for airway management should be
A: awake intubation via fibrinoscopy, preserving spontaneous breathing to avoid hypoxia and prevent more severe bronchospasm from stimulation during conventional laryngoscopic manipulation
B: Rapid sequential induction with preoxygenation with 100% pure oxygen, cricoid cartilage compressions, application of lidocaine 1 mg/kg, ketamine 1.5 mg/kg, succinylcholine
(succinylcholine) 1 mg/kg
C: slow induction, i.e., propofol 0.5 mg/kg repeated intravenous infusions until manual ventilation is easy, followed by IV succinylcholine to relax chest wall muscles
D: morphine 2.5 mg IV infusion followed by pancuronium bromide 10 mg IV infusion
Ans: All patients in the emergency room are under extreme physiological stress. The stomach is full of contents and in an acidic environment, regardless of the time of the last meal. The classical approach at this point is to use rapid sequential induction (hypnotic medication followed immediately by fast-acting inotropic medication) with cricoid cartilage compression to avoid airway contamination and inadvertent aspiration. If a difficult airway is anticipated, awake and spontaneous breathing techniques (often via fiberoptic laryngoscopy) are often used. Tracheal intubation via fiberoptic bronchoscopy is not the preferred method of tracheal intubation in this patient, and although some physicians are skilled at performing tracheal intubation via fiberoptic bronchoscopy, it usually takes 10-15 minutes to complete. This patient is about to go into respiratory arrest, and the hypoxia is already very severe! Second, even with careful surface anesthesia, airway irritation is inevitable and may exacerbate bronchospasm. Morphine at a dose of 2.5 mg has no amnestic effect and is likely to fail to reduce the characteristic airway hyperresponsiveness of asthmatics. Another reason to avoid pushing morphine is that it may lead to histamine release and thus exacerbate bronchospasm. During tracheal intubation, pancuronium is not the ideal choice of inotropic drug. It has a slow onset of maximal efficacy (4-5 min), a long interval for incomplete inotropy, the possibility of progressive hypoxia if ventilation is not performed, the possibility of aspiration during ventilation, and the strong vagal blocking effect of pancuronium, which may lead to tachyarrhythmias.
Obviously you made the most prudent choice, but unfortunately the patient went into cardiac arrest immediately after intubation …… Repeat laryngoscopy to confirm tracheal intubation position
Physical examination
ECG shows narrow QRS waves, heart rate 150/min; bilateral hypopnea and jugular venous filling (up to the angle of the jaw)
Targeted treatment should include
A: Immediate defibrillation to restore cardiac rhythm and ensure perfusion
B: Intensive manual ventilation to correct hypoxia and CO2 retention
C: Chest compressions to support circulation, IV epinephrine, and rapid fluid infusion while ventilation is stopped for 30 seconds and perfusion status is observed
D: Salbutamol 5 mg administered via tracheal intubation
E: Respiratory perfusionist helps to establish femoral vein-femoral vein cardiopulmonary bypass (VA-ECMO)
A: This is a PEA (pulseless electrical activity), indicating negligible cardiac output. However, based on the heart rhythm you determine that there should be some perfusion. The etiology includes structural and metabolic. The focus is on diagnosis and treatment of the etiology, as well as circulatory and neurological support through CPR and epinephrine. Electrical defibrillation is rarely applied. Reasons for pulseless electrical activity at the start of positive pressure ventilation often include: dynamic overfilling/endogenous PEEP, sedation-induced vasodilation, and relative hypovolemia; hyperventilation after tracheal intubation may exacerbate pre-existing gas trapping (secondary to airway edema/mucus plug), resulting in very high intrathoracic pressure with minimal venous return and therefore very low cardiac output; prolonged expiratory time may allow lung emptying to residual air volume level (when ventilating with pure oxygen), which is diagnostic if perfusion pressure is quickly restored.
You’re a smart kid, aren’t you? This method did not work
pulse: absent; blood pressure: undetectable; heart rhythm: wide QRS wave, HR 38/min, no p wave; patient’s whole body has turned dark gray-blue
Physical examination: the patient’s eyelids, lips and neck are visibly swollen
What to do?
A: Place bilateral chest tubes after placing 14 G catheters in the second intercostal space in the midclavicular line
B: Immediate CXR check for etiology
C: High-dose epinephrine (0.1 mg/kg) for vasoconstriction/bronchodilation
D: isoproterenol infusion at a dose of 10 ug/min
E: Immediate open-chest cardiac massage under direct vision (extracardiac compressions are not effective in such patients with overfilled lungs)
Ans: In clinical practice, bilateral tension pneumothorax is sometimes difficult to distinguish from dynamic overfilling (very low breath sounds bilaterally, centered trachea, elevated jugular venous pressure), therefore, if there is no response after a short period of termination of ventilation, the most rapid method of empirical chest drainage is indicated, and the chest tube should be left in a water-sealed bottle with negative pressure maintained at -10 cmH2O until the chest radiograph confirms that the lungs have re-inflated and there is no persistent gas Exposure. Intravenous epinephrine has a very strong bronchodilating effect and can significantly improve the outcome of CPR by redistributing blood flow to the cardiovascular bed; however, this dying patient in cardiac arrest required more targeted treatment. Due to the lack of data confirming its efficacy and the multiple reports of lethal arrhythmias, myocardial ischemia and lethal myocardial necrosis. Therefore, isoprenaline is no longer used in almost all cases. More seriously, isoprenaline has a strong vasodilating effect and can exacerbate hypotension in patients already in relative hypovolemia (reduced intake, increased nondisplaced loss, endogenous PEEP, etc.). In fact, CPR is more effective in patients who are overfilled because large fluctuations in intrathoracic pressure are better transmitted to the vessels. The American Heart Association does not consider persistent asthma as an indication for open-heart cardiac massage
You finally make it through, but the patient is still not out of danger.
The patient does not respond to verbal stimuli, but exhibits limb flexion and slow eye opening with painful stimuli; you can easily see the auxiliary respiratory muscles involved in the respiratory maneuver and there is still thoracoabdominal paradoxical breathing; the ventilator high pressure alarm often sounds (sometimes the peak inspiratory pressure can be as high as 90 cm H2O)
Physical examination
P94, sinus; BP 85/44; SpO2 86%
In addition to continued fluid resuscitation and aggressive bronchodilator/anti-inflammatory therapy, the next logical step in treatment should be
A: pancuronium (pancuronium) 5 mg IV push followed by continuous IV infusion 5 mg/hr with fentanyl (fentanyl) 25 μg IV/hr for sedation
B: Sedation with intravenous ketamine, propofol, or midazolam/fentanyl, followed by continuous inotropic medication as appropriate, followed by a permissive hypercapnic ventilation strategy
C: Increase minute ventilation to 13.5 lpm (50% increase from 9 lpm) to normalize PaCO2 and pH
Adjust midazolam dose according to efficacy, and IV morphine 50 ug/kg, with inotropes as necessary to achieve normal PaCO2 and minimal plateau pressure
D: Sedation and inotropes are administered only when necessary. Reduce the minute ventilation to less than 100 ml/kg/min and maintain the plateau pressure below 30 cmH2O. Apply exogenous PEEP (20% higher than endogenous PEEP) to avoid small airway collapse and gas trapping
E: Immediate bilateral alveolar bronchial lavage to aid sputum clearance
Ans: There is no significant difference in the clinical prognosis and complications of this patient with any mode of controlled ventilation (assisted controlled ventilation, pressure controlled ventilation, synchronized intermittent command ventilation, pressure-regulated volume-controlled ventilation), and the mode most familiar to your ward should be used. Deep sedation before deciding to start inotropic ventilation (no evidence yet on which drug is better) is important due to concerns that patients may be awake, increased incidence of deep vein thrombosis/pulmonary embolism and significant muscle atrophy. Setting exogenous PEEP at approximately 20% below endogenous PEEP reduces inspiratory work in patients with severe airflow obstruction and distal airway collapse (COPD) by a complex mechanism, but it is assumed that exogenous PEEP keeps the distal airway open to avoid gas trapping in overcompliant lung tissue. However, in patients with asthma, where the distal airways are stiffer than normal, any exogenous PEEP can lead to further lung volume increase, hemodynamic disturbances, and barotraumatic injury; therefore, exogenous PEEP is best set to 0. Although a few case reports have shown significant improvement in diffuse mucus plug in patients with intractable asthma who did not undergo tracheal intubation and underwent bilateral alveolar bronchial lavage (BAL). However, fiberoptic bronchoscopy occupies a large portion of the cross-sectional area of the tracheal intubation (and also produces airway irritation!) This is very dangerous for this patient who is difficult to ventilate effectively and has CO2 trapping.
What are the appropriate ventilator parameters to achieve this goal?
Tidal volume 8 ml / kg Inspiratory flow 80 l / min Respiratory rate 12 brths / min PEEP: 0 Flow time waveform: square
The patient’s condition improved: the patient’s SBP increased to 120, urine output increased to 100 ml in the previous hour, and her limbs were warm and red. No signs of subcutaneous emphysema, bilateral respiratory sounds are symmetrical. ECG is normal sinus rhythm with no ectopic rhythm. saO2 96%, ABG: pH 7.32, PaO2 87, PaCO2 50. spO2 96%; BP 134/88; P 88, sinus; peak pressure 40; plateau pressure 28. patient is easily aroused and neuromuscular function returns to normal. The patient tolerated controlled ventilation well and his spontaneous breathing disappeared.
Practical and effective methods to monitor dynamic overfilling or endogenous PEEP in this patient include.
A: Addition of exogenous PEEP to determine the lowest PEEP that resulted in elevated peak airway pressure
B: Based on peak airway pressure
C: Determining the total amount of expiratory air from end-inspiration to FRC during a 20-60 second period of asphyxia
D: Periodic measurement of esophageal pressure changes at the termination of expiratory flow
E: Determine the plateau pressure under normal ventilation and then again after 20 seconds of asphyxia and calculate the difference between the two
Ans: VEI > 20 ml/kg is a good predictor of pneumatic injury. Peak airway pressure is not related to endogenous PEEP because the pressure-volume relationship in the lung is not linear at high volumes. Periodic measurement of esophageal pressure changes at expiratory flow termination in spontaneously breathing patients allows estimation of endogenous PEEP. because if a patient is spontaneously breathing, a high enough negative intrathoracic pressure needs to be generated to overcome endogenous PEEP, thus creating an airway-alveolar pressure difference that allows gas flow. However, the expiratory muscles are often involved in these patients, which affects the accuracy of the aforementioned measurement method, and thus has been rarely used.
Early the next morning (wait…it’s early morning now, right?) …… The patient had normal blood gas results, was conscious, had a spirometry of 1.4 L, and a maximum inspiratory pressure (MIP) of -40 cmH2O. 24 hours later the tracheal tube was successfully removed and the patient was transferred to the general ward 72 hours after admission. One week later, the patient was discharged home with a tapered corticosteroid dose.
Related Knowledge.
Learn about magnesium and helium oxygen mixture (Heliox) for asthma
IV Magnesium sulfate inhibits acetylcholine release at the neuromuscular junction, thereby relieving bronchospasm caused by increased sympathetic tone. Seven clinical trials have confirmed the clinical efficacy of magnesium sulfate, but all were clinical observations with a small number of patients. Only one double-blind randomized clinical trial (48 patients divided into 3 groups: 2 gm IV push for 2 min followed by continuous infusion, or IV push only, or saline control) found that the addition of magnesium sulfate to Beta agonist therapy did not significantly improve pulmonary function; however, female patients showed a trend toward improvement. The clinical significance of this finding and the place of magnesium sulfate in the management of acute asthma is unclear. Because of the few toxic side effects of magnesium sulfate (mild vasodilatory effect and enhanced neuromuscular blockade at high doses or rapid infusion) some physicians use it as an adjunctive therapy when conventional treatment does not respond. Only one clinical observation has described the use of a 60:40 helium-oxygen mixture in 7 asthmatic patients with tracheal intubation, with a significant increase in pulmonary compliance and a significant reduction in airway resistance within minutes of application (mean airway pressure decreased by 33 cmH2O and PaCO2 decreased by 35.7 mmHg). Further research is needed on the safe use of helium-oxygen gas mixtures
The value of arterial blood gas analysis in patients with severe asthma
In a patient with severe asthma whose condition has progressively deteriorated after treatment, the significance of arterial blood gas analysis is to document the severity of hypoxemia and respiratory alkalosis/acidosis. However, this patient is deteriorating rapidly and the results of arterial blood gas analysis will not change the current treatment. Hypercapnia alone is not an indication for tracheal intubation: many patients with hypercapnia have a clinical course similar to that of patients with normal PaCO2 and are able to avoid positive pressure ventilation with the strongest pharmacological interventions. Also, the absence of hypercapnia has a low expectation of negativity for mechanical ventilation. In patients with adequate peripheral perfusion, pulse oximetry can be prepared to provide continuous information about arterial oxygenation. The point is that it is dangerous to delay effective supportive therapeutic measures (airway control, positive pressure ventilation, continuation of aggressive bronchodilator drugs and anti-inflammatory therapy) when the diagnostic information provided by blood gases does not change the therapeutic decision!
Significance of peak expiratory flow measurement in patients with severe asthma
Objective evaluation of airflow obstruction often requires bedside measurements of FEV1 and/or PEFR, and can be used as a guide for initial treatment of mild to moderate bronchospasm (PEFR > 25% of normal) and assessment of response to therapy. In persistent asthma (severe patients who do not respond to treatment), PEFR measurement can exacerbate airway obstruction and even induce respiratory arrest. The point is that it is dangerous to delay effective supportive treatment measures (airway control, positive pressure ventilation, continuation of aggressive bronchodilator drugs and anti-inflammatory therapy) when the diagnostic information provided by peak flow measurement does not change the treatment decision!
The role of Bi-PAP in the treatment of asthma
CPAP or BiPAP (together called “non-invasive positive pressure ventilation”) has been successfully used for the short-term treatment of persistent asthma with significant improvement in dyspnea and airflow/gas exchange. However, this patient is currently in a near-death state, unconscious and on the verge of respiratory exhaustion, at which point noninvasive ventilation is an absolute contraindication. Many physicians believe that BiPAP improves airway collapse in the distal expiratory phase and avoids exacerbating the dynamic overfilling/gas trapping characteristic of asthmatics, thereby reducing respiratory effort.
More details on rapid sequence induction during persistent asthma
IV Magnesium sulfate inhibits acetylcholine release at the neuromuscular junction, thus relieving bronchospasm due to increased sympathetic tone. Magnesium sulfate also inhibits calcium channels in respiratory smooth muscle, and seven clinical trials have confirmed the clinical efficacy of magnesium sulfate, but all were clinical observations with small numbers of patients. Only one double-blind randomized clinical trial (48 patients divided into 3 groups: 2 gm IV push for 2 min followed by continuous infusion, or IV push only, or saline control) found that the addition of magnesium sulfate to Beta agonist therapy did not significantly improve pulmonary function; however, female patients showed a trend toward improvement. The clinical significance of this finding and the place of magnesium sulfate in the management of acute asthma is unclear. Due to the few toxic side effects of magnesium sulfate (mild vasodilatory effect and enhanced neuromuscular blockade at high doses or rapid infusion), some physicians use it as an adjunctive therapy when conventional treatment does not respond, and only one clinical observation has been described in seven asthmatic patients with tracheal intubation using a 60:40 helium-oxygen mixture, with a significant increase in pulmonary compliance and a significant reduction in airway resistance within minutes after application (mean The helium oxygen mixture was used in seven patients with asthma.) Further research is needed on the safe use of helium-oxygen gas mixtures.
Myopathy associated with neuromuscular blocking drugs in patients with asthma
In a study by Douglas et al. 19 of 25 patients mechanically ventilated with persistent asthma had elevated serum CK levels and 9 (36%) developed clinically significant myopathy. 22 patients on vecuronium had significantly longer duration of mechanical ventilation in all patients with elevated CK, regardless of whether they had significant myopathy. In a retrospective study of 90 mechanically ventilated patients, 14 (16%) developed significant quadriplegia, and all patients with this complication were on inotropic medication. No correlation was found between neuromuscular blocking drugs (i.e., steroid nucleus [steroid nucleus] and benzylisoquinolinium [benzylisoquinolinium]). None of the patients with hormone application alone (regardless of dose) showed clinical or EMG manifestations of myopathy and normal myokines. The current animal studies suggest that allowing intermittent recovery of neuromuscular junction activity (avoiding continuous infusion of inotropic drugs) may help prevent myopathy, but this has yet to be confirmed in clinical trials. Most physicians will use inotropic drugs if the patient continues to experience human-computer incoordination during deep sedation or is too hemodynamically unstable to tolerate deep sedation
Strategies for mechanical ventilation in patients with asthma
The key to a mechanical ventilation strategy to limit dynamic hyperinflation (DH) is to keep Te (expiratory time) as long as possible, most effectively by reducing Ve (minute ventilation), which is directly related to the degree of dynamic hyperinflation. Reducing Ve does not necessarily lead to hypercapnia, as it may simultaneously reduce dead space ventilation in overfilled lung tissue; however, PaCO2 is usually elevated, allowing it to rise no more than 90 mmHg and maintaining a systemic pH >7.2 (with alkaline supplementation if necessary), known as permissive hypercapnia. Although permissive hypercapnia is well tolerated by most patients, it should not be used in patients with severe pulmonary hypertension, elevated cranial pressure, decreased myocardial contractility, and ventricular arrhythmias, and permissive hypercapnia does not improve the clinical prognosis of patients with persistent asthma; however, historical analysis has shown that since the widespread implementation of this strategy, the mortality rate in patients with persistent asthma receiving mechanical ventilation has decreased to almost However, historical analysis shows that since the widespread implementation of this strategy, the mortality rate in patients with persistent asthma receiving mechanical ventilation has decreased to almost zero.