a. Ketamine.
b.Thiopentone.
c.Ether.
d. N2o
Ans: A
Thiopental: Controversy exists over the ability of thiopental to constrict the airways when given in lower doses.
Large doses may block bronchospasm induced by an irritating ETT but increase the risk of hypotension.
Although perhaps suitable for the elective intubation of a stable asthmatic, it may not be appropriate for a patient with severe status.
Ketamine: Ketamine causes bronchodilation predominantly due to its sympathomimetic effects. Inhibition of vagal pathways and direct relaxation of smooth muscle are other possible mechanisms of action.
It has been used successfully for intubation of asthmatic patients and to improve bronchospasm in ventilated and non ventilated patients. Exercise caution with regards to its cardiovascular effects when used with other sympathomimetics.
Many would consider this the induction agent of choice.
Oxygen should be administered to maintain normal saturations. Only those patients with chronic severe asthma and chronic hypercarbia are at risk for increasing hypercarbia with oxygen administration.
It is clear that the mainstays of acute asthma treatment are the b2 agonists. Appropriate MDI dosing is 4 - 20 puffs salbutamol per hour.
Inhaled bronchodilators can be given by MDI or by WN. Considerable drug is wasted with WN as the predominant part of respiration is expiration hence as little as 1% of drug may actually reach the lungs.
A large amount of drug (5-10 mg salbutamol) should be therefore be given frequently (q 15-30 min.).Salbutamol may be given continuously by WN although this may increase risk for toxicity.
Whether intubated or not, the dosing of b2 agonists should be "titrated to effect" using objective and clinical signs of airflow limitation.
Anticholinergic agents, although not first line therapy may be of benefit in mild to moderate asthma, and should be used, in addition to b2 agonists in severe asthma.
In the severely obstructed patient drug deposition tends to be in the more proximal airways which is where cholinergic receptors are located. Ipratropium may be given by MDI (4-8 puffs q15 min.) or by WN (0.25-0.5 mg).
The maximum effect is probably reached with 0.5 mg, although more may be required in ventilated patients.
Glycopyrrolate and atropine both produce bronchodilation if given IV (atropine 20 mg/kg, glycopyrrolate 10 mg/kg), although there is a high incidence of side effects. They may also be nebulized (glycopyrrolate 1.0 mg, atropine 1.2-2.0 mg) which diminishes the incidence of side effects, particularly with glycopyrrolate.
Corticosteroids are invaluable in acute asthma but take 6-12 hours to show an effect - so give early!
Methylprednisolone has less mineralocorticoid activity and is cheaper than hydrocortisone.
Dexamethasone is cheaper again. Doses shown to be effective are 10-15 mg/kg/day of hydrocortisone or its equivalent (120-180 mg methylprednisolone/day, i.e. 40mg q6h). There may be slight improvements with 125 mg q6-8h. Smaller doses may be as effective although firm data is not available.
There is no role for inhaled steroids during an acute severe asthma attack.
Aminophylline is second line therapy. It is a weak bronchodilator, has a low therapeutic index, and a high incidence of potentially serious side effects.
A recent meta anlaysis and several subsequent studies have not shown significant improvement in PFT's when aminophylline is added to conventional treatment (b2 agents plus steroids).
Although it has little additive bronchodilatory effect, its other possible actions including increased diaphragm contractility, diuresis, mucociliary clearance, and antiinflammatory action may offer some benefit. If other first line therapy has been unsuccessfully tried, some clinicians will add aminophylline (loading dose of 3-6 mg/kg, infusion of 0.2-0.9 mg/kg/hr).
Magnesium Sulfate: There are several small studies that demonstrate improved bronchodilation with the addition of intravenous magnesium to conventional therapy. Overall, most studies show only modest improvements in PFT's, and there are also some negative studies.
In the doses given (10-12 mmol/20 min) it appears to be a relatively safe agent and can be considered in those not responding to conventional treatment.
Magnesium inhibits catecholamine induced arrhythmias. In theory it may not only improve the efficacy of b2 agonists, but also their safety.
Cromolyn and Nedocromil prevent the release of mediators from mast cells. They are of no benefit during an acute asthma attack although they may be of use in the preoperative preparation of a known asthmatic. They are devoid of any significant cardiovascular effects.
Intubation
With early and aggressive management the majority of asthma attacks can be managed without the need for intubation and ventilation.
Ventilation can be life saving but there is an associated high incidence of morbidity and mortality. Williams has reviewed 28 publications on ventilation in asthma and found a range of mortalities from 0-38% (mean 13%).
Mortality and morbidity figures seem to be decreasing in recent years with the advocation of controlled hypoventilation.
The decision as to who and when to intubate is more of an art than a science.
--Progressive exhaustion,
--Respiratory arrest,
--Decreased level of consciousness,
--Persistent respiratory acidosis (pH<7.2), AND
--UNREMITTING HYPOXEMIA (SATS<90) ARE CLEAR INDICATIONS FOR INTUBATION.
Hypercarbia, although a marker of severe disease, is not an indication for intubation and ventilation. Studies show that the majority of patients with hypercarbia will improve with aggressive use of bronchodilators.
Recommendations vary regarding the optimum route and technique of intubation. Intubation can be a marked stimulus for bronchospasm. This may be diminished with "deep" anesthesia rather than just "light" sedation.
When positive pressure is initiated the markedly negative pleural pressures seen during spontaneous inspiration will become positive, venous return drops, and precipitous hypotension may occur.
This can be aggravated by induction agents.
Large bore IV's should be in place (some advocate fluid bolusing prior to intubation) and vasopressors should be immediately available.
It would seem reasonable to avoid agents that may release histamine.
A large ETT is preferred to facilitate suctioning and possible bronchoscopy. Once intubated, many patients will require sedation and paralysis.
Thiopental: Controversy exists over the ability of thiopental to constrict the airways when given in lower doses.
Large doses may block bronchospasm induced by an irritating ETT but increase the risk of hypotension.
Although perhaps suitable for the elective intubation of a stable asthmatic, it may not be appropriate for a patient with severe status.
Ketamine: Ketamine causes bronchodilation predominantly due to its sympathomimetic effects. Inhibition of vagal pathways and direct relaxation of smooth muscle are other possible mechanisms of action.
It has been used successfully for intubation of asthmatic patients and to improve bronchospasm in ventilated and non ventilated patients. Exercise caution with regards to its cardiovascular effects when used with other sympathomimetics.
Many would consider this the induction agent of choice.
Lidocaine: Intravenous lidocaine can reduce irritant induced bronchospasm by blocking airway reflexes (1-2 mg/kg). IV infusions of 1-4 mg/min. may also be helpful. Topical application may induce bronchospasm.
Propofol: Propofol's effect on airway tone and reactivity are not clear. There are case reports of its successful use in decreasing bronchospasm in ventilated COPD patients (? direct smooth muscle relaxation). It may be preferable to thiopental for induction and a good choice for sedation of the ventilated asthmatic patient.
Anticholinergics: As discussed above the anticholinergic agents (ipratropium and glycopyrrolate) may help block irritant induced bronchospasm via either the IV or inhaled routes (less side effects).
Benzodiazepines: Benzodiazepines are commonly used for intubation and sedation and appear to be safe.
Narcotics: With the usual caveat of avoiding histamine release there appears to be no major concern with the use of narcotics as an adjunct to intubation or sedation.
Neuromuscular Blocking Agents: NMBs can theoretically induce bronchospasm by inducing histamine release or by reacting with muscarinic receptors. It has been suggested that those NMBs that cause histamine release (dtc, atracurium), or that block M2 muscarinic receptors be avoided in the treatment of the acute asthmatic.
There has been recent concern over profound muscle weakness developing in asthmatic patients who have received both NMBs and corticosteroids. Although guidelines do not exist, it would be prudent to monitor CPKs, and to minimize the dose and duration of administered NMBs.
Cholinesterase inhibitors may provoke bronchospasm by increasing acetylcholine at parasympathetic nerve terminals. Muscarinic receptor antagonists can prevent this, although it may be advisable to avoid using cholinesterase inhibitors if possible.
Ventilation
The goals of mechanical ventilation in acute asthma are to oxygenate, rest the patient, rest the respiratory muscles, correct acidemia, and do no harm.
Most of the morbidity and mortality that occurs in ventilated asthmatics are related to the consequences of "dynamic hyperinflation" (DHI). This occurs as a consequence of severe airflow obstruction leading to excessive positive end expiratory pressure within the lungs (auto-PEEP).
The result is barotrauma (pneumo-mediastinum, pneumothorax, air embolism, etc.), and volutrauma (decreased venous return and increased RV afterload leading to hypotension and shock).
Darioli and Perret achieved 100% survival in their series of 34 patients using the concept of "controlled hypoventilation".
Their goals of treatment were to keep:
1, Peak inspiratory pressures (PIP) < 50 CM H2O (TO AVOID BARO/VOLUTRAUMA)
2. MAINTAIN NORMAL OXYGENATION, AND
3. TO ACCEPT HYPERCARBIA IF NECESSARY.
THE SUCCESS OF THIS APPROACH HAS LED TO MANY RECOMMENDATIONS TO KEEP PIP BELOW 50 CM H2O. Others feel that due to high airway resistance PIP was a poor predictor of alveolar pressures and of subsequent barotrauma, and that controlled hypoventilation decreases barotrauma due to it's effect on DHI rather than PIP. If this is true, attention should therefore be paid to measures of DHI rather than PIP.
Hypercarbia and subsequent acidosis are usually well tolerated.
In theory, respiratory acidosis may cause myocardial depression and increased CBF (which may be inappropriate in a patient suffering from hypoxia brain injury).
The acidosis can be treated with bicarbonate (? treat pH < 7.2).
BICARBONATE ADMINISTRATION UNFORTUNATELY INCREASES CO2 PRODUCTION (? CLINICAL SIGNIFICANCE), INCREASES INTRACELLULAR ACIDOSIS, AND CAN POSSIBLY CAUSE METABOLIC ALKALOSIS WHEN THE CO2 IS CORRECTED.
Tuxen et al have described a relatively simple way of estimating DHI.
They measured the volume of gas that was exhaled during a prolonged apnea (40-60 sec) following a normal ventilator delivered tidal breath. This "volume at end inspiration" (VEI) appears to reflect the severity of DHI (composed of tidal volume and trapped gas). They found that VEI was more predictive of barotrauma than PIP.
The most critical factor in determining DHI was minute ventilation (VE).
Decreasing the inspiratory flow rate (VI) decreased PIP, but the subsequent obligatory shortening of expiratory time caused an increase in Pplat, VEI, and DHI.
Slowing the respiratory rate, or increasing VI prolonged expiratory time (TE) and decreased DHI.
It can be misleading to focus on I:E ratios rather than TE. For example, a patient with a VE of 15 lpm (VT1000 x 15) and VI of 60 lpm has an I:E ratio of 1:3.
Increasing VI to 120 lpm will impressively increase the I:E ratio to 1:7 but only increase TE from 3 to 3.5 seconds.
Decreasing the respiratory rate to 12 and maintaining the VI at 60 will "only" improve the I:E to 1:4 but will increase TE to 4 seconds.
PEEP: The role of PEEP in acute asthma is controversial. There are both positive and negative case reports.
In theory PEEP will splint open airways during exhalation. If the applied external PEEP is less than auto-PEEP there should be little increase in alveolar pressure, and obstructed units could empty due to decreased dynamic airway compression. The risk is increased DHI. Overall there is little evidence to support use of PEEP in the sedated, paralyzed, mechanically ventilated patient. There may be an advantage to using low to moderate levels of PEEP in spontaneously breathing patients as it decreases WOB.
Initial respirator settings may be as follows:
· FiO2 = 1.0
· Tidal volume = 6-8 ml/kg
· Rate = 6-8/min.
· Inspiratory flow = 60-100 lpm
· PEEP < 5 CM H2O
· Keep PIP < 50 CM H2O
· Square wave flow (increases VI)
On occasion profound hypotension will occur with ventilated asthmatic patients. This may be a result of barotrauma (pneumothorax) or volutrauma. If due to the latter, disconnecting the patient from the ventilator (apnea) may reduce the DHI and the BP should improve.
After intubation it may be physically impossible to ventilate a patient. The position and patency of the ETT should be determined and pneumothorax ruled out. If severe bronchospasm is the likely problem then adrenaline can be administered via IV or ETT. If related to extreme hyperinflation then repeated intermittent chest compression during expiration may increase exhaled gas volume and decrease DHI
