Normal VC is approximately 60 mL per kg. Inspiratory capacity IC is the maximum amount of gas that can be inhaled from the resting expiratory position afte r a normal exhalation.
Normal IC is 3, Functional residual capacity FRC is the remaining lung volume at the end of a normal quiet expiration. Normal FRC is 2,mL. Total lung capacity TLC is the lung volume at the end of a maximum insp iration. It is the sum of VC and RV. Normal TL C is 5, to 6, mL. Lumb AB. Nunn's applied respiratory physiology , 6th ed. Philadelphia: Elsevier Butterworth- Heinemann, — What are flow—volume loops? Draw flow—volume loops in a healthy subject, in a patient with COPD, and in a patient with restrictive lung disease.
Flow—volume loops provide a graphic analysis of flow at various lung volumes. This is immediately followed by maximum inhalation as fast as possible back to TLC Fig. This ratio is particularly useful in identifying the presence of upper airway obstruction. In patients with restrictive lung disease such as pulmonary fibrosis and scoliosis,. The TLC is markedly reduced, and. A variable obstruction is defined as a lesion with influence that vari es with the phase of respiration.
In variable extrathoracic obstructions such as vocal cord paralysis or tracheal stenosis, during forced inspiration the respiratory flow is reduced because the negative transmural pressure inside the airway tends to collapse the airway.
During expiration, the expiratory flow is reduced far less and may be normal because the positive pressure inside the airway tends to decrease the obstruction Fig. On the contrary, in variable intrathoracic obstruction, the expiratory flow is markedly reduced because the high positive intrapleural pressures during forced expiration decrease airway diameter, and the inspiratory flow is far less reduced because the negative intrapleural pressure tends to increase the diameter of the airway.
Also see Fig. Goudsouzian N, Karamanian A. Physiology for the anesthesiologist , 3rd ed. Norwalk, CT:. Appleton-Century-Crofts, — Miller RD, ed.
Miller's anesthesia , 6th ed. Philadelphia: Elsevier Churchill Livingstone,. Define closing capacity CC and closing volume CV. What is the normal value of CV? CC is the lung volume at which the small airways in the dependent parts of the lung begin to close. CV is the gas volume expelled during phase IV of the single-breath nitrogen test; it denotes the lung volume from the beginning of airway closure to the end of maximum expiration.
CV and CC increase with age. CV is increased in patients with small airway disease and in chronic smokers. Buist AS. The single-breath nitrogen test. N Engl J Med ; Closing volume [Editorial].
Lancet ; Philadelphia: Elsevier Butterworth- Heinemann, FRC is either independent of age in adults or increases very slightly with age, increasing by around 16 mL per year. CC, however, increases with age. Normally, CC becomes equal to FRC at the age of 66 in the upright position and at the age of 44 in the supine position. CC, on the other hand, is independent of body position.
It is important to remember that the effects of age on CC and posture on FRC determine whether airway closure exists. Philadelphia: Elsevier Butterworth- Heinemann, , Airway closure.
This is due to changes in the chest wall shape and diaphragm position. After induction of general anesthesia, a reduction occurs in the cross- sectional area of the rib cage corresponding to a decrease in lung volume of approximately mL. Recent studies have consistently shown a cephalad movement of the dependent regions of. However, the change in. FRC that can be ascribed to changes in diaphragm is on average less than 30 mL. Contribution of the closure of pulmonary units to impaired oxygenation.
Pag e 11 of Closing capacity measurements during general anesthesia. Closing capacity in awake and anesthetized-paralyzed man. J Appl Physiol ; Why is the FRC im portant in oxygenation? First, when FRC is decreased to below CC, airways close in the dependent parts of the lung during certain periods of normal tidal ventilation. Airway closure results in shunting of pulmonary blood flow through the unventilated alveoli. Second, pulmonary circulation and alveolar gas exchange are continuous during both inspiratory and expiratory phases of respiration.
Irrespective of whether there is airway closure or not, blood oxygenation during the expiratory phase is mainly dependent on the remaining lung volume, which is FRC.
Therefore, when the FRC is high, blood oxygenation is better and there is more time for oxygenation before hypoxemia occurs during apnea. FRC is decreased in the supine position during general anesthesia and in patients with acute respiratory distress syndrome.
Are there methods to m easure FRC and closing volume? FRC may be measured by helium dilution, nitrogen washout, and body plethysmography. CV may be determined by two techniques, the single-breath nitrogen test residual gas technique and the bolus technique with an inert tracer gas such as helium, xenon, or argon.
Philadelphia: Elsevier Butterworth- Heinemann, —37, 52— What are their normal values? Pag e 12 of Interpret the following arterial blood gases: pH, 7.
We assume the blood is. The blood gases show mild hypoxemia and respiratory acidosis, compensated by metabolic alkalosis. The blood gases are compatible with COPD. What are the common physiologic causes of hypoxemia? From the shunt equation, arterial oxygen content is related to the change in pulmonary capillary oxygen content, venous oxygen content, and venous admixture. It is easier to classify hypoxemia into the following three categories. Decreased Pulmonary Capillary Oxygen Tension.
Pag e 13 of Malley WJ. Clinical blood gases, assessment and intervention , 2nd ed. Louis: Elsevier Saunders, — Clinical application of blood gases , 5th ed. Chicago: Year Book Medical Publishers, — Would you order any special preoperative preparations for asthmatic patients with COPD? The preoperative preparation should include the following:.
Bishop MJ. Bronchospasm, avoiding an anesthetic disaster. In: Barash PG, ed. ASA refresher courses in anesthesiology. How long would you post pone elective surgery if the patient had a recent URI? Respiratory tract infections are the most common stimuli that evoke acute exacerbations of.
Pag e 14 of The airway responsiveness of even healthy subjects to nonspecific stimuli is transiently. Increased airway responsiveness can last from 2 to 8 weeks. Recently Cohen and Cameron. In addition, Tait and Knight found that laryngospasm and. Therefore, it has been recommended to wait for 2 to 3 weeks after clinical recovery from a URI.
ASA refresher. American Society of Anesthesiologists, — Should you cancel the operation when a child has an upper respiratory. Anesth Analg ;— Intraoperative respiratory complications in patients with upper respiratory. Can J Anaesth ;— What medicines would you expect the patient to have taken in the past or to be taking at the present time? The asthmatic patient might take bronchodilators such as methylxanthines and. Special attention is requ ired if the patient has taken systemic.
Recently, aerosol therapy has become quite popular because it provides optimal local therapeutic effects and minimizes the system ic side effects. Would you order preoperative steroid preparation? It is recommended that preoperative glucocorticoid replacement therapy be given to all patients. Patients who have been treated with high-dose. The human. It is.
The night. In addition, a. Postoperatively, hydrocortisone phosphate, mg intravenously, is given every 8. The biologic half-life of. If the patient had less than 1 week of systemic steroid therapy. Pag e 15 of However, intravenous steroid preparations should be available in the operating room in case intractable hypotension from adrenal insufficiency occurs during surgery.
The increasing emphasis on reactive airways as an inflammatory disease has led to greater appreciation of the importance of steroids in controlling the incidence of attacks and in aborting acute attacks. It has been recommended that systemic steroid preparation be used preoperatively in patients with moderate to severe asthma and a history of a need for steroids in the past. One day of high-dose steroids should not significantly affect wound healing.
In the face of ongoing wheezing and scheduled elective surgery, a steroid course in the week or weeks before surgery may be useful.
The concern that steroids will increase the rate of wound-healing problems or infection are not well founded. A recent study of asthmatics treated with steroids preoperatively found no increase in the incidence of wound infections or wound-healing problems. Editorial views: preoperative corticosteroids for reactive airway. Bronchospasm: successful management. Low complication rate of corticosteroid-treated asthmatics undergoing surgical procedures. Arch Intern Med ;— Sheffer AL. Expert panel on the management of asthma.
J Allergy Clin Immunol ; —. Corticosteroids and inhaled salbutamol in patients with reversible airway obstruction markedly decrease the incidence of bronchospasm after tracheal intubation. Anesthesiology ;— What is the onset of action of intravenous steroid therapy in asthma? The bronchial effects of intravenous steroids are not immediate and may not be seen for 6 to 12 hours after the initial administration. When severe bronchospasm does not resolve despite intense optimal bronchodilator therapy, intravenous corticosteroid administra tion is indicated.
A loading dose of hydrocortisone, 4 mg per kg, is given to achieve plasma cortisol levels above. Alternatively, methylprednisolone, 60 to. Time related decrea se in airway reactivity by corticosteroids [Abstract]. Anesthesiology ;A What are the effects of cimetidine on asthmatic patients? Cimetidine is an H 2 -receptor antagonist. Nathan et al. Pag e 16 of H 2 -receptors are thought to be. Cimetidine may potentiate histamine H 1 -receptor bronchoconstrictions. It should be avoided in as thmatic patients.
Cimetidine also slows clearing of theophylline by inhibiting microsomal metabolism. A comparison of the actions of H 1 and H 2 antihistamines on.
Allergy Clin Immunol ; How would you premedicate the patient? No good controlled studies have been performed on premedication used in asthmatic patients. The asthmatic patient may be premedicated with atropine and diphenhydramine alone or in. Atropine is an anticholinergic drug. It decreases airway resistance,. Diphenhydramine is an H1-receptor—. It inhibits histamine-mediated bronchoconstriction and possesses a sedative. The sedative effect of diphenhydramine may prevent bronchospasm induced by.
Hydroxyzine hydrochloride Vistaril is a frequently used alternative because. Inhaled or systemic steroids may be given to patients with moderate to severe asthma to. Anesthesia And co-existing disease , 4th ed. Intraoperative Management. What are the disadvantages of administering atropine to the asthmatic patient?
Some physicians consider atropine relatively contraindicated because it causes drying of. However, atropine blocks the formation of cyclic guanosine monophosphate GMP and therefore has a bronchodilation effect. Barrett JP. Editorial views: clinical epilog on bronchomotor tone. Anesthesiology ; 1—3. If the patient had a severe asthmatic atta ck in the operating room before the induction of anesthesia, would you put the patient to sleep or postpone the surgery?
Pag e 17 of First of all, medical treatment should be given to relieve the as thmatic attack. El ective surgery should be postponed and the patient should be reevaluated carefully and better prepared preoperatively. In case of emergency surgery such as acute appendicitis, the surgery can be performed after the asth matic attack is terminated with medical treatment. During surgery, the medical treatment should be continued. The patient did not have an asthmatic attack in the operating room.
How would you induce anesthesia? Would you use an LMA instead of an endotracheal tube? The principles of anesthetic management for the asthmatic patient are threefold: to block airway reflexes before laryngoscopy and intubation, to relax airway smooth muscle, and to prevent release of biochemical mediators. Before induction of anesthesia, I would like to ask the patient to take two to three puffs of al buterol from a metered- dose inhaler MDI.
Methohexital is used for induction. Then oxygen and a potent inhalation agent, such as halothane, sevoflurane, or isoflurane, are administered by mask to achieve adequate depth of anesthesia before endotracheal intubation after injection of succinylcholine or other muscle relaxants. Topical endotracheal spray of 80 to mg of lidocaine through a laryngotracheal anesthesia LTA kit may be used before intubation to suppress the cough reflex induced by intubation, but the introduction of lidocaine itself may cause the cough reflex when the depth of anesthesia is light.
As a supraglottic airway, the LMA seems to be suitable for asthmatic patien ts. The LMA provides a unique opportunity for the clinician to control the airway without having to introduce a foreign body into the trachea.
Therefore, it may be an ideal airway tool in the asthmatic patient who is not at risk of reflux and aspiration. However, the patient is undergoing cholecystectomy, which may need manipulating and packing of stomach and bowels; the patient is at risk of regurgitation and aspiration. Meanwhile, the patient may need a nasogastric tube for decompression of gastrointestinal tract.
I would not choose a classic LMA instead of an endotracheal tube for this procedure. However, the introduction of the LMA-ProSeal with a gastric drain tube and larger cuff reduces both the risk of gastric inflation and the risk of aspiration of refluxed gastric contents. Can J Anaesth ; Why would you use methoh exital instead of thiopental? Hirshman et al. Thiopental and thiamylal are thiobarbiturates, and methohexital and pentobarbital are oxybarbiturates.
This suggests that the sulfur atom is important in barbiturate-induced histamine release. Moreover, they further found that thiobarbiturates, but not oxybarbiturates, constricted guinea pig tracheas and that this constriction was mediated by thromboxane. Therefore, methohexital may be preferred as the induction agent in patients showing extreme sensitivity to histamine asthmatics or increased histamine releasability atopics.
However, thiopental itself does not cause bronchospasm. Because it provides only a light plane of anesthesia, airway instrumentation under thiopental anesthesia alone may trigger bronchospasm. Therefore, clinically, both barbiturates have been used successfully in the asthmatic patient, provided that an adequate depth of anesthesia is.
Pag e 18 of In: ASA annual meeting refresher course lectures. Contractile responses of guinea pig trachea to oxybarbiturates and thiobarbiturates. Lorenz W, Doenicke A. Editorial views: anaphylactoid reactions and histamine release by barbiturate induction agents: clinical relevance and pathomechanisms.
Thiobarbiturate-induced histamine release. Would you use propofol, etomidate, or ketamine for induction? Propofol may be the induction agent of choice for the patient with re active airways who was hemodynamically stable.
A recent report found that induction of asthmatics with 2. Another study found that in unselected patients, propofol resulted in a significantly lower respiratory resistance after tracheal intubation than induction with thiopental or etomidate. Etomidate does not depress myocardial function. Therefore, it provides hemodynamic stability in critically ill patients. Although it was advertised as an ideal agent for asthmatic patients, little evidence supports the claim except that etomidate does not release histamine.
A recent study suggests that neither etomidate nor thiopental prevents wheezing after intubation, as opposed to the marked protection afforded by propofol.
Ketamine produces bronchodilation both through neural mechanisms and through release of catecholamines. In an ac tively wheezing patient, ketamine is the induction agent of choice, particularly when hemodynamics are unstable. Comparison of the effects of etomidate, propofol, and.
Anesthesiology ;—. Wheezing during induction of general anesthesia in patients with and without asthma. A randomized, blind trial. Anesthesiology ; — Would you use lidocaine for intubation? Intravenous lidocaine, 1 mg per kg, may be given 1 to 2 minutes before intubation to prevent reflex-induced bronchospasm.
Topical endotracheal spray of lidocaine must be used cautiously because it may provoke reflex bronchoconstriction if adequate depth of anesthesia has not been achieved. Lidocaine infusion, 1 to 2 mg per kg per hour, may be used in cardiac or elderly patients with COPD whose airways need more anesthesia than their cardiovascular system can.
Pag e 19 of Hirshman CA. Anesthesia and bronchospastic disease. Chicago: American Society of Anesthesiologists, — Lidocaine-induced bronchoconstriction in asthmatic patients. Relation to histamine airway responsiveness and effect of preservative. Chest ; —. If this is emergency surg ery and rapid sequence induction is indicated, how would you induce anesthesia in this patient? All the precautions to prevent aspiration of gastric contents and as thmatic attack must be considered simultaneously.
Rapid sequence induction and tracheal intubation using propofol, thiopental or methohexital, and succinylcholine are necessary to prevent aspiration, but light anesthesia may precipitate severe bronchospasm.
Ketamine, 2 mg per kg, may be the induction agent of choice in noncardiac asthmatic patients, because ketamine increases catecholamine release with resultant bronchodilation. Intravenous lidocaine, 1 to 2 mg per kg, given immediately before the administration of ketamine or fentanyl, and succinylcholine, are useful adjunct drugs to prevent reflex bronchospasm, particularly in an emergency situation when deep anesthesia cannot be achieved before intubation.
A full stomach should be emptied by a functioning nasogastric tube. The patient should be. Cisatracurium or vecuronium, 1 mg, should be given. If the patient has a wheezing attack before anesthesia, inhalation of sympathomimetics such as.
Anesth Analg ; Low-dose fentanyl blunts circulatory responses to tracheal intubation. What is your choice of agents for maintenance of anesthesia? We use inhalation agents such as sevoflurane, halothane, and isoflurane with nitrous oxide and oxygen. Sevoflurane, enflurane, and isoflurane are preferable to halothane, because halothane sensitizes the myocardium to arrhythmic effects of circulating catecholamines more than sevoflurane, enflurane, and isoflurane. However, some authorities prefer halothane and sevoflurane to isoflurane and desflurane because the latter anesthetics have a pungent odor that may cause airway irritation and trigger bronchospasm.
However, more. Pag e 20 of In addition, sevoflurane may have a more rapid onset of bronchodilation than isoflurane or halothane. The effect of isoflurane, halothane, sevoflurane and thiopental nitrous oxide on respiratory system resistance after tracheal intubation. What are the mechanisms of halothane that produce bronchodilation?
Increased cAMP may bind free calcium within bronchial myoplasm and thereby promote relaxation by a negative feedback mechanism. However, a study by Hirshman et al. Halothane may also have protective effects by acting on bronchial epithelium through a nonadrenergic, noncholinergic mechanism, possibly involving the nitric oxide pathway. Mechanism of action of inhalational anesthesia on airways. Interaction between halothane and the nonadrenergic, noncholinergic inhibitory system in porcine trachealis muscle.
Why would you choose an inhalational instead of an intravenous technique? First, inhalation agents such as sevoflurane, halothane, enflurane, and isoflurane have dose- related direct bronchodilator effects. Ketamine has an indirect bronchodila tor effect, wh ich is not dose related and not predictable. Large doses of morphine produce bronchoconstriction because morphine increases central vagal tone and releases histamine. Meperidine was shown to have a spasmolytic effect in asthmatic patients, but not in experimental dogs.
Fentanyl does not have a significant effect on bronchial tone. Second, cholinesterase inhibitors can induce bronchospasm. Inhalation agents potentiate muscle relaxants; therefore, lower doses of relaxants are needed for surgery. The use of cholinesterase inhibitors to reverse the effect of muscle relaxants may be avoided or decreased.
Pag e 21 of Is regional anesthesia better than general anesthesia in this situation? This issue is controversial. The use of regional anesthesia avoids the possibility of bronchospasm that may be induced by endotracheal tube stimulation.
However, if high levels of sensory and motor block are required, they may produce severe anxiety and actually incite bronchospasm. Another concern is the associated blockade of sympathetic input to the lungs.
Some case reports have speculated about a resultant increase in airway resistance. Low spinal, epidural, and caudal anesthesia for surgery of the perineum, lower extremities, and pelvic extraperitoneal organs resulted in fewer respiratory complications than did general anesthesia.
A study of patients with asthma demonstrated no differences between those anesthetized with high epidurals T and those undergoing general anesthesia with ketamine and isoflurane. Endotracheal general anesthesia is advantageous because it provides a controlled airway to deliver the desirable oxygen concentration, but the endotracheal tube may also induce bronchospasm during light anesthesia. In: ASA annual refresher course lectures.
Gold MI, Helrich M. A study of the complications related to anesthesia in asthmatic patients. Epidural anesthesia in asthmatic patients. Anesth Analg. Which muscle relaxants would you use?
Muscle relaxants that cause histamine release should be avoided Table 1. Pancuronium, rocuronium, cisatracurium, and vecuronium are the preferred relaxants because the histamine released is insignificant. Vecuronium, rocuronium, and cisatracurium may be better choices of relaxant because of their intermediate action durations, allowing early recovery without reversal. D-Tubocurarine can cause bronchospasm by histamine release.
Metocurine and succinylcholine also cause histamine release, but to a lesser extent. Gallamine has minimal histamine release but has been reported to cause bronchospasm in patients.
Atracurium, mivacurium, and doxacurium in high doses increase histamine release. Therefore, they are not the relaxants of choice. Pag e 22 of Basta SJ. Modulation of histamine release by neuromuscular blocking drugs. Curr Opin Anesth. Atracurium versus vecuronium in asthmatic patients. A blinded, randomized comparison of adverse events. Mechanism of action of atracurium on airways. In the middle of surgery, the patient developed a severe wheezing attack.
How do you manage it? Pag e 23 of First, deepen the level of anesthesia and increase FIO 2. Remember that th e patient is under. The most common cause of asthmatic attack during surgery is. The asthmatic patient has an extremely sensitive tracheobronchial tree. When the level of anesthesia is too light, he may develop bucking, straining, or coughing as a.
First the blood pressure is taken to ensure it is normal or high, and then. At the. The patient should be continuously ventilated with a volume-cycled ventilator. Second, relieve mechanical stimulation. Pass a catheter through the endotracheal tube to.
Occasionally, the endotracheal tube slips down and stimulates the carina of the. Surgical stimulation, such as. Third, medical intervention is necessary if the previously mentioned treatment cannot break the. When severe bronchospasm is not resolving despite intense optimal. Fourth, bring in an intensive care unit ICU ventilator. Anesthesia ventilators are not designed. It is impossible to deliver adequate alveolar ventilation. With low tubing compliance, littl e ventilation is.
High inspiratory flow rate allows for shorter inspir atory time with. The major disadvantage of an ICU ventilator. However, the Siemens D anesthesia machine. It may be ideal for this. Attenuation of histamine-induced airway constriction by albuterol.
What is its mechanism of action on asthma? In the past it was fashionable to treat episodes of severe asth ma with intravenous. What problems may. Pag e 24 of This approach no longer appears justifiable. Isoproterenol infusions can induce ventricular arrhythmias during halothane anesthesia. MDI adapters or small-volume jet nebulizers to the anesthetic circuit.
The best-seller is still a guide for research selection for residents and licensed anesthesiologists. It uses a practical question and answer format to present more than 60 real-world cases. In the process of guiding you to reasonably determine an effective patient care plan, You provide logical guidance.
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