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Chapter: Essential Anesthesia From Science to Practice : Applied physiology and pharmacology : Anesthesia and the lung

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Anesthesia in the patient with pulmonary disease

Patients with lung disease arrive at respiratory patterns optimal for their condition.

Anesthesia in the patient with pulmonary disease

Patients with lung disease arrive at respiratory patterns optimal for their condition. This can include the recruitment of auxiliary muscles, changes in inspiratory and expiratory flow rates, respiratory rate, and arterial carbon dioxide tension. Because anesthesia can disturb these delicate adjustments, many anesthesiol-ogists prefer to resort to regional anesthesia, where practical. Two major issues must be considered, however:

·           The potential respiratory effects of the intended regional anesthetic. For exam-ple, a thoracic-level epidural anesthetic block begins to compromise inter-costal muscle activity, reduces FRC, limits the patient’s ability to cough, and theoretically can stimulate bronchospasm by blocking dilatory sympathetic innervation to the bronchi. Some approaches to the brachial plexus have a high incidence of unilateral phrenic nerve paralysis and an occasional pneu-mothorax. While the average patient can tolerate the loss of intercostal mus-cles, a “pulmonary cripple,” who at rest uses accessory muscles to breathe, might be left with inadequate respiratory muscle strength.

·           The respiratory depressant effects of sedative medications might be accen-tuated in these patients. While it is preferable to attempt an anesthetic that avoids airway instrumentation, this preference turns into a liability if the need for emergent tracheal intubation arises should the patient slip into respiratory failure.

Asthma

The patient with well-controlled asthma should sail through general anesthe-sia without much difficulty. All asthma medications, and particularly steroids, should be continued pre-operatively. Nebulized albuterol (or another 2 ago-nist) administered in the pre-operative holding area provides bronchodilation just before anesthesia. Because instrumentation of the airway can stimulate bronchospasm, patients with refractory asthma might benefit from anesthetic techniques that avoid airway manipulation, such as regional or local anesthesia with gentle intravenous sedation. Should general anesthesia be required, several options for induction and airway management are available. Small doses of either thiopental or propofol can ease the patient to sleep, at which point one of the halogenated inhalation anesthetics can be slowly introduced. These agents are bronchodilators. Ketamine is a bronchodilator as well and may be used, provided its potential side effects can be accepted. A laryngeal mask airway (LMA) is a lesser stimulus to bronchospasm than an endotracheal tube. When tracheal intubation becomes necessary, the goal at induction will be to completely block the airway reflexes that stimulate bronchospasm. Intravenous lidocaine (0.5–1.0 mg/kg) can prove helpful. Intravenous opioids (but not morphine which tends to release histamine) can be used. But remember that some patients develop respiratory difficulties (a “stiff chest”) in response to large doses of opioids, the treatment of which requires muscle relaxation.

Intra-operatively, warm and humidified gases can reduce bronchospasm. Mechanical ventilation requires consideration of the pulmonary pathology. Asth-matics have a prolonged expiratory phase. If we do not give them enough time for exhalation, they will trap air (“dynamic hyperinflation”), resulting in increased intrathoracic pressures. This “auto-PEEP” reduces venous return and cardiac out-put. A prolonged expiratory time allows for full exhalation. Simply lengthening the exhalation time steals time from inhalation, which in turn might require high inspiratory pressures (the same tidal volume must be given over a shorter time).

Reducing the tidal volume and/or respiratory rate would help, but will necessarily reduce minute ventilation and entail the potential for hypercarbia. “Permissive hypercapnea” can become necessary when minute ventilation cannot be main-tained without risk of barotrauma (pneumothorax).

Because stimulation of the trachea can trigger bronchospasm, removal of the endotracheal tube may be best accomplished during deep anesthesia. This is only appropriate in patients at low risk for aspiration and obstruction of the upper airway. Prophylactic supplemental oxygen in the post-operative period can prevent hypoxia-induced airway reactivity.

Obstructive sleep apnea

Obstructive sleep apnea (OSA) occurs when the soft tissues of the pharynx collapse during sleep, obstructing the airway and resulting in hypoxemia. Sleep apnea plagues obese patients who snore heavily with intermittent bouts of obstruction to the point of apnea (reported by partner) and repeated awakening. During the day, they are often somnolent. The apneic periods cause hypoxemia and hypercar-bia, resulting in (i) cardiac irritability with bradycardia and premature ventricular contractions (PVCs), (ii) vasoconstriction, both peripherally (leading to increased systemic vascular resistance and hypertension) and in the pulmonary circulation (with pulmonary hypertension and potentially right heart failure), and (iii) ery-thropoeisis (resulting in polycythemia). Because of the potential of thrombosis and unfavorable rheology, a polycythemic patient should be phlebotomized if the hematocrit is too high (>55%).

Should you obtain a history of OSA during the anesthesia pre-operative evalu-ation, you may have to order further studies including ECG and possibly echocar-diogram to look for evidence of pulmonary hypertension and right heart compro-mise. In a subset of patients (“Pickwickians”), ABG analysis might demonstrate daytime CO2 retention with potentially impaired hypercarbic respiratory drive. Therapeutic interventions include nasal CPAP during sleep, weight loss, and surgi-cal correction. OSA patients are particularly sensitive to opioids and sedatives and can develop airway obstruction with even low doses of respiratory depressants. Finally, patients with excess pharyngeal tissue and obesity present difficulties with airway management. Not only can intubation be tough, we may be unable to mask–ventilate or even use an LMA. Thus ventilation may be very difficult to provide once we render the patient unconscious and paralyzed.


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