Ebstein’s Anomaly

-A rare congenital cardiac abnormality.

-The septal and posterior cusps of the tricuspid valve are displaced downwards and are elongated, such that a varying amount of the right ventricle effectively forms part of the atrium. Its wall is thin and it contracts poorly. The remaining functional part of the right ventricle is therefore small.

-The foramen ovale is patent, or defective, in 80% of cases.

-The degree of abnormality of right ventricular function, and the size of the ASD, are probably the main determinants of the severity of the condition, which varies considerably.

-The right ventricular systolic pressure is low, and the RVEDP is elevated. Tricuspid incompetence can occur.

-There may be a right to left shunt, with cyanosis, on effort, and pulmonary hypertension and right heart failure may supervene.

-The natural history of the disease is very variable. Fifty percent of cases present in infancy with cyanosis, and 42% die in the first 6 weeks of life.

-In those who survive to adulthood, symptoms may be precipitated by the onset of arrhythmias, or by pregnancy. A few patients remain asymptomatic, even as adults, although once symptoms develop, the disability can increase rapidly.

-A cardiothoracic ratio of ≥ 0.65 is a better predictor of sudden death than the symptomatic state, and those who developed atrial fibrillation died within 5 years. It has therefore been suggested that tricuspid surgery should be undertaken before the cardiothoracic ratio reaches 0.65.

Preoperative Abnormalities:

1. There may be a right to left shunt, with dyspnea and cyanosis at rest, or on moderate exertion. Alternatively, the patient may be asymptomatic.

2. Episodes of tachyarrhythmias occur in 25% of patients. Some provoke syncopal attacks.

3. The ECG may show varying abnormalities, including large peaked P waves, a long P–R interval, Wolff–Parkinson–White syndrome, RBBB, and right heart strain. Paroxysmal supraventricular tachycardia occurs in 15%, usually because of the presence of WPW syndrome.

4. Chest X-ray may show cardiomegaly, with a prominent right heart border, and poorly perfused lung fields.

5. Paradoxical systemic embolism and bacterial endocarditis may occur.

6. Many other lesions of the tricuspid valve or right ventricle may mimic Ebstein’s anomaly, therefore the discriminating clinical and echocardiographic features for correct diagnosis have been enumerated.

Anesthetic Problems:

These will depend upon the anatomical abnormality, the degree of right to left shunt, and the presence or absence of right heart failure.

1. Induction time is prolonged, because of the pooling of drugs in the large atrial chamber.

2. Intracardiac catheter insertion may be hazardous because it can provoke serious cardiac arrhythmias.

3. Air entering peripheral venous lines or any open veins at subatmospheric pressure may cause paradoxical air emboli.

4. Tachycardia is poorly tolerated because of impaired filling of the functionally small right ventricle.

5. Hypotension may increase the right to left shunt if present.

6. Hypoxia causes pulmonary vasoconstriction, which also increases a right to left shunt.

7. There is a risk of bacterial endocarditis, especially if a CVP line is in place.

8. Deterioration may occur in pregnancy because of a decrease in right ventricular function, and an increase in blood volume and cardiac output, or with the onset of arrhythmias.

Management:

1. The severity of the lesion must be assessed. In the presence of maternal cyanosis or arrhythmias during pregnancy, there should be close monitoring of both mother and fetus. Deterioration may occur, despite previous successful pregnancies.

2. Treatment of heart failure and arrhythmias.

3. Antibiotic prophylaxis against bacterial endocarditis.

4. If a CVP is used for monitoring, its tip should be kept within the superior vena cava. The use of intracardiac catheters should probably be avoided.

5. Techniques should aim to minimize tachycardia and hypotension.

6. Oxygen therapy increases pulmonary vasodilatation. Long-term maternal therapy is required during pregnancy from 14 weeks, to treat fetal hypoxia that is demonstrated by umbilical venous blood gases.

7. Several anesthetic techniques have been described. A two-catheter epidural technique can be used for vaginal delivery to minimize hypotension. Bupivacaine doses must be fractionated and saline rather than air used to site the epidural, to avoid paradoxical air emboli. Cesarean section under general anesthesia, preceded by fentanyl, and a neurolept analgesic technique for hysterectomy, have been described.

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Acquired C1 Esterase Inhibitor Deficiency

-This may be a familial or, more rarely, an acquired disorder involving the complement system.

-The acquired form is mostly associated with a B-lymphocyte malignancy, and antibodies have been detected against abnormal immunoglobulins present on the malignant B-cells. The reaction between the two causes C1 activation, which in turn produces a secondary reduction in the concentrations of C1, C2, and C4 and reduced functional activity of the C1 esterase inhibitor.

-This form must be distinguished from the physical forms of angioedema that occur in response to food, drugs, or insect bites, or in association with connective tissue disorders.

-Recently, many patients have developed angioedema in response to treatment with ACE inhibitors, particularly enalapril and captopril. Substantial increases in plasma bradykinin have been demonstrated during attacks of hereditary, acquired, and captopril-induced angioneurotic edema.

Preoperative Abnormalities:

1. Intermittent attacks of angioneurotic edema that can involve any part of the body, and result from extravasation of intravascular fluid and protein into subcutaneous and mucosal structures.

2. As with hereditary angioneurotic edema, there is a low level of C1 esterase inhibitor, and sometimes life-threatening episodes of edema of the upper airway may develop in response to stress or local trauma, particularly dental treatment. However, attacks of edema may occur without any obvious reason, and recurrent abdominal pain may be a presenting feature.

3. As with the hereditary form, epinephrine (adrenaline), antihistamines, and steroids are ineffective for prophylaxis, and for treatment of these attacks.

4. The two conditions may be distinguished by the fact that in the acquired form the onset is late, no family history is elicited, no complement abnormalities are found in the patient’s blood relatives, and the underlying malignancy may already have been diagnosed.

5. Differentiation may now be made on measurement of the C1q subunit of C1; patients with acquired deficiency have a decreased level of C1q, compared with those with the hereditary form, in whom the C1 level is normal.

Anesthetic Problems:

1. Tracheal intubation and manipulation of the upper airway may precipitate local angioneurotic edema, for which treatment with epinephrine (adrenaline), steroids, and antihistamines is ineffective. Edema may also occur after dental extractions.

2. Although tranexamic acid has been recommended to prevent attacks in both forms, venous thrombosis has been reported after its prophylactic use during surgery in the acquired disease.

Management:

1. Progestogen derivatives: Increase the hepatic synthesis of a C1 esterase inhibitor. Its prophylactic value is acquired and hereditary disorders have been reported.

a) Danazol (200 mg TDS) should be given preoperatively but may take several days to become effective.

b) Stanozolol (0.5–8 mg/day) can also be used.

-The lower levels will be required for maintenance, whilst higher levels may be needed in the initial stages. A patient with autoimmune C1 EI, who was known to be carrying a male fetus, was given short-term therapy at 40 weeks of gestation.

2. Tranexamic acid: It should be avoided in the acquired form, especially in the presence of a thrombocytosis.

3. Fresh frozen plasma, and C1 esterase inhibitor concentrate: Used as preoperative prophylaxis and treatment.

Read more ☛ Angioneurotic Edema

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Dexmedetomidine

Mechanism of Action:

-It is an imidazole derivative and is a specific alpha-2 adrenoceptor agonist that acts via post-synaptic alpha-2 receptors primarily in the locus ceruleus to increase conductance through K+ channels.

Uses and Dose:

-Its main actions are sedation, anxiolysis, and analgesia

-It is a clear, colorless isotonic solution containing 100 g/ml of dexmedetomidine base and 9 mg/ml of sodium chloride in water. The solution is preservative-free and contains no additives.

-Dexmedetomidine can be administered intravenously, intramuscularly, and transdermally.

1. ICU Sedation:

-Used for sedation of initially intubated and mechanically ventilated patients in ICU.

-Loading: 1 mcg/kg IV over 10 minutes; loading dose may not be required for adults converted from other sedative therapy.

-Maintenance 0.2-0.7 mcg/kg/h. continuous IV infusion; not to exceed 24 h.

-The duration of use should not exceed 24 hours.

-Dexmedetomidine has been infused in mechanically ventilated patients before, during, and after extubation; it is not necessary to discontinue dexmedetomidine before extubation.

2. Procedural Sedation:

Indicated for sedation of non-intubated patients before and/or during surgical and other procedures.

Loading: 1 mcg/kg IV over 10 minutes.

Maintenance 0.6 mcg/kg/h. IV titrate to effect (usually 0.2-1 mcg/kg/h.).

3. Awake Fiberoptic Intubation:

Loading: 1 mcg/kg IV over 10 minutes.

Maintenance 0.7 mcg/kg/hr IV until endotracheal tube secured.

Dosage Modifications:

-Dose reduction may be required if co-administered with other concomitant anesthetics, sedatives, hypnotics, or opioids.

-Consider dose reduction in patients with hepatic impairment or aged ≥ 65 y.; clearance decreases with increasing severity of hepatic impairment.

-Renal impairment: No dosage adjustment required.

Pharmacokinetics

Distribution: It is 94% protein-bound in the plasma; the volume of distribution is 1.33 l/kg. The distribution half-life is 6 minutes.

Metabolism: The drug undergoes extensive hepatic metabolism to methyl and glucuronide conjugates.

Excretion: 95% of the metabolites are excreted in the urine. The elimination half-life is 2 hours, and the clearance is 39 l/hour.

Pharmacodynamics:

1. Cardiovascular System: It causes a predictable decrease in the mean arterial pressure and heart rate.

2. Respiratory System: It causes a slight increase in PaCO₂ and a decrease in minute ventilation, with minimal change in the respiratory rate—these effects are not clinically significant.

3. Central Nervous System: The drug is sedative and anxiolytic—ventilated patients remain easily arousable and cooperative during treatment. Reversible memory impairment is an additional feature.

4. Metabolic / Other: It causes a decrease in plasma epinephrine and norepinephrine concentrations. It does not impair adrenal steroidogenesis when used in the short term.

Side Effects:

Hypotension, bradycardia, nausea, and a dry mouth are the most commonly reported side effects of the drug.

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Angioneurotic Edema

-A general term applied to the development of acute edema in the subcutaneous or submucous tissues.

-Anesthetic help may be sought during an attack, when edema of the lips, tongue, or larynx may cause respiratory problems.

Causes:

-Angioedema may be secondary to the release of histamine, or many other vasoactive substances such as bradykinins, prostaglandins, or leukotrienes.

-It is thought that pediatric and adult angioedemas differ. Children are less likely to require intubation or tracheostomy than adults. Recent work in adults has shown substantial increases in plasma bradykinin during attacks of hereditary, acquired, or captopril-induced angioedema.

-The development of edema may be:

1. Part of a general anaphylactoid or anaphylactic reaction to a drug, bite, sting, or the ingestion of a substance.

2. A manifestation of hereditary angioneurotic edema, a condition caused by a deficiency of C1 esterase inhibitor.

3. A result of an acquired form of C1 esterase inhibitor deficiency which usually occurs in association with a B-lymphocyte malignancy.

4. A known side effect of a drug. Recently, there have been several cases of angioedema reported, usually involving the tongue, floor of the mouth, epiglottis, and aryepiglottic folds, secondary to treatment with ACE inhibitors. Most occur in the first week of treatment but may be delayed for up to a year. Can be associated with elevated serum bradykinin levels.

Presentation:

1. There may be a history of a predisposing factor. This can be ingestion of food or a drug, an infection, bite or sting, a family history of angioedema, or a B-lymphocytic malignancy.

2. Edema of subcutaneous tissue may occur alone or be accompanied by hypotension.

3. Patients taking ACE inhibitors have developed problems in the perioperative period. Angioedema of the tongue occurred 15 min after tracheal tube removal.

4. A patient with acquired C1 esterase inhibitor deficiency undergoing cardiopulmonary bypass had massive activation of the common pathway, coagulopathy, pulmonary edema, and circulatory collapse.

Management:

1. Assessment of severity of airway obstruction.

2. If the angioedema is part of an anaphylactic or anaphylactoid reaction:

a) Give epinephrine (adrenaline) IV or IM, 0.1–0.5 mg depending on the severity.

b) If the condition is severe and involves the glottis, an airway should be established, either by tracheal intubation, cricothyroidotomy, or tracheostomy.

c) Second-line treatment includes IV fluids, chlorpheniramine IV 10–20 mg, and steroids.

3. Hereditary angioneurotic edema, or acquired C1 esterase inhibitor deficiency. These do not respond to epinephrine (adrenaline) or antihistamines, but to replacement of the deficient inhibitor by either:

a) An infusion of fresh frozen plasma.

b) Purified C1 esterase inhibitor concentrate.

Read more ☛ Acquired C1 Esterase Inhibitor Deficiency

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Jugular Venous Oximetry

Jugular Venous Oximetry (JVO)

-It provides insight into the metabolic and oxygenation state of the brain.

-It provides information about the balance of oxygen supply and demand, for a larger portion, if not the complete brain.

Indications:

-During cardiopulmonary bypass

-Neurosurgery

-After traumatic brain injury.

Figure 1: JVO Catheterization Technique

Technique:

-A catheter is inserted into the jugular vein in a retrograde fashion (using Seldinger’s technique) so that its tip sits at the base of the skull in the jugular bulb. This allows continuous pressure monitoring as well as intermittent withdrawal of a jugular venous blood sample for gas analysis (Fig. 1).

-Continuous monitoring: can be achieved using an oximetry catheter inserted via a conduit sheath.

-Confirmation of location: can be made with a lateral cervical spine x-ray (Fig. 2).

Figure 2: JVO Catheter Lateral Cervical Spine X-Ray 

Identification of the dominant Jugular vein:

For the best representation of the metabolic state of the brain, the catheter should be placed in the dominant jugular vein, most commonly the right side. Confirmed by:

-In patients who have had a cerebral angiogram, the venous phase of the study will provide information on dominant venous drainage.

-The intra-arterial contrast will drain almost exclusively through one jugular vein, regardless of the side of injection.

-Side dominance can also be predicted using ultrasound where the dominant vein may be larger. In the absence of this information, the right side is preferred.

The pressure gradient between the jugular venous pressure and the central venous pressure:

-Pressure transduction of the jugular bulb catheter allows comparison with the central venous pressure to rule out potential venous obstruction.

-In a supine patient with a neutral neck position, there should be no pressure gradient between the tip of the jugular bulb and the central venous catheter.

-Although rare, a significant gradient (> 4 mmHg) can occasionally develop during positioning if there is significant twisting or bending of the neck.

-This gradient indicates venous obstruction, potentially causing brain edema or ischemia.

-The head should be repositioned until the gradient resolves.

Interpretation of blood gas analysis of jugular venous blood sample:

-The saturation of jugular venous blood (SjvO₂) demonstrates whether cerebral blood flow (CBF) is sufficient to meet the cerebral metabolic rate for oxygen (CMRO₂) of the brain (Lower values of SjvO₂ reflecting greater uptake by the brain and therefore less blood flow).

-It is essential that blood samples from the retrograde catheter be drawn slowly to avoid contamination from non-cerebral venous blood.

-A normal value is between 65-75 %. Desaturation (SjvO₂ < 55 %) indicates impending cerebral ischemia (e.g., caused by hypotension, hypocapnia, increasing cerebral edema).

-In traumatic brain injury, SjvO₂ below 50% for more than 10 min. is undesirable and associated with poor outcomes. However, it has low sensitivity, (a relatively large volume of tissue must be affected, approximately 13 % before SjvO₂ levels decreased below 50 %).

-Intraoperative hyperventilation will lower SjvO₂ as it decreases CBF.

-In the setting of a non-traumatized brain that is exposed to moderate hyperventilation for the duration of a neurosurgical procedure, the acceptable level for SjvO₂ is unknown.

-In the absence of other demands, it is reasonable to guide intraoperative hyperventilation by maintaining SjvO₂ > 50%.

-Measurement of simultaneous arterial and jugular venous samples allows the determination of lactate output from the brain, the presence of which indicates the occurrence of anaerobic metabolism.

Disadvantages & Limitations:

-It is a global monitor that could easily miss small areas of regional ischemia.

-If CBF & O₂ consumption both decreased (e.g., in severe brain injury, SjvO₂ may be unchanged.

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Oculo-cardiac Reflex and Oculo-respiratory Reflex

1-Oculo-cardiac Reflex

Definition:

Bradycardia following traction on the extraocular muscles, especially the medial rectus.

The reflex is particularly active in children. Bradycardia may be severe and may lead to asystole. Other arrhythmias may occur, e.g. ventricular ectopics or junctional rhythm.

Bradycardia may also follow pressure on/or around the eye, fixation of facial fractures, retrobulbar block (pressure associated with local infiltration), ocular trauma, or manipulation of tissue in orbital apex after enucleation,...etc. The reflex has been used to stop SVT with eyeball massage.

Pathway: (Figure 1)

Afferent pathways are via the trigeminal nerve (ciliary ganglion to the ophthalmic division of trigeminal nerve to Gasserian ganglion to the main trigeminal sensory nucleus).; efferents are via the vagus nerve (afferents synapse with the visceral motor nucleus of the vagus nerve located in the reticular formation and efferents travel to the heart and decrease output from the sinoatrial node).

Prophylaxis:

Reduced by anticholinergic drugs administered as premedication or on induction of anesthesia.

Management:

If it occurs, surgery should stop, and atropine or glycopyrrolate should be administered.

Retrobulbar block does not reliably prevent it; local infiltration of the muscles has been used instead.

Figure 1: Oculo-cardiac Reflex Pathway

2-Oculo-respiratory Reflex

Definition:

Hypoventilation following traction on the external ocular muscles. Reduced respiratory rate, reduced tidal volume, or irregular ventilation may occur.

Pathway:

Thought to involve the same afferent pathways as the oculocardiac reflex, but with efferents via the respiratory centers.

Heart rate may be unchanged, and the reflex is unaffected by atropine.

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Anesthesia for Electroconvulsive Therapy

Principle:

-The exact mechanism of Electroconvulsive Therapy (ECT) is unknown. Electrical stimuli (electroconvulsive shock) are usually administered until a therapeutic generalized seizure is induced (30–60 sec. in duration).

-A good therapeutic effect is generally not achieved until a total of 400–700 seizures have been induced, in several sessions, over 2-3 weeks. Progressive short memory loss often occurs with an increasing number of treatments.

Physiological Effects:

-Seizure activity is characteristically associated with an “initial parasympathetic” discharge characterized by bradycardia and increased secretions. Marked bradycardia (<30 beats/min.) and even transient asystole (up to 6s) are occasionally seen.

-This is followed by “sustained sympathetic” discharge. Hypertension and tachycardia that follow are typically sustained for several minutes.

-Transient autonomic imbalance can produce arrhythmias and T-wave abnormalities on the ECG. Cerebral blood flow and ICP, intragastric pressure, and intraocular pressure all transiently increase.

Contraindications:

• Recent MI (<3 months)

• Recent stroke (usually <1 month)

• Intracranial mass or increased ICP from any cause

• More relative contraindications include:

- Angina

- Poorly controlled heart failure

- Significant pulmonary disease

-Bone fractures, Severe osteoporosis

- Pregnancy

- Glaucoma and retinal detachment.

Anesthetic Considerations:

-Amnesia is required only for the brief period (1–5 min) from when the NMB is given to when a therapeutic seizure has been successfully induced. The seizure itself usually results in a brief period of anterograde amnesia, somnolence, and often confusion. Consequently, only a short-acting induction agent is necessary.

-Increases in seizure threshold are often observed with each subsequent ECT.

-Most induction agents (Barbiturates, Benzodiazepines, and Propofol) have anticonvulsant properties, small doses must be used. The seizure threshold is increased and seizure duration is decreased by all of these agents.

--Sodium pentothal (2–4 mg/kg) was the first induction agent used, it raises the seizure threshold and decreases its duration.

--Methohexital (0.5-1.0 mg/kg): has been the induction agent of choice (gold standard) because it has very little effect on seizure duration and has a rapid onset and recovery profile. Unfortunately, methohexital is no longer available.

--Benzodiazepines: raise the seizure threshold and decrease its duration.

--Propofol (1–1.5 mg/kg): but higher doses reduce seizure duration.

--Etomidate (0.15-0.6 mg/kg): lacks anticonvulsant properties, increases seizure duration, and prolongs recovery.

--Ketamine (1.5-2 mg/kg): lacks anticonvulsant properties, and increases seizure duration, but is generally not used because it also increases the incidence of delayed awakening, nausea, and ataxia and is also associated with hallucinations during emergence.

-Short-acting opioids: are not given alone because they do not consistently produce amnesia.

-Sevoflurane (5%–8% for induction, followed by 1–2 MAC): is the only inhalational agent in widespread use for induction in ECT, with comparable effects to intravenous (IV) agents. It is preferred for patients not cooperative with IV access. It has the advantage of attenuating uterine contractions following ECT and is used in the third trimester of pregnancy.

-Induction agents in the descending order of seizure duration after their use are:

[Etomidate > Ketamine > Methohexital > Sevoflurane > Thiopental > Propofol]

-Induction agents in descending order of seizure threshold reducing property are:

[Etomidate > Ketamine > Methohexital > Thiopental > Propofol]

-Neuromuscular blockade: required from the time of electrical stimulation until the end of the seizure. A short-acting agent, such as succinylcholine (0.25–0.5 mg/kg), is most often selected.

-Ventilation: Controlled “mask ventilation” (with a backup plan of LMA if concerned about effective ventilation), is required until spontaneous respirations resume. As ECT is usually administered 3-times a week, repeated intubations may lead to airway trauma and edema. Hyperventilation can increase seizure duration and is routinely employed in some centers.

Monitoring:

-Routine monitoring should be as with the use of any other general anesthetic.

-Seizure activity is monitored by an unprocessed EEG. It can also be monitored in an isolated limb: a tourniquet is inflated around one arm before injection of succinylcholine, preventing entry of the NMB and allowing observation of convulsive motor activity in that arm.

Precautions:

-Rubber bite block: to avoid dental, tongue, and lips injury.

-Exaggerated parasympathetic effects: should be treated with atropine. In fact, premedication with glycopyrrolate is desirable both to prevent the profuse secretions associated with seizures and to attenuate bradycardia.

-Sympathetic manifestations: Nitroglycerin, Nifedipine, and α- and β-adrenergic blockers have all been employed successfully for control. High doses of β-adrenergic blockers (Esmolol, 200 mg), however, are reported to decrease seizure duration.

-Patients with pacemakers: may safely undergo ECT treatments, but a method to convert the pacemaker to a fixed mode, if necessary should be readily available.

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How to avoid ALI after Thoracic Surgery

How to avoid Acute Lung Injury (ALI) after Thoracic Surgery

-Fortunately, Acute Lung Injury (ALI) occurs infrequently, with an incidence of 2.5 % of all lung resections combined, and an incidence of 8% after pneumonectomy. However, when it occurs, ALI is associated with a risk of mortality or major morbidity of about 40%.

Causes of ALI:

I. Ventilated Lung:

1-Hyperoxia: (Oxygen toxicity, Reactive oxygen species)

2-Hyperperfusion: (Endothelial damage, Increased pulmonary vascular pressure)

3-Ventilatory Stress: (Volutrauma, Barotrauma, Atelectrauma)

II. Collapsed Lung:

1-OLV: (Ischemia/Reperfusion, Reexpansion, Cytokine release, Altered redox status)

2-Surgery: (Manipulation trauma, Lymphatic disruption)

III. Systemic:

-Cytokine release, Reactive oxygen species, Complement activation, Overhydration, Chemotherapy/Radiotherapy.

Prophylaxis against ALI:

A) Protective Lung Ventilation Strategies:

I. Lower Tidal Volumes (6–8 mL/kg):

-The use of lower tidal volumes may lead to lung derecruitment, atelectasis, and hypoxemia. Lung derecruitment may be avoided by the application of external PEEP and frequent recruitment maneuvers.

II. PEEP (5–10 cm H₂O):

-Although PEEP may prevent alveolar collapse and development of atelectasis, it may cause a decrease in PaO₂ due to diversion of blood flow away from the dependent, ventilated lung and an increase in the total shunt.

-Thus, PEEP must be customized to the underlying disease of each patient, and a new application of PEEP will rarely be the appropriate way to treat hypoxemia that occurs immediately after the onset of one-lung ventilation.

-Patients with obstructive pathology may develop intrinsic PEEP. In these patients, the application of external PEEP may lead to unpredictable levels of total PEEP.

III. Lower FiO₂ (50-80%):

-Although the management of one-lung ventilation has long included the use of 100% oxygen, evidence of oxygen toxicity has accumulated both experimentally and clinically.

-Clinicians recommend titrating FiO₂ to maintain the O₂ saturation >90%, especially in patients who have undergone adjuvant therapy and are at risk of developing ALI.

IV. Lower Ventilatory Pressures:

-Plateau pressure <25 cm H₂O; and peak airway pressure <35 cm H₂O, through the use of pressure-controlled ventilation, may diminish the risk of barotrauma.

-The flow pattern results in a more homogenous distribution of the tidal volume and improved dead space ventilation.

V. Permissive Hypercapnia:

-Periodic ABG analysis is helpful to ensure adequate ventilation. End-tidal CO₂ measurement may not be reliable due to increased dead space and an unpredictable gradient between the arterial and end-tidal CO₂ partial pressure.

VI. At the end of the procedure:

-The operative lung is inflated gradually to a peak inspiratory pressure of less than 30 cm H₂O to prevent disruption of the staple line.

-During reinflation of the operative lung, it may be helpful to clamp the lumen of the dependent lung, to limit over-distension.

B) IV Fluids:

-Restrict IV fluids in pulmonary resection to avoid lower lung syndrome (Gravity-dependent transudation of fluid).

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