Anaesthesia facts from previous papers

* Inhalational anaesthesia causing BRONCHOCONSTRICTION ( ENT)

E-ETHER

N-NITROUS OXIDE

T-THIOPENTONE .

* Platelet dysfunction in uremia is probably multifactorial; causative factors include uremic toxins (hence performance of dialysis immediately before surgery is advisable), anemia, excessive parathyroid hormone, and aspirin use. Some patients with chronic renal disease are hypercoagulable; therefore, one should not assume that all dialysis patients are safe from acute venous thromboembolism.

Pain Management

         ACUTE PAIN MANAGEMENT

1. Pain is the fifth vital sign.
2. Good pain control may decrease postoperative complications.
3. Adjuvant drugs can be helpful.
4. Continuous femoral infusions are as good as epidural infusions for postoperative pain control after knee procedures.
5. Doses of morphine differ by a factor of 10 between intravenous, epidural, and intrathecal routes.

·         CHRONIC PAIN MANAGEMENT

1. Chronic pain is best treated using multiple therapeutic modalities. These include physical therapy, psychological support, pharmacological management, and the rational use of more invasive procedures such as nerve blocks and implantable technologies.
2. Patients suffering from cancer pain often exhibit complex symptomatology that includes various forms of nociceptive and neuropathic pain.
3. In patients suffering from chronic pain underlying psychological/psychiatric conditions should be addressed if any meaningful recovery is to be achieved.
4. Neuropathic pain is usually less responsive to opioids than pain originating from nociceptors.

·         CRPS stands for complex regional pain syndrome. It is a painful condition usually centered in an extremity in which different degrees of sympathetic dysfunction can be identified. CRPS usually presents with spontaneous pain, hyperalgesia, hyperpathia, and allodynia that is not restricted to the territory of a single nerve. Sympathetic dysfunction presents as variations in regional blood flow that can cause edema and cyanosis. Localized sweating and trophic changes in the skin and nails of the affected part of the body can be seen as the disease progresses. CRPS I (formerly known as RSD) can follow minor trauma, venipuncture, or carpal tunnel surgery; sometimes no identifiable cause can be found. CRPS II (formerly causalgia) follows damage to a peripheral nerve. Sympathetic blocks are very useful since they can facilitate physical therapy and help the patient regain some function in the affected extremity. Upper extremity sympathetic denervation is accomplished by blocking the stellate ganglion; for lower extremity sympathetic block a lumbar sympathetic block is performed.

·         Myofascial pain syndrome is a group of muscle disorders characterized by hypersensitive areas called trigger points that can occur in more than one muscle group. Trigger points when mechanically stimulated will be painful and will refer pain to an area called the reference zone. This reference zone does not correlate with any dermatome or peripheral nerve innervation area.

·         Fibromyalgia is a chronic pain condition characterized by widespread musculoskeletal pain, aches, and stiffness, soft tissue tenderness, general fatigue, and sleep disturbances. The most common sites of pain include the neck, back, shoulders, pelvic girdle, and hands, but any body part can be involved. Fibromyalgia patients experience a range of symptoms of varying intensities that wax and wane over time.

·         Melzack and Wall in 1965 proposed that the substantia gelatinosa in the spinal cord was the primary gate in the transmission of noxious and non noxious stimulus to the central nervous system. The pain gate is opened by information coming from slow unmyelinated C fibers and closed by the impulses from faster myelinated fibers such as A-ß. Since pain is transmitted by slow A-d and C fibers they reason that by activating faster fibers such as the ones that transmit proprioception the gate will be closed and the pain symptoms will improve. A practical application is the use of TENS units as well as spinal and peripheral nerve stimulators for the treatment of pain.

·         The most common indication for use of spinal cord stimulation in the United States is in the treatment of postlaminectomy pain syndromes. In Europe the most common indication is in the treatment of peripheral vascular disease. Among other uses are CRPS I and II, arachnoiditis, and intractable angina pectoris.

Regional Anasthesia

Caudal analgesia can be induced by injection of anesthetic through the sacral hiatus into the sacral epidural space of the vertebral canal well caudal to the termination of the dural sac.

The sacral hiatus represents the absence of a complete neural arch of the fifth sacral vertebra. The four anterior and posterior sacral foramina on either side of the midline join the intervertebral foramen and provide egress for the anterior and posterior primary rami of the sacral spinal nerves. The level to which the anesthesia blocks the spinal nerves is a function of the amount delivered.

·         Local anaesthetic drugs act by inhibiting sodium influx through sodium-specific ion channels in the neuronal cell membrane. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited.

Local anaesthetics (LA) are weak bases. They are either aminoamides or aminoesters. Aminoamides are degraded by hepatic enzymes and aminoesters by the plasma cholinesterase. Local anaesthetic activity can be enhanced by altering the pH of a drug preparation to maximise the amount of drug in the unionized (unprotonated) form. It is well established that local acidosis such as caused by wound infection greatly reduces the action of local anesthetics. Sodium bicarbonate makes LA more hydrophobic thereby increasing its cellular penetration. This increases its potency. The use of adrenaline causes vasoconstriction and decreases the rate of removal of LA by the blood.

·         SAB-associated bradycardia:

Bradycardia may occur secondary to unopposed vagal tone from a high sympathectomy, blockade of the cardioaccelerator fibers (T1-T4), and the Bezold-Jarisch reflex (slowing of the heart rate secondary to a decrease in venous return). Patients with underlying increased vagal tone (children and adults with resting heart rates < 60) are at increased risk. Bradycardia may be treated with anticholinergic agents (atropine) or beta-adrenergic agonists, such as ephedrine.

·         SPINAL ANESTHESIA

1. Loss of afferent sensory and motor stimulation renders a patient sensitive to sedative medications secondary to deafferentation. For the same reason, neuraxial anesthesia decreases the minimum alveolar concentration of volatile anesthetics.
2. Vagal predominance suggests a patient may be at risk for cardiovascular collapse during neuraxial anesthesia.
3. Patients with sympathectomies from regional anesthesia will require aggressive resuscitation, perhaps with unfamiliarly large doses of pressors, to reestablish myocardial perfusion after cardiac arrest.
4. Suspect TNS in a patient who has received a lidocaine spinal anesthetic and has postanesthetic complaints of pain in buttocks and dorsal lower extremities. Notably, there are no objective neurologic findings with this syndrome.

·         EPIDURAL ANALGESIA AND ANESTHESIA

1. Epidural anesthesia is segmental; that is, it has an upper and lower level. The block is most intense near the site of catheter insertion and diminishes with distance.
2. Advantages include avoidance of airway manipulation, decreased stress response, less thrombogenesis, improved bowel motility, awake patient, less postoperative nausea and sedation, better postoperative pain control, and faster turnover.
3. Disadvantages include slow initiation and higher failure rate than general anesthesia.
4. Contraindications include coagulopathy, hemodynamic instability, spinal instrumentation, and patient refusal.
5. Complications include hypotension due to sympathetic blockade, intravascular injection of local anesthetic, subarachnoid injection of a large volume of local anesthetic ("total spinal"), postdural puncture headache, and epidural hematoma.

Procedural Consideration

The peak oxygen consumption (VO2) during exercise appears to provide the most objective assessment of functional capacity in patients with heart failure and may be the best predictor of when to list an individual patient for cardiac transplantation.

·         Exercise tolerance is determined by three factors: pulmonary gas exchange, cardiac performance, and skeletal muscle metabolism. Exercise capacity can be quantified clinically by measurement of oxygen uptake (VO2), carbon dioxide production (VCO2), and minute ventilation.

·         After initial dissection, the patient is fully heparinized. The perfusion-sensitive organs (kidneys and liver) are removed before cardiectomy. The donor heart is excised via median sternotomy. After excision, the donor heart is placed in a plastic bag containing ice-cold saline and transported in an ice-filled cooler. Optimal myocardial function after transplantation is achieved when the donor heart ischemic time is less than 4 hours.

·         Post-CPB LV dysfunction may be a result of a prolonged donor heart ischemic time, inadequate myocardial perfusion, intracoronary embolization of intracavitary air, or surgical manipulation. The incidence of post-CPB LV dysfunction is greater in donors requiring prolonged, high-dose inotropic support before organ harvest.

Post-CPB RV failure is a significant cause of early morbidity and mortality, accounting for nearly 20% of early deaths. Therefore, prevention, diagnosis, and aggressive treatment of RV dysfunction after CPB are essential. Acute RV failure after cardiac transplantation may be due to preexistent pulmonary HTN in the recipient, transient pulmonary vasospasm, tricuspid or pulmonic valve insufficiency secondary to early postoperative RV dilation, and donor-recipient size mismatch. Additional factors that may contribute to postoperative RV dysfunction include a prolonged donor heart ischemic time, inadequate myocardial protection, and surgical manipulation of the heart.

·         In contrast to nonselective vasodilators such as nitroglycerin and sodium nitroprusside, which produce systemic hypotension, inhaled NO (20-80 ppm) selectively reduces PVR in the ventilated area of the lung, improving ventilation-perfusion (V/Q) mismatch. NO has little systemic effect because it is inactivated by hemoglobin and has a 5- to 10-second half-life.

·         three stages of liver transplantation:

The preanhepatic stage (stage 1) begins with the surgical incision and dissection and mobilization of the patient's diseased liver. During this stage, the surgeons identify the hepatic artery, portal vein, and the inferior vena cava, above and below the liver.

The anhepatic stage (stage 2) isolates the liver from the circulation and commences with the occlusion of the hepatic artery and portal vein. Occlusion of the inferior vena cava above and below the liver is performed so that the liver can be removed. During the anhepatic stage, the donated liver is reinserted into the circulation by anastomoses to the patient's vena cava, portal vein, and hepatic artery. The anhepatic stage concludes with removal of the vascular clamps resulting in reperfusion of the donor liver graft.

Stage 3 starts during reperfusion and extends to the conclusion of the operation. It mainly encompasses the process of biliary reconstruction and assessment of graft function.

·         Reperfusion syndrome during stage 2 of liver transplantation: is characterized by either a decrease of 30% or more in mean arterial pressure (from baseline) for greater than 1 minute and occurring within the first 5 minutes of reperfusion, or a mean arterial pressure less than 60 mmHg under the same circumstances. Following unclamping, approximately 30% of patients will exhibit profound cardiovascular collapse on reperfusion irrespective of attentive management during stage 2. The bradycardia, myocardial depression, and systemic vasodilation noted during reperfusion are secondary to rapid increases in serum potassium, decreases in temperature, acute acidosis, and release of vasoactive substances by the grafted liver. These vasoactive mediators include prostaglandins, kallikrein, platelet-activating factor, and leukotrienes. Increased age and larger donor organs also are considered risk factors.

Generally, treatment with calcium and/or epinephrine improves cardiovascular function. Fluid administration should be judicious because it can aggravate the already increased filling pressures (secondary to myocardial depression), resulting in impaired hepatic perfusion. Although the hemodynamic changes generally subside within 10-15 minutes, pulmonary hypertension, elevated central venous pressure (CVP), and hypotension may persist.

·         two basic types of oxygenators:

Bubble oxygenators work by bubbling oxygen (O2) through the patient's blood and then defoaming the blood to minimize air microemboli.

In membrane oxygenators, O2 and CO2 diffuse across a semipermeable membrane. Membrane units are generally preferable owing to a decreased risk of gas microemboli and less damage to blood elements.

·         There are differing opinions as to whether blood gases should be corrected for the temperature during CPB because the solubility of gases decreases with hypothermia. All blood gases are analyzed at 37%. In pH-stat measurements, the obtained value is corrected on a nomogram and the reported values refer to the partial pressure at the hypothermic temperatures. More commonly blood gases are reported uncorrected for temperature, a method referred to as alpha-stat blood gas management. Probably in terms of outcome, there is little difference in how blood gases are interpreted.

·          CARDIOPULMONARY BYPASS

1. There is no "best" anesthetic technique during CPB. Patients with a decreased ejection fraction will not tolerate propofol infusions or volatile anesthesia as well as patients with preserved stroke volume and will probably require an opioid-based technique.
2. Patients should be completely anticoagulated before initiating CPB or face the risk of massive intravascular clot formation.
3. The CPB reservoir should never be allowed to empty during CPB as massive air embolism is a consequence.
4. Factors involved in myocardial preservation include cardioplegia, hypothermia, preventing the heart from becoming warm from an adjacent structure, and ventricular venting and consequences of inadequate myocardial preservation include decreased cardiac output, ischemia, dysrhythmias, and failure to come off pump.
5. Always consider inadequate surgical technique for the patient failing to come off pump.
6. Neurologic complications, in particular neurocognitive deficits, are surprisingly common after CPB.

·         There are two basic techniques for lung isolation:

Double-lumen endotracheal tube (DLT), in which a bifurcated tube with both an endotracheal and endobronchial lumen can be used to isolate, selectively ventilate, or collapse the right or left lung independently according to the operative approach. This is the most common technique.

Blockade of a bronchus to allow lung collapse distal to the occluding bronchial blocker.

·         three methods of bronchial blockade:

Univent tube (Vitaid Airway Management, Williamsville, NY), also known as a torque control blocker

Wire-guided Endobronchial Blocker WEB (Cook Critical Care, Bloomington, IN), also known as an Arndt blocker

Fogarty embolectomy catheter (Baxter Healthcare Corporation, Irvine, CA)

·         SOMATOSENSORY-EVOKED POTENTIALS AND SPINAL SURGERY

1. SSEPs are used when spinal cord or brain parenchyma is at risk for ischemia during surgery.
2. Volatile anesthetics have the most profound effects on SSEP waveforms.
3. An anesthetic technique that minimizes volatile anesthetic exposure is best-an opiate-based technique with low-dose (< 1 MAC) volatile or a total intravenous anesthetic (TIVA).
4. During distraction of the spinal column in scoliosis surgery (or other critical parts of surgery), minimize interventions that will lower mean arterial blood pressure or deepen anesthetic levels acutely to allow differentiation of changes in SSEP waveforms from anesthetic effect.

·         SSEPs are the electrophysiologic responses of the nervous system to the application of a discrete stimulus at a peripheral nerve anywhere in the body. They reflect the ability of a specific neural pathway to conduct an electrical signal from the periphery to the cerebral cortex.

·         Deliberate hypotension is the intentional reduction of systemic perfusion pressure. The major indication for using a deliberate hypotensive technique is to reduce intraoperative blood loss and to produce a relatively bloodless surgical site. Deliberate hypotension decreases blood loss and thereby reduces the need for blood transfusion. This technique has been used in neurosurgical, orthopedic, vascular, and major craniofacial and other plastic procedures. Deliberate hypotension also may be used to help manage patients who refuse blood transfusions (e.g., for religious reasons).

·         DELIBERATE HYPOTENSION

1.       Deliberate hypotension is a technique that can limit blood loss and improve operative conditions but appropriate patient selection is necessary.

2.       Three signs of cyanide toxicity from SNP infusion include (1) the need for doses > 10 µg/kg/min, (2) tachyphylaxis occurring within 60 minutes, or (3) resistance to SNP.

3.       Treatment of cyanide toxicity includes stopping the infusion of SNP; delivery of 100% oxygen; administration of amyl nitrite by inhalation for 30 seconds every 2 minutes; administration of sodium nitrite, 10 mg/kg intravenously, followed by an infusion of 5 mg/kg over 30 minutes; and administration of sodium thiosulfate, 150 mg/kg, not to exceed 12.5 gm, immediately after sodium nitrite.

·         Postoperative visual loss (POVL), ranging from vision deficits to blindness, are catastrophic complications following surgery and anesthesia. Ischemic optic atrophy appears to be the final mechanism though numerous patient-related and intraoperative events have been implicated. Spine surgery and cardiac surgery are the most common procedures associated with POVL.

·         ANESTHESIA FOR MINIMALLY INVASIVE SURGERY

1. PaCO2 increases during CO2 pneumoperitoneum in laparoscopy because of CO2 absorption and ventilation-perfusion mismatch; if the patient is spontaneously breathing, ventilatory depression may also contribute to hypercapnia.
2. Hemodynamic changes during laparoscopy include increased systemic vascular resistance, mean arterial pressure, and left ventricular wall stress; cardiac output decreases initially, then gradually increases back to baseline.
3. Pulmonary changes during laparoscopy include increases in peak inspiratory pressure, intrathoracic pressure, and respiratory resistance and decreases in vital capacity, functional residual capacity, and pulmonary compliance.

·         Only nonelectrolyte solutions can be used for irrigation during TURP. Electrolyte solutions are avoided to minimize the dispersion of current throughout the bladder when electrocautery is used. Dissemination of electrocautery current would be uncomfortable for the patient and dangerous to both patient and surgeon. After completion of surgery and before the patient is moved to the postanesthesia care unit, bladder irrigation should be changed to normal saline. Because fluid absorption from continuous bladder irrigation may continue in the postoperative period, eliminating nonelectrolyte solutions reduces the risk of postoperative hyponatremia.

·         TRANSURETHRAL RESECTION OF THE PROSTATE

1. Hyponatremia secondary to TURP syndrome may present with restlessness, mental confusion, nausea, vomiting, dizziness, headache, unresponsiveness, transient visual changes, hypertension, hypotension, heart rate changes, cardiac arrhythmias, pulmonary edema, or cyanosis.
2. Prompt treatment of TURP syndrome is essential and includes terminating the procedure, changing the bladder irrigant to normal saline, infusing normal saline, evaluating serum sodium and other chemistries, administering diuretics, and considering the use of hypertonic saline in unstable patients.
3. The hyponatremia of TURP syndrome is due to fluid excess and not a loss of sodium.
4. The preferred anesthetic technique is subarachnoid block so that mental status can be followed as an early indicator of hyponatremia.

·         Laser light has three defining characteristics:

Coherence: All waves are in phase, both in time and in space

Collimation: The waves travel in parallel directions

Monochromaticity: All waves have the same wavelength

·         ELECTROCONVULSIVE THERAPY

1. Methohexital should be considered the drug of choice for the induction of anesthesia for ECT.
2. ECT causes pronounced sympathetic activity, which may result in myocardial ischemia or even infarction in patients with coronary artery disease.
3. To perform ECT safely it is necessary to complete a preoperative history and physical examination, use standard monitors, have readily available equipment and medications appropriate for full cardiopulmonary resuscitation, utilize an induction agent (e.g., methohexital) and muscle relaxant (e.g., succinylcholine), and have a beta blocker readily available (e.g., esmolol).

Systemic Diseases

         The resting CBF averages about 225 mL/min, which is 4-5% of the total cardiac output in normal adults. The CBF increases three- to fourfold to supply the extra nutrients needed by the heart at maximum exercise level. The CBF is determined by the pressure gradient between the aorta and the ventricles. There are phasic changes in CBF during systole and diastole in the left ventricle.

·         Myocardial ischemia occurs when coronary blood flow is inadequate to meet the needs of the myocardium. The main coronary artery epicardial branches have lumens that are 2-4 mm in diameter. In the absence of collaterals, exertional angina occurs when the lumen area is reduced to 1 mm2 (50-60% reduction in diameter or 75% reduction in cross-sectional area) and angina at rest occurs when the lumen area is reduced to 0.65 mm2 (75% reduction in diameter or 90% reduction in cross-sectional area). Most of the sclerotic lesions are eccentrically located so the remainder of the arterial wall is responsive to vasoactive stimuli and is capable of contraction. Therefore, the severity of the stenosis is dynamic and influenced by the vasomotor activity of the free arterial wall.

Nonstenotic causes of myocardial ischemia include aortic valve disease, left ventricular hypertrophy, ostial occlusion, coronary embolism, coronary arteritis, and vasospasm.

·         The ability to climb two to three flights of stairs without significant symptoms (angina, dyspnea, syncope) is usually an indication of adequate cardiac reserve > 4 metabolic equivalents (METs) exercise capacity (1 MET equals 3.6 mL/kg/min oxygen consumption at rest).

·         Clinical predictors for perioperative myocardial infarction include the following:

Major predictors include severe or unstable coronary syndromes, decompensated CHF, significant arrhythmias, and severe valvular disease.

Intermediate clinical predictors include mild angina pectoris, prior MI, compensated or prior CHF, and diabetes mellitus.

Minor clinical predictors include advanced age, abnormal ECG (LVH, LBBB, nonspecific ST-T abnormalities), rhythm other than sinus, low functional capacity, history of stroke, and uncontrolled systemic hypertension.

·         A pressure-volume loop plots left ventricular pressure against volume through one complete cardiac cycle. Each valvular lesion has a unique profile that suggests compensatory physiologic changes by the left ventricle.

·         VALVULAR HEART DISEASE

1. Hemodynamic goals in the patient with aortic stenosis include maintaining intravascular volume, contractility, peripheral vascular resistance, and sinus rhythm while avoiding extremes in heart rate. Arrhythmias associated with hypotension require emergent cardioversion.
2. Hemodynamic goals in the patient with aortic insufficiency include augmenting preload, supporting heart rate, maintaining contractility, and afterload reduction.
3. Hemodynamic goals in the patient with mitral stenosis include maintaining intravascular volume, sinus rhythm, a slower heart rate, and afterload. Avoid hypoxemia, hypercarbia, and acidosis because they may increase pulmonary vascular resistance. Sedative medications should be given with great care.
4. Hemodynamic goals in the patient with mitral regurgitation include maintaining intravascular volume, contractility, and an elevated heart rate while reducing afterload. As in mitral stenosis, avoid situations that will increase pulmonary vascular resistance.

·         INTRACRANIAL AND CEREBROVASCULAR DISEASE

1. Atherosclerosis at the bifurcation of the common carotid artery is the source of most cerebral ischemic events.
2. Cerebral autoregulation usually maintains cerebral blood flow relatively constant over a wide range of arterial pressures. It is critically important to maintain the blood pressure of the carotid endarterectomy patient because they have minimal or no autoregulatory reserve to counter anesthetic-induced reductions in blood pressure.
3. Normal cerebral vessels are highly sensitive to arterial carbon dioxide partial pressure, dilating in response to hypercapnia and constricting in response to hypocapnia. However, in ischemic and already maximally vasodilated areas of the brain, this relationship breaks down, and responses to hypercapnia and hypocapnia may be paradoxic.
4. In the normal brain, cerebral blood flow varies directly with the cerebral metabolic rate. Inhalational agents are said to "uncouple" this relationship in that they decrease the cerebral metabolic rate while concurrently dilating cerebral blood vessels and increasing cerebral blood flow.
5. No particular anesthetic technique for CEA has been shown to improve outcome.
6. None of the methods of monitoring cerebral blood flow during CEA has been demonstrated to improve outcome, and none has gained widespread acceptance as the monitor of choice.
7. Postoperative complications of CEA include blood pressure instability, potential for airway obstruction, cerebral hyperperfusion, and stroke.

·         Traditionally, vasospasm of SAH has been treated with hypertensive hypervolemic hemodilution (HHH).

·         The phenomenon of cerebral edema is also called "autoregulation breakthrough." It is commonly seen following AVM resection or embolization. With large AVMs, the high-flow, low-resistance shunt can lead to underperfusion of adjacent brain tissue so the vessels supplying the underperfused region of brain lose the ability to autoregulate. Once the shunt is excised, all of the blood flow is diverted to the previously marginally perfused tissues and the maximally dilated vessels are unable to vasoconstrict. This leads to the potential of cerebral edema, hyperperfusion, and hemorrhage into surrounding areas. The precise mechanism of how and why this occurs is not clear. Neurologic dysfunction following such episodes is a major cause of morbidity and mortality following AVM surgery. Treatment modalities of hyperperfusion include hyperventilation, osmotic diuresis (mannitol), head-up positioning, cautious use of deliberate hypotension, barbiturate coma, and moderate hypothermia.

·         New therapies for treating asthmatic patients in bronchospasm:

Magnesium sulfate: has been administered to patients in status asthmaticus. Hypothetically magnesium interferes with calcium-mediated smooth muscle contraction and decreases acetylcholine release at the neuromuscular junction. Magnesium reduces histamine- and methacholine-induced bronchospasm in controlled studies, but so far clinical studies have failed to show a significant response.

Heliox: a blend of helium and oxygen that decreases airway resistance, peak airway pressures, and PaCO2 levels when administered to spontaneously and mechanically ventilated patients. The mixture contains 60-80% helium and 20-40% oxygen and is less dense than air. The decrease in density allows less turbulent flow and significant declines in resistance to flow. The device for heliox administration in intubated patients is cumbersome unless the anesthesia machine is already equipped.

The Lita-Tube endotracheal tube allows intraoperative instillation of lidocaine at and below the cords of the intubated patient. This technique decreases airway stimulation from the endotracheal tube and may prevent reflex bronchospasm.

·         ASPIRATION

1.       For elective procedures, the most current fasting guidelines are as follows:

Clear liquids (water, clear juices): 2 hours

Nonclear liquids (Jell-O, breast milk): 4 hours

Light meal or snack (crackers, toast, liquid): 6 hours

Full meal (fat containing, meat): 8 hours

2.       Numerous patient subgroups are at increased risk of aspiration, including patients presenting for emergency surgery, those having had a recent meal, those with bowel obstruction or delayed gastric emptying, the obese, trauma or pregnant patients, those having pain or being treated with opioids, and those who cannot protect the airway, such as patients with a depressed level of consciousness or neuromuscular disease.

3.       Such patients may require prophylaxis to decrease the severity of aspiration, should it occur, and medications valuable for decreasing the acidity of gastric secretions include nonparticulate antacids, H2 blockers, and proton pump inhibitors, given at an interval prior to surgery appropriate to their onset of action. Patients with bowel obstruction should receive gastric decompression prior to anesthetic induction.

4.       Regional anesthetics are ideal for patients at risk for aspiration if appropriate. A rapid sequence induction with cricoid pressure is the technique of choice when general anesthesia is required in patients with manageable airways. Awake intubation may be necessary in patients with difficult airways.

5.       Should aspiration occur, the treatment is mostly supportive. Antibiotics should be given if aspiration with gram-negative or anaerobic organisms is suspected (e.g., bowel obstruction).

·         SMOKING CESSATION:

Cessation for 48 hours prior to surgery decreases carboxyhemoglobin levels. The oxyhemoglobin dissociation curve shifts to the right, allowing increased tissue oxygen availability.

Cessation for 4-6 weeks before surgery has been shown to decrease the incidence of postoperative pulmonary complications.

Cessation for 2-3 months before surgery results in all the above benefits plus improved ciliary function, improved pulmonary mechanics, and reduced sputum production.

·         Air trapping is known as auto-PEEP (positive end-expiratory pressure) and results from "stacking" of breaths when full exhalation is not allowed to occur. Auto-PEEP results in impairment of oxygenation and ventilation as well as hemodynamic compromise by decreasing preload and increasing pulmonary vascular resistance. Increasing expiratory time reduces the likelihood of auto-PEEP. This can be accomplished by increasing the expiratory phase of ventilation and decreasing the respiratory rate.

·         NECESSARY CRITERIA FOR ALI/ARDS

1. Acute onset.
2. PaO2/Fio2 ratio = 300 for ALI.
3. PaO2/Fio2 ratio = 200 for ARDS.
4. Chest radiograph with diffuse infiltrates.
5. Pulmonary capillary wedge pressure = 18 mmHg.

• CAUSES AND TREATMENT OF ARDS

1. Historically, sepsis has been identified as the most common risk factor for ARDS. Now Pneumonia ??
2. VALI is thought to be caused by two mechanisms:

Overdistention of normal aerated lung by using high tidal volumes.

Lung collapse that occurs as a result of ventilating the lungs with low end-expiratory volumes and pressures.

3. Mechanical ventilation settings for patients with ARDS or ALI include tidal volume at 6-8 mL/kg of ideal body weight and limiting plateau pressures to < 30 cm H2O.
4. PEEP should be adjusted to prevent end-expiratory collapse.
5. FiO2 should be adjusted to maintain oxygen saturations between 88% and 92%.

·         In general, the potential of an inhalational anesthetic agent to induce immune complexe hepatitis is related to the extent of metabolism. Generally, the degree of metabolism of agents is halothane > sevoflurane > enflurane > isoflurane > desflurane.

·         There is now considerable evidence that dopamine is not renoprotective (that is, improves renal perfusion), nor does it improve splanchnic perfusion. Two recent meta-analyses determined that low-dose dopamine did not prevent mortality or acute renal failure, result in improvement in serum creatinine, or decrease the need for dialysis. Dopamine redistributes renal blood flow to the renal cortex, putting the renal medulla at risk for hypoperfusion and acute renal failure. While dopamine is natriuretic and can increase urine output, this may be deceiving because overall renal function may be deteriorating, especially (but not exclusively) in hypovolemic patients. Dopamine also suppresses anterior pituitary hormonal function and blunts both hypercarbic and hypoxic ventilatory drive, increasing the risk of ventilator dependency.

·         AGENTS TO AVOID IN THE SETTING OF ELEVATED ICP

1.       Ketamine

2.       Etomidate

3.       Nitrous oxide

4.       Hypotonic or glucose-containing intravascular fluid

·         Masseter muscle rigidity (MMR) is defined as jaw muscle tightness with limb muscle flaccidity following a dose of succinylcholine. There is a spectrum of masseter response, from a tight jaw to a rigid jaw to severe spasticity, or trismus, otherwise described as "jaws of steel." Of concern, the mouth cannot be opened sufficiently to intubate the patient. If jaws of steel are present the incidence of MH susceptibility is increased. There is some controversy as to the management of patients experiencing MMR. Most pediatric anesthesiologists agree that if trismus occurs the triggering agent should be halted along with the surgical procedure if feasible. The patient should be admitted to the hospital for 24 hours of close observation. Creatine kinase levels should be followed every 6 hours. Creatine kinase levels greater than 20,000 have a 95% predictive value that the patient is MH susceptible.

·         Dantrolene pretreatment is no longer indicated providing a nontriggering agent and appropriate monitoring are used and an adequate supply of dantrolene is available. Dantrolene pretreatment may cause mild weakness in normal patients and significant weakness in patients with muscle disorders. MH-susceptible patients with an uncomplicated intraoperative course should be monitored for at least 4 hours postoperatively.

·         Only two disorders are clearly associated with a risk of MH:

Central core disease is a channelopathy that presents in infancy and is characterized by generalized muscle weakness. It is generally not debilitating and is autosomal dominant in inheritance.

King-Denborough syndrome is a very rare disorder characterized by myopathy, short stature, pigeon breasts, high forehead, and low-set ears.

Disorders with less convincing evidence of an association with MH include hypokalemic and hyperkalemic periodic paralysis, Charcot-Marie-Tooth disease, Smith-Lemli-Opitz syndrome, strabismus, sudden infant death syndrome, Hurler's syndrome, familial hereditary fever, Angelman's syndrome, and dermatomyositis.

               

·          Succinylcholine must be avoided in children with MD and should be avoided except in airway emergencies in young males.

·         Patients with MG are resistant to succinylcholine. However, the degree of resistance does not appear to be of great clinical significance, and increasing the dose of succinylcholine to 2 mg/kg results in satisfactory intubating conditions.

Myasthenic patients are more sensitive than nonmyasthenic persons to nondepolarizing relaxants. Dosing nondepolarizing relaxants should start at about one-tenth the usual recommended doses. Recovery time for these reduced doses is quite variable but may be quite prolonged. Relaxation should be reversed at case conclusion and the patient carefully evaluated for return of strength.

·         Regional anesthesia may be beneficial in the patient with MS because of a decreased stress response to surgery. Epidural block may be safer than spinal block because the local anesthetic concentration at the spinal cord is lower than following spinal block.

In patients with multiple sclerosis spinal anesthesia should be used with caution and only in situations where the benefits of spinal anesthesia over general anesthesia are clear.

·         CONCERNS IN PATIENTS TAKING COCAINE

1. Myocardial ischemia is not uncommon in cocaine-abusing patients, and selective beta2 blockade should be avoided because it may cause vasoconstriction and worsen the ischemia.
2. Severe hypertension and tachycardia are risks during airway management unless the patient is deeply anesthetized.
3. Cocaine sensitizes the cardiovascular system to the effects of endogenous catecholamines. Ketamine and pancuronium potentiate the cardiovascular toxicity of cocaine and should be avoided.

·         CONCERNS IN PATIENTS TAKING ECSTASY AND PCP

1. Hyperthermia and cardiovascular collapse with ecstasy.
2. Dissociative state, severe behavior disturbances, and enhanced sympathomimetic effects with PCP.

·         DIABETES MELLITUS

1. Careful attention to glucose control prior to, during, and after surgery is important to reduce risk of infection, promote more rapid healing, avoid metabolic complications, and shorten hospital stay.
2. The goal for insulin management during surgery is to maintain glucose between 120 and 200 mg/dL.
3. Intraoperative glucose control in all but the shortest cases is best achieved by using a glucose-insulin intravenous infusion.
4. Diabetic patients have a high incidence of coronary artery disease with an atypical or silent presentation. Maintaining perfusion pressure, controlling heart rate, continuous ECG observation, and a high index of suspicion during periods of refractory hypotension are key considerations.
5. The inability to touch the palmar aspects of index fingers when palms touch (the prayer sign) can indicate a difficult oral intubation in diabetic patients.

·         THYROID AND ADRENAL DISEASE

1. Perioperatively, mild to moderate hypothyroidism is of little concern even for elective surgery. Patients with severe, symptomatic hypothyroidism should be treated preoperatively.
2. Minimum alveolar concentration of volatile anesthetics is unchanged in both hypothyroid and hyperthyroid states.
3. Thyroid storm may mimic malignant hyperthermia. It is detected by an increased serum T4 level, and treated initially with beta blockade followed by antithyroid therapy.
4. Perioperative glucocorticoid supplementation should be considered for patients receiving exogenous steroids.
5. Chronic exogenous glucocorticoid therapy should not be abruptly discontinued. Doing so may precipitate acute adrenocortical insufficiency.

·         OBESITY

1. Morbidly obese patients have numerous systemic disorders, including restrictive lung disease, obstructive sleep apnea, coronary artery disease, diabetes mellitus, hypertension, cardiomegaly, pulmonary hypertension, and delayed gastric emptying, all of which increase the likelihood of anesthetic difficulties and postoperative complications.
2. Obese patients may be difficult to ventilate and difficult to intubate and backup strategies should always be considered and readily available before airway management begins.
3. Because of the increased mass and decreased oxygen reserves, obese patients also desaturate quickly postanesthetic induction, complicating airway management.
4. Because obese patients have altered volumes of distribution of anesthetic agents, these drugs should be titrated to affect and not dosed based on body weight.
5. Respiratory complications are particularly common in obese patients.

·         While the symptoms are indistinguishable from anaphylaxis, an anaphylactoid reaction is nonimmune mediated. Release of inflammatory mediators from mast cells and basophils results in activation of the complement cascade.

Perioperative Problems

*  Negative-pressure pulmonary edema: A phenomenon unique to the postextubation period and thus pertinent to the PACU is negative-pressure pulmonary edema. As with other causes of pulmonary edema, findings include coarse breath sounds and production of pink frothy sputum. Typically in the PACU setting hypoxia and hypertension precede the telltale physical signs.

·         Recruitment maneuver, Also known as a vital capacity (VC) maneuver, the technique consists of giving multiple manual positive-pressure "sigh" breaths and maintaining pressure at 40 cm H2O for 5-10 seconds in an effort to open, or "recruit," atelectatic alveoli. Nearly all patients experience atelectasis under general anesthesia. A VC maneuver resolves this atelectasis, but it will recur within 5 minutes or so of breathing 100% oxygen. Atelectasis recurs more slowly if a lower fraction of inspired oxygen (FiO2) is used (e.g., > 45 minutes for FiO2 of 0.30).

·         Diffusion hypoxia is a decrease in PO2 usually observed as the patient is emerging from an inhalational anesthetic where nitrous oxide (N2O) was a component. The rapid outpouring of insoluble N2O can displace alveolar oxygen, resulting in hypoxia. All patients should receive supplemental O2 at the end of an anesthetic and during the immediate recovery period.

·         Commonly cited criteria for intubation and mechanical ventilation in adults include the following:

PaO2/FiO2 ratio < 300 mmHg

PaCO2 > 50 mmHg in the absence of metabolic alkalosis (also consider chronicity)

Dead space to tidal volume ratio (Vd/Vt) > 0.6

Respiratory rate > 35

Insufficient negative inspiratory force (NIF) > -20 mm H2O

Tidal volume < 5 mL/kg

Vital capacity

·         Methylmethacrylate, a cement used in joint replacement, undergoes an exothermic reaction that causes it to adhere to imperfections in the bony surface. Hypotension usually occurs 30-60 seconds after placement of the cement but can occur up to 10 minutes later. Postulated mechanisms include tissue damage from the reaction, release of vasoactive substances when it is hydrolyzed to methacrylate acid, embolization, and vasodilation caused by absorption of the volatile monomer.

·         DIFFERENTIAL DIAGNOSIS FOR A NARROW COMPLEX TACHYCARDIA

Sinus tachycardia

Atrial flutter

Atrial fibrillation

Multifocal atrial tachycardia

Atrial tachycardia

Atrioventricular nodal reentrant tachycardia (AVNRT)

Atrioventricular reentrant tachycardia (AVRT)

Junctional tachycardia

·         Despite its short half-life, adenosine can provoke severe exacerbations of bronchospasm, and it should be used with caution in patients with a history of asthma or reactive chronic obstructive pulmonary disease.

·         DIFFERENTIAL DIAGNOSIS FOR A WIDE COMPLEX TACHYCARDIA

1. Ventricular tachycardia
2. Supraventricular tachycardia with aberrant conduction, such as with a bundle branch block
3. Tachycardia with activation of the ventricles via an accessory pathway (Wolff-Parkinson-White syndrome)

·         Monomorphic ventricular tachycardia is common in patients with structural heart disease (such as a previous Q wave myocardial infarction), but it is generally not due to acute ischemia. Polymorphic VT may be seen in a variety of settings. Patients may have a long QT interval associated with polymorphic ventricular tachycardia, commonly referred to as torsades de pointes. This may arise from medications, electrolyte derangements, a congenital predisposition (long QT syndrome), severe bradycardia, or myocardial ischemia.

·         TEMPERATURE DISTURBANCES

1. Hypothermia is an extremely common event in the operating room because the environment and the effects of anesthetics increase heat loss. Anesthetics also decrease the ability to generate a response to hypothermia (shivering and vasoconstriction).
2. Even mild hypothermia has a negative influence on patient outcome, increasing wound infection rates, delaying healing, increasing blood loss, and increasing cardiac morbidity threefold.
3. The best method to treat hypothermia is use of forced air warming blankets. Warm all fluids and blood products. Cover all body surfaces possible, including the head, to further reduce heat loss.

·         A phenomenon unique to the postextubation period and thus pertinent to the PACU is negative-pressure pulmonary edema. As with other causes of pulmonary edema, findings include coarse breath sounds and production of pink frothy sputum. Typically in the PACU setting hypoxia and hypertension precede the telltale physical signs. The cause of the edema is the patient's vigorous ventilatory effort against a partially closed glottis or occasionally a small endotracheal tube. The clinical presentation follows a rapid emergence, often when the patient has been intoxicated at the time of induction. This phenomenon should be anticipated in young muscular individuals but may occur in any patient with some degree of laryngospasm after extubation.