Curtis Sheldon, MD

• Assistant Professor of Surgery, University of Cincinnati
• Director, Pediatric Urology, Cincinnati Children? Hospital,
• Cincinnati, Ohio

Propofol increases collapsibility of the upper airway by inhibiting genioglossus and other muscles 1 discount 0.1mg clonidine with visa,17 and airway obstruction may occur with sedative doses or during emergence from propofol anesthesia heart attack early symptoms buy 0.1 mg clonidine. When compared with thiopental heart attack xbox purchase clonidine master card, propofol decreases the incidence of wheezing after induction of anesthesia and tracheal intubation in healthy and asthmatic patients arteria zygomaticoorbitalis discount clonidine 0.1 mg overnight delivery. Similar to thiopental and unlike volatile anesthetics pulse pressure 67 proven 0.1mg clonidine, propofol probably does not enhance neuromuscular blockade from neuromuscular blocking drugs hypertension 80 mg purchase clonidine us. Yet, propofol often provides excellent clinical conditions for endotracheal intubation without the use of neuromuscular blocking drugs. Unexpected arrhythmias or electrocardiogram changes occurring during propofol anesthesia should prompt laboratory evaluation for possible metabolic acidosis, rhabdomyolysis, or hyperkalemia (propofol infusion syndrome). The dose should be decreased in the elderly, especially those who have a reduced cardiovascular reserve, or after premedication with benzodiazepines or opioids. Obese patients require a larger total dose compared with nonobese patients of similar height and age, but boluses for morbidly obese patients should be calculated per kilogram of lean body weight rather than total body weight to avoid excess hypotension. The required plasma concentration is 1 to 2 g/mL, which normally requires a continuous infusion rate between 25 and 75 g/kg/min. Because of its pronounced respiratory depressant effect and its narrow therapeutic range, propofol should be administered only by individuals trained in airway management. Spontaneous ventilation is usually preserved in children at quite rapid propofol infusion rates (200 to 250 g/kg/ min), making it a good choice for pediatric procedures such as magnetic resonance imaging scans24 (also see Chapter 34). As mentioned earlier, the lipid emulsion formulation of propofol has several disadvantages including pain on injection, risk of bacterial contamination, and hypertriglyceridemia with prolonged infusion. Intense research has therefore focused on finding alternative formulations or related drugs to address some of these problems. Given the kinetics previously described, fospropofol in theory should cause less hypotension31 and less respiratory depression than propofol. Common side effects of fospropofol include a perineal burning sensation and pruritus. Small trials have demonstrated safety and efficacy of fospropofol for sedation during colonoscopy, bronchoscopy, and minor surgical procedures. Hence, fospropofol should be administered only by personnel trained in airway management. It is metabolized by alkaline phosphatase in a reaction producing propofol, phosphate, and formaldehyde. Aldehyde dehydrogenase in the liver and in erythrocytes rapidly metabolizes formaldehyde to produce formate, which is further metabolized by 10-formyltetrahydrofolate dehydrogenase. Pharmacokinetics Because fospropofol is a prodrug that requires metabolism to form the active compound propofol, the pharmacokinetics are complex. Multicompartment models with two compartments for fospropofol and three for propofol have been used to describe the kinetics. In theory, a fospropofol bolus should yield lower peak plasma levels and a delayed time-to-peak compared with propofol. Based on their substitution at position 2, barbiturates can be grouped into thiobarbiturates, substituted with a sulfur (thiopental), or oxybarbiturates, substituted with an oxygen (methohexital). Hypnotic, sedative, and anticonvulsant effects, as well as lipid solubility and onset time, are determined by the type and position of substitution. Thiopental and methohexital are formulated as sodium salts mixed with anhydrous sodium carbonate. Although this property prevents bacterial growth and helps increase the shelf life of the solution after reconstitution, it will lead to precipitation when mixed with acidic drug preparations such as neuromuscular blocking drugs. These precipitates can irreversibly block intravenous delivery lines if mixing occurs during administration. Furthermore, accidental injection into an artery or infiltration into paravenous tissue will cause extreme pain and may lead to severe tissue injury. Several barbiturates, including thiopental and methohexital, have optical isomers with different potencies. However, the available formulations are racemic mixtures, and their potencies reflect the summation of the potencies of the individual isomers. Through stimulation of aminolevulinic acid synthetase, the production of porphyrins is increased. Therefore, barbiturates should not be administered to patients with acute intermittent porphyria. Methohexital is cleared more rapidly by the liver than thiopental and thus has a shorter elimination half-time. This accounts for faster and more complete recovery after methohexital administration. Although thiopental is metabolized slowly and has a long elimination half-time, recovery after a single bolus administration is comparable to methohexital and propofol because it depends on redistribution to inactive tissue sites rather than metabolism. The resulting metabolites are inactive and excreted through urine and, after conjugation, through bile. Subsequently, thiopental is redistributed to skeletal muscles (red line) and, to a lesser extent, to fat (pink line). Ultimately, most of the administered dose of thiopental undergoes metabolism (green line). For the same reason, methohexital is also a popular choice for anesthesia to facilitate electroconvulsive therapy (also see Chapter 38). Although barbiturates blunt the baroreceptor reflex, compensatory increases in heart rate limit the magnitude and duration of hypotension. Moreover, dilation of peripheral capacitance vessels leads to pooling of blood and decreased venous return, thus resulting in reduced cardiac output and systemic arterial blood pressure. Indeed, exaggerated decreases in blood pressure are likely to follow the administration of barbiturates to patients with hypovolemia, cardiac tamponade, cardiomyopathy, coronary artery disease, or cardiac valvular disease because these groups are less able to compensate for the effects of peripheral vasodilation. The negative inotropic effects of barbiturates, which are readily demonstrated in isolated heart preparations, are usually masked in vivo by baroreceptor reflex-mediated responses. Furthermore, they may provide neuroprotection from focal cerebral ischemia (stroke, surgical retraction, temporary clips during aneurysm surgery) but probably not from global cerebral ischemia (cardiac arrest). Anesthetic induction doses of thiopental and methohexital typically induce transient apnea, which is more pronounced in the presence of other respiratory depressants. Suppression of laryngeal reflexes and cough reflexes is not as profound as after propofol administration, which makes barbiturates an inferior choice for airway instrumentation in the absence of neuromuscular blocking drugs. Furthermore, stimulation of the upper airway or trachea (secretions, laryngeal mask airway, direct laryngoscopy, tracheal intubation) during inadequate depression of airway reflexes may result in laryngospasm or bronchospasm. This phenomenon is not unique to barbiturates but is true in general Chapter 8 Intravenous Anesthetics when the dose of anesthetic is inadequate to suppress the airway reflexes. Side Effects Accidental intra-arterial injection of barbiturates results in excruciating pain and intense vasoconstriction, often leading to severe tissue injury involving gangrene. One approach to treatment is blockade of the sympathetic nervous system in the involved extremity (stellate ganglion block). Barbiturate crystal formation probably results in the occlusion of distal, small-diameter arterioles. Crystal formation in veins is less hazardous because of the ever-increasing diameter of veins. Accidental subcutaneous injection (extravasation) of barbiturates results in local tissue irritation, thus emphasizing the importance of using dilute concentrations (2. In some situations, the anesthesia provider may choose a "rapid-sequence induction" of anesthesia, typically when a patient is at increased risk for aspiration of gastric contents. The classic drug regimen for rapid-sequence induction is a barbiturate, usually thiopental, followed by succinylcholine in rapid succession. Important advantages of this technique are avoidance of bag-mask ventilation and early tracheal intubation with a cuffed tube. Although thiopental was the traditional drug used for rapid-sequence induction, propofol is currently the more frequent choice. For patients who are not at increased risk of aspirating gastric contents, intravenous barbiturates may be used to initiate a gradual induction. The induction can then be completed by delivering an inhaled agent such as sevoflurane. This type of slow induction helps titrate the anesthetic effect more carefully and avoids exaggerated hemodynamic responses. A gradual induction can also be accomplished by careful titration of intravenous anesthetics alone, but propofol is probably a more logical choice for this application because it has a shorter context-sensitive half-time. When used as an anesthetic for electroconvulsive therapy, methohexital may allow for longer seizure duration when compared with propofol. The utility of barbiturates can be illustrated by describing several different techniques for anesthesia induction. In a large registry of patients undergoing repair of acute type A aortic dissection, there was no benefit from barbiturates for preventing permanent neurologic dysfunction,42 and these drugs are unlikely to be of benefit during cardiac surgery. Physicochemical Characteristics the chemical structure of the benzodiazepines contains a benzene ring fused to a seven-member diazepine ring, hence their name. The three benzodiazepines commonly used in the perioperative setting are all highly lipophilic, with midazolam having the highest lipid solubility. Although they are used as parenteral formulations, all three drugs are absorbed after oral administration. Other possible routes of administration include intramuscular, intranasal, and sublingual. Exposure of the acidic midazolam preparation to the physiologic pH of blood causes a change in the ring structure that renders the drug more lipid soluble, thus speeding its passage across the blood-brain barrier and its onset of action. Metabolism of benzodiazepines occurs in the liver through microsomal oxidation (N-dealkylation and aliphatic hydroxylation) and glucuronide conjugation. Microsomal oxidation, the primary pathway for metabolism of midazolam and diazepam, is more susceptible to external factors such as age, diseases (hepatic cirrhosis), and the administration of other drugs that modulate the efficiency of the enzyme systems. Lorazepam is one of few benzodiazepines that does not undergo oxidative metabolism and is excreted after a single-step conjugation to glucuronic acid. Diazepam undergoes hepatic metabolism to active metabolites (desmethyldiazepam and oxazepam) that may contribute to the prolonged effects of this drug. Whereas 1-hydroxymidazolam has sedative effects similar to the parent compound, it undergoes rapid glucuronidation and clearance. Furthermore, the short duration of action of a single dose of midazolam is due to its lipid solubility and rapid redistribution as prevously described. Of the three commonly used intravenous benzodiazepines, midazolam has the shortest context-sensitive halftime, making it the most suitable for continuous infusion. Remimazolam contains a carboxylic ester group that is rapidly hydrolyzed by tissue esterases, analogous to remifentanil (also see Chapter 9). Indeed, the magnitude of depression of ventilation and the development of hypotension after the administration of benzodiazepines are lower than that observed when barbiturates are used for induction of anesthesia (Table 8. Spectrum of Effects Safety Profile Benzodiazepines have a very favorable side effect profile. When administered alone, these drugs cause only minimal depression of ventilation and the cardiovascular system, making them relatively safe even in larger doses. Central Nervous System (Also See Chapter 30) the wide spectrum of effects of benzodiazepines is similar for all drugs in this class, although potencies for individual effects may vary between drugs. The site of action for muscle relaxation is in the spinal cord, and this effect requires much larger doses. They are potent anticonvulsants for the treatment of status epilepticus, alcohol withdrawal, and local anesthetic-induced seizures. Pain during intravenous injection and subsequent thrombophlebitis are most pronounced with diazepam and reflect the poor water solubility of this benzodiazepine. It is the organic solvent, propylene glycol, required to dissolve diazepam that is most likely responsible for pain during intramuscular or intravenous administration, as well as for the unpredictable absorption after intramuscular injection. Midazolam is more water soluble (but only at low pH), thus obviating the need for an organic solvent and decreasing the likelihood of exaggerated pain or erratic absorption after intramuscular injection or pain during intravenous administration. Decreased Decreased Decreased Decreased Decreased Decreased Decreased Decreased Yes No No No Unchanged No No Unchanged to Increased decreased Unchanged Unchanged Unchanged to Unchanged decreased Decreased Decreased Decreased Unchanged Yes Yes No No Decreased Yes No Unchanged Increased to unchanged Increased to unchanged Increased to unchanged Yes No Yes Yes Unchanged No No Adrenocortical suppression No Pain on injection *May Bolus Yes cause direct myocardial depression and hypotension in critically ill or catecholamine-depleted patients. Clinical Uses Benzodiazepines are used for (1) preoperative medication, (2) intravenous sedation, (3) intravenous induction of anesthesia, and (4) suppression of seizure activity. The slow onset and prolonged duration of action of lorazepam limit its usefulness for preoperative medication or induction of anesthesia, especially when rapid and sustained awakening at the end of surgery is desirable. Preoperative Medication and Sedation (Also See Chapter 13) the amnestic, anxiolytic, and sedative effects of benzodiazepines are the basis for the use of these drugs 114 for preoperative medication. Many patients who receive preoperative midazolam do not recall the operating room, and some have no memory of the preoperative holding area. Although awareness during anesthesia is rare (also see Chapter 47), benzodiazepines seem Chapter 8 Intravenous Anesthetics to be superior to ketamine and barbiturates for prevention of recall. However, the combination of these drugs also exacerbates respiratory depression and may lead to airway obstruction or apnea. Only the racemic mixture of ketamine (10, 50, 100 mg/mL) is available in the United States. After its initial introduction, ketamine was for a time established as a safe anesthetic. However, the popularity of ketamine has since declined, and its unpleasant psychomimetic side effects have limited its use in anesthesia. Still, the unique features of ketamine (potent analgesia with minimal respiratory depression) make it a very valuable alternative in certain settings.

The relationship of age to the pharmacokinetics of early drug distribution: the concurrent disposition of thiopental and indocyanine green blood pressure what do the numbers mean cheap clonidine 0.1mg line. Although treatment of chronic systemic hypertension is sometimes necessary blood pressure chart for 70+ year olds best buy clonidine, acute hypotension is often a problem with many anesthetics arteria thoracoacromialis clonidine 0.1mg free shipping. Hypotension can be of sufficient magnitude to jeopardize organ perfusion blood pressure medication make you gain weight purchase generic clonidine canada, causing injury and an adverse outcome blood pressure medication questions buy discount clonidine line. Organs of most immediate concern are the heart and brain arrhythmia word breakdown discount generic clonidine canada, followed by the kidneys, liver, and lungs. Intraoperative hemodynamic instability has long been thought to result in worse outcomes after surgery. Whether a change in anesthetic management will alter these risks needs future study. Systemic Vascular Resistance hyperdynamic states, such as sepsis and liver failure, are associated with decreased systemic blood pressure. Although the amount of blood pumped by the right side and left side of the heart can differ in the presence of certain congenital heart malformations, these amounts are usually the same. On the other hand, hypertension nearly always involves excessive vasoconstriction. Most of the resistance to blood flow in the arterial side of the circulation is in the arterioles. Loss of sinus rhythm and atrial contraction results in decreased ventricular filling. Atrial contraction constitutes a significant percentage of preload, even more so in patients with a poorly compliant ventricle. Preload refers to the amount the cardiac muscle is "stretched" before contraction. The relationship between pressure and volume of the heart in diastole is depicted by ventricular compliance curves. Likewise, trying to fill a "stiff" left ventricle to a normal volume may increase intracardiac and pulmonary capillary pressures excessively. At higher points on the curve, little additional benefit is derived from increases in preload. The "stiff" heart shows a steeper rise of pressure with increased volume than the normal heart. Venodilation occurs with general anesthesia and may be even more prominent in the presence of neuraxial anesthesia (also see Chapter 17). Additional causes of decreased preload include tension pneumothorax and pericardial tamponade, which prevent ventricular filling due to increased pressure around the heart, even though blood volume and filling pressures are adequate. Pathologic problems on the right side of the heart may prevent filling of the left ventricle. Pulmonary embolism and other causes of pulmonary hypertension prevent the right side of the heart from pumping a sufficient volume to fill the left side of the heart. The interventricular septum may be shifted, further constricting filling of the left side of the heart. Filling pressure can be measured as left atrial pressure or pulmonary capillary wedge pressure. At low preload, augmentation of filling results in significantly increased cardiac output. It can be measured for research purposes by the rate at which pressure develops Afterload is the resistance to ejection of blood from the left ventricle with each contraction. When the pressure decreases below left atrial pressure, the mitral valve opens, and diastolic filling begins. The systolic pressure-volume relationship (black line) can be constructed from a family of curves under different loading conditions. The red dashed line suggests the transition to the new cardiac cycle shown in blue. A clinical understanding of cardiac reflexes is based on the concept that the cardiovascular system in the brainstem integrates the signal and provides a response through the autonomic nervous system. This finding may suggest that preload rather than afterload is the cause of hypotension. Such 56 Autonomic Nervous System the heart and vascular systems are controlled by the autonomic nervous system. Sympathetic and parasympathetic efferents innervate the sinoatrial and atrioventricular nodes. Conduction through the atrioventricular node is increased and decreased by Chapter 5 Clinical Cardiac and Pulmonary Physiology sympathetic and parasympathetic nervous system innervation, respectively. Baroreceptors Baroreceptors in the carotid sinus and aortic arch are activated by increased systemic blood pressure that stimulates stretch receptors to send signals through the vagus and glossopharyngeal nerves to the central nervous system. The sensitivity of baroreceptors to systemic blood pressure changes varies and is significantly altered by longstanding essential hypertension. Vagal stimulation and decreases in sympathetic nervous system activity also decrease myocardial contractility and cause reflex vasodilatation. This carotid sinus reflex can be used therapeutically to produce vagal stimulation that may be an effective treatment for supraventricular tachycardia. The atria and ventricles are innervated by a variety of sympathetic and parasympathetic receptor systems. Stimulation of the chemoreceptors in the carotid sinus has respiratory and cardiovascular effects. Arterial hypoxemia results in sympathetic nervous system stimulation, although more profound and prolonged arterial hypoxemia can result in bradycardia, possibly through central mechanisms. The Cushing reflex includes bradycardia in response to increased intracranial pressure. Many anesthetics blunt cardiac reflexes in a dosedependent fashion, with the result that sympathetic nervous system responses to hypotension are reduced. The blunting of such reflexes represents an additional mechanism by which anesthetic drugs contribute to hypotension. Endogenous regulators of coronary blood flow include adenosine, nitric oxide, and adrenergic stimulation. With coronary artery stenosis, compensatory vasodilatation downstream can maintain coronary blood flow until about 90% stenosis, when coronary reserve begins to become exhausted. Instantaneous flow through the coronary arteries varies throughout the cardiac cycle, peaking during systole. The heart is fundamentally different from other organs, because the myocardial wall tension developed during systole can completely stop blood flow in the subendocardium. The right ventricle, with its lower intramural pressure, is perfused during diastole and systole. The bronchial circulation supplies nutrients to lung tissue and empties into the pulmonary veins and left atrium. The pulmonary circulation differs substantially from the systemic circulation in its regulation, normal pressures (Table 5. Pulmonary hypertension has idiopathic causes and may accompany several common diseases. It is associated with significant anesthetic-related morbidity and mortality rates. The consequence of this physiology is that the heart cannot increase oxygen extraction as a reserve mechanism. In cases of threatened oxygen supply, vasodilatation to increase blood flow is the primary compensatory mechanism of the heart. Coronary reserve is the ability of the coronary circulation to increase flow more than the baseline state. During blood flow through the pulmonary circulation, resistance is thought to occur in the larger vessels, small arteries, and capillary bed. Vessels within the alveoli and the extra-alveolar vessels respond differently to forces within the lung. The most useful physiologic model for describing changes in the pulmonary circulation is the distention of capillaries and the recruitment of new capillaries. With large lung volumes, intra-alveolar vessels can be compressed, whereas extraalveolar vessels have lower resistance. Sympathetic nervous system stimulation can cause pulmonary vasoconstriction, but the effect is not large, in contrast to the systemic circulation, in which neurohumoral influence is the primary regulator of vascular tone. Nitric oxide is an important regulator of vascular tone and can be given by inhalation. Common forms of emboli are blood clots and air, but they also include amniotic fluid, carbon dioxide, and fat emboli. Arteriolar Thickening Arteriolar thickening occurs in several clinical circumstances. Primary pulmonary hypertension is an idiopathic disease associated with arteriolar hyperplasia. Gravity determines the way pressures change in the vascular system relative to the measurement at the level of the heart. Position can also be used therapeutically to decrease blood flow to abnormal areas of the lung, such as unilateral pneumonia, and thereby improve gas exchange. Blood flow through the collapsed lung during one-lung ventilation is also reduced by this physiologic effect. Pulmonary Edema Intravascular fluid balance in the lung depends on hydrostatic driving forces. Excessive pulmonary capillary pressures cause fluid to leak into the interstitium and then into alveoli. Although the pulmonary lymphatic system is very effective in clearing fluid, it can be overwhelmed. Hydrostatic pulmonary edema is expected with high left ventricular filling pressures. Pulmonary edema can also occur with "capillary leak" from lung injury, such as acid aspiration of gastric contents, sepsis, or blood transfusion. The higher Pco2 and the lower pH of venous blood cause a rightward shift of the curve and facilitate unloading of oxygen in the tissues (blue). Arterial hypoxemia is defined as a low partial pressure of oxygen in arterial blood (Pao2). An arbitrary definition of arterial hypoxemia (Pao2 < 60 mm Hg) is commonly used but not necessary. Occasionally, arterial hypoxemia is used to describe a Pao2 that is low relative to what might be expected based on the inspired oxygen concentration (Fio2). Arterial hypoxemia (which reflects pulmonary gas exchange) is distinguished from hypoxia, a more general term including tissue hypoxia, which also reflects circulatory factors. Anoxia, a nearly complete lack of oxygen, is potentially fatal and is often associated with permanent neurologic injury, depending on its duration. Arterial hypoxemia is most significant when anoxia is threatened, such as with apnea, and the difference between the two may be less than 1 minute. Oxyhemoglobin Dissociation Curve Measurements of arterial blood oxygen levels include Pao2, oxyhemoglobin saturation (Sao2), and arterial oxygen content (Cao2). Understanding the oxyhemoglobin dissociation curve is facilitated by the ability to measure continuous oxyhemoglobin saturation with pulse oximetry (Spo2) and measurement of Pao2 with arterial blood gas analysis. Rightward and leftward shifts of the oxyhemoglobin dissociation curve provide significant homeostatic adaptations to changing oxygen availability. P50, the Po2 at which hemoglobin is 50% saturated with oxygen, is a measurement of the position of the oxyhemoglobin dissociation curve. Other points on the curve, such as the normal venous point and points for 80% and 90% oxygen saturations may also be clinically useful. A rightward shift causes little change in conditions for loading oxygen (essentially the same Sao2 at Po2 of 100 mm Hg), but it allows larger amounts of oxygen to dissociate from hemoglobin in the tissues. Carbon dioxide and metabolic acid shift the oxyhemoglobin dissociation curve rightward, whereas alkalosis shifts it leftward. Most blood gas machines are now combined with oximeters so that the Sao2 provided is a true measured value, not calculated. This is called the functional saturation, which is the percent oxyhemoglobin saturation relative to hemoglobin available to bind oxygen. Oxygen content at the plateau of the curve (Po2 > 100 mm Hg) continues to rise because dissolved oxygen still contributes a small, but not negligible, quantity. Although amounts of dissolved oxygen are fairly trivial at normal Po2 levels, at high Fio2 dissolved oxygen can be physiologically and clinically important. Although under normal conditions only a fraction (25%) of the oxygen on hemoglobin is used, all of the added dissolved oxygen added while giving supplemental oxygen can be used. For example, if Hb = 15 g/dL and Pao2 = 100 mm Hg, resulting in nearly 100% saturation, the value of Cao2 is calculated as follows: CaO2 = 1. The oxygen cascade depicts the passage of oxygen from the atmosphere to the tissues. Multiwavelength Pulse Oximetry Complete measurement of oxygen parameters are derived not just from analysis of arterial blood gases (Pao2) but 60 the alveolar gas equation describes the way in which inspired oxygen and ventilation determine Pao2. One clinical consequence of this relationship is that supplemental oxygen can easily compensate for the adverse effects of hypoventilation. Modern anesthesia machines have safety mechanisms to prevent delivery of hypoxic gas mixtures. Nevertheless, death from delivery of gases other than oxygen is still occasionally reported because of errors in pipe connections made during construction or remodeling of operating rooms. Current anesthesia machines have multiple safety features to prevent delivery of hypoxic gas mixtures. Delivery of an inadequate Fio2 may occur when oxygen tanks run out or with failure to recognize accidental disconnection of a self-inflating bag (Ambu) from its oxygen source. Apnea is an important cause of arterial hypoxemia, and storage of oxygen in the lung is of prime importance in delaying the appearance of arterial hypoxemia in humans.

The anion gap is the difference between measured cations (sodium) and measured anions (chloride and bicarbonate) and represents the concentration of anions in serum that are unaccounted for in this equation hypertension 3rd trimester buy 0.1mg clonidine. A normal anion gap value is 8 to 12 mEq/L and is mostly composed of anionic serum albumin blood pressure how to take buy discount clonidine on line. An increase in the anion gap occurs when the anion replacing bicarbonate is not one that is routinely measured blood pressure quitting drinking order 0.1 mg clonidine with mastercard. Metabolic acidosis with a normal anion gap occurs when chloride replaces the lost bicarbonate such as with a bicarbonate-wasting process in the kidneys (renal tubular acidosis) or gastrointestinal tract (diarrhea) blood pressure medication pictures generic clonidine 0.1mg visa. Aggressive fluid resuscitation with normal saline (>30 mL/ kg/h) will induce a nongap metabolic acidosis secondary to excessive chloride administration heart attack normal ekg clonidine 0.1mg line, which impairs bicarbonate reabsorption in the kidneys blood pressure normal readings clonidine 0.1 mg fast delivery. Henderson-Hasselbalch) is the inclusion of the serum albumin concentration in the Stewart approach, which provides some increase in accuracy in certain clinical settings. If changes in serum albumin concentration are accounted for in measurement of the anion gap, the more complex Stewart approach does not appear to offer a clinically significant advantage over the traditional approach to acid-base disturbances. Chronic metabolic acidosis, as seen with chronic renal failure, is commonly associated with loss of bone mass because buffers present in bone are used to neutralize the nonvolatile acids. Treatment of metabolic acidosis is based on whether an anion gap is present or not. Intravenous administration of sodium bicarbonate is often given for a nongap metabolic acidosis because the problem is bicarbonate loss. Management of an anion gap metabolic acidosis is guided by diagnosis and treatment of the underlying cause in order to remove the nonvolatile acids from the circulation. Tissue hypoxia leading to lactic acidosis should be corrected if possible with oxygen, fluid resuscitation, and circulatory support. Minute ventilation can be increased in a patient who is mechanically ventilated to compensate until more definitive treatment takes effect. Bicarbonate therapy is more controversial, but may be considered in the setting of extreme metabolic acidosis as a temporizing measure, particularly when a patient is hemodynamically unstable. Sodium bicarbonate administration generates carbon dioxide, which, unless eliminated by ventilation, can worsen any intracellular and extracellular acidosis. A common approach is to administer a small dose of sodium bicarbonate, and then repeat the pH measurement and monitor hemodynamics to determine the impact of treatment. Alkalinizing drugs, because of their osmotic properties, introduce the risk of causing hypervolemia and hypertonicity. The loss of hydrogen ions is usually from the gastrointestinal tract or the kidney. The stimulus for bicarbonate reabsorption or gain is usually from hypovolemia, hypokalemia, or hyperaldosteronism (Box 21. In hypovolemia, because of insufficient chloride ions, bicarbonate is reabsorbed with sodium. The efficiency of the renal compensatory mechanism is dependent on the presence of cations (sodium, potassium) and chloride. Lack of these ions impairs the ability of the kidneys to excrete excess bicarbonate and results in incomplete renal compensation. Respiratory compensation for pure metabolic alkalosis, in contrast to metabolic acidosis, is never more than 75% complete. As a result, the pH remains increased in patients with primary metabolic alkalosis. Diagnosis the diagnosis of an acid-base disorder should occur in a structured fashion. Step 3 looks at whether the cause is from a primary metabolic or respiratory process. Metabolic processes involve a change in bicarbonate concentration from 24 mEq/L, and respiratory processes involve a change in Pco2 from 40 mm Hg. If the primary process is respiratory in origin, then step 4 assesses whether the abnormality is chronic or acute (Box 21. If a metabolic alkalosis is present, then the next step is to skip to step 7 and determine whether appropriate respiratory compensation is present (Box 21. If the measured Pco2 is more than expected, a concurrent respiratory acidosis is present. If the measured Pco2 is less than expected, then a concurrent respiratory alkalosis is present. If a metabolic acidosis is present, then an anion gap should be calculated (step 5). The gap is the excess anion gap (anion gap minus 12) added back to the serum bicarbonate level. If the number is less than 22 mEq/L, then a concurrent nongap metabolic acidosis is present. If the number is more than 26 mEq/L, then a concurrent metabolic alkalosis is present. The last step, step 7, determines whether an appropriate respiratory compensation is present for the metabolic acidosis. If the measured Pco2 is more than expected [as calculated by the formula Pco2 = (0. If the measured Pco2 is less than calculated, then a concurrent respiratory alkalosis is present. If measured Pco2 < calculated Pco2, then concurrent respiratory alkalosis is present. Ventilation Paco2 reflects the adequacy of ventilation for removing carbon dioxide from blood. A measured Paco2 above 45 mm Hg suggests that a patient is hypoventilating relative to carbon dioxide production, whereas a Paco2 below 35 mm Hg suggests that a patient is hyperventilating. Increased dead space ventilation markedly decreases the efficiency of ventilation. The Vd/Vt ratio is the fraction of each tidal volume that is involved in dead space ventilation. Arterial hypoxemia may be caused by (1) a low Po2 in the inhaled gases (altitude, accidental occurrence during anesthesia), (2) hypoventilation, or (3) venous admixture with or Chapter 21 Acid-Base Balance and Blood Gas Analysis A 23-year-old man with insulin-dependent diabetes presents to the emergency room with somnolence, influenza-like symptoms, nausea, vomiting, and anorexia. Acute hypoxemia causes activation of the sympathetic nervous system with endogenous catecholamine release, which augments blood pressure and cardiac output despite the vasodilating effects of hypoxemia. The increased cardiac output will increase oxygen delivery from the lungs to peripheral tissues. Alveolar Gas Equation decrease in alveolar oxygen concentration by subtracting an amount equal to the carbon dioxide divided by the respiratory quotient. Alveolar-Arterial Gradient the alveolar gas equation estimates the partial pressure of alveolar oxygen by accounting for barometric pressure, water vapor pressure, and the inspired oxygen concentration. Atmospheric oxygen is a constant 21% of barometric pressure; however, barometric pressure diminishes with altitude such that the decrease in inspired oxygen can become significant. Hypoventilation leads to increased Pco2, which encroaches on the space available in the alveolus for oxygen and dilutes the oxygen concentration. The alveolar gas equation estimates this Calculation of the alveolar-arterial (A-a) gradient provides an estimate of venous admixture as the cause of hypoxemia. Venous admixture refers to deoxygenated venous blood mixing with oxygenated arterial blood through shunting. The A-a gradient formula calculates the difference in oxygen partial pressure between alveolar (Pao2) and arterial (Pao2) blood. Normally, the A-a gradient is less than 15 mm Hg while breathing room air as a result of shunting via the thebesian and bronchial veins. Vasodilating drugs (nitroglycerin, nitroprusside, inhaled anesthetics), which inhibit hypoxic pulmonary vasoconstriction and increase ven tilation/perfusion (V/Q mismatch), can also increase the A-a gradient. Larger A-a gradients suggest the presence of pathologic shunting, such as right-to-left intrapulmonary shunts (atelectasis, pneumonia, endobronchial intubation) or intracardiac shunts (congenital heart disease). A patient may have an Sao2 of 100% but have a Pao2 of only 90 mm Hg while breathing 100% oxygen. Significant shunting secondary to a pulmonary or cardiac process has occurred despite the reassuring pulse oximeter reading. In patients with large shunts (>50%), administration of 100% oxygen will be unable to raise Pao2. To estimate the amount of shunt present, when Pao2 is higher than 150 mm Hg, the shunt fraction is approximately 1% of cardiac output for every 20 mm Hg difference in the A-a gradient. When Pao2 is less than 150 mm Hg or when cardiac output is increased relative to metabolism, this guideline will underestimate the actual amount of venous admixture. Cardiac Output Estimates Normal mixed venous Po2 (PvO2) is 40 mm Hg and is a balance between oxygen delivery and tissue oxygen consumption. A true PvO2 should reflect blood from the superior and inferior vena cava and the heart. The PvO2 will decrease when there is inadequate cardiac output because the peripheral tissues have to increase oxygen extraction for aerobic metabolism. Fick Equation the Pao2/Fio2 (P/F) ratio is a simple alternative to the A-a gradient to communicate the degree of hypoxemia. Patients 374 If Pao2, PvO2, and hemoglobin are measured, the cardiac output can then be calculated by using the Fick equation. The total amount of oxygen in the blood is the amount bound to hemoglobin and the amount dissolved in solution. Because the vast majority of the oxygen content in blood is bound to hemoglobin, the amount dissolved can often be left out of the equation in order to simplify calculations. The amount dissolved becomes important in situations such as severe anemia, when the amount carried by hemoglobin is low. With further reductions in oxygen delivery, a critical point is reached when oxygen consumption becomes proportional to delivery. Correlation of central venous and arterial blood gas measurements in mechanically ventilated trauma patients. Comparison of pH-stat versus alphastat during hypothermic cardiopulmonary bypass in the prevention and control of acidosis in cardiac surgery. Cardiopulmonary effects of permissive hypercapnia in the management of adult respiratory distress syndrome. Diagnosing metabolic acidosis in the critically ill: bridging the anion gap, Stewart, and base excess methods. Choices in fluid type and volume during resuscitation: impact on patient outcomes. Trends but not individual values of central venous oxygen saturation agree with mixed venous oxygen saturation during varying hemodynamic conditions. Physiologic hemostasis involves a complex interplay of four components: vascular endothelium, platelets, coagulation factors, and the fibrinolytic system. This intricate system of checks and balances allows blood to maintain its fluidity within a vessel, promotes clot at the site of vessel injury, dismantles clot, and prevents thrombus formation at other sites. If dysfunction of one component or imbalance between components occurs, abnormal bleeding or pathologic thrombosis may occur. Both congenital and acquired disease states, as well as medications, can disrupt the equilibrium of this complex system and lead to bleeding or thrombosis. Under normal conditions and blood flow, platelets do not adhere to the endothelial surface or aggregate with each other, but with vascular injury, the endothelial matrix is exposed. Greg Stratmann for contributing to this chapter in the previous edition of this work. Traditionally, the clotting cascade has been described as consisting of intrinsic, extrinsic, and common pathways. Although this view is useful for providing a structural framework to understand coagulation and to interpret in vivo coagulation tests. Factor Xa then complexes with and activates factor V (which is released from platelet granules during platelet activation) forming the prothrombinase complex. The tenase complex activates additional factor X, leading to increased production of the prothrombinase complex and increased thrombin formation. Once sufficient levels of thrombin are available, fibrin is generated from fibrinogen. Plasmin that is unbound to the fibrin clot and circulating is inhibited by 2-antiplasmin. If plasmin activation goes unchecked, systemic fibrinolysis and massive hemorrhage may develop. This is the result of a disruption of the hemostatic process and involves a complex interaction between coagulation factors, platelets, fibrinolysis, and vascular integrity. Patients with less than 20% to 30% normal coagulation factor values or platelet counts of less than 50,000 cells/L are more likely than patients with normal values to have uncontrolled intraoperative bleeding. Bleeding diatheses vary in clinical presentation depending on what component of the hemostatic system is affected. Diseases involving coagulation factor deficiencies may present in early childhood with subcutaneous, intramuscular, or intra-articular hemorrhage after only minor trauma. Diseases involving decreased or dysfunctional platelets are typically associated with mucosal bleeding, epistaxis, prolonged bleeding after dental procedures, and menorrhagia. A careful history and physical examination, laboratory evaluation, and consultation with a hematologist when appropriate are necessary to evaluate any patient with suspected bleeding disorders. Endogenous heparin is found on normal endothelial cell surface and prevents spontaneous clot formation, thus limiting the coagulation process to only damaged endothelium. Protein C becomes activated when thrombin binds to thrombomodulin on the endothelial cell surface as clot progresses. The thrombin-thrombomodulin complex no longer promotes platelet activation or the formation of fibrin, but instead activates protein C. Fibrin is cleaved by plasmin into soluble products (D-dimer, fibrin degradation products), which also inhibit thrombin activity. Hemophilia A and hemophilia B are X-linked recessive disorders that are the most common inherited deficiencies of specific coagulation factors.

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During a "cannot intubate heart attack 85 year old order clonidine master card, cannot ventilate" situation in which supraglottic airway placement has also failed pulse pressure in athletes buy online clonidine, what are the relative advantages and disadvantages of cricothyrotomy versus transtracheal jet ventilation What are the most common complications after endotracheal extubation in adults and children What are the major differences between the airway anatomy of an infant compared to an adult When an uncuffed endotracheal tube is used in an infant hypertension food purchase clonidine visa, what steps should be taken to determine the appropriate size Predicting difficult intubation in apparently normal patients: a meta-analysis of bedside screening test performance arteria world aion clonidine 0.1mg sale. The diagnostic value of the upper lip bite test combined with sternomental distance arrhythmia atrial fibrillation generic clonidine 0.1 mg amex, thyromental distance arrhythmia or dysrhythmia purchase 0.1mg clonidine mastercard, and interincisor distance for prediction of easy laryngoscopy and intubation: a prospective study. Criteria for estimating likelihood of difficulty of endotracheal intubation with the Macintosh laryngoscope. Incidence, predictors, and outcome of difficult mask ventilation combined with difficult laryngoscopy: a report from the multicenter perioperative outcomes group. The difficult airway with recommendations for management-part 2-the anticipated difficult airway. The difficult airway with recommendations for management-part 1-difficult tracheal intubation encountered in an unconscious/induced patient. Critical hemoglobin desaturation will occur before return to an unparalyzed state following 1 mg/kg intravenous succinylcholine. Preoxygenation is more effective in the 25 degrees head-up position than in the supine position in severely obese patients: a randomized controlled study. Noninvasive ventilation and alveolar recruitment maneuver improve respiratory function during and after intubation of morbidly obese patients: a randomized controlled study. Evolution of the extraglottic airway: a review of its history, applications, and practical tips for success. Supraglottic airways in difficult airway management: successes, failures, use and misuse. Predictors and clinical outcomes from failed laryngeal mask airway unique: a study of 15,795 patients. Difficult and failed intubation: incident rates and maternal, obstetrical, and anesthetic predictors. Glidescope video-laryngoscopy versus direct laryngoscopy for endotracheal intubation: a systematic review and meta-analysis. Review article: video-laryngoscopy: another tool for difficult intubation or a new paradigm in airway management Routine clinical practice effectiveness of the glidescope in difficult airway management: an analysis of 2,004 glidescope intubations, complications, and failures from two institutions. Awake fiberoptic or awake video laryngoscopic tracheal intubation in patients with anticipated difficult airway management: a randomized clinical trial. Brief review: supplementing oxygen through an airway exchange catheter: efficacy, complications, and recommendations. Endotracheal tube cuff pressure in three hospitals, and the volume required to produce an appropriate cuff pressure. Cricoid pressure results in compression of the postcricoid hypopharynx: the esophageal position is irrelevant. Evaluation of Seldinger technique emergency cricothyroidotomy versus standard surgical cricothyroidotomy in 200 cadavers. Percutaneous emergency airway access; prevention, preparation, technique and training. Transtracheal jet ventilation in 50 patients with severe airway compromise and stridor. A randomized comparison of the laryngeal mask airway supreme and laryngeal mask airway unique in infants and children: does cuff pressure influence leak pressure Cuffed endotracheal tubes in infants and children: should we routinely measure the cuff pressure Prospective randomized controlled multi-centre trial of cuffed or uncuffed endotracheal tubes in small children. Cuffed versus uncuffed endotracheal tubes in pediatric anesthesia: the debate should finally end. Correlations between controlled endotracheal tube cuff pressure and postprocedural complications: a multicenter study. Inspiratory stridor after tracheal intubation with a MicroCuff(R) tracheal tube in three young infants. Pediatric video laryngoscope versus direct laryngoscope: a meta-analysis of randomized controlled trials. A prospective randomized equivalence trial of the GlideScope cobalt video laryngoscope to traditional direct laryngoscopy in neonates and infants. Significant technical, physiologic, and pharmacologic differences exist between the techniques, although all result in one or a combination of sympathetic, sensory, and motor blockade. Spinal anesthesia requires a small amount of drug to produce rapid, profound, reproducible, but finite sensory analgesia. In contrast, epidural anesthesia progresses more slowly, is commonly prolonged using a catheter, and requires a large amount of local anesthetic, which may be associated with the editors and publisher would like to thank Drs. Indwelling long-term spinal catheters may be inserted for chronic malignant and nonmalignant pain. Combined spinal and epidural techniques blur some of these differences but add flexibility to clinical care. This distal termination varies from L3 in infants to the lower border of L1 in adults. The spinal cord lies within the bony vertebral column, surrounded by three membranes: from innermost to outermost the pia mater, the arachnoid mater, and the dura mater. Surrounding the dura is the epidural space, extending from the foramen magnum to the sacral hiatus. Single-injection spinal or epidural anesthesia is commonly used for surgery to the lower abdomen, pelvic organs. Continuous catheter-based epidural infusions are used for obstetric labor analgesia and to provide postoperative pain relief for days after major surgery. Neuraxial analgesia can reduce pulmonary and possibly cardiac morbidity, although the mortality benefits appear minimal. Caudal blocks are mostly performed for surgical anesthesia and analgesia in children (also see Chapter 34) and for therapeutic analgesia in adults with chronic pain (also see 274 Chapter 17 Spinal, Epidural, and Caudal Anesthesia Spinous process Cervical Lamina Superior articular process Transverse process Vertebral foramen (spinal canal) Pedicle Thoracic Vertebral body. The ligamentum flavum (the so-called "yellow ligament") also extends from the foramen magnum to the sacral hiatus. Although classically portrayed as a single ligament, it is actually composed of the right and left ligamenta flava, which join to form an acute midline angle with a ventral opening. The vertebral canal is triangular and largest in area at the lumbar levels, and it is circular and smallest in area at the thoracic levels. Immediately posterior to the ligamentum flavum are either the lamina of vertebral bodies or the interspinous ligaments (that connect the spinous processes). Finally there is the supraspinous ligament, which extends from the external occipital protuberance to the coccyx and attaches to the vertebral spines. The vertebrae are joined together anteriorly by the fibrocartilaginous joints with central disks containing the nucleus pulposus, and posteriorly by the zygapophyseal (facet) joints. Thoracic spinous processes are angulated more steeply caudad as opposed to the almost horizontal angulation of the lumbar spinous processes. The differences between the caudal and lumbar spinous processes are clinically important for needle insertion and advancement. The sacral canal contains the terminal portion of the dural sac, which typically ends at S2 in adults and lower in children. Spinal Nerves Dorsal (afferent) and ventral (efferent) nerve roots merge distal to the dorsal root ganglion to form spinal nerves. There are 31 pairs of spinal nerves (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal). The nerves pass through the intervertebral foramen, becoming ensheathed by the dura, arachnoid, and pia, which, respectively, become the epineurium, the perineurium, and the endoneurium. One of the largest anastomotic feeder arteries to the anterior system is the artery of Adamkiewicz, which arises from the aorta and enters an intervertebral foramen between T7 and L4 on the left. Ischemia within the anterior system leads to anterior spinal artery syndrome, manifested as anterior horn motor neuron injury along with disruption of pain and temperature sensation below the level affected. Ischemia may result from any one or a combination of profound hypotension, mechanical obstruction, vasculopathy, or hemorrhage. Longitudinal anterior and posterior spinal veins communicate with segmental anterior and posterior radicular veins before draining into the internal vertebral venous plexus in the medial and lateral components of the epidural space. The increased angle of needle insertion during thoracic epidural cannulation may provide a slightly longer distance of "needle travel" before entering the epidural space (A). Similarly, the epidural space is more segmented and less uniform than previously believed, which Dura mater Arachnoid Pia mater Ventral roots Ventral root Spinal nerve Ventral ramus Dorsal roots Dorsal ramus Dorsal root ganglion Dorsal root. Preganglionic efferent fibers travel in the ventral root and then via the white ramus communicans to paravertebral sympathetic ganglia or more distant sites such as the celiac ganglion. Afferent fibers travel via the white ramus communicans to join somatic nerves, which pass through the dorsal root to the spinal cord. Finally, contents of the epidural space also vary and can influence the volume of local anesthetic required. Nerves in the subarachnoid space are easily anesthetized, even with a small dose of local anesthetic, compared with the extradural nerves, which are often ensheathed by dura mater (the "dural sleeve"). The speed of neural blockade depends on the size, surface area, and degree of myelination of the nerve fibers exposed to the local anesthetic. The small preganglionic sympathetic fibers (B fibers, 1 to 3 m, minimally myelinated) are most sensitive to local anesthetic blockade. The A-beta fibers (5 to 12 m, myelinated), which conduct touch sensation, are the last sensory fibers to be affected. The larger A-alpha motor fibers (12 to 20 m, myelinated) are the most resistant to local anesthetic blockade. Local anesthetic also diffuses through the pia mater and penetrates through the spaces of Virchow-Robin (extensions of the subarachnoid space accompanying the blood vessels that invaginate the spinal cord from the pia mater) to reach the deeper dorsal root ganglia. A portion of the subarachnoid drug diffuses outward to enter the epidural space, and some is taken up by the blood vessels of the pia and dura maters. Other local anesthetic spreads by bulk flow longitudinally and circumferentially within the epidural space. Factors that may enhance the distribution of local anesthetic within the epidural space are small caliber (greater spread in the thoracic space), decreased epidural space compliance, decreased epidural fat content, decreased local anesthetic leakage through the intervertebral foramina. Spread is mostly cephalad in the lumbar and low thoracic region, but caudad after a high thoracic injection. Increased spread exposes the drug to a larger area for vascular absorption and thus a shorter duration of action. Therefore, cold sensation (also an approximate level of sympathetic blockade) is most cephalad and is on average one to two spinal segments higher than the level of pinprick anesthesia, which in turn is one to two segments higher than anesthesia to touch. The degree to which arterial blood pressure decreases with either spinal or epidural technique depends on multiple factors. However, in studies that demonstrated a decrease in cerebral perfusion,12 there was no postoperative change in cognitive function in any of the patients. The sympathectomy typically extends for two to six dermatomes above the sensory block level with spinal anesthesia but the same level with epidural anesthesia. Cardiac Output Respiratory Alterations in pulmonary variables during neuraxial block are usually of little clinical importance. A decrease in vital capacity follows a reduction in expiratory reserve volume related to paralysis of the abdominal muscles necessary for forced exhalation rather than a decrease in phrenic or diaphragmatic function. These changes are more marked in obese patients and may affect patients with severe respiratory disease. Because 75% of the total blood volume resides in the venous system, the venodilation effect predominates and stroke volume is reduced. Despite a compensatory baroreceptor-mediated sympathetic response (vasoconstriction and increased heart rate) above the level of blockade, the reduction in venous return and right atrial filling reduce signal output from intrinsic atrial and great vein chronotropic stretch receptors,9 thereby increasing parasympathetic activity. The two opposing responses result in a minimal change in heart rate unless neuraxial anesthesia is extended to the T1 level when blockade of the cardioaccelerator fibers (in addition to a marked reduction in venous return) may result in severe bradycardia and even asystole. The BezoldJarisch reflex can also cause profound bradycardia and circulatory collapse after spinal anesthesia, especially in the presence of hypovolemia, when a small endsystolic left ventricular volume may trigger a mechanoreceptor-mediated bradycardia. Atropine is effective in treating nausea associated with extensive (T5) subarachnoid anesthesia. Renal Despite a predictable decrease in renal blood flow accompanying neuraxial blockade, this decrease is of little physiologic importance. The belief that neuraxial blocks frequently cause urinary retention is questionable (see "Complications" later in the chapter). It may also be indicated when patients wish to remain conscious or when some comorbid condition, such as severe respiratory disease or an airway that may be difficult to manage, increases the risks of using general anesthesia. Epidural anesthesia allows for more prolonged surgical anesthesia by catheter-based local anesthetic delivery. Indwelling catheter-based spinal anesthesia is less conventional, but may be useful when insertion of an epidural catheter is challenging or in the setting of severe cardiac disease when the reliability of a single-shot spinal anesthetic must be combined with more hemodynamically stable incremental dosing. Chronic low back pain without neurologic deficit is not a contraindication to neuraxial blockade. Spinal Stenosis There is an association between the presence of spinal stenosis and nerve injury following neuraxial techniques,23 but the relative contribution of surgical factors and natural history of the spinal disease itself is unknown. Spine Surgery Neuraxial Analgesia Intrathecal or epidural local anesthetics along with other additives, such as opioids either alone or in combination, can provide excellent quality, long-lasting intraand postoperative analgesia in labor and delivery15 (also see Chapter 33), during and after hip16 or knee replacement17 (also see Chapter 32), in laparotomy,18 in thoracotomy (also see Chapter 37),19 and increasingly even in cardiac surgery (also see Chapter 25). Previous spine surgery does not predispose patients to an increased risk of neurologic complications. Depending on the severity of the neural tube defect the potential for traumatic needle injury to the spinal cord may be increased. In any of these circumstances, a careful evaluation of neurologic status must first be undertaken and noted along with documentation of the discussion of the risks and benefits. Cardiac (Also See Chapter 25) Aortic Stenosis or Fixed Cardiac Output Relative Relative contraindications can be approached by system and must be weighed against the potential benefits of neuraxial blockade. A catheterbased neuraxial anesthetic with repeated small doses of local anesthetic may allow better hemodynamic control. Chapter 17 Spinal, Epidural, and Caudal Anesthesia Hypovolemia An exaggerated hypotensive response because of vasodilatory effects may occur. Inherited Coagulopathy Hemorrhagic complications after neuraxial techniques in patients with known hemophilia, von Willebrand disease, or idiopathic thrombocytopenic purpura appear infrequently when factor levels are more than 0. The minimum safe factor levels and platelet count for neuraxial blockade remain undefined in both the obstetric and general populations.

Patient position affects lumbar epidural injections blood pressure medication coreg order clonidine cheap, with preferential spread and faster onset to the dependent side in the lateral decubitus position blood pressure medication start with l order clonidine 0.1mg without a prescription. Needle bevel direction and speed of injection do not appear to influence the spread of a bolus injection prehypertension due to anxiety 0.1mg clonidine mastercard. Prior to preservative-free preparations blood pressure medication muscle weakness buy 0.1mg clonidine visa, large volumes of chloroprocaine had been associated with deep arteria lusoria definition order generic clonidine on-line, burning lumbar back pain blood pressure medication recall buy 0.1 mg clonidine amex. The 2% preparation has an onset time similar to that for lidocaine of approximately 15 minutes, but a slightly longer duration (up to 200 minutes with epinephrine). Long-Acting Local Anesthetics Tetracaine is not widely used because of unreliable block height and, in larger doses, systemic toxicity. More dilute concentrations such Chapter 17 Spinal, Epidural, and Caudal Anesthesia Table 17. However, disadvantages include cardiac and central nervous system toxicity and potential motor block from larger doses. Levobupivacaine administered epidurally has the same clinical characteristics as bupivacaine and is less cardiotoxic. It is associated with a superior safety profile compared with bupivacaine, with a higher seizure threshold and less cardiotoxicity. Epidural Additives Vasoconstrictors Epinephrine reduces vascular absorption of local anesthetics in the epidural space. The effect is greatest with lidocaine,56 mepivacaine, and chloroprocaine (up to 50% prolongation); less with bupivacaine and levobupivacaine; and limited with ropivacaine, which already has intrinsic vasoconstrictive properties (see Table 17. Fentanyl and sufentanil are also readily absorbed into the systemic circulation, which may be the principal analgesic mechanism. Epidural morphine can be administered as a bolus (duration of up to 24 hours) or continuously. Epidural fentanyl and sufentanil have a faster onset but a shorter duration (only 2 to 3 hours). Depodur is an extended-release liposomal formulation of morphine used as a single-shot lumbar epidural dose, potentially avoiding issues of continuous local anesthetic infusions and indwelling catheters. Opioid-related side effects are dosedependent and there appears to be a therapeutic ceiling effect above which only side effects increase. Clonidine may also reduce immune stress and cytokine response, but side effects include hypotension, bradycardia, dry mouth, and sedation. Dexmedetomidine can reduce intraoperative anesthetic requirements, improve postoperative analgesia, and prolong both sensory and motor block. Other Drugs Ketamine, neostigmine, midazolam, tramadol, dexamethasone, and droperidol have all been studied but are not commonly used. C7 T7 L1 L4 S2 Inferior angle of scapula Iliac Posterior crest superior iliac spine. Although this may theoretically increase the speed of onset and quality of the block by producing more rapid intraneural diffusion and more rapid penetration of connective tissue surrounding the nerve trunk, data suggest that there are no clinical advantages for carbonated solutions. They are usually 16 to 18 G and have a shaft marked in 1-cm intervals with a 15- to 30-degree curved, blunt Huber needle tip designed to both reduce the risk of accidental dural puncture and guide the catheter cephalad. The catheter is made of a flexible, calibrated, radiopaque plastic with either a single end hole or multiple side orifices near the tip. Multiple orifices can improve analgesia but may increase epidural vein cannulation in parturients. Position Technique Preparation Patient preparation as previously described for spinal anesthesia must equally be applied to epidural anesthesia, namely consent, monitoring, resuscitation equipment, and intravenous access. Sterility is arguably even more important than spinal anesthesia because a catheter is often left in situ. The nature and the duration of surgery must be understood so that the epidural may be inserted at the appropriate level (Table 17. Tuohy needles are most commonly used 292 the sitting and lateral decubitus positions necessary for epidural puncture are the same as those for spinal anesthesia, and success rates are comparable. As with spinal anesthesia, epidurals are ideally performed with the patient awake. Chapter 17 Spinal, Epidural, and Caudal Anesthesia A variety of different needle approaches exist: midline, paramedian, modified paramedian (Taylor approach), and caudal. A midline approach, in which the angle of approach is only slightly cephalad, is commonly chosen for lumbar and low thoracic approaches. In the midthoracic region, the approach should be more cephalad because of the significant downward angulation of the spinous processes. The needle should be advanced in a controlled fashion with the stylet in place through the supraspinous ligament and into the interspinous ligament, at which point the stylet can be removed and the syringe attached. This method may increase the chance of a false loss-of-resistance, possibly because of defects in the interspinous ligament. Air or saline (or a combination) is commonly used to detect a loss-of-resistance when identifying the epidural space. Usually the ligamentum flavum is identified as a tougher structure with increased resistance, and when the epidural space is subsequently entered, the pressure applied to the syringe plunger allows the solution to flow without resistance into the epidural space. Air is likely less reliable in identifying the epidural space, results in a possible chance of incomplete block, and may cause both pneumocephalus (which can result in headaches) and even venous air embolism in rare cases. Nevertheless, adverse outcomes in obstetric patients do not vary when air versus saline was studied. With the hanging-drop technique, a drop of solution such as saline is placed within the hub of the needle after the needle is placed in the ligamentum flavum. When the needle tip reaches the epidural space, the solution is "sucked in" as a result of subatmospheric pressure inside the epidural space. When a lumbar midline approach is used, the depth from skin to the ligamentum flavum in most (80%) patients is between 3. When the epidural space is identified, the depth should be noted, the syringe removed, and a catheter gently threaded to leave 4 to 6 cm in the space. Less than 4 cm in length in the epidural space may increase the risk of catheter dislodgement and inadequate analgesia. Threading more catheter increases the likelihood of catheter malposition or complications. The needle is inserted into the ligamentum flavum, and a syringe containing saline and an air bubble is attached to the hub. After compression of the air bubble is obtained by applying pressure on the syringe plunger, the needle is carefully advanced until its entry into the epidural space is confirmed by the characteristic loss of resistance to syringe plunger pressure, and the fluid enters the space easily. The Taylor approach is a modified paramedian approach via the L5-S1 interspace, which may be useful in trauma patients who cannot tolerate or are not able to maintain a sitting position. Before initiating an epidural local anesthetic infusion, a test dose may be administered. Another advantage is the ability to administer a low dose of intrathecal local anesthetic, and, if necessary, use the epidural catheter to extend the block. Adding either local anesthetic or saline alone to the epidural space via the catheter compresses the dural sac and increases the block height. Needle insertion is completed by insertion and withdrawal in a stepwise fashion (inset, so-called "1-2-3 insertion") until the needle can be advanced into the caudal canal and the solution can be injected easily (without creation of a subcutaneous "lump" of fluid). The separate needle insertion technique65 has the advantage of being able to confirm that the epidural catheter is functional before spinal anesthesia is administered but does theoretically risk shearing the in situ epidural catheter. Pharmacology the local anesthetics used are similar to those described for epidural anesthesia and analgesia. In adults, approximately twice the lumbar epidural dose is required to achieve a similar block with the caudal approach. In adults, caudal anesthesia is unpredictable when upper abdominal or thoracic spread is required. Therefore its indications in adults are the same as those for lumbar epidural anesthesia. Technique Patient preparation as described before applies equally to caudal anesthesia. The prone position, lateral decubitus position, and the knee-chest position may be used. The posterior superior iliac spines should be located, and by using the line between them as one side of an equilateral triangle, the location of the sacral hiatus can be approximated. A decrease in resistance to needle insertion should be appreciated as the needle enters the caudal canal. In male patients, this angle is almost parallel to the coronal plane; in female patients, a slightly steeper angle (15 degrees) is necessary. In adults, the tip should never be advanced beyond the S2 level (approximately 1 cm inferior to the posterior superior iliac spine), which is the level to which the dural sac extends. Additional advancement increases the risk of dural puncture and unintentional intravascular cannulation. Bleeding within the vertebral canal can cause ischemic compression of the spinal cord and lead to permanent neurologic deficit if not recognized and evacuated expeditiously. Many risk factors have been associated with the development of an epidural hematoma, including difficult or traumatic needle or catheter insertion, coagulopathy, elderly age, and female gender. Direct needle trauma to the spinal cord is possible, but the intrathecal injectate can be neurotoxic. In the early 1980s, several patients developed adhesive arachnoiditis, cauda equina syndrome, or permanent paresis possibly related to a combination of low pH and the antioxidant sodium bisulfite preservative used in early (and discontinued) preparations of the short-acting ester local anesthetic chloroprocaine. Anterior spinal artery syndrome, characterized by potentially irreversible, painless loss of motor and sensory function with sparing of proprioception was described earlier. The incidence is approximately 1% in spinal anesthesia and is minimized by using smaller gauge, noncutting tip spinal needles and orientating the needle bevel parallel with the axis of the spine. Symptoms usually begin within 3 days of the procedure, and 66% start within the first 48 hours. Spontaneous resolution usually occurs within 7 days in the majority (72%) of cases, whereas 87% of cases resolve by 6 months. It is recommended inserting the blood patch needle at or caudad to the level of the dural puncture, with 20 mL of blood being a reasonable starting target volume. Symptoms occur within 24 hours of the resolution of an otherwise uneventful spinal anesthetic and are not associated with any neurologic deficits or laboratory abnormalities. Pain can be mild or severe but typically resolves spontaneously in less than 1 week. Nonsteroidal antiinflammatory drugs are the first line of treatment, but opioids may be required. Infection Bacterial meningitis and epidural abscess are rare but potentially catastrophic complications. The presence of a concomitant systemic infection, diabetes, immunocompromised states, and prolonged maintenance of an epidural (or spinal) catheter are risk factors. Chlorhexidine in an alcohol base is the most effective antiseptic for the purposes of neuraxial techniques. Cardiovascular Hypotension Hypotension is more likely with peak block height higher than or equal to T5, at an age of 40 years or older, baseline systolic blood pressure less than 120 mm Hg, combined spinal and general anesthesia, spinal puncture at or above the L2-L3 interspace, and the addition of phenylephrine to the local anesthetic. Bradycardia the mechanism has been described earlier but factors that may increase the likelihood of exaggerated bradycardia include baseline heart rate less than 60 beats/min, age younger than 37 years, male gender, nonemergency status, -adrenergic blockade, and prolonged duration of surgery. Cardiac Arrest Backache There is no association between epidural analgesia and new-onset back pain up to 6 months postpartum. This event is rare, and the cause of sudden cardiac arrest after spinal anesthesia is not understood. Hypoxemia and oversedation may be a factor in the severe bradycardia and asystole that can occur suddenly during well-conducted spinal anesthesia. Curiously, these rare events are associated with spinal anesthesia rather than epidural techniques. Nausea and Vomiting Nausea and vomiting may be secondary to either direct exposure of the chemoreceptor trigger zone in the brain to emetogenic drugs. Nausea or vomiting after spinal anesthesia is more likely with the addition of phenylephrine or epinephrine to the local anesthetic, peak block height more than or equal to T5, baseline heart rate more rapid than 60 beats/min, use of procaine, history of motion sickness, and the development of hypotension during spinal anesthesia. Intrathecal morphine has the highest risk of opioid-induced nausea or vomiting, whereas fentanyl and sufentanil carry the lowest risk. Respiratory the risk of respiratory depression associated with neuraxial opioids is dose-dependent, with a reported frequency that approaches 3% after the administration of 0. With lipophilic anesthetics, respiratory depression is generally an early phenomenon occurring within the first 30 minutes (and has not been reported after 2 hours), whereas with intrathecal morphine late respiratory depression may occur up to 24 hours after injection. Respiratory monitoring for the first 24 hours after the administration of intrathecal morphine is recommended. Patients with sleep apnea can be especially sensitive and considerable caution must be exercised in this group. Local anesthetic blockade of the S2, S3, and S4 nerve roots inhibits urinary function as the detrusor muscle is weakened. Neuraxial opioids can further complicate urinary function by suppressing detrusor contractility and reducing the sensation of urge. Along with male gender and age, intrathecal morphine has also been linked to urinary retention after neuraxial anesthesia. Naloxone, naltrexone, or the partial agonist nalbuphine can be used for treatment. Yet, when an epidural block is performed and a higher-than-expected block develops 15 to 30 minutes after injection, subdural placement of local anesthetic must be considered. Through these windows the hyperechoic dura (a bright line), the subarachnoid space, and the posterior aspect of the vertebral body may be visualized. Visualization of the ligamentum flavum and epidural space is often more difficult. Ultrasound facilitates identification of the optimal location for needle insertion and an estimation of the skin-to-dura distance.