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Please refer to the chapter on extrapulmonary causes of respiratory failure for guidelines on how to monitor for the adequacy of ventilation and when to consider endotracheal intubation (Chapter 165); and to the chapter on invasive mechanical ventilation for guidelines on how to ventilate patients with respiratory failure due to neuromuscular diseases trusted clonidine 0.1 mg blood pressure 152 over 90. For adults and older children purchase clonidine 0.1 mg line blood pressure medication upset stomach, passive immunization with equine antitoxin should be administered as soon as botulism is diagnosed discount 0.1mg clonidine fast delivery heart attack or gas. Timely administration minimizes subsequent nerve damage and severity of disease but will not reverse existing paralytic damage [21]. Patients should be skin tested prior to antitoxin administration and desensitized using the protocol enclosed with the antitoxin if there is any evidence of a wheal and flare reaction. This is explained by the shorter half-life of the heptavalent preparation and ongoing toxin production from the intestinal bacterium [23]. This is not an issue with the more common food-borne cases in which continued toxin production does not occur. Equine antitoxin is not recommended for treatment of infants suspected of botulism because of the potential serious side effects of serum sickness and anaphylaxis. However, a 2006 study found that the administration of human botulism immune globulin intravenous within 72 hours of hospitalization for suspected infant botulism decreased illness severity, shortened hospital stays, and reduced costs [24]. Patients with wound botulism also require aggressive wound debridement regardless of how well the wound appears as toxin is produced until the infection is eliminated. Aminoglycosides and clindamycin should be avoided because of the potential for neuromuscular blockade [25,26]. Because botulinum toxin is not absorbed through intact skin, standard precautions should be undertaken when caring for patients suspected of botulism. A number of potential vaccine candidates remain investigational with no phase 3 studies reported to date. Center for Disease Control: Botulism in the United States 1899–1996: Handbook for Epidemiologists, Clinicians and Laboratory Workers. Clinically, tetanus presents with skeletal muscle rigidity and spasms that classically involve the muscles of the face (lockjaw). However, tetanus still occurs frequently in the third world, and in individuals who have never been or have been inadequately vaccinated in the setting of a wound infection or another portal of entry. Diagnosis is based on clinical suspicion and the exclusion of other entities because of a lack of timely confirmatory testing. Treatment relies mainly on respiratory support and symptomatic management of the muscular rigidity and spasms and the autonomic manifestations of the disease. Mature organisms develop spores that are widely distributed in soil and dust as well as in the intestines and feces of animals. Although this toxin can exert an excitatory effect, it acts primarily by blocking the release of neurotransmitters such as glycine and gamma-amino butyric acid, which normally act to inhibit the transmission of motor nerve impulses. Specifically, the toxin degrades synaptobrevin, a protein required for contact of inhibitory neurotransmitter vesicles with their release site on the presynaptic membrane [3]. As the effect of the toxin on a synapse does not appear reversible, recovery from tetanus depends on the generation of new nerve terminals and new synapse formation. Tetanus is a rare disease in the developed world with morbidity and mortality in the United States declining steadily, due to the availability of tetanus vaccines, improved wound management and the use of tetanus immunoglobulin for postexposure prophylaxis [4]. Age ≥ 65 years old remained the highest risk factor for fatal tetanus with a case fatality rate of 31. Sporadic cases of tetanus have been reported in those with a tetanus antibody level adequate for protective immunity [6]. The first nerves affected are the shortest, accounting for the early symptoms of facial distortion and neck stiffness. Clinical tetanus can present in three forms—local, cephalic, and generalized—with 80% of cases being generalized. Cephalic tetanus develops after a traumatic head injury, but has been reported after otitis media when C. Generalized tetanus typically presents with involvement of facial musculature, starting with masseter rigidity (lockjaw or trismus) and risus sardonicus (orbicularis oris), and then progresses in a descending fashion with difficulty swallowing and abdominal rigidity [1]. Spasms, which are often triggered by sensory stimuli, are common and may resemble seizures with flexion of the arms and the extension of legs (opisthotonus). Laryngospasm and respiratory compromise may result from vocal cord or diaphragmatic spasms and upper airway obstruction. Fractures of the spine or the long bones, dislocations, and rhabdomyolysis may occur as a result of spasms. Spasms occur within the first 2 weeks of illness followed by autonomic disturbances such as extremes in blood pressure and cardiac arrhythmias including sinus tachycardia and cardiac arrest [12,13]. Individuals with tetanus are at high risk of nosocomial pneumonia with an incidence of approximately 35%. Neonatal tetanus, more often seen in developing countries, is a form of generalized tetanus that commonly arises when an unhealed umbilical stump becomes infected after an incision with an unsterile instrument and if the mother had not been adequately immunized [1,9]. Diagnosis is clinical and primarily based on the presence of trismus, dysphagia, muscular rigidity, and spasm. Unusual presentations such as meningitis should be considered in the setting of risk factors such as a history of a contaminated wound [15]. Few other conditions present with muscular rigidity and sympathetic hyperreactivity except for strychnine poisoning. Unlike tetanus, however, the sudden contraction of all striated muscles is usually followed by complete relaxation of these muscles. Additional conditions that can mimic the spasms seen in tetanus include hypocalcemia and reactions to certain medications including neuroleptic drugs and central dopamine antagonists. Autonomic nervous system dysfunction has been shown to predict a poor outcome in mild to moderate cases of tetanus [17]. Individuals suspected of generalized tetanus should be observed in an intensive care setting with minimal stimuli. Initial management consists of airway stabilization and general intensive care support including mechanical ventilation, nutritional support, and deep venous thrombosis prophylaxis. Propofol (alone or in combination with benzodiazepines) and intrathecal baclofen are alternative options that have been used [19,20]. Intravenous diazepam and lorazepam contain propylene glycol, which may increase the risk of lactic acidosis at the recommended doses of treatment [21]. If the muscle spasms cannot be controlled with these agents, a neuromuscular paralytic agent such as vecuronium can be added [1]. Botulinum toxin acts mainly on lower motor neurons by inhibiting acetylcholine release and muscle activity. Direct injection of botulinum toxin into the muscle has been successfully used in a small number of patients to reduce tetanus induced rigidity and spasm [22]. If a portal of entry can be identified, the wound should be debrided and an antibiotic active against anaerobic organisms should be administered with metronidazole for 7 to 10 days now considered to be the first line of therapy. Treatment courses of 7 to 10 days using regimens of penicillin, either as a single-dose intramuscular benzathine dose or intravenous benzyl penicillin are alternative regimens [1,23]. Alternative regimens such as doxycycline, clindamycin, vancomycin, and chloramphenicol are likely to be effective given susceptibility data against C. In a randomized clinical trial, patients treated with intrathecal rather than intramuscular administration of human antitetanus immunoglobulin showed better clinical progression including fewer respiratory complications and significantly shorter duration of spasms [26], though methodical issues with the study have been raised [7].

Thrombotic events order clonidine online pills blood pressure 7850, when they do occur purchase cheap clonidine line hypertension headaches, may be a result of the patient’s immobility owing to coma and muscle rigidity rather than to any temperature-mediated change 0.1mg clonidine sale white coat hypertension xanax. Mild elevations of lactate dehydrogenase, serum glutamic oxaloacetic acid transaminase, serum glutamic pyruvic transaminase, and alkaline phosphatase are common. This criterion requires independent validation before its use can be recommended in clinical practice. Differential Diagnosis A thorough examination and diagnostic evaluation for other causes of hyperthermia should be conducted (see Table 185. Acute lethal catatonia presents with psychotic excitement and automatisms a few weeks before motor deficit [174]. If catatonia has been induced or exacerbated by neuroleptics, withdrawal of the neuroleptic drug should aid in clarifying the diagnosis. Heat stroke must be considered when temperature elevation develops in a patient taking neuroleptics during periods of high ambient temperature or after vigorous exercise. In the rare circumstance in which the two syndromes cannot be distinguished, attempts at paralysis with curare or pancuronium may aid diagnosis. Idiosyncratic drug reactions and anaphylaxis accompanying severe hyperthermia may usually be diagnosed by their distinct clinical presentations. Monoamine oxidase inhibitors may produce hyperthermia, especially when administered with meperidine, linezolid, or dextromethorphan [177–180]. Specific agents used to decrease thermogenesis by reducing muscle contracture include dantrolene, curare, pancuronium, amantadine, bromocriptine, and L-dopa (Table 185. Dantrolene therapy does carry a risk of hepatotoxicity, but in patients with temperatures greater than 40°C, its use is specific and should be beneficial. Paralysis with curare or pancuronium should produce a similar prompt decrease in temperature, but this treatment necessitates mechanical ventilation and extensive support [161]. Bromocriptine, amantadine, and carbidopa/L-dopa increase central dopaminergic tone; this decreases the central drive, reducing muscular rigidity and thermogenesis. The use of dantrolene, bromocriptine, and amantadine has yet to be shown to reduce mortality significantly [123]. Electroconvulsive therapy has been successful for several patients [131,132,189,190] and is the only therapeutic modality that may be used successfully to treat simultaneously hyperthermia, the extrapyramidal side effects, and the underlying neuropsychiatric disorder for which the neuroleptic drug was prescribed. Because of several reports of cardiovascular collapse among patients undergoing electroconvulsive therapy, this therapy should be given only to patients at low risk of cardiovascular disease who have failed other therapy. Less-specific agents, such as diphenhydramine, benztropine, diazepam, and trihexyphenidyl, have been used successfully [127,130,134,137,139,146] but more typically have not been helpful [121,134,140,141,161,187,188]. Rechallenge with neuroleptics may cause the syndrome to recur, but this occurs much more frequently during the first 2 weeks [201,202], concomitant use of lithium, high potency drugs, and parenteral neuroleptics. Although mortality rates as high as 20% to 30% have been reported [115], this rate can probably be reduced to less than 10% with appropriate support and treatment. Mortality rate does appear to be influenced by peak temperature, inciting neuroleptic drug, and renal failure. Death has been reported as a result of cardiovascular collapse [126], pneumonia [131,161], renal failure [129,145], and hepatic failure [145]. The development of renal failure is particularly ominous; in some series, 46% of patients with myoglobinuria and 56% of those with renal failure died [123]. Drugs that blunt cardiovascular performance, such as β-blockers, or alter heat dissipation, such as chlorpromazine, are widely used and can contribute to temperature elevation. This section focuses on drugs that independently produce significant elevations of temperature (Table 185. Commonly abused street drugs may result in severe hyperthermia without other pharmacologic or environmental stimuli. Although all these drugs have a low incidence of producing severe hyperthermia, owing to the prevalence of their use, they may account for a large percentage of cases of hyperthermia presenting to an emergency department. Common prescription drugs that alter central serotonin levels and lysergic acid diethylamine, a serotonin analog, may result in hyperthermia greater than 41°C [209]. Monoamine oxidase inhibitors and selective serotonin reuptake inhibitors may produce hyperthermia, especially when administered with meperidine or dextromethorphan [177–179], tricyclic antidepressant [177,215], or each other. For example, a postoperative patient who receives linezolid, a weak monoamine oxidase inhibitor, and tramadol, a weak serotonin reuptake inhibitor, may present with fever, confusion, and clonus. In addition, abrupt withdrawal of baclofen, especially after intrathecal administration, has resulted in severe sequelae including hyperpyrexia and potential multiorgan failure and death [180]. Pathogenesis These drugs are thought to cause hyperthermia as a result of muscular contracture or hypermetabolism. Cocaine, amphetamine, phencyclidine, and hallucinogens appear to produce hyperthermia by centrally and peripherally inducing vigorous muscle contractions [218,219]. Selective serotonin reuptake inhibitors, dextromethorphan, and meperidine inhibit serotonin reuptake and, in susceptible patients, increase already high serotonin levels and trigger a hyperthermic crisis [200]. In general, a 2-week, drug-free period after stopping a monoamine oxidase inhibitor before starting a selective serotonin reuptake inhibitor is indicated. Some patients may exhibit exertional heat stroke, in that they are frequently found running in an agitated or confused manner. Rise in temperature is frequently rapid, and multiple organ failure rapidly ensues with prolonged elevation of temperature. Patients, however, may also be affected by the direct toxic action of the drug, and it may be difficult to separate the sequelae of hyperthermia from those of direct drug toxicity. Hyperthermia can be assumed to have the same physiologic sequelae in these patients as others, but prompt correction of temperature may not be adequate to ensure survival. Diagnosis In most case reports, patients are described as agitated, hyperexcited, and diaphoretic and have increased muscle tone. Because nonexertional heat stroke is uncommon in youth, hyperthermia at a young age always suggests possible drug intoxication. The onset of symptoms is within 2 hours of medication ingestion in 50% of cases and within 24 hours in 75% of cases [222]. Treatment For all cases, treatment should be directed at minimizing the toxicity of the causative drug. Treatment in general parallels that for exertional heat stroke and is extensively outlined in that section. Evaporative cooling and external cooling with ice are the preferred methods of cooling and should be instituted in any patient with a temperature above 39°C. Because the temperature appears to be generated from muscular contraction, paralysis or use of dantrolene would appear to be useful therapy. Paralysis and support with mechanical ventilation should be considered in any patient with a temperature above 40°C not responding promptly to symptomatic cooling. Because hyperthermia may be mediated by central serotonin receptors, doses of cyproheptadine high enough to block central receptors, 20 to 50 mg, should be considered [227]. Prognosis Hyperthermia owing to amphetamine overdose appears to be well tolerated, with 10 of 11 patients reported in the literature surviving [205,206,228,229].

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Rivers E 0.1 mg clonidine otc wykladzina arteria 95, Nguyen B buy discount clonidine 0.1 mg line pulse pressure greater than 50, Havstad S purchase clonidine 0.1 mg overnight delivery heart attack 720p, et al: Earlygoal-directed therapy in the treatment of severe sepsis and septic shock. Vieillard-Baron A, Caille V, Charron C, et al: Actual incidence of global left ventricular hypokinesia in adult septic shock. Jardin F, Fourme T, Page B, et al: Persistent preload defect in severe sepsis despite fluid loading: a longitudinal echocardiographic study in patients with septic shock. Poelaert J, Declerck C, Vogelaers D, et al: Left ventricular systolic and diastolic function in septic shock. Tsuchihashi K, Ueshima K, Uchida T, et al: Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction: angina pectorismyocardial infarction investigations in Japan. Kyuma M, Tsuchihashi K, Shinshi Y, et al: Effect of intravenous propranolol on left ventricular apical ballooning without coronary artery stenosis (ampulla cardiomyopathy): three cases. The goal of respiratory monitoring in any setting is to allow the clinician to ascertain the status of the patient’s ventilation and oxygenation. As with all data, it is imperative to remember that interpretation and appropriate intervention are still the onus of the clinician, who must integrate these data with other pieces of information in order to make a final intervention. For the critically ill patient, the principal intervention with regard to respiratory function and monitoring usually involves the initiation, modification, or withdrawal of mechanical ventilatory support. These simplified goals of mechanical ventilation are achieved in spite of complex and dynamic interactions of mechanical pressure with the physical properties of the respiratory system, namely, elastance (E ) and resistance (R ). Therefore, this chapter will focus on three specific areas of monitoring for the mechanically ventilated patient: (a) the evaluation of gas exchange, (b) respiratory mechanics, and (c) respiratory neuromuscular function. Inadequate ventilation and oxygenation within the intensive care setting are typically caused by hypoventilation, diffusion impairment, and ventilation–perfusion ( V. Fortunately, the institution of mechanical ventilatory support readily corrects hypoventilation while the underlying cause is determined and corrected. Diffusion impairment is the result of inadequate exchange of oxygen across the capillary-alveolar membrane, resulting in hypoxemia. This may occur due to pathological thickening of the membrane or high cardiac output states such as sepsis. This is because the hypoxemia that results from the acute exacerbation of diffusion impairment is usually corrected by supplemental oxygen therapy. Ventilation–perfusion mismatch is the result of an inequality of the normal ventilation to perfusion ratio within the lung. The true shunt fraction is the proportion of the cardiac output that results in venous blood mixing with end-arterial blood without participating in gas exchange. This has little effect on carbon dioxide tension; however, increases in shunt result in worsening hypoxemia. The absolute oxygen content of arterial and mixed venous blood is calculated according to the oxygen content equation: Cx = (1. The clinical significance of true shunt is the fact that it is not amenable to supplemental oxygen therapy. Shunted blood re-enters the circulation and dilutes oxygenated blood, resulting in a lower partial pressure of oxygen (PaO ) in the2 arterial system. Increasing the FiO will not improve oxygenation since2 the shunted fraction of blood does not meet alveolar gas. As with most monitors, sources of error abound at many points as gases flow according to their concentration gradients. However, the limitations of blood gas analysis as a tool for monitoring gas exchange are numerous, including the fact that it is invasive, wasteful (blood), expensive, and intermittent (i. Pulse Oximetry Without question, pulse oximetry has been the most significant advance in respiratory monitoring in the past several decades. A detailed explanation of pulse oximetry including the physics and limitations is provided in the Chapter “Routine Monitoring of Critically Ill Patients” (Chapter 27). Expired Carbon Dioxide Measurements Capnometry is the quantification of the carbon dioxide concentration in a sample of gas. The inhaled and exhaled carbon dioxide is displayed on the monitor along with its corresponding numerical measurement. For a detailed explanation of capnography and its uses, please refer to Chapter 27, “Routine Monitoring of Critically Ill Patients. Measurement of dead space is a marker of respiratory efficiency with regard to carbon dioxide elimination. Anatomic dead space is the sum of the inspiratory volume that does not reach the alveoli and therefore, does not participate in gas exchange. For mechanically ventilated patients, the anatomic dead space includes the proximal airways, trachea, endotracheal tube, and breathing circuit components from the Y-adapter to the endotracheal tube. In healthy human subjects, anatomic dead space in cubic centimeters is approximately 2 to 3 times the ideal body weight in kilograms, or 150 to 200 mL. Alveolar dead space is the conceptual sum of all alveoli that are ventilated but not participating in gas exchange, otherwise described as “West Zone 1” [10]. Integration of these measurements allows assessment of the mechanical components of the respiratory system. The mechanical components are influenced by various disease states, and understanding these relationships could promote the delivery of more appropriate ventilator support as well as pharmacologic management. The airway pressure (Paw) is described by the equation of motion and must be equal to all opposing forces. For the relaxed respiratory system ventilating at normal frequencies, the major forces that oppose Paw are the elastive and resistive properties of the respiratory system as they relate to the tidal volume (V ) and flow ( V. Constant flow inflation in a relaxed, ventilator- dependent patient produces a typical picture as depicted in ure 30. The Pplat measured at the airway represents the static end-inspiratory recoil of the entire respiratory system [16]. It is important that the Pplat measurement is preformed when the patient is passive as any inspiratory or expiratory efforts will create an error in the obtained value. Therefore, pleural pressures have often been estimated via an esophageal balloon catheter measuring the pressure in the esophagus (Pes), which lies in close proximity to the pleura at the mid-lung level. Transpulmonary pressure has been estimated as the difference between these pressures with specific assumptions. Compliance and Elastance the static compliance (Cst, rs) of the respiratory system and its reciprocal, elastance (Est, rs), are easily measured at the bedside using the aforementioned end-inspiratory airway occlusion method to produce zero flow and thus negate the resistive forces within the system. Both of these will lead to an additional increase in the elastance of the total respiratory system (Est, rs) as a result of an increase in the elastance of the chest wall (Ecw). Resistance According to Ohm’s law, resistance is a function of the airway pressure gradient (ΔPaw) divided by flow ( V. Respiratory system resistance is a complex and dynamic construct that relates the difference of alveolar to airway opening pressures to airflow. Airway resistance can be measured for ventilator-dependent patients by using the technique of rapid airway occlusion during constant flow inflation. Recognizing that airway resistance is abnormally high suggests that airway tube position and patency should be verified, airway contents removed by suctioning or cleaning the tube, and that the bronchodilator administration may be indicated. However, the actual pressure remaining in the alveoli and ventilator circuit at end-exhalation may be higher due to flow limitations or early closing capacity within a patient’s lungs. Such patients often have high resistance to both inhalation and exhalation and may not complete exhalation prior to the next inspiratory cycle.

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Complete air evacuation buy cheap clonidine 0.1mg online prehypertension symptoms, even after specific and meticulous venting techniques purchase clonidine 0.1 mg zofran arrhythmia, is nearly impossible to achieve [1] clonidine 0.1mg on-line hypertension blood pressure. The resultant pressure decrease is transmitted to the coronary arterial circulation, thus allowing air entry via the coronary arteriotomy site, with subsequent passage into the aortic root or the left ventricle. Any gases trapped in a proximal coronary artery or in a distally attached vein graft may also pass into the aortic root in the absence of venting if the graft is injected under pressure, as occurs commonly during the administration of cardioplegic hypothermia. Transcranial Doppler monitoring of the middle cerebral artery during open-heart operations has confirmed the occurrence of cerebral gas embolization [1]. The mode of air entry after percutaneous lung puncture, penetrating or blunt lung trauma, or with positive-pressure mechanical ventilation is via production of a bronchovenous fistula. For patients with preexisting pulmonary fibrosis, one should expect an increased frequency and severity of systemic embolism because of the inability of the injured veins to retract and constrict. This low-flow rate is approximately 5- to 25-fold less than the reported “safe range” of previous work [1]. Because the true “safe” amount of air that can remain in an arterial flush catheter without the risk of retrograde embolization remains unknown, medical personnel need to be vigilant and meticulous in ensuring removal of any entrapped air in arterial flush lines. Percutaneous Transluminal Coronary Angioplasty/Coronary Artery Stents Most coronary artery gas emboli resulting from percutaneous transluminal coronary angioplasty or stenting of a coronary artery are reportedly extremely small, and they do not result in symptoms or hemodynamic consequences [1]. For almost all patients, these effects resolve spontaneously within 5 to 10 minutes, similar to findings from experimental models. Gas bubbles distribute themselves throughout the body primarily directed by the relative blood flow at the time. Bubble buoyancy is actually a minor factor unless there is a significant depression of forward systemic flow [1]. Because the heart, lung, and brain receive the greatest amount of blood flow, the consequences of embolization are most frequently reported for these organs. Systemic Mechanical and Biophysical Effects Bubble formation results in two broad categories of effects: mechanical— physical obstruction to blood flow with distortion or tearing of tissues as the bubble forms and expands, and biophysical—where the blood–gas, blood–tissue, or gas–endothelial interfaces stimulate a cascade of leukocyte, platelet, coagulation, fibrinolytic, and complement-mediated activations [1]. Research over the last few decades now recognizes the importance of oxidative stressors causing impairment of endothelium- dependent vasorelaxation (i. Unlike the situation when bubbles are trapped in a vein, an arterial occlusion may have an immediate clinical impact. Uptake and release of inert gas by a particular tissue depends on the rate of blood flow to that tissue, as well as the rate of gas diffusion out of the blood into the tissue. When bubbles do form, the inert gas becomes isolated from the circulation, and it cannot be removed by blood flow until it diffuses back into tissues. The speed of diffusion is the result of the difference between the N partial pressure in the air bubble and the N partial pressure in the2 2 tissue. Injury is probably more a result of damage from endothelial mediators, oxidant stress, and neuronal hypoxia rather than being directly a result of vascular obstruction or edema. After 5 to 30 seconds of arrested cerebral blood flow, most gas bubbles easily pass through the pial arteries. Cerebral air emboli have been shown to persist in the circulation for 40 hours after initial insult [5]. In the latter group, the initial presentation is that of stable respiratory and heart rates, but with a wide spectrum of neurologic signs and symptoms. There may be loss of consciousness, convulsions, visual disturbances (including blindness), headache, confusion or other mental status changes, coma, vertigo, nystagmus, aphasia, sensory disturbances, weakness or hemiparesis, or even focal or more widespread paralysis. The air may dissect along the perivascular sheaths into the mediastinum, causing pneumomediastinum, usually associated with a substernal aching or tightness that may have a pleuritic nature and may radiate to the neck, back, or shoulders. There may be coexistent subcutaneous emphysema and a notable “crunching” sound with each heartbeat (Hamman’s sign) caused by air in the pericardium. Tension pneumothorax may occur in patients on positive-pressure mechanical ventilation or during decompression. Pneumopericardium and air in the retroperitoneum and subcutaneous tissues of the neck, trunk, or limbs may also occur. This extra-alveolar gas also has access to torn pulmonary blood vessels when the intrathoracic pressure decreases during normal inspiration after barotrauma has occurred. Once egress into the pulmonary venous circulation has occurred, migration to the left side of the heart and then to the arterial circulation may follow. Hemoptysis has often been mentioned as a cardinal sign of dysbaric air embolism, but it actually occurs in a minority (approximately 5%) of patients [1]. Appropriate therapy involves prompt recognition, initial stabilization (with emphasis on preventing further damage), and definitive specific therapy (Table 177. Therefore, it cannot be emphasized strongly enough that a high index of suspicion for these diagnoses is one of the most important elements of care. Like many other true medical emergencies, therapeutic interventions should not be delayed to implement diagnostic testing. Any rapid lowering of ambient pressure, regardless of the initial pressure level or saturation of inert gas, results in the release of bubbles of inert gas into the blood and tissues. This is equally true for too quick a return to a normobaric state after a hyperbaric exposure (as in diving or compressed air mining), or for rapid progression from a normobaric state into a hypobaric exposure (as in aviators, astronauts, or mountain climbers). Haldane also formulated the concept that the tissues of the body absorb nitrogen at varying rates, depending on the type of tissue and its vascularity. There is an important inter- and intraindividual variation in the degree of “bubbling” after a dive, indicating a significant, but as yet poorly characterized, influence of personal factors affecting gas saturation and desaturation [1,8]. Modern airline transportation has minimized these risks by pressurizing aircraft to maintain cabin pressures equivalent to 8,000 ft. Astronauts performing activities outside their space vehicles are decompressed from a cabin pressure equivalent to sea level, down to a suit pressure equivalent of approximately 30,000 ft. This table also demonstrates the reduction of pressure and volume expansion that accompanies increases of altitude. As a scuba diver ascends slowly from depth, pressure in the lungs equalizes with ambient pressure as long as proper exhalation is achieved. The fragility of alveoli is not generally appreciated, but it is highlighted by the fact that with the lungs fully expanded on compressed air, a pressure differential of only 95 to 110 cm H O (equivalent to an ascent from a depth of only 4 to 6 ft. Dalton’s law of partial pressures states that the total pressure exerted by a mixture of gases is equal to the sum of the partial pressures of its constituent gases. The composition of gases that make up our atmosphere remains essentially constant up through an altitude of approximately 70,000 ft. N is more soluble in2 fat than in water, which suggests that during decompression, bubbles more likely form in lipophilic tissues such as bone marrow, fat, and spinal cord. Henry’s law of gas solubility states that the amount of gas that dissolves in a fluid is directly proportional to the pressure of that gas on that fluid. The deeper one descends underground or in the ocean, the greater the driving pressure for the gas on the blood and the bodily fluids. The total accumulation of dissolved N into the tissues of the body, therefore,2 depends on the depth achieved and the time spent at that depth. The site of origin of intravascular bubbles is controversial, but overwhelming human and animal experimental evidence shows that gas bubbles are first detected in the venous circulation during decompression.