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The aminoglycoside antibiotics and amphotericin B are particularly difficult to avoid because they are effective antimicrobials discount 100 mg kamagra mastercard erectile dysfunction genetic, with few available alternatives purchase kamagra australia erectile dysfunction drugs forum. Their effect can be additive with other nephrotoxic factors causing impairment of kidney function. Hypovolemia, fever, renal vasoconstriction, and concomitant therapy with other nephrotoxic agents should be avoided wherever possible. Electrolyte disorders such as hypercalcemia, hypomagnesemia, hypokalemia, and metabolic acidosis can further enhance nephrotoxic damage to the kidney. Cyclosporin A and tacrolimus are indispensable components of many immunosuppressive drug regimens, but in combination with other nephrotoxins and clinical factors, they can cause acute and exacerbate chronic 3527 kidney injuries in transplant recipients. Radiocontrast dye has effects on renal49 function that develop 24 to 48 hours after exposure and peak at 3 to 5 days. Myoglobin seems to be a more potent nephrotoxin than hemoglobin because it is more readily filtered at the glomerulus and can be reabsorbed by the renal tubules, where it chelates nitric oxide and thus induces medullary vasoconstriction and ischemia. These goals may be accomplished by expanding the intravascular fluid volume with crystalloid infusion, stimulating an osmotic diuresis with mannitol, and increasing the urine pH with intravenous bicarbonate therapy. Though high-quality evidence is lacking, forced mannitol-alkali diuresis is recommended as the second step in the preventive treatment of myoglobinuria, with urine flow rates of up to 300 mL/hour and a urine pH above 6. However, peak fluoride levels during administration of these agents seldom reach toxic levels, and there are few reports describing volatile agent–induced nephrotoxicity. The potential of sevoflurane-induced nephrotoxicity has56 been related to the production of compound A during prolonged, low-fresh- gas-flow sevoflurane anesthesia. Although there are insufficient data to57 conclude that sevoflurane-induced kidney injury occurs in the human population, even during low-gas-flow anesthesia, it is probably prudent to maintain a fresh gas flow of at least 2 L/min during sevoflurane anesthesia. Evidence of increased rates of renal replacement therapy in critically ill and septic patients receiving hydroxyethyl starches resulted in the elimination of these fluids from routine clinical practice. Thus, optimal63 fluid management in the perioperative period, in both the type and amount of fluid, has significant effects on renal function. Patients with decreased renal reserve are often asymptomatic and frequently do not have elevated blood levels of creatinine or urea. It results in inability of the kidney to perform its two major functions: regulation of the volume and composition of the extracellular fluid and excretion of waste products. Situations predisposing patients with renal failure to hyperkalemia are presented in Table 50-2. Both render patients susceptible to an endogenous acid load such as may occur in shock states, hypovolemia, or with an increase in catabolism. Cardiovascular complications of the uremic syndrome are primarily due to volume overload, high renin–angiotensin activity, autonomic nervous system hyperactivity, acidosis, and electrolyte disturbances. Together with volume overload, acidemia, anemia, and possibly the presence of high-flow arteriovenous fistulae created for dialysis access, hypertension may contribute to the development of myocardial dysfunction and heart failure. Pericarditis may occur secondary to uremia or dialysis, with pericardial tamponade developing in 20% of the latter group. Pulmonary edema and restrictive pulmonary dysfunction are commonly seen in patients with renal failure and are usually responsive to dialysis. Hypervolemia, heart failure, reduced serum oncotic pressure, and increased pulmonary capillary permeability are relevant factors in the development of pulmonary edema. Platelet dysfunction may aggravate blood loss, but it is responsive to dialysis, cryoprecipitate administration, and desmopressin acetate (or 1-deamino-8-D-arginine vasopressin). Unfortunately, clearance of most medications involves a more complex combination of both hepatic and renal functions, and drug level measurement or algorithms for specific drugs are often recommended. However, plasma protein binding is highly variable, with acidic drugs having reduced binding and basic agents (e. Importantly, for drugs with less binding, “normal” drug levels may reflect dangerously high active (unbound) drug levels. For example, therapeutic phenytoin levels are typically reported as being in the range of 10 to 20 mg/mL normally but 4 to 10 mg/mL in cases of renal failure. Anesthetic Agents in Renal Failure With the exception of methoxyflurane and possibly enflurane, anesthetic agents do not directly cause renal dysfunction or interfere with the normal compensatory mechanisms activated by the stress response. The nephrotoxicity of methoxyflurane appears to be due to its metabolism, which results in release of the fluoride ions believed responsible for the renal injury. It has been suggested that renal, not hepatic, metabolism of65 methoxyflurane may be responsible for generating fluoride ions locally that contribute to nephrotoxicity. Enflurane nephrotoxicity may also occur but66 67 is of minor clinical importance, even in patients with pre-existing renal dysfunction. Although direct anesthetic effects on the kidney are usually not harmful, indirect effects may combine with hypovolemia, shock, nephrotoxin exposure, or other renal vasoconstrictive states to produce renal dysfunction. If the chosen anesthetic technique causes a protracted reduction in cardiac output or sustained hypotension that coincides with a period of intense renal vasoconstriction, renal dysfunction or failure could result. There are no comparative studies demonstrating superior renal protection or improved renal outcome with 3533 general versus regional anesthesia. Significant renal impairment may affect the disposition, metabolism, and excretion of the commonly used anesthetic agents. Inhalation anesthetics are, of course, an exception to the rule that drugs with central nervous system activity (which generally are lipid soluble) must be converted to more hydrophilic compounds by the liver before being excreted by the kidney. The water-soluble metabolites of agents that are not inhaled may accumulate in renal failure and display prolonged pharmacodynamic effects if they possess even a small percentage of the pharmacologic activity of the parent drug. Many drugs used in anesthesia are highly protein bound and may demonstrate exaggerated clinical effects when protein binding is reduced by uremia. Burch and Stanski showed that the free fraction of an68 induction dose of thiopental is almost doubled in patients with renal failure. Ketamine is less extensively protein bound than thiopental, and renal failure appears to have less influence on its free fraction. Redistribution and hepatic metabolism are largely responsible for termination of the anesthetic effects, with less than 3% of the drug excreted unchanged in the urine. Norketamine, the major metabolite, has one-third the pharmacologic activity of the parent drug and is further metabolized before it is excreted by the kidney. The decrease in protein binding70 does not seem to alter the clinical effects of etomidate anesthetic induction in patients with renal failure. Propofol undergoes extensive rapid hepatic biotransformation to inactive metabolites that are renally excreted. Certain benzodiazepine metabolites are pharmacologically active and have the potential to accumulate with repeated administration of the parent drug to anephric patients. For example, 60% to 80% of midazolam is excreted as its (active) α-hydroxy metabolite, which72 accumulates during long-term infusions in patients with renal failure. Volunteers with renal impairment receiving dexmedetomidine experienced a longer-lasting sedative effect than subjects with normal kidney function. The most likely explanation is that less protein binding of dexmedetomidine occurs in subjects with renal dysfunction.

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J Am Coll Cardiol 54:312–321 that this text has further elucidated the incidence kamagra 100 mg online erectile dysfunction blogs, 9 generic 50 mg kamagra otc impotence over the counter. Interact Cardiovasc device with the device thrombogenicity emulation- Thorac Surg 20(6):743–748. Horstmanshof D, Adamson R, Boyle A, Zucker M, Rogers Ann Thorac Surg 100(3):884–889. Eur J Cardiothorac Surg events after left ventricular assist device implanta- 23(3):328–333. Ann Thorac Surg 97(6):2097– Predictors of cerebrovascular events in patients sub- 2103. Tis defnition for patients showed in this respect no signifcant dif- gastrointestinal bleeding as an adverse event is ferences within 2-year postoperative follow-up. Most frequently the bleeding is patients with a continuous-fow assist device, located in the upper gastrointestinal tract 48% which implicates anticoagulation with vitamin K (until Treitz band) and in 22% in the lower gastro- antagonist in combination with inhibitor of plate- intestinal tract. Notably, a high percentage is contrast to patients with a pulsatile assist device of caused by angiodysplasias. Terefore older patients with an age > 65 years endoscopy is not successful, a capsule endoscopy is show a 1. Te results of the capsule study may indicate tiles of pulsatility index subsets demonstrated in a the further need for therapeutic intervention by a study from Wever-Pizon et al. Upper 40 endoscopy had the highest yield for a source of bleeding, 30 signifcantly higher than that seen with colonoscopy or enteroscopy. The number of 20 capsule endoscopy (5) and radiologic procedures (8) 10 performed was limited 0 Upper Colonoscopy ush Capsule Radiologic endoscopy enteroscopy endoscopy procedures 492 A. Te emic etiology of heart failure which were further administration of fresh frozen plasma and coagula- confrmed in other series [1, 12]. Due to the chronic a complex highly secretory endocrine organ that antiplatelet therapy, application of platelet concen- can regulate insulin sensitivity and infammation trates should be considered. Te soma- Gastrointest Endosc 80(3):435–446 e431 tostatin analogue reduces the portal venous pres- 5. Crow S, John R, Boyle A, Shumway S, Liao K, Colvin- Adams M, Toninato C, Missov E, Pritzker M, Martin C sure and decreases the splanchnic blood fow. Te et al (2009) Gastrointestinal bleeding rates in recipi- side efects were diarrhea and abdominal pain [21]. Dig Liver Dis 43(7): lial vasomotor dysfunction of visceral adipose arteri- 515–522 oles in human obesity. Ann Thorac Surg 93(5): implications for left ventricular assist device-associ- 1534–1540 ated bleeding. Areas ascending aorta, sometimes the descending of fow stagnation represent preferred thrombus aorta in the case of less-invasive developing sites as well as areas with recirculation implantation procedures, in rare cases also vortices. Tis would be called bearings, ofen are subjected to thrombus buildup post-pump thrombosis or graf thrombosis. Tis also applies thrombosis: thrombus development around the to running the device in the specifed optimal apical infow section of the pump or the infow range of operation. Kinks and other causes wound or the textured part of the infow cannula, obstructing the fow path like cannula most ofen seen at the transition from a struc- malposition have to be avoided. A small tured section (titanium sintered) to the smooth, clearance of the apical infow cannula to the polished section toward the tip of the infow. In a position of the infow opening close to the lat- the following, the detection of pump thrombosis is eral or the septal wall causing narrowing of the focused on implantable rotary blood pumps sup- lumen. Heat efects in 48 extreme pump thrombosis situations requiring If the thrombotic material is of considerable size driving power of up to or more than 20 W so far and thus is narrowing the fow path in one or have not been investigated but may very well be more sections of the device, the pumping capac- existent. With magnetic or hydrodynamic bearings, Clinically this would lead to low pump fow, thus thrombus on the impeller may cause substantial reducing unloading of the lef ventricle, and as a rotor displacement resulting in contact of the consequence the patient will show signs of heart rotor with the housing producing scratch marks. Dyspnea, weakness, or dizziness may At these no longer highly polished surfaces of the occur, and ultimately, if there is no sufcient rotor secondary thrombus formation is likely, residual capacity of the patient’s heart, it would aggravating the situation. Trombi adhering to the impeller of a rotary blood pump may change the hydrodynamic properties of the pump. Sometimes hemolysis is the most impressive result and thus an indicator of pump thrombosis 48. Dark urine If thrombus material is flling the gap between the output may be the frst sign to be recognized in rotating impeller and the pump housing, friction an outpatient and requires immediate reaction: will result. To overcome this energy loss, more hospitalization for a thorough investigation of power is required in order to keep the preset rota- the situation. If culated out of the created pressure head, whose no blood is passing through the pump, it cannot level is retrieved from rotor displacement data be damaged by high shear rates. In-pump thrombosis thus of the Sound of the is likely to create false high fow readings. To Running Pump complicate the situation, these two efects of fow decrease and power increase may compensate Trombotic material adhering to the impeller of a for each other, resulting in unsuspicious fow rotary blood pump will cause an imbalance. Like 499 48 Pump Thrombosis an imbalanced tire on a car, high rotational speeds create specifc noise. If measured and com- will excite vibration of the whole system, causing pared to existing acoustic spectra of a specifc an alteration of the sound produced by the run- pump (acoustic footprint), this was indicative of ning pump. One efect is an intensifed volume of thrombus formation in an in vitro setting as well. Another efect is the excitation of a dif- However, clinical application of this method so ferent acoustic spectrum or pattern. Tese efects far was not possible but it could be promising if may be small if the rotor is forced to rotate stably obstacles like a poor signal-to-noise ratio could by means of mechanical bearings. Te methods which can be applied to detect locate the onset of changes in the system param- pump thrombosis depend on the respective sys- eters usually is not successful in capturing the tem or pump technology. Because the hemodynamics is a big gap between the magnetic feld created in of individual patients can difer a lot, an independent the stator coils and the magnet of the rotor. To test protocol is necessary to evaluate the actual state create the necessary magnetic fux, the magnetic of the pump functionality, the so-called ramp test. Trombus material consumption compensating friction, which may adhering to the impeller circumference will cause lead to the assumption of good unloading of the lef an imbalance of the magnetically levitated impel- ventricle, together with opening of the aortic valve ler. To compensate this and stabilize the rotation, or large size of the lef ventricle at the same time are the magnetic levitation requires stronger mag- suspicious. Tough quency and low number of patients on device, up to now there is no plausible and clinically con- the specifc aspects of thrombus detection, expla- frmed explanation of these power spikes, they do nation of the efects, and treatment options are not qualify as indicative for thrombus formation. However, although the techni- Only together with signs of fow impairment and cal aspects are quite diferent compared to those hemolysis, respective treatment is advisable. Single experiences indicate that changes in these parameters will very likely indi- 48. Analysis and inter- extends only over some days and has irregular pretation of these levitation log fles is not feasi- sample points.

In 1885 cheap kamagra generic impotence clinic, O’Dwyer designed a series of metal laryngeal tubes order kamagra 50mg fast delivery erectile dysfunction miracle, which he inserted blindly between the vocal cords of children suffering a diphtheritic crisis. Three years later, O’Dwyer designed a second rigid tube with a conical tip that occluded the larynx so effectively that it could be used for artificial ventilation when applied with the bellows and T-piece tube designed by George Fell. The Fell– O’Dwyer apparatus, as it came to be known, was used during thoracic surgery by Rudolph Matas of New Orleans. Matas was so pleased with it that he predicted, “The procedure that promises the most benefit in preventing pulmonary collapse in operations on the chest is … the rhythmical maintenance of artificial respiration by a tube in the glottis directly connected with a bellows. From 1900 until 1912, Kuhn148 published several articles and a classic monograph, “Die perorale Intubation,” which were not well known in his lifetime but have since become widely appreciated. His work might have had a more profound impact if it had been translated into English. Kuhn described techniques of oral and nasal intubation that he performed with flexible metal tubes composed of coiled tubing similar to those now used for the spout of metal gasoline cans. After applying cocaine to the airway, Kuhn introduced his tube over a curved metal stylet that he directed toward the larynx with his left index finger. Although he was aware of the subglottic cuffs that had been used briefly by Victor Eisenmenger, Kuhn preferred to seal the larynx by positioning a supralaryngeal flange near the tube’s tip before packing the pharynx with gauze. Kuhn even monitored the patient’s breath sounds continuously through a monaural earpiece connected to an extension of the tracheal tube by a narrow tube. Intubation of the trachea by palpation was an uncertain and sometimes traumatic act; surgeons even believed that it would be anatomically impossible to visualize the vocal cords directly. This misapprehension was overcome in 1895 by Alfred Kirstein in Berlin, who devised the first direct- vision laryngoscope. Kirstein was motivated by a friend’s report that a30 patient’s trachea had been accidentally intubated during esophagoscopy. Kirstein promptly fabricated a handheld instrument that at first resembled a shortened cylindrical esophagoscope. Kirstein could now examine the larynx while standing behind his seated patient, whose head had been placed in an attitude approximating the currently termed “sniffing position. Endoscopy was refined by Chevalier Jackson in Philadelphia, who designed a U-shaped laryngoscope by adding a handgrip that was parallel to the blade. The Jackson blade has remained a standard instrument for endoscopists but was not favored by anesthesiologists. Two laryngoscopes that closely resembled modern L-shaped instruments were designed in 1910 and 1913 by two American surgeons, Henry Janeway and George Dorrance, but neither instrument achieved lasting use despite their excellent designs. This challenge was made somewhat easier, however, with the advent of laryngoscope blades specifically designed to increase visualization of the vocal cords. Robert Miller of San Antonio, Texas, and Robert Macintosh of Oxford University created their respectively named blades within an interval of 2 years. In 1941, Miller brought forward the 64 slender, straight blade with a slight curve near the tip to ease the passage of the tube through the larynx. Although Miller’s blade was a refinement, the technique of its use was identical to that of earlier models as the epiglottis was lifted to expose the larynx. Sir Robert Macintosh later described the circumstances of its discovery in an appreciation writing regarding the career of his technician, Mr. As Sir Robert recalled, “A Boyle-Davis gag, a size larger than intended, was inserted for tonsillectomy, and when the mouth was fully opened the cords came into view. This was a surprise since conventional laryngoscopy, at that depth of anaesthesia, would have been impossible in those pre-relaxant days. Within a matter of hours, Salt had modified the blade of the Davis gag and attached a laryngoscope handle to it; and streamlined (after testing several models), the end result came into widespread use. The most distinguished innovator in tracheal intubation was the self- trained British anesthetist Ivan (later, Sir Ivan) Magill. In 1919, while34 serving in the Royal Army as a general medical officer, Magill was assigned to a military hospital near London. Although he had only rudimentary training in anesthesia, Magill was obliged to accept an assignment to the anesthesia service, where he worked with another neophyte, Stanley Rowbotham. Together, Magill and Rowbotham attended casualties35 disfigured by severe facial injuries who underwent repeated restorative operations. These procedures required that the surgeon, Harold Gillies, have unrestricted access to the face and airway. These patients presented formidable challenges, but both Magill and Rowbotham became adept at tracheal intubation and quickly understood its current limitations. Because they learned from fortuitous observations, they soon extended the scope of tracheal anesthesia. They gained expertise with blind nasal intubation after they learned to soften semirigid insufflation tubes for passage through the nostril. Even though their original intent was to position the tips of the nasal tubes in the posterior pharynx, the slender tubes frequently ended up in the trachea. Stimulated by this chance experience, they developed techniques of deliberate nasotracheal intubation. In 1920, Magill devised an aid to manipulating the catheter tip, the “Magill angulated forceps,” which continues to be manufactured according to his original design over 90 years ago. With the war over, Magill entered civilian practice and set out to develop a wide-bore tube that would resist kinking but be conformable to the contours of the upper airway. While in a hardware store, he found mineralized red 65 rubber tubing that he cut, beveled, and smoothed to produce tubes that clinicians around the world would come to call “Magill tubes. Magill also rediscovered the advantage of applying cocaine to the nasal mucosa, a technique that greatly facilitated awake blind nasal intubation. In 1926, Arthur Guedel began a series of experiments that led to the introduction of the cuffed tube. Guedel transformed the basement of his Indianapolis home into a laboratory, where he subjected each step of the preparation and application of his cuffs to a vigorous review. He fashioned36 cuffs from the rubber of dental dams, condoms, and surgical gloves that were glued onto the outer wall of tubes. Using animal tracheas donated by the family butcher as his model, he considered whether the cuff should be positioned above, below, or at the level of the vocal cords. He recommended that the cuff be positioned just below the vocal cords to seal the airway. Ralph Waters later recommended that cuffs be constructed of two layers of soft rubber cemented together. These detachable cuffs were first manufactured by Waters’ children, who sold them to the Foregger Company. He first filled the mouth of an anesthetized and intubated patient with water and showed that the cuff sealed the airway. Even though this exhibition was successful, he searched for a more dramatic technique to capture the attention of those unfamiliar with the advantages of intubation. He reasoned that if the cuff prevented water from entering the trachea of an intubated patient, it should also prevent an animal from drowning, even if it were submerged under water. To encourage physicians attending a medical convention to use his tracheal techniques, Guedel prepared the first of several “dunked dog” demonstrations (Fig.

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Nevertheless buy discount kamagra 50 mg on-line erectile dysfunction before 30, ventilation and perfusion are not matched perfectly 100mg kamagra for sale erectile dysfunction treatment in tampa, and various V˙/Q˙ ratios result throughout the lung. The ideal V˙/Q˙ ratio of 1 is believed to occur at approximately the level of the third rib. Above this level, ventilation occurs slightly in excess of perfusion, whereas below the third rib the V˙/Q˙ ratio becomes less than 1 (Fig. In a simplified model, gas exchange units can be divided into normal (V˙/Q˙ 1:1), dead space (V˙/Q˙ = 1:0), shunt (V˙/Q˙ = 0:1), or a silent unit (V˙/Q˙ = 0:0) (Fig. Although this model is helpful in understanding V˙/Q˙ relationships and their influences on gas exchange, V˙/Q˙ really occurs as a continuum. In the lungs of a healthy, upright, spontaneously breathing individual, the majority of alveolar–capillary units are normal gas exchange units. The V˙/Q˙ ratio varies between absolute shunt (in which V˙/Q˙ = 0) to absolute dead space (in which V˙/Q˙ = ∞). Rather than absolute shunt, most units with low V˙/Q˙ mismatch receive a small amount of ventilation relative to blood flow. Similarly, most dead space units are not absolute, but rather are characterized by low blood flow relative to ventilation. During acute lung injury and adult respiratory distress syndrome, areas of low V˙/Q˙ matching commonly lie adjacent to areas of high V˙/Q˙ matching. Thus, the West lung50 zone model should be used to aid the understanding of pulmonary physiology and not be regarded as an incontrovertible anatomic truism. In Zone 2, arterial pressure exceeds alveolar pressure, but alveolar pressure exceeds pulmonary venous pressure (Ppv). Flow in Zone 2 is determined by 967 the arterial–alveolar pressure difference (Ppa − P ), which steadily increases down theA zone. In Zone 3, pulmonary venous pressure exceeds alveolar pressure, and flow is determined by the arterial–venous pressure difference (Ppa − Ppv), which is constant down this pulmonary zone. However, the pressure across the vessel walls increases down the zone so their caliber increases, as does flow. Distribution of blood flow in isolated lung: Relation to vascular and alveolar pressures. Because blood flow falls more rapidly than ventilation with distance up the lung, ventilation—perfusion ratio rises, slowly at first, then rapidly. Hypoxic pulmonary vasoconstriction, stimulated by alveolar hypoxia, severely decreases blood flow. Furthermore, decreased regional pulmonary blood flow results in bronchiolar constriction and diminishes the degree of dead space ventilation. Many pulmonary diseases result in both physiologic shunt and dead space abnormalities. However, most disease processes can be characterized as producing either primarily shunt or dead space in their early stages. Increases in dead space ventilation primarily affect carbon dioxide elimination and have little influence on arterial oxygenation until dead space ventilation exceeds 80% to 90% of minute ventilation ( ). Similarly, physiologic shunt primarilyE affects arterial oxygenation with little effect on carbon dioxide elimination until the physiologic shunt fraction exceeds 75% to 80% of the cardiac 968 output. Defective to absent gas exchange can be the net effect of either abnormality in the extreme. Physiologic Dead Space Each inspired breath is composed of gas that contributes to alveolar ventilation (V ) and gas that becomes dead space ventilation (V ). In the normal, spontaneously breathing person, theA D ratio of alveolar-to-dead space ventilation (V /V ) for each breath is 2:1. A D Conveniently, the rule of “1, 2, 3” applies to normal, spontaneously breathing persons. For each breath, 1 mL/lb (lean body weight) becomes V , 2 mL × lbD −1 becomes V , and 3 mL × lb−1 constitutes the Vt. Gas exchange is maximally effective in normal lung units and only partially effective in shunt and dead space effect units. Anatomic dead space ventilation, approximately 2 mL/kg ideal body weight, accounts for the majority of physiologic dead space. It arises from ventilation of structures that do not exchange respiratory gases: the oronasopharynx to the terminal and respiratory bronchioles. Clinical conditions that modify anatomic dead space include tracheal intubation, tracheostomy, and large lengths of ventilator tubing between the tracheal tube and the ventilator Y- piece. It is important to note that ventilation occurs because gas flows into 969 and out of the alveoli. In contrast, the inspiratory or expiratory limb of the anesthesia circle system has unidirectional flow, and therefore, is not a component of anatomic dead space ventilation. Alveolar dead space ventilation arises from ventilation of alveoli with inadequate or no perfusion. Since disease produces little change in anatomic dead space, physiologic dead space is primarily influenced by changes in alveolar dead space. Rapid changes in physiologic dead space ventilation most often arise from changes in pulmonary blood flow, resulting in decreased perfusion to ventilated alveoli. The most common etiology of acutely increased physiologic dead space is an abrupt decrease in cardiac output. Another pathologic condition that interferes with pulmonary blood flow, and thereby creates dead space, is pulmonary embolism, whether due to thrombus, fat, air, or amniotic fluid. Although there may be obstruction to blood flow with some types of pulmonary emboli, the greatest decrease in pulmonary blood flow is due to vasoconstriction induced by locally released vasoactive substances such as leukotrienes. Finally, therapeutic or supportive manipulations such as positive-pressure ventilation or positive airway pressure therapy can increase alveolar dead space because depressed venous return to the right heart will decrease cardiac output and blood flow through the pulmonary vasculature, leading to decreased perfusion of the alveoli despite improved ventilation with positive-pressure therapy. Occasionally, therapeutics which create intrapulmonary positive pressure may increase physiologic shunt, when blood flow to a previously silent area of V˙/Q˙ matching now receives blood redistributed by positive pressure from more compliant areas of the lung. Assessment of Physiologic Dead Space As the lung receives nearly 100% of the cardiac output, assessment of physiologic dead space ventilation in the acute setting yields valuable 970 information about pulmonary blood flow and, ultimately, about cardiac output. If pulmonary blood flow decreases, the most likely cause is a decreased cardiac output. Thus, it is clinically useful to be able to readily assess the degree of physiologic dead space ventilation. Because positive-pressure ventilation increases alveolar pressure, the mechanically ventilated patient with normal lungs has a dead space to alveolar ventilation ratio (V /V ) of 1:1 (more West Zone 1) rather than 1:2,D A as during spontaneous ventilation. If mechanical Vt is 1,000 mL, 500 mL contributes to V , and 500 mL contributes to V. During spontaneous breathing, the requiredA V˙ would be 6,300 mL/min, but during mechanical ventilation V˙ would haveE E to be 8,400 mL/min.

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