The management of critically ill patients has one universal goal: to maintain adequate levels of tissue oxygenation and sustain aerobic metabolism. However, much of what is done in the name of aerobic support is based on traditional beliefs rather than documented need because there is no direct measure of tissue oxygenation.
Shock is best defined as inadequate tissue perfusion and thereby an impairment of oxygen delivery. A primary goal in resuscitation is to detect these changes in tissue oxygenation before cardiovascular collapse. During this phase of compensated shock, better endpoints are needed to guide resuscitation efforts and to determine when to stop resuscitation. The complications of over-resuscitation have been well documented, and include abdominal compartment syndrome, acute respiratory distress syndrome and organ failure. The ideal endpoint should be readily obtainable, easily interpretable and have a high degree of consistency across the population.
TENEMOS QUE REVISAR LOS COMPONENTES DEL PROCESO FISIOLOGICO DE LA OXIGENACION TISULAR QUE SON EL INTERCAMBIO DE GAS, LA ENTREGA Y EL CONSUMO LA EVAUACION TIENE 2 OBJETIVOS, 1 SABER COMO ESTA LA OXIGENACION EN TERMINOS GLOBALES Y 2 SABER CUAL ES EL PROCESO QUE SE DEBE MANIPULAR PARA MEJORAR LA MISMA
Dysoxia is inadequacy of tissue oxygenation, The condition when O2 levels are so low that mitochondrial respiration can no longer be sustained . It is assumed that tissue dysoxia and O2 debt are major factors in the development and the propagation of multiple organ failure in critically ill patients. Dysoxia is the result of an abnormal relationship between O2 supply (DO2) and O2 demand. In order
Describir el metabolismo aerobico con el numero de ATPproducido y lo que sucede en el funcionamiento celular cuando hay paso a metabolismo anaerobio con poca produccion de ATP. Blood lactate levels are also commonly used clinically for monitoring systemic Do2. When Do2 is adequate and there is no tissue oxygen deficit, adequate ATP (38 mol/L) is produced from glucose via the tricarboxylic acid cycle to support the metabolic functions of the cell. During hypovolemic shock, the energy source for the cell turns primarily to anaerobic glycolysis, which produces only 2 mol/L of ATP. Instead of entering the tricarboxylic acid cycle, pyruvate is converted to lactate. Blood lactate begins to accumulate, and in the presence of increased hydrogen ion (H) from hydrolysis of ATP, lactic acidosis ensues. The lactate level in arterial blood during lactic acidosis is usually elevated above the normal 2 mmol/L. The lactate level in the blood, however, is also influenced by the elimination and the distribution of lactate. The liver plays a central role in eliminating lactate from the blood, so in patients with poor liver function ( eg, cirrhosis), the blood lactate level can increase without lactic acidosis. Lactic acidosis may also be present without an increase in blood lactate level. This may occur when the blood flow to an organ is completely blocked ( eg, limb ischemia). Transient increases in blood lactate are only observed after successful reperfusion because of washout of lactate from the ischemic tissues. Thus, it is usually more advantageous to follow the changes in the blood lactate level rather than the absolute values. A continuous fall in the blood lactate level during resuscitation from hypovolemic shock is usually a favorable sign and is associated with survival. Persistent increase in blood lactate, however, almost always indicates the continuous presence of ischemic tissues and correlates with multiorgan system failure and poor outcome . clear improvement in blood lactate clearance is also a good and minimally invasive indicator of adequate resuscitation . The blood lactate concentration alone fails to discriminate between dysoxia and aerobiosis . Although more reliable, the time course of lactate levels is not an ideal marker [2,7,9]. The limitations of lactate were recently reviewed . Diabetes mellitus, liver dysfunction, tissue reperfusion, catecholamine infusion, cellular metabolic alterations and inhibition of pyruvate dehydrogenase can all result in a marked increase in blood lactate concentrations, despite improvement in tissue dysoxia.
CaO2 is calculated according to the formula in Table 5. Normal CaO2 is 20 mL O2/dL. PaO2 contributes minimally to overall DO2 and is frequently omitted from the calculation. Global DO2 depends more on SaO2 than PaO2. Therefore, there is little extra benefit from increasing PaO2 above 90 mmHg due to the shape of the oxyhemoglobin dissociation curve when over 90% of Hb is already saturated with oxygen. Increasing Hb through blood transfusion may seem to be an appropriate intervention to optimize CaO2. However, blood viscosity increases with Hb 10 g/dL and can impair blood flow. Although blood transfusion to polycythaemic levels might seem an appropriate way to increase DO2, blood viscosity increases markedly above 100 g/l. This impairs flow and oxygen delivery, particularly in smaller vessels and when the perfusion pressure is reduced, and will therefore exacerbate tissue hypoxia.1 Recent evidence suggests that even the traditionally accepted Hb concentration for critically ill patients of approximately 100 g/l may be too high since an improved outcome was observed if Hb was maintained between 70 and 90 g/l with the exception of patients with coronary artery disease in whom a level of 100 g/l remains appropriate.2 With the appropriate Hb achieved by transfusion, and since the oxygen saturation (SaO2) can usually be maintained above 90% with supplemental oxygen (or if necessary by intubation and mechanical ventilation), cardiac output is the variable that is most often manipulated to achieve the desired global DO2 levels.
Normal DO2 is 950 to 1150 mL/min or 500 to 600 mL/min/m2.15
La perdida de consciencia correlaciona con hipoxemia, el llenado capilar es un mal indicador por su baja sensibilidad, la frialdad de la piel correlaciona con otros marcadores como BE,ac lactico y SvO2. marcadores como la FC y gasto urinario son poco confiables porque su manifestacion puede ser tardia y ademas hay casos de adecuado gasto urinario con compromiso d ela perfusion de otros tejidos
Oxygen consumption (VO2) is the amount of oxygen that is actually being used by the tissues per minute. Normally, VO2 is 200 to 250 mL/min/ or 120 to 160 mL/min/m2
La formula inversa de fick subestima el valor del VO2 porque no tiene en cuenta la circulacion bronquial y las venas de tabesio que serian de gran importancia en el aumento del VO2 cuando hay enfermedad pulmonar El metodo de fick por su parte es episodico y no refleja una tendencia del VO2 actual indirect calorimetry measurements are 8 to 27% higher than measurements made using the Fick method. Por eso esos dos metodos no son intercambiables
The cellular metabolic rate determines VO2. The metabolic rate increases during physical activity, with shivering, hyperthermia and raised sympathetic drive (pain, anxiety). Similarly, certain drugs such as adrenaline4 and feeding regimens containing excessive glucose increase VO2.Mechanical ventilation eliminates the metabolic cost of breathing which, although normally less than 5% of the total VO2, may rise to 30% in the catabolic critically ill patient with respiratory distress. It allows the patient to be sedated, given analgesia and, if necessary, paralysed, further reducing VO2.
The amount of oxygen consumed as a fraction of oxygen delivered defines the oxygen extraction ratio (O2ER). The O2ER estimates the balance between oxygen delivery and oxygen consumption and is calculated as O2ER = VO2/DO2. As VO2 increases or DO2 decreases the O2ER rises to maintain aerobic metabolism. An O2ER greater than 0.35 implies an excessively high extraction of oxygen to meet metabolic demands and is often associated with shock states.9 Tissue hypoxia, either because DO2 is inadequate or cells do not extract and use oxygen normally, may be a contributor to organ failure in critical illness
EL VO2 SE MANTIENE EN UN RANGO DEL DO2 PORQUE SE AUMENTA LA TASA DE EXTRACCION DE O2 CON EL FIN DE MANTENER EL VO2 CONSTANTE, SIN EMBARGO SE LLEGA UN NIVEL CRITICO, A PARTIR DEL CUAL EL VO2 SE VUELVE DEPEDIENTE DEL DO2 Y NO PUEDE SER AUMENTADO POR MAS QUE SE AUMENTE LA TASA DE EXTRACCION DE O2, AQUÍ INICIA EL METABOLISMO ANAERÓBICO. EN ESTE PUNTO, SE DISMINUYE LA SvO2 , SE ELEVA EL LACTATO Y LA BASE EXCESO. The relationship between global DO2 and VO2 in critically ill patients has received considerable attention over the past two decades. Shoemaker and colleagues demonstrated a relationship between DO2 and VO2 in the early postoperative phase that had prognostic implications such that patients with higher values had an improved survival.7 A subsequent randomised placebo controlled trial in a similar group of patients showed improved survival if the values for DO2 (>600 ml/min/m2) and SvO2 (>70%) that had been achieved by the survivors in the earlier study were set as therapeutic targets (“goal directed therapy”). This evidence encouraged the use of “goal directed therapy” in patients with established (“late”) septic shock and organ dysfunction in the belief that this strategy would increase VO2 and prevent multiple organ failure. DO2 was increased using vigorous intravenous fluid loading and inotropes, usually dobutamine. The mathematical linkage caused by calculating both VO2 and DO2 using common measurements of Qt and CaO2 3 and the “physiological” linkage resulting from the metabolic effects of inotropes increasing both VO2 and DO2 were confounding factors in many of these studies.9 This approach was also responsible for a considerable increase in the use of pulmonary artery catheters to direct treatment. However, after a decade of conflicting evidence from numerous small, often methodologically flawed studies, two major randomised controlled studies finally showed that there was no benefit and possibly harm from applying this approach in patients with established “shock”. Interestingly, these studies also found that those patients who neither increased their DO2 spontaneously nor in response to treatment had a particularly poor outcome. This suggested that patients with late “shock” had “poor physiological reserve” with myocardial and other organ failure caused by fundamental cellular dysfunction. These changes would be unresponsive to Shoemaker’s goals that had been successful in “early” shock
For all systems, VO2 is the difference between the input flow and the output flow. For the whole body circulation, the input flow is the arterial oxygen delivery (DaO2) and the output flow is the venous oxygen delivery. If one considers the oxygen extraction ratio (EO2) to be the ratio between VO2 and DaO2, then VO2 can be represented by the product DaO2 × EO2. The simple equation VO2 = DaO2 × EO2 is conventionally used to represent the macrocirculatory balance. T he VO2 observed (oVO2) by a clinician (either measured or calculated) is the product of an observed DO2 and an observed EO2, such that oVO2 = oDO2 × oEO2. Similarly, the specific patient’s requirements (nVO2) may be formulated as the product of the needed DO2 and the needed EO2: nVO2 = nDO2 × nEO2. The ratio between these two equations represents the balance between what the doctor sees and That the patient needs: oVO2/nVO2 = oDO2/nDO2 × oEO2/nEO2. Any change in oDO2/nDO2 must be balanced by an inverse change in oEO2/nEO2 to maintain oVO2/nVO2 = 1 and vice versa. When oVO2/nVO2 = 1 cannot be maintained, dysoxia occurs. Consequently, three indices of performance may be described: oVO2/nVO2 is an index of global performance, with a value below 1 indicating shock; oDO2/nDO2 is an index of circulatory performance, with a value below 1 indicating circulatory failure; and oEO2/nEO2 is an index of tissue performance, with a value below 1 indicating tissue failure
In a normal adult, V o2 is approximately 250 mL/min if the CO is 5 L/min. Thus, under normal resting conditions, the tissues extract about 25% of oxygen delivered to them. This ratio of V˙ o2/Do2, termed the oxygen extraction ratio (OER), can increase during exercise, 2 congestive heart failure, or severe anemia, leading to a lower Cvo2. The OER can decrease in disease states such as sepsis leading to a higher Cvo2. Because each organ has its own characteristic metabolic needs, individual organ OERs vary. Resting blood and oxygen supply of various organs are shown in Table 1.3 Brain tissue and cardiac muscle extract much more oxygen from the blood than other organs. These two organs also are most susceptible to oxygen deprivation, and their functions are critically dependent on adequate delivery of oxygen. Oxygen content in a mixed venous blood sample is a blood flow-weighted average of venous oxygen content of different organs, and thus may not accurately reflect changes in tissue V˙ o2 and OER
Assessment of the VO2/DO2 relationship is a theoretical means of evaluating the gap between actual VO2 and needed VO2. A DO2 challenge can be performed easily at the bedside by increasing cardiac output (CO) , increasing low hemoglobin concentration (Hb) [11, 17], or increasing low SaO2 . When DO2 increases, an increase in VO2 argues for inadequate O2 supply. In contrast, a stable VO2 value when DO2 increases suggests either that VO2 matches needs when associated with decreasing lactate levels [11, 13, 14, 15], or that VO2 is limited by other mechanisms than O2 supply, when associated with increasing lactate levels [19, 20, 21].
Two mechanisms delay achievement of the VO2 plateau and account for a rightward shift in the critical DO2 point (Fig. 1). When VO2 needs are excessive (uncoupling and/or increased metabolic activity), the VO2 plateau is reached at a higher level of VO2 [22, 23]. When O2 tissue diffusion is impaired (impaired microcirculation and/or impaired O2 mitochondrial use), the slope of the dependent part of the VO2/DO2 relationship is decreased
LOS ESTADOS DE HIPOXIA TISULAR DONDE HAY BAJA ENTREGA Y UTILIZACION DE O2 POR LOS TEJIDOS DEBE DIFERENCIARSE DE TERMINOS COMO HIPOXEMIA, ANEMIA, ISQUEMIA E HIPOXIA HISTOTOXICA Q SON FENOMENOS QUE LLEVAN A LA HIPOXIA TISULAR.
Of the various forms of circulatory shock, two distinct groups can be defined: those with hypovolaemic, cardiogenic, and obstructive forms of shock (group 1) have the primary problem of a low cardiac output impairing DO2; those with septic, anaphylactic, and neurogenic shock (group 2) have a problem with the distribution of DO2 between and within organs—that is, abnormalities of regional DO2 in addition to any impairment of global DO2. Sepsis is also associated with cellular/metabolic defects that impair the uptake and utilisation of oxygen by cells. Prompt effective treatment of “early” shock may prevent progression to “late” shock and organ failure. In group 1 the peripheral circulatory response is physiologically appropriate and, if the global problem is corrected by intravenous fluid administration, improvement in myocardial function or relief of the obstruction, the peripheral tissue consequences of prolonged inadequacy of global DO2 will not develop. However, if there is delay in instituting effective treatment, then shock becomes established and organ failure supervenes. Once this late stage has been reached, manipulation of the “global” or convective components of DO2 alone will be ineffective. Global DO2 should nonetheless be maintained by fluid resuscitation to correct hypovolaemia and inotropes to support myocardial dysfunction.
Es necesario entender que asi como bajo condiciones normales, hay un aumento de aporte regional de O2 en condiciones como el ejercicio donde se da el fenómeno llamado consumo dirige entrega, donde se abren vasos para aumentar el aporte de O2, se puede presentar en condiciones patológicas la hipoxia global o hipoxia regional. It is therefore important to distinguish between global and regional DO2 when considering the cause of tissue hypoxia in specific organs. Loss of normal autoregulation in response to humoral factors during sepsis or prolonged hypotension can cause severe “shunting” and tissue hypoxia despite both global DO2 and SvO2 being normal or raised.18 In these circumstances, improving peripheral distribution and cellular oxygen utilisation will be more effective than further increasing global DO2. Regional and microcirculatory distribution of cardiac output is determined by a complex interaction of endothelial, neural, metabolic, and pharmacological factors. endothelium not only maintains a physical barrier between the blood and body tissues but also modulates leucocyte migration, angiogenesis, coagulation, and vascular tone through the release of both constrictor (endothelin) and relaxing factors (nitric oxide, prostacyclin, adenosine).20 The differential release of such factors has an important role in controlling the distribution of regional blood flow during both health and critical illness.
Until recently the endothelium had been perceived as an inert barrier but it is now realised that it has a profound effect on vascular homeostasis, acting as a dynamic interface between the underlying tissue and the many components of flowing blood. In concert with other vessel wall cells, the endothelium not only maintains a physical barrier between the blood and body tissues but also modulates leucocyte migration, angiogenesis, coagulation, and vascular tone through the release of both constrictor (endothelin) and relaxing factors (nitric oxide, prostacyclin, adenosine). The differential release of such factors has an important role in controlling the distribution of regional blood flow during both health and critical illness. The endothelium is both exposed to and itself produces many inflammatory mediators that influence vascular tone and other aspects of endothelial function. For example, nitric oxide production is increased in septic shock following induction of nitric oxide synthase in the vessel wall. Similarly, capillary microthrombosis following endothelial damage and neutrophil activation is probably amore common cause of local tissue hypoxia than arterial hypoxaemia . tissue hypoxia show that the fall in cellular oxygen resulting from an increase in intercapillary distance is more severe if the reduction in tissue DO2 is caused by “hypoxic” hypoxia (a fall in PaO2) rather than “stagnant” (a fall in flow) or “anaemic” hypoxia (fig 5).27 Studies in patients with hypoxaemic respiratory failure have also shown that it is PaO2 rather than DO2—that is, diffusion rather than convection—that has the major influence on outcome. Thus, tissue oedema due to increased vascular permeability or excessive fluid loading may result in impaired oxygen diffusion and cellular hypoxia, particularly in clinical situations associated with arterial hypoxaemia. In these situations, avoiding tissue oedema may improve tissue oxygenation. Figure 5 Influence of intercapillary distance on the effects of hypoxia, anaemia, and low flow on the oxygen delivery-consumption relationship. With a normal intercapillary distance illustrated in the top panels the DO2/VO2 relationship is the same for all interventions. However, in the lower panels an increased intercapillary distance, as would occur with tissue oedema, reducing DO2 by progressive falls in arterial oxygen tension results in a change in the DO2/VO2 relationship with VO2 falling at much higher levels of global DO2. This altered relationship is not seen when DO2 is reduced by anaemia or low blood flow.
This situation mandates a careful reappraisal of the theoretical limitations of bedside calculations of DO2 and VO2, including a re-evaluation of the clinical situations in which these calculations are valid. Three levels of complexity can be distinguished when analysing a patient’s hemodynamic status: 1) simple cases where investigations can be limited to clinical monitoring, including lactate changes over time; 2) intermediate situations requiring invasive investigations in which continuous monitoring of VO2-related variables such as cardiac output and mixed venous oxygen saturation often provide enough information to guide clinical decision; and 3) complex situations where assessment of VO2 and VO2/ DO2 analysis might be recommended.
Resuscitation goals should be the same regardless of the etiology of shock. These goals include: (1) restoration of adequate oxygen delivery, (2) resolution of existing oxygen debt, and (3) elimination of anaerobic metabolites. Appropriate patient-centered resuscitation endpoints should be used to evaluate the effectiveness of therapeutic interventions. Identification of the most appropriate endpoints of resuscitation still remains controversial. Newer endpoints are evolving, as additional technologies are becoming available to the clinician at the bedside. Early detection and aggressive management of tissue hypoxia will assist in decreasing complications, limiting organ dysfunction, and improving outcomes.11
Blood pressure (BP) is one of the most commonly measured endpoints of resuscitation. It plays an important role in the determination of perfusion to various organs including the brain, heart, gut, and kidneys. Mean arterial pressure (MAP) is considered a more reliable indicator of tissue perfusion than systolic (SBP) or diastolic (DBP) because it more closely reflects the autoregulatory limits of organ blood flow.2,5,6 Blood pressure may not always be the best indicator of organ perfusion due to activation of protective compensatory mechanisms, such as increased HR and contractility and vasoconstriction. These compensatory mechanisms are activated when there are abnormalities in blood flow or vascular resistance. Consequently, BP may remain normal until compensatory mechanisms are exhausted. In trauma patients, the reliance on arterial BP as a therapeutic endpoint may mask the existence of hypovolemia that can only be detected by direct measurements of flow or other tissue perfusion markers, such as mixed venous or central venous oxygen saturation, lactate, and base deficit.7 Blood pressure alone often fails to identify hemodynamic instability early in shock states HR is a nonspecific indicator of inadequate perfusion. Many factors and clinical conditions can prevent HR changes indicative of poor perfusion states, including the use of medications, such as beta blockers and calcium channel blockers, or the presence of a pacemaker.2 Conditioned athletes may not initially manifest tachycardia. ADEMAS OTRAS SITUACIONES COMO DOLOR, ANSIEDAD, FIEBRE, PUEDEN ELEVAR LA FC. Decreased mental status is suggestive of cerebral hypoperfusion. Unfortunately, there are many other conditions that may affect mental status during shock, such as the presence of a head injury, use of illicit drugs, or alcohol intake. The ability to perform serial mental status exams is also lost when patients are intubated or receiving medications, such as sedatives and analgesic agents . Urine output is a valuable indicator of renal perfusion and vital organ blood flow. During shock states, compensatory mechanisms are activated, causing vasoconstriction and redistribution of blood flow. Blood is preferentially shunted to the vital organs, such as the brain and heart. Thus, a significant drop in UOP indicates reduced renal blood flow. Unfortunately, an adequate UOP will not always indicate a successful resuscitation. Other factors may affect UOP, such as the use of drugs including mannitol and other diuretics. Preexisting conditions, such renal failure, may also affect the reliability of this index of the adequacy of resuscitation. ESTOS ELEMENTOS CORRELACIONAN POBREMENTE CON LA PERFUSION Y OXIGENACION TISULAR TODOS ESOS PARAMETROS NO SON NI ESPECIFICOS NI SENSIBLES, ADEMAS APARECEN DE MANERA LENTA POR LOS MECANISMOS COMPENSADORES INICIALES, ENTONCES CUANDO APARECEN SE ENCUENTRAN EN UNA FASE TARDIA DE DISMINUIDO DO2
Because of the regional differences in the circulatory response during shock, measurement of global Do2 andV˙ o2 may not adequately reflect oxygenation status in individual tissues and organs. For example, splanchnic organ blood flow may be disproportionately reduced during shock without affecting global tissue oxygenation.6,10 During periods of hypoperfusion, gut barrier functions may become compromised, increasing its permeability and resulting in the introduction of endotoxin, microorganisms, and inflammatory cytokines into the systemic circulation, contributing to multiple organ failure.5 The ability to monitor the adequacy of local tissue Do2 thus may allow early detection of oxygen deprivation and early intervention that might prevent the progression to multiple organ failure. Base deficit and lactate levels are commonly used serum markers for altered perfusion. These values have clinical relevance as endpoints, but the clinician must also understand their limitations. Current limitations include that they: (1) may normalize in the presence of ongoing regional tissue ischemia, (2) are subject to time delays, and (3) are not currently available as continuous measurements. Many global indicators of oxygen transport, including blood lactate levels, base deficit, DO2, VO2, SvO2, and ScvO2 are currently used in clinical practice as endpoints for resuscitation. These indicators reflect overall body tissue perfusion, but provide little insight into the adequacy of cellular oxygenation.70 However, oxygen consumption and the distribution of blood flow will vary between different tissue beds within the body. Measurement of regional tissue oxygenation has some distinct advantages over evaluation of global tissue oxygenation. First, the metabolic activity is different among various tissue beds during and after shock. Monitoring of specific tissue beds, such as the gut, may assist in the identification of patients at risk for the development of systemic inflammatory response syndrome (SIRS) and organ failure
El deficit de base es sensible como marcador de disminucion de DO2 en pacientes con trauma y su valor es un indice de mortalidad siendo mayor mortalidad en valor menor de menos de -15 en menores de 55 años. En mayores de 55 años, el valor menor de -8. En otras patologias diferentes a trauma no se ha encontrado correlacion con mortalidad ni relacion con el ac lactico. Davis et al.  classified base deficit according to severity: mild (2–5mmol/l), moderate (6–14mmol/l) or severe (above 15mmol/l). The severity of the deficit directly correlated with the volume of crystalloid and blood replaced within the first 24 h. Failure to normalize the base deficit also correlated directly with mortality
Limitations of base deficit exist and clinicians should consider this in the interpretation of these data. Administration of sodium bicarbonate, hypothermia, and hypocapnea can affect base deficit. Certain conditions that result in a metabolic acidosis, unrelated to lactic acidosis, can produce a base deficit that does not reflect DO2/VO2 balance. These include hyperchloremic acidosis as a result of infusions of large volumes of normal saline,115 preexisting renal failure, acute ingestion of certain substances (ie, alcohol, cocaine, aspirin), conditions associated with chronic CO2 retention (emphysema), and diabetic ketoacidosis.
Initial serum lactate levels in patients in shock have been demonstrated to correlate with outcome and have been utilized extensively to guide resuscitation . Lactate trends over timeare, however, more predictive of mortality than initial values. In a review of trauma patients resuscitated to supranormal oxygen delivery values, patients whose lactate normalized (serum levels below 2 mmol/l) by 24 h had a 0–10% mortality; those who normalized by 24–48 h had a 25% mortality; those who normalized above 48 h after injury had an 80–86% mortality Singhal et al.  found that lactate was an independent predictor of mortality with a sensitivity of87%and a specificity of80%, and significantly correlated with base deficit. Lactate is a widely used as serum marker of tissue hypoxia in the critically ill and has been found to be a better predictor of morbidity and mortality than base deficit
however, is also influenced by the elimination and the distribution of lactate. The liver plays a central role in eliminating lactate from the blood, so in patients with poor liver function ( eg, cirrhosis), the blood lactate level can increase without lactic acidosis. Lactic acidosis may also be present without an increase in blood lactate level. This may occur when the blood flow to an organ is completely blocked ( eg, limb ischemia). Transient increases in blood lactate are only observed after successful reperfusion because of washout of lactate from the ischemic tissues. Thus, it is usually more advantageous to follow the changes in the blood lactate level rather than the absolute values. A continuous fall in the blood lactate level during resuscitation from hypovolemic shock is usually a favorable sign and is associated with survival. Persistent increase in blood lactate, however, almost always indicates the continuous presence of ischemic tissues and correlates with multiorgan system failure and poor outcome. Lactate can be influenced by glycolysis, protein catabolism, and liver dysfunction.35 Serum lactate levels are increased not only in shock states, but also in other conditions unrelated to shock. Elevated lactate levels indicate that the anaerobic threshold has been reached.31 Physical exertion from seizures, shivering, and even agitation can cause lactate levels to increase beyond normal. Fortunately, lactate levels from these conditions normalize rapidly within half an hour; whereas in shock, lactate is usually not cleared for at least 12 hours. shock states, a high lactate levels is related to a poor prognosis.32,38,39 Early clearance of lactate in response to resuscitation has been found to be a positive prognostic indicator. Bakker et al38 found that serum lactate levels were better prognostic indicators than oxygen transport variables, such as DO2 and VO2 . Lactate levels are currently being used as endpoints for resuscitation, as well as a method to stratify the severity of illness in the critically ill
The blood lactate concentration is an unreliable indicator of tissue hypoxia. It represents a balance between tissue production and consumption by hepatic and, to a lesser extent, by cardiac and skeletal muscle.30 It may be raised or normal during hypoxia because the metabolic pathways utilising glucose during aerobic metabolism may be blocked at several points. Inhibition of phosphofructokinase blocks glucose utilisation without an increase in lactate concentration. In contrast, endotoxin and sepsis may inactivate pyruvate dehydrogenase, preventing pyruvate utilisation in the Krebs cycle resulting in lactate production in the absence of hypoxia.32 Similarly, a normal DO2 with an unfavourable cellular redox state may result in a high lactate concentration, whereas compensatory reductions in energy state [ATP]/[ADP][Pi] or [NAD+]/ [NADH] may be associated with a low lactate concentration during hypoxia
Lactate can be influenced by glycolysis, protein catabolism, and liver dysfunction.35 Serum lactate levels are increased not only in shock states, but also in other conditions unrelated to shock. Elevated lactate levels indicate that the anaerobic threshold has been reached.31 Physical exertion from seizures, shivering, and even agitation can cause lactate levels to increase beyond normal. Fortunately, lactate levels from these conditions normalize rapidly within half an hour; whereas in shock, lactate is usually not cleared for at least 12 hours. Although both pathologic dysoxia and exercise may be characterized as type A lactic acidosis, only the former is associated with generalized decreases in perfusion and impending doom. High blood lactate concentrations may be found without evidence of dysoxia, the result of increased substrate flux through the glycolytic pathway (type B lactic acidosis).
La saturacion venosa mixta no esta sujeto a retraso de tiempo como el deficit de base y el lactato. Pvo2 (or Svo2) is another parameter that is used clinically to monitor systemic Do2. Svo2 can be measured in the pulmonary artery blood samples O tained from a pulmonary artery catheter. For a given rate of V˙ o2, Svo2 is determined by CO, hemoglobin concentration, and Sao2. Svo2 is reduced in low Do2 (low CO, hypoxia, severe anemia) or increased V˙ o2 (fever, thyrotoxicosis). It is increased in sepsis and cytotoxic tissue hypoxia ( eg, cyanide poisoning). Svo2 can now be monitored continuously via an intravascular sensor in a specialized pulmonary arterial catheter. Decreases in Svo2 may be an earliest signs that the clinical condition of the patient is deteriorating.
Mixed venous oxygen saturation (SvO2) is used as a global indicator of the balance between oxygen delivery and oxygen consumption. The SvO2 is measured intermittently by withdrawing a blood sample from the distal port of a PA catheter or continuously by using a fiberoptic PA catheter. Continuous measurement of SvO2 provides for rapid, ongoing monitoring and evaluation of tissue oxygenation at the bedside, which allows for minute to minute evaluation of clinical responses to interventions. The SvO2 is not subject to the time delays that are seen with evaluation of serum tissue markers, such as base deficit and lactate. The SvO2 reflects the overall, mixed venous oxygen saturation of blood returning from the inferior vena cava (lower body), superior vena cava (upper body), and the coronary sinus (heart). Clinically, SvO2 is used during resuscitation to indicate the presence of ongoing global tissue hypoxia in the critically ill.28 The SvO2 is affected by the cardiac output, SaO2, Hb and VO2. The SvO2 decreases when oxygen delivery falls or when tissue oxygen demand and consumption are increased. A SvO2 value of 60% to 75% is considered normal under most circumstances and indicates adequate balance between oxygen delivery and consumption. 42 High SvO2 values result from increased oxygen delivery or decreased consumption and demand. It may also result from obstruction and maldistribution of blood flow, reflecting that the tissues have not received oxygen or that they are unable to utilize the oxygen that has been delivered to them.43 During shock states, an elevated SvO2 value may not always be indicative of a successful resuscitation. The increase in SvO2 may have resulted from maldistribution of blood flow to tissues unable to utilize oxygen.43 In this situation, it is important to interpret the SvO2 within the context of the entire clinical picture. On the other hand, a low SvO2 value will generally always indicate an incomplete resuscitation. The major benefit of using SvO2 as an endpoint during resuscitation is that it provides the clinician with a rapid, real-time, continuous method for evaluating tissue oxygenation and response to resuscitation at the bedside. However, in many situations it may not be feasible to place a PA catheter, such as early in resuscitation or in other settings outside the ICU.
Central venous catheterization is a commonly performed procedure and considered standard of care for most critically ill patients.52 It is easier to perform and has less associated risks than placement of a PA catheter. This new technology allows for measurement of central venous oxygen saturation (ScvO2) in the superior vena cava (SVC), which has been shown to trend with SvO2. en shock la ScvO2 sobreestima la mixta en 5 a 18% . This difference suggests that the presence of a low ScvO2 indicates an even lower SvO2. La saturacion venosa mixta mide la saturacion d ela vena cava superior e inferior y el seno coronario y normalmente es más alta (porque la saturacion de la vena cava inferior es más alta que la superior) que la saturación venosa central que es medida en la vena cava superior (que representaria la de la parte superior del cuerpo). This relationship changes in pathologic states, such as severe sepsis, circulatory shock, cardiac shock, heart failure, and head injury.in these situations, ScvO2 is generally higher than SvO2. During shock states, blood flow to the vital organs, including the brain and heart, is maintained due to the activation of compensatory mechanisms. At the same time, there is redistribution of blood flow away from the renal and mesenteric circulations. Oxygen saturation in the IVC is reduced, and ScvO2 becomes greater than SvO2.In shock, ScvO2 has been found to overestimate SvO2 by 5% to 18%. This relationship changes in pathologic states, such as severe sepsis, circulatory shock, cardiac shock, heart failure, and head injury. In these situations, ScvO2 is generally higher than SvO2. During shock states, blood flow to the vital organs, including the brain and heart, is maintained due to the activation of compensatory mechanisms. At the same time, there is redistribution of blood flow away from the renal and mesenteric circulations. Oxygen saturation in the IVC is reduced, and ScvO2 becomes greater than SvO2. About 10–30% of central venous catheters are inserted into the right atrium. It might be therefore possible that blood drawn from a central venous catheter also to some degree contains blood from the inferior vena cava. Furthermore, the catheter tip may be moved depending on the position of the patient. When a patient is moved from a supine to upright position, the
Estas son las condiciones que cambian la relación de SvO2 y SvcO2 haciendo esta última más alta que la otra
Initially, gastric tonometry was accomplished by placing a modified oral or nasogastric tube into the stomach. This tube had a saline-filled balloon at the tip, and following placement and a period of equilibration, the PCO2 of the saline sample was analyzed. The complex nature of this initial technology led to the development of an infrared CO2 meter that measured gastric PCO2 in air, rather than in saline. Inicialmente se calculaba el pH a partir de dichas formulas que incluian la PCO2 de la mucosa y se asumia que el HCO3 arterial era el mismo de la mucosa lo cual fue muy controvertido. Posteriormente de asumio el calculo del GAP DE CO2 que es la diferencia entre el PCO2 de la mucosa gastrica y el arterial
When blood flow limits oxygen availability to the gut, the decrease in pHi parallels the decrease in oxygen levels. Splanchnic hypoperfusion may be present even when systemic hemodynamic and metabolic parameters are within normal limits. Patients with splanchnic hypoperfusion may develop subsequent bacterial translocation and SIRS. Gastric tonometry, which measures gastric Pco2 and calculates gastric intramucosal pH (pHi), was developed based on the principle that fluid in a hollow organ can be used to measure the gas tension of the surrounding tissue.15,16 During periods of oxygen debt, anaerobic metabolism produces organic acids, but regional acidosis is difficult to measure directly because of the acid-buffering capacity of plasma and other fluids. However, one can measure Pco2 in the intramucosal fluid and calculate the local pH based on this value and the arterial bicarbonate concentration using the Henderson-Hasselbalch equation: pHi 6.1 log10HCO3 /0.03 Pco2 where 6.1 is the negative logarithm of ionization constant of carbonic acid, [HCO3 – ] is the concentration of bicarbonate ion in arterial plasma; and 0.03 is the solubility of carbon dioxide in plasma. In practice, intraluminal Pco2 is measured by introducing a carbon dioxide-permeable balloon into the gut and filling it with saline solution. After an equilibrium period, the saline solution is sampled anaerobically, and Pco2 in the saline solution is measured by standard methods. Animal experiments have shown that this indirect estimate of pHi within the stomach correlates well with pHi measured directly with a microelectrode ( r2 0.76),17 and that pHi of the intact intestine calculated by tonometry falls as Do2 is reduced below a critical level.18 Clinical studies have been performed to validate the use of gastric tonometry in surgical and critically ill patients. Fiddian-Green and Baker19 measured stomach wall pH in 85 patients undergoing elective cardiac surgery and found that decreased pHi was a sensitive predictor of complications. In a prospective study of 83 consecutive critically ill patients, Maynard and colleagues10 reported that mortality was higher in patients with low gastric pHi ( 7.35) on admission to the ICU than in those who had admission gastric pHi in the normal range (59% vs 21% mortality, p 0.001). Abnormal gastric pHi was a better predictor of outcomes than other global measures of Do2 and utilization ( eg, arterial pH, Do2, V˙ o2, arterial lactate concentration). Although gastric tonometry may provide the physician with additional information regarding the metabolic state of the gastric mucosa, the accuracy and reliability of pHi measurement is affected by several local factors, including equilibration time, choice of buffer in the balloon, and the secretion of hydrogen ions by the parietal cells.20 The measurement is also intermittent. Newer methods that measure Pco2 in the air circulating through a gastric balloon may allow for automatic and continuous determination of pHi.20,21 Despite frequent study, no clinical data have demonstrated that outcome in critically ill patients is improved by the use of gastric tonometry
There is little doubt that tissue PCO2 increases with ischemia. In a porcine model,. This rise correlated with tissue lactate and occurred long before energy stores of phosphocreatine and ATP decreased. More difficult to ascertain is whether the increase in PCO2 results from tissue dysoxia (the condition in which aerobic ATP production cannot satisfy cellular energy requirements) or from decreases in blood flow and the accumulation of CO2 produced in the tricarboxylic acid (Krebs) cycle. Dubin et al. [46.] lowered oxygen delivery in sheep intestine by decreasing flow (ischemic hypoxia) or by lowering arterial oxygen saturation (hypoxic hypoxia). They noted that intestinal venous PCO2 increased during ischemic hypoxia but not during hypoxic hypoxia. Given that both preparations were subjected to similar decreases in DO2, this finding suggests that blood flow, not dysoxia, is the primary determinant of increases in tissue PCO2. hay mayor correlacion entre la elevacion del CO2 del intestino por hipoxa isquémica que por hipoxia hipoxica
Gastric tonometry analysis is, however, hindered by endogenous gastric acid secretion, H2 blockers and nasogastric enteral nutrition [34,35]. Furthermore, there is significant variability in tissue pCO2 levels within a population of normal individuals, making standardization of this technique difficult.
Sublingual capnography was developed to overcome some of the limitations in gastric tonometry. Sublingual capnography is noninvasive and portable, and data are available within minutes. It correlates well with gastric PCO2 Sublingual PCO2 is measured by placing a tonometric catheter under the tongue using a hand-held portable device.87 During shock, there is a rise in both sublingual PCO2 and gastric PCO2. A PCO2 70 mm Hg indicates poor blood flow to the sublingual mucosa. This is consistent with global tissue ischemia.86 Several studies84,85 have found that sublingual PCO2 is a good prognostic indicator of tissue perfusion in septic patients, unstable ICU patients, and cardiogenic shock patients. Marik and colleagues84,85 demonstrated its ease of use, reproducibility, and positive correlation with gastric intramucosal PCO2. These authors investigated the clinical utility and prognostic value of using sublingual PCO2 as a marker of tissue perfusion in hemodynamically unstable ICU. They compared sublingual PCO2 to both lactate levels and SvO2. Sublingual PCO2 was found to be more predictive of outcome. They suggested that sublingual PCO2 may be a sensitive marker of tissue perfusion and a useful endpoint for resuscitation in the ED and ICU. Weil and colleagues86 demonstrated a high correlation between sublingual PCO2, gastric PCO2, arterial blood lactate levels, and cardiac index in all types of shock patients. One limitation of this technology is that the senor must be securely placed under the tongue for measurement of sublingual PCO2. This may become problematic in uncooperative uncooperative patients or those with facial injuries or edema. Secondly, it is only an intermittent measurement Ruffolo DC, Headley JM. Regional carbon dioxide monitoring: A different look at tissue perfusion. AACN Clin Issues. 2003;14: 168-175. 130. Boswell SA, Scalea TM. Sublingual capnography: An alternative to gastric tonometry for the management of shock resuscitation. AACN Clin Issues. 2003;14:176-184 Marik PE, Bankov A. Sublingual capnometry versus traditional markers of tissue oxygenation in critically ill patients. Crit Care Med. 2003;31(3):818–822. 85. Marik PE. Sublingual capnograpahy: a clinical validation study. Chest. 2001;120:923–927. 86. Weil MH, Nakagawa Y, Tang W, et al. Sublingual capnometry: a noninvasive measurement for diagnosis and quantitation of severity of circulatory shock. Crit Care Med. 1999;27:1225–1229.
Near-infrared spectroscopy (NIRS) is a continuous, noninvasive technology used to determine tissue oxygen saturation (StO2), oxygen utilization at the cellular level, and local tissue blood flow.88 It uses the principles of light transmission and absorption to measure deoxygenated and oxygenated Hb, as well as the redox state of cytochrome aa3.89 NIRS can be used to measure skeletal muscle oxygenation because light in the near-infrared region (700 to 1000 nm) is transmitted through muscle, bone, and skin with little attenuation. A major limitation of this technology is contamination of the light transmission by scatter and absorption, which may limit the systems ability to make quantitative measurements in the clinical setting
RECENTLY, increasing attention has been directed to the hemodynamic treatment of critically ill patients, because it has been observed in several studies that patients who survived had values for the cardiac index and oxygen delivery that were higher than those of patients who died and, more important, higher than standard physiologic values. 1-3 Cardiac-index values greater than 4.5 liters per minute per square meter of body-surface area and oxygen-delivery values g reater than 650 ml per minute per square meter — derived empirically on the basis of the median values for patients who previously survived critical surgical illness — are commonly referred to as supranormal hemodynamic values. However, there is no agreement about the clinical benefit of a treatment strategy intended to achieve supranormal values, since the few randomized studiesavailable have produced conflicting results. Two studies of surgical patients 5,6 have shown significant decreases in mortality associated with such therapy, whereas studies of patients with sepsis 7 and mixed groups of critically ill patients 8,9 have failed to show significant differences in mortality. In addition, because mixed venous oxygen saturation (SvO ) reflects the balance between oxygen delivery and oxygen consumption 10,11 and because it can be monitored continuously, we thought that targeting therapy to achieve a normal SvO 2( 70 percent) could result in a hemodynamic treatment better
1. ALCANZAR LOS PARAMETRSO HEMODINAMICOS ES MAS DIFICIL EN EL GRUPO DE GC Q EN SVO2 Y CONTROL. APARENTEMENTE LA EDAD PUEDE INFLUENCIAR NEGATIVAMENTE EL LOGRO DE LAS METAS 2. ENTRE LOS PACIENTES QUE LOGRAGRON LAS METAS, NO HABIA DIFERECIA SIGNIFICATIVA EN CUANTO A LA MORTALIDAD Y LA MORBILIDAD. 3. EL CURSO DE PARAMETROS HEMODINAMICOS ENTRE EL GRUPO CONTROL Y EL DE SVO2 FUERON SIMILARES, DE MODO Q NO HAY DIFERENCIA ENTRE UNA U OTRA ESTRATEGIA
Anemia triggers a number of adaptive mechanisms that collectively serve to maintain DO2 even at very low hemoglobin levels (22). Anemia results in increased cardiac output due to reduced blood viscosity and increased sympathetic outflow. Lowering of viscosity as hematocrit falls may also result in fewer inflammatory nteractions between activated platelets and the endothelium (23). As discussed earlier, selective vasoconstriction promotes blood flow to critical organs, whereas oxygen-deprived tissue cells undergo specific hypoxia-induced adaptations. Through increased production of 2,3-diphosphoglycerate in red blood cells, anemia results in a shift in the oxyhemoglobin dissociation curve to the right, thereby facilitating oxygen unloading at the level of the tissue. The extent of new red blood cell production depends on the balance of positive and negative influences. On one hand, reduced DO2 to the tubular epithelial cells of the kidney provides a signal for increased expression of erythropoietin expression and secondary stimulation of erythroid production in the bone marrow. On the other hand, the acute inflammatory response, commonly associated with trauma and shock, blocks hypoxiamediated induction of erythropoietin, blunts the response of erythroid progenitor cells to erythropoietin, and leads to a functional iron deficiency state.
There was a trend toward decreased 30-day mortality among patients who were treated according to the restrictive transfusion strategy. The significant differences in mortality rates during hospitalization, rates of cardiac complications, and rates of organ dysfunction all favored the restrictive strategy. We also found that maintaining hemoglobin concentrations in the range of 7.0 to 9.0 g per deciliter decreased the average number of red-cell units transfused by 54 percent and decreased exposure to any red cells after randomization by 33 percent. number of randomized, controlled clinical trials have addressed the hypothesis that oxygen delivery should be increased or maintained at high levels to minimize the effects of tissue hypoxia caused by disease processes that interfere with oxygen delivery or the body’s ability to extract oxygen. In our study, red-cell transfusions, used as a means of augmenting oxygen delivery, did not offer any survival advantage in patients with normovolemia when hemoglobin concentrations exceeded 7.0 g per deciliter. On the basis of our results, we recommend that critically ill patients receive red-cell transfusions when their hemoglobin concentrations fall below 7.0 g per deciliter and that hemoglobin concentrations should be maintained between 7.0 and 9.0 g per deciliter. The diversity of the patients enrolled in this trial and the consistency of the results suggest that our conclusions may be generalized to most critically ill patients, with the possible exception of patients with active coronary ischemic syndromes.
Figure 1 illustrates the values of the 14 randomized studies whose control group mortalities were 20%. Seven early studies whose optimal therapy was completed before organ failure occurred had marked and significant overall reduction in the mortality rate of 0.23 0.07 ( p .05). Of the seven late studies of patients who had organ failure before initiation of the studies, the overall mortality rate difference was 0.01 0.06, indicating no significant improvement with therapy. Shoemaker et al.  observed that in critically ill trauma patients, survivors had above-normal oxygen delivery and oxygen consumption values. Based on these results, it was hypothesized that ‘driving’ the physiology of severely injured patients to supranormal values would increase survival. This has become known as ‘supranormal resuscitation’, and it aims to maintain CI>4.5 l/min/m2, DO2I>600 ml/min/m2 and VO2I>170 ml/min/m2. Several authors have advocated that this regimen reduces morbidity and mortality in critically ill patients [41,42]. Recently, Pearse et al.  randomized high-risk surgical patients to supranormal resuscitation or conventional management. Patients resuscitated to supranormal endpoints received more fluids and vasoactive medications. They had fewer complications and a reduced hospital stay, although there was no difference in mortality. A recent meta-analysis by Poeze et al.  supported these findings. Reviewing 30 randomized controlled trials in adults, they found that supranormal oxygen delivery resuscitation resulted in decreased mortality, but this was not seen in patients with sepsis or organ failure. The majority of the studies, however, focused on perioperative surgical patients, which when pooled demonstrated a survival benefit. Studies of patients with sepsis and overt organ failure demonstrated no benefit with supranormal resuscitation Overall, the meta-analysis concluded that hemodynamic optimization strategies might be beneficial, but there were no significant differences in outcomes between groups . Shoemaker in 1988, Velmahos et al.  concluded in 2000 that patients who achieved supranormal oxygen delivery goals had a better survival; however, this was not a function of the supranormal resuscitation, but rather the patient’s own ability to achieve these parameters independent of forced hemodynamic optimization. Earlier reports by Gattinoni et al. and McKinley et al. In randomized controlled trials, and Heyland et al. in a metaanalysis demonstrated that no such benefit of supranormal oxygen delivery existed [46–48]. Furthermore, supranormal resuscitation can be associated with significant complications. Improvements in blood pressure and cardiac performance by vasoactive drugs can be negated by reduced tissue perfusion and can worsen ongoing tissue ischemia. The use of dobutamine to augment oxygen delivery in critically ill patients may actually increase mortality, while the increased administration of intravenous fluids can result in abdominal compartment syndrome, coagulopathy and congestive heart failure. In summary, supranormal resuscitation may offer a survival benefit when initiated in the perioperative period, but no survival advantage has been observed in trauma or patients with sepsis. Furthermore, supranormal resuscitation utilizes significantly greater volumes of fluid and has been associated with numerous complications
Of the 263 enrolled patients, 130 were randomly assigned to early goal-directed therapy and 133 to standard therapy; there were no significant differences between the groups with respect to base-line characteristics. In-hospital mortality was 30.5 percent in the group assigned to early goal-directed therapy, as compared with 46.5 percent in the group assigned to standard therapy (P=0.009). During the interval from 7 to 72 hours, the patients assigned to early goaldirected therapy had a significantly higher mean (―SD) central venous oxygen saturation (70.4―
Despite the large number of endpoints available to the clinician, none are universally applicable and none have independently demonstrated improved survival when guiding resuscitation. Only with frequent re-evaluation of endpoint parameters can the resuscitation be tailored specifically to the individual patient and change a ‘nonresponder’ into a ‘responder’. Which endpoint is used to guide resuscitation is less important than how the results are interpreted and how the therapy is altered to return the patient to adequate global tissue oxygenation.
KATHERYNE CHAPARRO M. RESIDENTE ANESTESIOLOGÍA
<ul><li>Objetivo global de manejo del paciente crítico: </li></ul><ul><li>Mantener oxigenación tisular </li></ul><ul><li>Sostener metabolismo aeróbico </li></ul><ul><li>Evitar disfunción de órganos </li></ul>
<ul><li>Inadecuada perfusión tisular </li></ul><ul><li>Compromiso entrega de oxígeno </li></ul><ul><li>Metas de reanimación </li></ul>Measurement of acid–base resuscitation endpoints: lactate, base deficit, bicarbonate or what?. Curr Opin Crit Care 12:569–574. 2006 DEFICIT REANIMACION SOBRE REANIMACION
<ul><li>Revisión de fenómenos fisiopatológicos </li></ul><ul><li>Identificación de métodos de medición </li></ul><ul><li>Descripción de intervenciones médicas </li></ul>
CONVECCION DIFUSION DIFUSION CONVECCION Diagnostic Measures o Evaluate Oxygenation in Critically Ill Adults. AACN Clinical Issues. 2004: Volume 15, Vumber 4, pp. 506–524
<ul><li>Estado de inadecuada oxigenación tisular, donde los niveles de O2 son tan bajos que no se puede mantener la respiración mitocondrial </li></ul>Assessment of tissue oxygenation in the critically-ill. European Journal of Anaesthesiology 2000, 17, 221±229
Assessment of tissue oxygenation in the critically-ill. European Journal of Anaesthesiology 2000, 17, 221±229 38 ATP
Measurement of acid–base resuscitation endpoints: lactate, base deficit, bicarbonate or what? Curr Opin Crit Care . 2006: 12:569–574. Monitoring Oxygen Delivery in the Critically. Chest 2005;128;554S-560S
<ul><li>DO2: Entrega de O 2 </li></ul>DO2 = GC x CaO2 CaO2 = 1,34 x Hb x SaO2 + 0.003 PaO2 <ul><li>VO2: utilización de O 2 </li></ul>VO2 = GC x (CaO2 – CvO2) CvO2 = 1,34 x Hb x SvO2 + 0.003 PvO2
<ul><li>CaO2 = 1,34 x Hb x SaO2 + 0.003 PaO2 </li></ul>GASTO CARDIACO Diagnostic Measures o Evaluate Oxygenation in Critically Ill Adults. AACN Clinical Issues. 2004: Volume 15, Vumber 4, pp. 506–524 ANEMIA DESATURACIÓN DE O2
<ul><li>Normal 1000 ml/min </li></ul><ul><li>600 ml/min/m 2 </li></ul><ul><li>Sensibilidad variable de tejidos a DO2 </li></ul>Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316 The pulmonary physician in critical care c 2: Oxygen delivery and consumption in the critically ill Thorax 2002;57;170-177 Más sensibles, cardiomiocitos, neuronas, cel renales. Tolerancia 15 a 20 min hipoxia riñón e hígado 60 a 90 musculo esquelético Musculo liso vascular 24 a 72 h Pelo y uñas pueden seguir creciendo
<ul><li>Estado de conciencia </li></ul><ul><li>Llenado capilar (sensibilidad 6%, especificidad 93%) </li></ul><ul><li>Frialdad de piel </li></ul><ul><li>Frecuencia cardiaca </li></ul><ul><li>Gasto urinario </li></ul>Diagnostic Measures o Evaluate Oxygenation in Critically Ill Adults. AACN Clinical Issues. 2004: Volume 15, Vumber 4, pp. 506–524
<ul><li>VO2 normal 250 ml/min </li></ul><ul><li>130 ml/min/m2 </li></ul><ul><li>No hay parámetros clínicos para su valoración </li></ul><ul><li>Medición en relación al DO2 </li></ul>Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316 Diagnostic Measures o Evaluate Oxygenation in Critically Ill Adults. AACN Clinical Issues. 2004: Volume 15, Vumber 4, pp. 506–524
<ul><li>Calorimetría indirecta </li></ul><ul><li>Formula inversa de Fick </li></ul><ul><li>Subestima el valor </li></ul><ul><li>Diferencia con calorimetría 8 – 27% </li></ul>Diagnostic Measures o Evaluate Oxygenation in Critically Ill Adults. AACN Clinical Issues. 2004: Volume 15, Vumber 4, pp. 506–524
<ul><li>TASA METABÓLICA </li></ul><ul><li>Actividad física </li></ul><ul><li>Escalofrio, hipertermia </li></ul><ul><li>Actividad simpática elevada </li></ul><ul><li>Medicamentos: adrenalina </li></ul><ul><li>Régimen alimentario rico en glucosa </li></ul><ul><li>Distres respiratorio </li></ul>The pulmonary physician in critical care c 2: Oxygen delivery and consumption in the critically ill Thorax 2002;57;170-177
<ul><li>DO2 1000 ml/min </li></ul><ul><li>VO2 250 ml/min </li></ul><ul><li>Extracción 25% </li></ul><ul><li>TEO2 crítico 60 – 70% </li></ul>Diagnostic Measures o Evaluate Oxygenation in Critically Ill Adults. AACN Clinical Issues. 2004: Volume 15, Vumber 4, pp. 506–524 Tasa de extracción es la cantidad O2 consumido en relación a la fracción de O2 entregado TASA DE EXTRACCIÓN = VO2 / DO2
180 a 330 mL/min The pulmonary physician in critical care c 2: Oxygen delivery and consumption in the critically ill Thorax 2002;57;170-177 Matching total body oxygen consumption and delivery: a crucial objective? Intensive Care Med (2004) 30:2170–2179
Oxygen uptake-to-delivery relationship: a way to assess adequate flow. Critical Care 2006, 10(Suppl 3):S4 VO2 = DO2 x EO2 VO2o/ VO2n = DO2o/DO2n x EO2o/EO2N INDICES: VO2o/VO2n = Función global, < 1 disoxia, shock DO2o/DO2n = función circulatoria, < 1 falla EO2o/EO2N = función tisular, < 1 falla tisular
<ul><li>Reposo EO2: 25% </li></ul>Monitoring Oxygen Delivery in the Critically. Chest 2005;128;554S-560S Bajo CvO2 Alta CvO2
Monitoring Oxygen Delivery in the Critically. Chest 2005;128;554S-560S
Matching total body oxygen consumption and delivery: a crucial objective? Intensive Care Med (2004) 30:2170–2179
Incremento de VO2, desacople o aumento de TM Deterioro de la difusión de O2: alt microvascular o edema tisular Matching total body oxygen consumption and delivery: a crucial objective? Intensive Care Med (2004) 30:2170–2179
HIPOXIA ANEMIA ISQUEMIA HIPOXIA HISTOTOXICA Tissue Hypoxia. How to detect, how to correct, how to prevent. Am J. Respir Crit Care Med. Vol 154. pp 1573-1578. 1996. Assessment of tissue oxygenation in the critically-ill. European Journal of Anaesthesiology 2000, 17, 221±229 HIPOXIA TISULAR VO2 = CO x Hb x 1.39 x SaO2 x ERO2
The pulmonary physician in critical care c 2: Oxygen delivery and consumption in the critically ill Thorax 2002;57;170-177 Caída del DO2 primariamente por caída del GC Problema de distribución de DO2 entre y dentro de los órganos Defecto de uptake y consumo de O2
B. Vallet, E. Wiel, and G. Lebuffe. Resuscitation from circulatory shock: an approach based on oxygen –derived parameters. Yearbook of intensive Care and Emergency Medicine. 2005
<ul><li>Trastorno global de DO2 </li></ul><ul><li>Trastornos de flujo regional entre y dentro de los órganos </li></ul><ul><li>Endotelio órgano activo </li></ul>The pulmonary physician in critical care c 2: Oxygen delivery and consumption in the critically ill Thorax 2002;57;170-177
The pulmonary physician in critical care c 2: Oxygen delivery and consumption in the critically ill Thorax 2002;57;170-177
<ul><li>SIMPLES: monitoria clínica y lactato </li></ul><ul><li>INTERMEDIOS: Variables relacionadas con VO2 </li></ul><ul><li>COMPLEJOS: valoración VO2 y relación VO2/DO2 </li></ul>Matching total body oxygen consumption and delivery: a crucial objective?. Intensive Care Med (2004) 30:2170–2179
<ul><li>Restauración de una adecuada entrega de O2 </li></ul><ul><li>Resolución de la deuda de oxígeno </li></ul><ul><li>Eliminación de los metabolitos anaeróbicos </li></ul>Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316
Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316 <ul><li>Adecuado aporte de O2 </li></ul><ul><li>Resolver la deuda de O2 </li></ul><ul><li>Eliminar metabolismo anaerobio </li></ul>1 . Puede haber isquemia regional 2. Retraso 3. No disponible para medición continua
<ul><li>Cantidad de base (mMol) requerida para titular 1 L de sangre arterial a un pH 7,4, con la muestra completamente saturada de O2, T 37 o C y pCO2 40 mmHg </li></ul><ul><li>BD = - (HCO3 – 24,8 + (16,2 x (pH - 7,4)) </li></ul><ul><li>Normal -3 a 3 </li></ul><ul><li>>3 alcalosis < -3 acidosis </li></ul>Diagnostic Measures o Evaluate Oxygenation in Critically Ill Adults. AACN Clinical Issues. 2004: Volume 15, Vumber 4, pp. 506–524
<ul><li>Sensible con grado y duración de DO2 inadecuado en pacientes con tx </li></ul><ul><li>Mortalidad alta > -15 en < 55 años </li></ul>Diagnostic Measures o Evaluate Oxygenation in Critically Ill Adults. AACN Clinical Issues. 2004: Volume 15, Vumber 4, pp. 506–524 Measurement of acid–base resuscitation endpoints: lactate, base deficit, bicarbonate or what? Curr Opin Crit Care . 2006: 12:569–574. Leve -2 a -5 mMol Moderado -6 a -14 mMol Severo > - 15 mMol
<ul><li>Se puede alterar con hipocapnia, bicarbonato y hipotermia </li></ul><ul><li>Otras condiciones diferentes al VO2/DO2 lo pueden alterar: enf renal, ac. Hiperclorémica, intoxicaciones, cetoacidosis, enfisema </li></ul>Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316 Déficit de base no asociado a aumento de Ac láctico no se relaciona con mortalidad Measurement of acid–base resuscitation endpoints: lactate, base deficit, bicarbonate or what? Curr Opin Crit Care . 2006: 12:569–574.
<ul><li>Marcador de inadecuada oxigenación tisular </li></ul><ul><li>Normal < 2 mMol/L </li></ul><ul><li>Duración y magnitud de la elevación marcador de mortalidad </li></ul><ul><li>Sen 87% y Esp 80% predictor de mortalidad </li></ul>Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316 Measurement of acid–base resuscitation endpoints: lactate, base deficit, bicarbonate or what? Curr Opin Crit Care . 2006: 12:569–574. Don’t take vitals, take a lactate. Intensive Care Med (2007) 33:1863–1865 Lactate as a marker of energy failure in critically ill patients: hypothesis. Critical Care December 2005 Vol 9 No 6
<ul><li>Componente del metabolismo normal </li></ul><ul><li>Niveles = producción / depuración </li></ul><ul><li>INFLUENCIA: glicolisis, metabolismo proteico, disfunción hepática </li></ul><ul><li>Temprana depuración en shock: buen pronóstico </li></ul>
Monitoring oxygen transport and tissue oxygenation. Curr Opin Anaesthesiol 17:107–117. 2004
<ul><li>Cambio de relación por cambio en perfusión tisular </li></ul>Menor SvO2 en V. cava sup Menor SvO2 en V. cava inferior
<ul><li>Se mide por extracción de sangre del puerto distal del catéter SG o medición continua por fibroóptico </li></ul><ul><li>Mide SvO2: sangre cava sup, inf y seno coronario </li></ul><ul><li>Representa balance VO2/DO2 </li></ul><ul><li>Normal 60 – 75% </li></ul>Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316
<ul><li>SvO2 : VO2 aumentado o DO2 disminuido </li></ul><ul><li>Baja SvO2 siempre representa incompleta resucitación </li></ul><ul><li>Alta SvO2 no utilización de O2 o mal distribución sanguínea </li></ul><ul><li>Medición sin retraso </li></ul>Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316 The value of venous oximetry. Curr Opin Crit Care. 2005 11:259—263. <ul><li>MAL PRONÓSTICO SvO2 BAJA: </li></ul><ul><li>Enfermedad cardiopulmonar </li></ul><ul><li>• Choque séptico </li></ul><ul><li>• Choque cardiogénico </li></ul><ul><li>• Postoperatorio de cirugía </li></ul><ul><li>cardiovascular </li></ul>
<ul><li>SvO2: V. cava sup, inferior y seno coronario </li></ul><ul><li>SvcO2: V cava superior </li></ul><ul><li>Muestra tendencia de SvO2 </li></ul><ul><li>Menor riesgo que SG </li></ul><ul><li>Correlación con SvO2 es 7 ± 4% </li></ul>Mixed vs Central Venous Oxygen Saturation May Be Not Numerically Equal, But Both Are Still Clinically Useful. CHEST / 129 / 3 / MARCH, 2006
<ul><li>Anestesia </li></ul><ul><li>Trauma cráneo encefálico </li></ul><ul><li>Shock (5-18%) </li></ul><ul><li>Shunt de microcirculación </li></ul>Mas que valores precisos de SvO2, cuales cambios de SvO2 reflejan alteración hemodinámica y como el tratamiento se refleja en la SvcO2c The value of venous oximetry. Curr Opin Crit Care. 2005 11:259—263.
Tonometría salina Analizador de gases Tonometría aire infrarojo Gastric Tonometry The Hemodynamic Monitor of Choice (Pro). CHEST / 123 / 5 / MAY, 2003
<ul><li>Predictor de severidad y resultado de estados de Shock </li></ul><ul><li>Hipoperfusión gástrica H+, lactato, CO2 </li></ul><ul><li>Diferencia CO2 gástrico y arterial < 10 mmHg </li></ul><ul><li>Gap amplio indica hipoperfusión esplácnica </li></ul>Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316 Gastric Tonometry The Hemodynamic Monitor of Choice (Pro). CHEST / 123 / 5 / MAY, 2003
Monitoring oxygen transport and tissue oxygenation. Curr Opin Anaest. 2004: 17:107–117.
<ul><li>El PCO2 se aumenta con acides gástrica y reflujo duodenal </li></ul><ul><li>Se afecta por anti H2, sonda de alimentación, secreción gastrica endógena </li></ul><ul><li>Variabilidad de pCO2 entre individuos </li></ul>Measurement of acid–base resuscitation endpoints: lactate, base deficit, bicarbonate or what? Curr Opin Crit Care . 2006: 12:569–574. Valor diagnóstico de hipoperfusión, valor pronóstico. No cambio en el resultado de pacientes como herramienta terapéutica Gastric Tonometry The Hemodynamic Monitor of Choice (Pro). CHEST / 123 / 5 / MAY, 2003
<ul><li>Dispositivo sublingual </li></ul><ul><li>Mide tensión de CO2 </li></ul><ul><li>pCO2 >70 mmHg correlaciona con hipoperfusión sublingual </li></ul><ul><li>Correlación con tonometría gástrica y marcadores séricos </li></ul><ul><li>Requiere colaboración del paciente </li></ul><ul><li>Medición intermitente </li></ul>Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316
<ul><li>Mide diferencia de absorción de cromóferos (Hb) </li></ul><ul><li>Monitoriza consumo de O2 mitocondrial via citocromo aa3 </li></ul><ul><li>Falla en mostrar sobrevida </li></ul>Saturación de O2 tisular Utilización de O2 celular Flujo sanguíneo tisular Endpoints of Resuscitation What Should We Be Monitoring? AACN Advanced Critical Care 2006: Volume 17, Number 3, pp.306–316 Measurement of acid–base resuscitation endpoints: lactate, base deficit, bicarbonate or what? Curr Opin Crit Care . 2006: 12:569–574.
<ul><li>Efecto de la anemia: compensación mantener DO2 </li></ul><ul><li>Aumento GC, menor viscosidad, aumento simpático </li></ul><ul><li>Poca interacción inflamatoria </li></ul>Oxygen delivery. Crit Care Med 2003 Vol. 31, No. 12 (Suppl.)
<ul><li>Disminución de la mortalidad </li></ul><ul><li>Terapia temprana </li></ul><ul><li>Antes de inicio de falla orgánica </li></ul>
Disminución de mortalidad 30 v.s 46.5% Menor disfunción multiorgánica Mayor logro de metas
<ul><li>No hay un marcador universalmente aplicable </li></ul><ul><li>Ninguno ha mostrado independientemente mejorar la sobrevida </li></ul><ul><li>Cual end point es usado para guiar la resucitación es menos importante que como se interpretan y como cambian la terapia </li></ul>