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Approach to the Patient with Critical Illness: Introduction The care of critically ill patients requires a thorough understanding of pathophysiology and is centered initially on resuscitation of patients at extremes of physiologic deterioration. This resuscitation is often fast-paced and occurs early without a detailed awareness of the patients chronic medical problems. While physiologic stabilization is taking place, intensivists attempt to gather important background medical information to supplement the real-time assessment of the patients current physiologic conditions. Numerous tools are available to assist intensivists in the accurate assessment of pathophysiology and management to incipient organ failure, offering a window of opportunity for diagnosing and treating underlying disease(s) in a stabilized patient. Indeed, the use of invasive interventions such as mechanical ventilation and renal replacement therapy is commonplace in the intensive care unit. An appreciation of the risks and benefits of such aggressive and often invasive interventions is vital to assure an optimal patient outcome. Nonetheless, intensivists must recognize when patients chances for recovery are remote or impossible and counsel and comfort dying patients and their significant others. Critical care physicians often must redirect the goals of care from resuscitation and cure to comfort when the resolution of an underlying illness is not possible. Assessment of Severity of Illness Categorization of a patients illness into grades of severity occurs frequently in the intensive care unit (ICU). Numerous severity-of-illness (SOI) scoring systems have been developed and validated over the last two decades. Although these scoring systems have been validated as tools to assess populations of critically ill patients, their utility in predicting individual patient outcomes is not clear. SOI scoring systems are important for defining populations of critically ill patients. This allows effective comparison of groups of patients enrolled in clinical trials. To be assured that a purported benefit of a therapy is real, investigators must be assured that different groups involved in a clinical trial have similar illness severities. SOI scores are also useful in guiding hospital administrative policies. Allocation of resources such as nursing and ancillary care can be directed by such scoring systems. SOI scoring systems also can assist in the assessment of quality of ICU care over time. Scoring system validations are based on the premise that increasing age, the presence of chronic medical illnesses, and increasingly severe derangements from normal physiology are associated with increased mortality rates. All currently existing SOI scoring systems are derived from patients who already have been admitted to the ICU. There are no established scoring systems available that purport to direct clinicians decision-making regarding criteria for admission to an ICU. Currently, the most commonly utilized scoring systems are the APACHE (acute physiology and chronic health evaluation) system and the SAPS (simplified acute physiology score) system. These systems were designed to predict outcomes in critical illness and use common variables that include age; vital signs; assessments of respiratory, renal, and neurologic function; and an evaluation of chronic medical illnesses. Apache II Scoring System The APACHE II system is the most commonly used SOI scoring system in North America. Age, type of ICU admission (after elective surgery vs. nonsurgical or after emergency surgery), a chronic health problem score, and 12 physiologic variables (the most severely abnormal of each in the first 24 h of ICU admission) are used to derive a score. The predicted hospital mortality is derived from a formula that takes into account the APACHE II score, the need for emergency surgery, and a weighted, disease-specific diagnostic category (Table Q-1). The relationship between APACHE II score and mortality is illustrated in Fig. Q-1. Updated versions of the APACHE scoring system (APACHE III and APACHE IV) have been published. APACHE III is derived from a larger database than APACHE II and utilizes a daily clinical update protocol to provide daily modification of predicted mortality. APACHE IV uses a modified statistical model of logistic regression; it is the most recently released version of this scoring system. Table Q–1. Calculation of Acute Physiology and Chronic Health Evaluation II (APACHE II)a Score 4 3 2 1 0 1 2 3 4 Rectal temperature, °C ≥41 39.0–40.9 38.5–38.9 36.0–38.4 34.0–35.9 32.0–33.9 30.0–31.9 ≤29.9 Mean blood pressure, mmHg ≥160 130–159 110–129 70–109 50–69 ≤49 Heart rate ≥180 140–179 110–139 70–109 55–69 40–54 ≤39 Respiratory rate ≥50 35–49 25–34 12–24 10–11 6–9 ≤5 Arterial pH ≥7.70 7.60–7.69 7.50–7.59 7.33–7.49 7.25–7.32 7.15–7.24 <7.15 Oxygenation If FIO2 > 0.5, use (A – a) DO2 ≥500 350–499 200–349 <200 If FO2 ≤0.5, use PaO2 ≥70 61–70 55–60 <55 Serum sodium, meqL ≥180 160–179 155–159 150–154 130–149 120–129 111–119 ≤110 Serum potassium, L ≥7.0 6.0–6.9 5.5–5.9 3.5–5.4 3.0–3.4 2.5–2.9 <2.5 Serumcreatinine, mg dL ≥3.5 2.0–3.4 1.5–1.9 0.6–1.4 <0.6 Hematocrit ≥60 50–59.9 46–49.9 30–45.9 20–29.9 <20 WBCcount, 103 mL ≥40 20–39.9 15–19.9 3–14.9 1–2.9 <1 GlasgowComa Scoreb,c Eye Opening Verbal (Nonintubated) (Intubated) Motor Activity 4—Spontaneous 5—Oriented and talks 5—Seems able to talk 6—Verbal command 3—Verbal stimuli 4—Disoriented talks 3—Questionable ability talk 5—Localizes pain 2—Painful stimuli 3—Inappropriate words 1—Generally unresponsive 4—Withdraws pain 1—No response 2—Incomprehensible sounds 3—Decorticate 1—No response 2—Decerebrate 1—No response Points Assigned Age Chronic Disease as Part of the APACHE II Score Age, Years <45 0 45–54 2 55–64 3 65–74 5 ≥75 6 Chronic Health (History Conditions) Score None 0 If patient is admitted after elective surgery 2 If emergency surgery or for reason other than surgery 5 a score sum acute physiology (vital signs, oxygenation, laboratory values), Glasgow coma score, age, chronic health points. Worst values during first 24 h in ICU should be used. b (GCS) =eye-opening + verbal (intubated nonintubated) motor score. c For GCS component subtract from 15 obtain points assigned. d conditions: liver, cirrhosis with portal hypertension encephalopathy; cardiovascular, class IV angina (at rest minimal self-care activities); pulmonary, hypoxemia hypercapnia, polycythemia, ventilator dependent; kidney, peritoneal hemodialysis; immune, immunocompromised host. Note: (A – a) DO2, alveolar-arterial oxygen difference; WBC, white blood (cell) count. (Critical Illness) Figure Q-1 : PACHE survival curve. Blue, nonoperative; green, postoperative. The Saps Scoring System The SAPS used more frequently Europe, was derived a manner similar scores. This not disease-specific but, rather, incorporates three underlying disease variables (AIDS, metastatic cancer, hematologicmalignancy). Severity illness scoring systems cannot predict individual patients. Accordingly, these direct therapy clinical decision-making recommended at present. Instead, tools important data complement bedside decision-making. SHOCK Fully elaborated Shock chapter. Initial Evaluation Shock common condition necessitating admission occurring course critical care. defined by presence multisystem end organ hypoperfusion. Clinical indicators include reduced mean arterial pressure (MAP), tachycardia, tachypnea, cool skin extremities, altered mental status, oliguria. Hypotension usually, though always, The result multiorgan hypoperfusion tissue hypoxia, often clinically manifested lactic acidosis. Since MAP product cardiac output systemic vascular resistance (SVR), reductions can caused decreased SVR. initial evaluation hypotensive an assessment adequacy output; this part earliest clinician once shock contemplated (Fig. Q-2). evidence diminished includes narrow pulse pressure—a marker that correlates stroke volume—and extremities delayed capillary refill. Signs increased widened (particularly diastolic pressure), warm bounding pulses, rapid has signs output, one infer SVR. Figure Q-2 Approach shock. EGDT, early goal-directed therapy; JVP, jugular venous pulse. In patients intravascular volume status appropriate. A may have history suggesting hemorrhage losses (e.g., vomiting, diarrhea, polyuria). (JVP) such patient, although change right atrial function spontaneous respiration better predictor fluid responsiveness Q-3). Patients fluid-responsive (i.e., hypovolemic) also manifest large changes positive-pressure mechanical ventilation Q-4). dysfunction S3 S4 gallops on examination, extremity edema, crackles lung auscultation. chest x-ray show cardiomegaly, widening pedicle,Kerley B lines, pulmonary edema. Chest pain electrocardiographic consistent ischemia noted . Fig. Q-3 Right who will increase response intravenous administration. decreases 7 mmHg 4 mmHg. horizontal bar marks time inspiration. Fig. Q-4 Pulse (systolic minus pressure) septic shock. In search causes SVR most cause high hypotension sepsis. Other liver failure, severe pancreatitis, burns trauma elicit inflammatory syndrome (SIRS), anaphylaxis, thyrotoxicosis, peripheral arteriovenous shunts. In summary, categories are hypovolemic, cardiogenic, (high-output hypotension). Certainly overlap occur simultaneously hypovolemic shock). The outlined above take only few minutes. It aggressive, resuscitation instituted based assessment, particularly since cardiogenic improve (see below). yields equivocal confounding data, objective assessments echocardiography invasive monitoring useful. goal reestablish adequate perfusion prevent minimize injury. Mechanical Ventilatory Support During shock, principles advanced life support followed. obtunded unable protect airway, airway mandatory Early intubation required. Reasons institution endotracheal hypoxemic respiratory failure ventilatory which accompany Acute edema well those pneumonia distress (ARDS). occurs load system. present form metabolic acidosis (often acidosis) compliance lungs (“stiff” lungs) Inadequate muscles setting another ventilation. Normally, receive very small percentage output. However, reasons listed above, dedicated tenfold more. Lactic acid production inefficient muscle activity presents additional load. Mechanical relieve work breathing allow redistribution limited vital organs, improvement demonstrate number including inability speak full sentences, accessory muscles, paradoxical abdominal activity, extreme tachypnea (>40 breaths/min), and decreasing respiratory rate despite an increasing drive to breathe. When patients with shock are treated with mechanical ventilation, a major goal of ventilator settings is to assume all or the majority of work of breathing, facilitating a state of minimal respiratory muscle work. With the institution of mechanical ventilation for shock, further declines in MAP are frequently seen. The reasons for this include impeded venous return with positive-pressure ventilation, reduced endogenous catecholamine secretion once the stress associated with respiratory failure abates, and the actions of drugs used to facilitate endotracheal intubation (e.g., barbiturates, benzodiazepines, opiates), all of which may result in hypotension. Accordingly, hypotension should be anticipated after endotracheal intubation and positive-pressure ventilation. Many of these patients have a component of hypovolemia, which may respond to IV volume administration. Fig. 267-2 summarizes the diagnosis and treatment of different types of shock. For further discussion of individual forms of shock, see Shock chapter in detail. Respiratory Failure Respiratory failure is one of the most common reasons patients are admitted to the ICU. In some ICUs, ≥75% of patients require mechanical ventilation during their stay. Respiratory failure can be categorized mechanistically, based on pathophysiologic derangements in respiratory function. Accordingly, four different types of respiratory failure can be described, based on these pathophysiologic derangements. Type I, Acute Hypoxemic Respiratory Failure This occurs when alveolar flooding and subsequent intrapulmonary shunt physiology occur. Alveolar flooding may be a consequence of pulmonary edema, pneumonia, or alveolar hemorrhage. Pulmonary edema can be further categorized as occurring due to elevated pulmonary microvascular pressures as seen in heart failure and intravascular volume overload or ARDS (“low-pressure pulmonary edema”; and represents an extreme degree of lung injury. This syndrome is defined by diffuse bilateral airspace edema seen on chest radiography, the absence of left atrial hypertension, and profound shunt physiology (Fig. Q-5) in a clinical setting in which this syndrome is known to occur, including sepsis, gastric aspiration, pneumonia, near-drowning, multiple blood transfusions, and pancreatitis. The mortality rate of patients with ARDS was traditionally very high (50–70%), although recent changes in ventilator management strategy have led to reports of mortality rates closer to 30% (see below). Fig. Q-5 : Chest radiograph of a patient with ARDS. ARDS, acute respiratory distress syndrome. For many years, physicians have suspected that mechanical ventilation of patients with acute lung injury and ARDS may propagate lung injury. Cyclical collapse and reopening of alveoli may be partly responsible for this. As seen in Fig. Q-6, the pressure-volume relationship of the lung in ARDS is not linear. Alveoli may collapse at very low lung volumes. Animal studies have suggested that stretching and overdistention of injured alveoli during mechanical ventilation can further injure the lung. Concern over this alveolar overdistention, termed ventilator-induced “volutrauma,” led to a multicenter, randomized, prospective trial to compare traditional ventilator strategies for acute lung injury and ARDS (large tidal volume—12 mL/kg ideal body weight) to a low tidal volume (6 mL/kg ideal body weight). This study showed a dramatic reduction in mortality rate in the low tidal volume group (large tidal volume—39.8% mortality rate versus low tidal volume—31% mortality rate) and confirmed that ventilator management could affect outcomes in these patients. In addition, a “fluid conservative” management strategy [maintaining a relatively low central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP)] is associated with the need for fewer days of mechanical ventilation compared with a “fluid liberal” management strategy (maintaining a relatively high CVP or PCWP) in acute lung injury and ARDS. Figure Q-6 : Pressure-volume relationship of the lungs of a patient with ARDS. At the lower inflection point, collapsed alveoli begin to open, and the lung compliance changes. At the upper deflection point, alveoli become overdistended. The shape and size of alveoli are illustrated at the top. ARDS, acute respiratory distress syndrome. Type II Respiratory Failure This type of respiratory failure occurs as a result of alveolar hypoventilation and results in the inability to eliminate carbon dioxide effectively. Mechanisms by which this occurs are categorized by impaired central nervous system (CNS) drive to breathe, impaired strength with failure of neuromuscular function in the respiratory system, and increased load(s) on the respiratory system. Reasons for diminished CNS drive to breathe include drug overdose, brainstem injury, sleep-disordered breathing, and hypothyroidism. Reduced strength can be due to impaired neuromuscular transmission (e.g., myasthenia gravis, Guillain-Barré syndrome, amyotrophic lateral sclerosis, phrenic nerve injury) or respiratory muscle weakness (e.g., myopathy, electrolyte derangements, fatigue). The overall load on the respiratory system can be subclassified into increased resistive loads (e.g., bronchospasm), loads due to reduced lung compliance [e.g., alveolar edema, atelectasis, intrinsic positive end-expiratory pressure (autoPEEP)—see below], loads due to reduced chest wall compliance (e.g., pneumothorax, pleural effusion, abdominal distention), and loads due to increased minute ventilation requirements (e.g., pulmonary embolus with increased dead space fraction, sepsis). The mainstays of therapy for type II respiratory failure are treatments directed at reversing the underlying cause(s) of ventilatory failure. Noninvasive positive-pressure ventilation using a mechanical ventilator with a tight-fitting face or nasal mask that avoids endotracheal intubation often can stabilize these patients. This approach has been shown to be beneficial in treating patients with exacerbations of chronic obstructive pulmonary disease. Noninvasive ventilation has been tested less extensively in other types of type II respiratory failure but may be attempted nonetheless in the absence of contraindications (hemodynamic instability, inability to protect airway, respiratory arrest). Type III Respiratory Failure This form of respiratory failure occurs as a result of lung atelectasis. Because atelectasis occurs so commonly in the perioperative period, this is also called perioperative respiratory failure. After general anesthesia, decreases in functional residual capacity lead to collapse of dependent lung units. Such atelectasis can be treated by frequent changes in position, chest physiotherapy, upright positioning, and aggressive control of incisional and/or abdominal pain. Noninvasive positive-pressure ventilation may also be used to reverse regional atelectasis. Type IV Respiratory Failure This form results from hypoperfusion of respiratory muscles in patients in shock. Normally, respiratory muscles consume <5% of the total cardiac output and O2 delivery. Patients in shock often experience respiratory distress due to pulmonary edema (e.g., patients in cardiogenic shock), lactic acidosis, and anemia. In this setting, up to 40% of the cardiac output may be distributed to the respiratory muscles. Intubation and mechanical ventilation can allow redistribution of the cardiac output away from the respiratory muscles and back to vital organs while the shock is treated. Care of the Mechanically Ventilated Patient Whereas a thorough understanding of the pathophysiology of respiratory failure is essential to optimize patient care, recognition of a patients readiness to be liberated from mechanical ventilation is similarly important. Several studies have shown that subjecting patients to daily spontaneous breathing trials can identify those ready for extubation. Accordingly, all intubated, mechanically ventilated patients should undergo a daily screening of respiratory function. If oxygenation is stable (i.e., PaO2/FIO2 >200 and PEEP ≤5 cmH2O), cough and airway reflexes are intact, and no vasopressor agents or sedatives are being administered, the patient has passed the screening test and should undergo a spontaneous breathing trial. This trial consists of a period of breathing through the endotracheal tube without ventilator support [both continuous positive airway pressure (CPAP) of 5 cmH2O and an open T-piece breathing system can be used] for 30–120 min. The spontaneous breathing trial is declared a failure and stopped if any of the following occur: (1) respiratory rate >35/min for >5 min, (2) O2 saturation <90%, (3) heart rate >140/min or a 20% increase or decrease from baseline, (4) systolic blood pressure <90 mmHg or>180 mmHg, (5) increased anxiety or diaphoresis. If, at the end of the spontaneous breathing trial, the ratio of the respiratory rate and tidal volume in liters (f/VT) is <105, the patient can be extubated. Such protocol-driven approaches to patient care can have an important impact on the duration of mechanical ventilation and length of stay in the ICU. In spite of such a careful approach to liberation from mechanical ventilation, up to 10% of patients will develop respiratory distress after extubation and may require resumption of mechanical ventilation. Many of these patients will require reintubation. The use of noninvasive ventilation in patients who fail extubation may be associated with worse outcomes compared with immediate reintubation. Mechanically ventilated patients frequently require sedatives and analgesics. Most patients undergoing mechanical ventilation experience pain, which can be elicited by the presence of the endotracheal tube and endotracheal suctioning. Accordingly, early attention to pain control is extremely important. Opiates are the mainstay of therapy for pain control in mechanically ventilated patients. After adequate pain control has been assured, additional indications for sedation for mechanically ventilated patients include anxiolysis; treatment of subjective dyspnea; psychosis; facilitation of nursing care; reduction of autonomic hyperactivity, which may precipitate myocardial ischemia; and reduction of total O2 consumption (VO2). Neuromuscular blocking agents are occasionally needed to facilitate mechanical ventilation in patients with profound dyssynchrony with the ventilator despite optimal sedation. The use of neuromuscular blocking agents may result in prolonged weakness—a myopathy known as the postparalytic syndrome. For this reason, these agents typically are used as a last resort when aggressive sedation fails to achieve patient-ventilator synchrony. Because neuromuscular blocking agents result in pharmacologic paralysis without altering mental status, sedative-induced amnesia is mandatory when these agents are administered. Amnesia can be achieved reliably with benzodiazepines such as lorazepam and midazolam as well as the IV anesthetic agent propofol. Outside the setting of pharmacologic paralysis, there are few data supporting the idea that amnesia is mandatory in all patients who require intubation and mechanical ventilation. Since many of these patients have impaired hepatic and renal function, sedatives and opiates may accumulate in critically ill patients when they are given for prolonged periods. A protocol-driven approach to sedation of mechanically ventilated patients with daily interruption of sedative infusions paired with daily spontaneous breathing trials has been shown to prevent excessive drug accumulation and shorten the duration of mechanical ventilation and length of stay in the ICU. Multiorgan System Failure The syndrome of multiorgan system failure is a common problem associated with critical illness. This syndrome is defined by the simultaneous presence of physiologic dysfunction and/or failure of two or more organs. Typically, this occurs in the setting of severe sepsis, shock of any kind, severe inflammatory conditions such as pancreatitis, and trauma. The fact that multiorgan system failure occurs commonly in the ICU is a testament to our current ability to stabilize and support single-organ failure. The ability to support single-organ failure aggressively (e.g., mechanical ventilation for respiratory failure, renal replacement therapy for acute renal failure) has affected rates of early mortality in critical illness greatly. As a result, it is uncommon for critically ill patients to die in the initial stages of resuscitation. Instead, many patients succumb to critical illness later in the ICU stay, after the initial presenting problem has been stabilized. Although there is debate regarding specific definitions of organ failure, several general principles governing the syndrome of multiorgan system failure apply. First, organ failure, no matter how defined, must persist beyond 24 h. Second, mortality risk increases as patients accrue additional failing. Third, prognosis is worsened by increased duration of organ failure. These observations remain true across various critical care settings (e.g., medical versus surgical). SIRS is a common basis for multiorgan system failure. Although infection is a common cause of SIRS, “sterile” triggers such as pancreatitis, trauma, and burns often are invoked to explain multiorgan system failure. Monitoring in the ICU Because respiratory and circulatory failure occurs commonly in critically ill patients, monitoring of the respiratory and cardiovascular systems is undertaken frequently in the ICU. Evaluation of respiratory gas exchange is routine in critical illness. The “gold standard” remains arterial blood-gas analysis, in which pH, partial pressures of O2 and CO2, and O2 saturation are measured directly. With arterial blood-gas analysis, the two main functions of the lung—oxygenation of arterial blood and elimination of CO2—can be assessed directly. Importantly, the blood pH, which has a profound effect on the drive to breathe, can be assessed only by sampling arterial blood. Though sampling of arterial blood is generally safe, it may be painful and cannot provide continuous information for clinicians routinely. In light of these limitations, noninvasive monitoring of respiratory function is often employed in the critical care setting. Pulse Oximetry This is the most commonly utilized noninvasive monitor of respiratory function. This technique takes advantage of differences in the absorptive properties of oxygenated and deoxygenated hemoglobin. At wavelengths of 660 nm, oxyhemoglobin reflects light more effectively than does deoxyhemoglobin, whereas the reverse is true in the infrared spectrum (940 nm). A pulse oximeter passes both wavelengths of light through a perfused digit such as a finger, and the relative intensity of light transmission at these two wavelengths is recorded. This allows the derivation of the relative percentage of oxyhemoglobin. Since arterial pulsations produce phasic changes in the intensity of transmitted light, the pulse oximeter is designed to detect only light of alternating intensity. This allows distinction of arterial and venous blood O2 saturations. Respiratory System Mechanics These can be measured in patients during mechanical ventilation. When volume-controlled modes of mechanical ventilation are used, accompanying airway pressures can be easily measured, assuming the patient is passive. The peak airway pressure is determined by two variables: airway resistance and respiratory system compliance. At the end of inspiration, inspiratory flow can be stopped transiently. This end-inspiratory pause (plateau pressure) is a static measurement, affected only by respiratory system compliance, not airway resistance. Therefore, during volume-controlled ventilation, the difference between the peak (airway resistance + respiratory system compliance) and plateau (respiratory system compliance only) airway pressures provides a quantitative assessment of airway resistance. Accordingly, during volume-controlled ventilation, patients with increases in airway resistance typically have increased peak airway pressures as well as abnormally high gradients between peak and plateau airway pressures (typically >15 cmH2O). The compliance of the respiratory system is defined by the change in pressure of the respiratory system per unit change in volume. The respiratory system can be divided further into two components: the lungs and the chest wall. Normally, respiratory system compliance is ~100 mL per cmH2O. Pathophysiologic processes such as pleural effusions, pneumothorax, and increased abdominal girth from ascites all reduce chest wall compliance. Lung compliance may be reduced by pneumonia, pulmonary edema from any cause, or autoPEEP. Accordingly, patients with abnormalities in compliance of the respiratory system (lungs and/or chest wall) typically have elevated peak and plateau airway pressures but a normal gradient between peak and plateau airway pressures. AutoPEEP occurs when there is insufficient time for emptying of alveoli before the next inspiratory cycle. Since the alveoli have not decompressed completely, alveolar pressure remains positive at end exhalation (functional residual capacity). This phenomenon results most commonly from critical narrowing of distal airways in disease processes such as asthma and chronic obstructive pulmonary disease. AutoPEEP with resulting alveolar overdistention may result in diminished lung compliance, reflected by abnormally increased plateau airway pressures. Modern mechanical ventilators allow breath-to-breath display of pressure and flow, which may allow detection of problems such as patient-ventilator dyssynchrony, airflow obstruction, and autoPEEP (Fig. Q-7). Fig.Q-7 : Increased airway resistance with autoPEEP. The top waveform (airway pressure vs. time) shows a large difference between the peak airway pressure (80 cmH2O) and the plateau airway pressure (20 cmH2O). The bottom waveform (flow vs. time) demonstrates airflow throughout expiration (reflected by the flow tracing on the negative portion of the abscissa) that persists up to the next inspiratory effort. Oxygen delivery (Qo2) is a function of cardiac output and the content of O2 in the arterial blood (Cao2). The Cao2 is determined by the hemoglobin concentration, the arterial hemoglobin saturation, and dissolved O2 not bound to hemoglobin. For normal adults: It is apparent that the vast majority of O2 delivered to tissues is bound to hemoglobin and that the dissolved O2 (PaO2) contributes very little to O2 content in arterial blood or O2 delivery. Normally, the content of O2 in mixed venous blood (Cvo2) is 15.76 mL O2 per dL blood, since the mixed venous blood is 75% saturated. Therefore, the normal tissue extraction ratio for O2 is Cao2 – Cvo2/Cao2 ([21.16–15.76]/21.16) or ~25%. A pulmonary artery catheter allows measurements of O2 delivery and O2 extraction ratio. The mixed venous O2 saturation allows assessment of global tissue perfusion. A reduced mixed venous O2 saturation may be caused by inadequate cardiac output, reduced hemoglobin concentration, and/or reduced arterial O2 saturation. An abnormally high O2 consumption (Vo2) may also lead to a reduced mixed venous O2 saturation if O2 delivery is not concomitantly increased. Abnormally increased Vo2 by peripheral tissues may be caused by a multitude of problems, such as fever, agitation, shivering, and thyrotoxicosis. The pulmonary artery catheter originally was designed as a tool to guide therapy in acute myocardial infarction but is currently used in the ICU for evaluation and treatment of a variety of other conditions, such as ARDS, septic shock, congestive heart failure, and acute renal failure. This device has never been validated as a tool associated with reduction in morbidity and mortality rates. Indeed, despite numerous prospective studies, there has been no report of mortality or morbidity rate benefit associated with the use of the pulmonary artery catheter in any setting. Accordingly, it appears that the routine use of pulmonary artery catheterization is not indicated as a monitor to characterize the circulatory status in most critically ill patients. Recent data suggest that static measurements of circulatory parameters (e.g., CVP, PCWP) do not provide reliable information on the circulatory status of critically ill patients. In contrast, dynamic assessments measuring the impact of breathing on the circulation are more reliable predictors of responsiveness to IV fluid administration. A decrease in CVP of >1 mmHg during inspiration in a spontaneously breathing patient has been shown to predict an increase in cardiac output after IV fluid administration. Similarly, a changing pulse pressure during mechanical ventilation has been shown to predict an increase in cardiac output after IV fluid administration in patients with septic shock. Prevention of Complications of Critical Illness Sepsis in the Critical Care Unit Sepsis is a significant problem in the care of critically ill patients. It is the leading cause of death in noncoronary ICUs in the United States, with case rates expected to increase as the population ages with a greater percentage of people vulnerable to infection. Many therapeutic interventions in the ICU are invasive and predispose patients to infectious complications. These interventions include endotracheal intubation, indwelling vascular catheters, nasally placed enteral feeding tubes, transurethral bladder catheters, and other catheters placed into sterile body cavities (e.g., tube thoracostomy, percutaneous intraabdominal drainage catheters). The longer such devices remain in place, the more prone to these infections patients become. For example, ventilator-associated pneumonia (VAP) correlates strongly with the duration of intubation and mechanical ventilation. Therefore, an important aspect of preventive care is the timely removal of invasive devices as soon as they are no longer needed. Multidrug-resistant organisms are commonplace in the ICU. An important aspect of critical care is infection control in the ICU. Simple measures such as frequent hand washing are effective but underutilized strategies. Protective isolation of patients with colonization or infection by drug-resistant organisms is another frequently used strategy in the critical care setting. A recent study utilizing silver-coated endotracheal tubes reported a significant reduction in VAP incidence. Studies evaluating multifaceted, evidence-based strategies to decrease catheter-related bloodstream infections have shown improved outcomes from using measures such as hand washing, full-barrier precautions during insertion, chlorhexidine skin preparation, avoidance of the femoral site, and timely catheter removal. Deep Venous Thromboses (Dvts) All ICU patients are at high risk for this complication because of their predilection for being immobile. Therefore, all should receive some form of prophylaxis against DVT. The most commonly employed forms of prophylaxis are subcutaneous low-dose heparin injections and sequential compression devices for the lower extremities. Observational studies report an alarming incidence of the occurrence of DVTs despite the use of these standard prophylactic regimens. Heparin prophylaxis may result in heparin-induced thrombocytopenia (HIT), another relatively common nosocomial complication in critically ill patients. Low-molecular-weight heparins such as enoxaparin are more effective than unfractionated heparin for DVT prophylaxis in high-risk patients, such as those undergoing orthopedic surgery, and they have a lower incidence of HIT. Fondaparinux, a selective factor Xa inhibitor, is even more effective than enoxaparin in high-risk orthopedic patients. Stress Ulcers Prophylaxis against stress ulcers is frequently administered in most ICUs; typically, histamine-2 antagonists are given. Currently available data suggest that high-risk patients, such as those with coagulopathy, shock, or respiratory failure requiring mechanical ventilation, benefit from such prophylactic treatment. Nutrition and Glycemic Control These are important issues in critically ill patients that may be associated with respiratory failure, impaired wound healing, and dysfunctional immune response. Early enteral feeding is reasonable, though no data are available to suggest that this improves patient outcome per se. Certainly, enteral feeding, if possible, is preferred over parenteral nutrition, which is associated with numerous complications, including hyperglycemia, fatty liver, cholestasis, and sepsis. In addition, enteral feeding may prevent bacterial translocation across the gut mucosa. Tight glucose control is another area of controversy in critical care. Although one study showed a significant mortality benefit when glucose levels were aggressively normalized in a large group of surgical ICU patients, more recent data suggest that tight glucose control in a large population of both medical and surgical ICU patients resulted in increased rates of mortality. ICU-Acquired Weakness This occurs frequently in patients who survive critical illness. It is particularly common in those with SIRS and/or sepsis. Neuropathies and myopathies both have been described, most commonly after ~1 week in the ICU. The mechanisms behind ICU-acquired weakness syndromes are poorly understood. Intensive insulin therapy may reduce polyneuropathy of critical illness. A recent study of very early physical and occupational therapy in mechanically ventilated critically ill patients reported significant improvements in functional independence at hospital discharge, as well as reduced duration of mechanical ventilation and delirium. Anemia This is a common problem in critically ill patients. Studies have shown that the vast majority of ICU patients are anemic. Furthermore, most have anemia of chronic inflammation. Phlebotomy contributes significantly to anemia in ICU patients. Studies have demonstrated that erythropoietin levels are inappropriately reduced in most ICU patients and that exogenous erythropoietin administration may reduce transfusion requirements in the ICU. The hemoglobin level that merits transfusion in critically ill patients has been a long-standing area of controversy. A large, multicenter study involving patients in many different ICU settings challenged the conventional notion that a hemoglobin level of 100 g/L (10 g/dL) is needed in critically ill patients. Red blood cell transfusion is associated with impairment of immune function and increased risk of infections as well as acute lung injury and volume overload, all of which may explain the findings in this study. A conservative transfusion strategy should be the rule in managing critically ill patients who are not actively hemorrhaging. Acute Renal Failure This occurs in a significant percentage of critically ill patients. The most common underlying etiology is acute tubular necrosis, usually precipitated by hypoperfusion and/or nephrotoxic agents. Currently, there are no pharmacologic agents available for prevention of renal injury in critical illness. A recent study showed convincingly that low-dose dopamine is not effective in protecting the kidneys from acute injury. Neurologic Dysfunction in Critically Ill Patients Delirium This state is defined by (1) an acute onset of changes or fluctuations in the course of mental status, (2) inattention, (3) disorganized thinking, and (4) an altered level of consciousness (i.e., other than alert). Delirium is reported to occur in over 80% of mechanically ventilated ICU patients and can be detected by the Confusion Assessment Method (CAM)-ICU. This assessment asks patients to answer simple questions and perform simple tasks and can be completed by the bedside nurse in 2 min. The differential diagnosis of delirium in ICU patients is broad and includes infectious etiologies (including sepsis), medications (particularly sedatives and analgesics), drug withdrawal, metabolic/electrolyte derangements, intracranial pathology (e.g., stroke, intracranial hemorrhage), seizures, hypoxia, hypertensive crisis, shock, and vitamin deficiencies (particularly thiamine). Patients with ICU delirium have increases in hospital length of stay, time on mechanical ventilation, cognitive impairment at hospital discharge, and 6-month mortality rate. Interventions to reduce ICU delirium have been described recently. The use of the novel sedative dexmedetomidine was associated with reduced ICU delirium compared with midazolam. In addition, as mentioned above in the section “ICU-Acquired Weakness,” very early physical and occupational therapy in mechanically ventilated patients also has been demonstrated to reduce delirium. Anoxic Cerebral Injury This condition is common after cardiac arrest and often results in severe and permanent brain injury in patients whose cardiac arrest is resuscitated. Active cooling of patients after cardiac arrest has been shown to improve neurologic outcomes. Therefore, patients who present to the ICU after circulatory arrest from ventricular fibrillation or pulseless ventricular tachycardia should be actively cooled with cooling blankets and ice packs if necessary to achieve a core body temperature of 32–34°C. Stroke See also in Stroke chapter for details . This is a common cause of neurologic critical illness. Hypertension must be managed carefully, since abrupt reductions in blood pressure may be associated with further brain ischemia and injury. Acute ischemic stroke treated with tissue plasminogen activator (tPA) has an improved neurologic outcome when treatment is given within 3 h of onset of symptoms. The mortality rate is not improved when tPA is compared with placebo, despite the improved neurologic outcome. Cerebral hemorrhage is significantly higher in patients given tPA. A treatment benefit is not seen when tPA therapy is given beyond 3 h. Heparin has not been shown to demonstrate improved outcomes convincingly in patients with acute ischemic stroke. Subarachnoid Hemorrhage See also in Subarachnoid Hemorrhage for details . This may occur secondary to aneurysm rupture and is often complicated by cerebral vasospasm, rebleeding, and hydrocephalus. Vasospasm can be detected by either transcranial Doppler assessment or cerebral angiography; it is typically treated with the calcium channel blocker nimodipine, aggressive IV fluid administration, and therapy aimed at increasing blood pressure, typically with vasoactive drugs such as phenylephrine. The IV fluids and vasoactive drugs (hypertensive hypervolemic therapy) are used to overcome the cerebral vasospasm. Early surgical clipping of aneurysms is advocated by most authorities to prevent complications related to rebleeding. Hydrocephalus, typically heralded by a decreased level of consciousness, may require ventriculostomy drainage. Status Epilepticus See in chapter Status Epilepticus for details. Recurrent or relentless seizure activity is a medical emergency. Cessation of seizure activity is required to prevent irreversible neurologic injury. Lorazepam is the most effective benzodiazepine for treating status epilepticus and is the treatment of choice for controlling seizures acutely. Phenytoin or fosphenytoin should be given concomitantly since lorazepam has a short half-life. Other drugs, such as gabapentin, carbamazepine, and phenobarbital, should be reserved for patients with contraindications to phenytoin (e.g., allergy or pregnancy) or ongoing seizures despite phenytoin. Brain Death See also in chapter Brain Death for details. Though critically ill patients usually die from irreversible cessation of circulatory and respiratory function, a diagnosis of death also may be established by irreversible cessation of all functions of the entire brain, including the brainstem, even if circulatory and respiratory function remains intact on artificial life support. Patients must demonstrate absence of cerebral function (unresponsive to all external stimuli) and brainstem functions [e.g., unreactive pupils, absent ocular movement to head turning or ice water irrigation of ear canals, positive apnea test (no drive to breathe)]. Absence of brain function must have an established cause and be permanent without possibility of recovery (e.g., must confirm the absence of sedative effect, hypothermia, hypoxemia, neuromuscular paralysis, or severe hypotension). If there is uncertainty about the cause of coma, studies of cerebral blood flow and electroencephalography should be performed. Withholding and Withdrawing Care Withholding and withdrawing of care occurs commonly in the ICU setting. The Task Force on Ethics of the Society of Critical Care Medicine reported that it is ethically sound to withhold or withdraw care if a patient or surrogate makes such a request or if the goals of therapy are not achievable according to the physician. Since all medical treatments are justified by their expected benefits, the loss of such an expectation justifies the act of withdrawing or withholding such treatment. Thus, the act of withdrawing care is fundamentally similar to the act of withholding care. An underlying stipulation derived from this report is that an informed patient should have his or her wishes respected with regard to life-sustaining therapy. Implicit in this stipulation is the need to ensure that patients are thoroughly and accurately informed regarding the plausibility and expected results of various therapies. The act of informing patients and/or surrogate decision makers is the responsibility of the physician and other health care providers. If a patient or surrogate desires therapy deemed futile by the treating physician, the physician is not obligated ethically to provide such treatment. Rather, arrangements may be made to transfer the patients care to another care provider. Whether the decision to withdraw life support should be initiated by the physician or left to surrogate decision makers is not clear. A recent study reported that slightly more than half of surrogate decision makers preferred to receive such a recommendation, whereas the rest did not. Critical care providers should meet regularly with patients and/or surrogates to discuss prognosis when the withholding or withdrawal of care is being considered. After a consensus among caregivers has been reached regarding withholding or withdrawal of care, this should be relayed to the patient and/or surrogate decision maker. If a decision to withhold or withdraw life-sustaining care for a patient has been reached, aggressive attention to analgesia and anxiolysis is needed. Opiates and benzodiazepines are typically used to achieve these goals.
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