12
Shock & Acute Pulmonary Failure in Surgical Patients
James W. Holcroft, MD
John T. Anderson, MD
Matthew J. Sena, MD
INITIAL TREATMENT OF SHOCK
Cardiovascular failure, or shock, can be caused by (1) depletion of the vascular volume; (2) compression of the heart or great veins; (3) intrinsic failure of the heart itself or failure arising from excessive hindrance to ventricular ejection; (4) loss of autonomic control of the vasculature; (5) severe untreated systemic inflammation; and (6) severe but partially compensated systemic inflammation. If the shock is decompensated, the mean blood pressure or the cardiac output (more precisely, the product of the pressure and output) will be inadequate for peripheral perfusion. In compensated shock, the perfusion will be adequate but only at the expense of excessive demands on the heart. Depending on the type and severity of cardiovascular failure and on response to treatment, shock can go on to compromise other organ systems. This chapter discusses the cardiovascular and pulmonary disorders associated with shock.
HYPOVOLEMIC SHOCK
Diagnosis
Hypovolemic shock (shock caused by inadequate circulating blood volume) is most often caused by bleeding but may also be a consequence of protracted vomiting or diarrhea, sequestration of fluid in the gut lumen (eg, bowel obstruction), or loss of plasma into injured or burned tissues. Regardless of the etiology, the compensatory responses, mediated primarily by the adrenergic nervous system, are the same: (1) constriction of the venules and small veins in the skin, fat, skeletal muscle, and viscera with displacement of blood from the peripheral capacitance vessels to the heart; (2) constriction of arterioles in the skin, skeletal muscle, gut, pancreas, spleen, and liver (but not the brain or heart); (3) improved cardiac performance through an increase in heart rate and contractility; and (4) increased sodium and water reabsorption through renin-angiotensin-aldosterone as well as vasopressin release. The result is improved cardiac filling, increased cardiac output (both directly by the increase in contractility and indirectly through increased end-diastolic volumes), and increased blood flow to organs with no or limited tolerance for ischemia (brain and heart).
The symptoms and signs of hypovolemic shock are many and can be caused either by the inadequate blood volume or by the compensatory responses. Some signs manifest themselves early, in mild forms of shock. Some present late and only in severe forms of shock. The goal is to pick up on the early signs. Doing so can save a life.
As early signs of shock, the physician might find it difficult to gain intravenous access. The skin might be cold (a nonspecific sign, but an early sign). But, by far and away, the most important, that is, most sensitive, of all the early signs of hypovolemic shock is diminished blood flow to the skin and subcutaneous tissues. It is a sign that needs to be elicited with care. It can be missed. It is best detected in the skin on the plantar surface of the foot, an area without pigmentation, with the color determined solely by the blood contained in the tissues. One begins by compressing the skin over the plantar surface of a toe with intense pressure, just short of being painful, followed by milking of the blood contained in the compressed area proximally, to the skin over the metatarsal phalangeal joint. The compression is then suddenly released. The previously compressed area will be profoundly pale, but will fill quickly, within a few seconds, if the patient is not in shock (and does not have peripheral vascular disease). In a hypovolemic patient, the refill takes longer. The test is usually done with the foot at the level of the heart, but if the patient is reasonably stable and if the lower extremities are not injured, it is more sensitive if it can be done with the foot raised above the level of the heart, to a height of perhaps 30 cm. Although the toe is usually used, one can also use the skin over the heel. The heel affords a larger surface for observation. One has to use different criteria, however. If the toe is used, color should begin to return within 4 seconds; if the heel is used, color should return in 2 seconds.
Postural hypotension—a fall in the systolic blood pressure of more than 10 mm Hg that persists for more than 1 minute when the patient sits up—can be a sign of early or mild shock. It is very useful in patients who are suspected of being hypovolemic from either dehydration or occult internal blood loss (eg, in a patient who might have gastrointestinal bleeding). It cannot be used, however, in very ill patients and in injured patients, who might not tolerate changes in position.
Low filling pressures in the right atrium are always present in hypovolemic shock, even in cases of mild shock, assuming there is no accompanying cardiac compression. Filling pressures high enough to distend the neck veins when the patient’s head, neck, and torso are elevated 30 degrees, in the absence of cardiac compression, rule out hypovolemic shock. Failure to see the veins suggests, but is not diagnostic of, hypovolemia.
Oliguria is a consistent finding in early shock, in the absence of a hyperosmolar-induced diuresis. A bladder catheter should be inserted in any patient suspected of being hypovolemic. Urine output is considered to be potentially inadequate if it is less than 0.5 mL/kg/h in an adult, less than 1 mL/kg/h in a child, or less than 2 mL/kg/h in an infant. The sign, if present, is both sensitive and specific. One must wait, however, for 30 minutes or so, before one knows that the sign is present.
The hematocrit will fall within minutes in the bleeding patient, or in the patient who has bled, even when the blood loss is mild, if the patient has been given asanguineous fluids. In the absence of fluid administration, however, the fall can take hours—restitution of the intravascular volume from interstitial albumin and water and electrolytes, takes time. One can make an estimate of the blood loss, if the patient has been given asanguineous fluids, by the magnitude of the fall in the hematocrit. A hematocrit fall of 3%-4% indicates that the blood volume was depleted by about 10%; a fall of 6%-8% indicates a depletion of about 20% (or 1 L in an average adult). These calculations assume that the patient has been given enough fluid to correct the hypovolemia. They also assume that the patient was not dehydrated, prior to the hemorrhage, and that the patient did not have large loses of plasma into the extravascular spaces, as in a patient with large burns, prior to a possible hemorrhage. The hematocrit in these patients can be normal in the face of even substantial bleeding.
Hypovolemic shock is easier to recognize when it becomes more severe. In moderate cases (a deficit of 20%-30% of the blood volume), the patient can be thirsty. Hypotension can be present, even in the supine position. A metabolic acidemia, usually with a compensatory rapid respiratory rate, can develop after initial resuscitation. (The acidemia is usually not present before resuscitation. The products of anaerobic metabolism in the ischemic tissues are only flushed into the circulating blood volume once some degree of reperfusion has been achieved.)
In profound hypovolemic shock (a deficit of more than 30% of blood volume), the blood pressure will always be low, even in the supine position. Cerebral and cardiac perfusion can become inadequate. Signs of the former include changes in mental status, restlessness, agitation, confusion, lethargy, or the appearance of inebriation; signs of the latter include an irregular heartbeat or electrocardiographic evidence of myocardial ischemia, such as ST–T segment depression and, over time, the appearance of Q waves. A metabolic acidemia will always be present, after initial resuscitation.
There are many pitfalls in making the diagnosis of hypovolemic shock, and every clinician will miss the diagnosis on occasion. In some patients, especially children and young adults, strong compensatory mechanisms can maintain the blood pressure at normal levels in the setting of mild to moderate shock. In other patients, one might not know if the observed pressure is abnormally low—a young patient might normally have systolic pressures in the low 100s; the same pressure in a chronically hypertensive patient might precede catastrophe. Pain-producing injuries in the absence of blood loss should produce hypertension; a normal pressure in a patient with a pain-producing injury suggests hypovolemia. Administration of a sedative or narcotic in the face of hypovolemia can produce hypotension but usually has no effect on the pressure in a normovolemic subject—one should not ascribe hypotension to sedatives or narcotics until the possibility of hypovolemia has been ruled out.
The heart rate is notoriously unreliable as a sign of hypovolemic shock. Although it increases in response to graded hemorrhage in anesthetized animals, the correlation between hypovolemia and heart rate in unanesthetized human beings is poor. Unanesthetized hypovolemic human beings often have normal heart rates. Severe hypovolemia can even produce bradycardia, as the cardiovascular system makes a last attempt to allow filling of the ventricles during diastole. A normal heart rate provides no assurance that the patient is not in shock. (A rapid heart rate, however, has to be taken seriously. It might be the only indication of shock. The pitfall is in the assumption that a normal heart rate rules out shock.)
There are at least three other pitfalls that can lead to missing the diagnosis of shock: (1) the cutaneous vasoconstriction of hypovolemic shock can be ablated by the vasodilation induced by alcohol or other pharmacologic agents, both therapeutic and recreational; the patient might have well-perfused skin even when hypovolemic; (2) the oliguria of shock can be overcome by an osmotic diuresis induced by high blood alcohol or glucose levels; and (3) shock can cause alterations in mental status that resemble intoxication with drug use or inebriation. If so, the patient might be in a preterminal state, in which the shock is so severe that cerebral blood flow becomes inadequate. The diagnosis of drug or alcohol use, as the cause of the mental abnormalities, should only be made after shock has been ruled out.
Treatment
Resuscitation of patients in hypovolemic shock, either hemorrhagic or nonhemorrhagic, begins with ensuring adequacy of the airway. In many patients in shock, especially severe shock, this means preemptive intubation and mechanical ventilation. The physician cannot let uncertainty about the airway interfere with evaluation and resuscitation of other problems in the often confusing picture of shock. A patient who later turns out to need no support for the airway or ventilation can easily be extubated; failure to intubate a patient who later loses control of an airway or who can no longer ventilate means, at the least, an emergency intubation under difficult conditions and, at the worse, anoxic brain damage or death. This approach is different from the approach for medical patients with decompensated chronic obstructive lung disease, in whom intubation can mean prolonged mechanical ventilation and perhaps even failure to ever extubate. Those patients have such severe underlying pulmonary disease that even under baseline conditions they have trouble breathing. The baseline condition in surgical patients is usually perfectly adequate pulmonary function. Once the possible surgical problems are ruled out or dealt with, there is usually no problem with extubation.
If the patient requires mechanical ventilation, and almost all patients intubated for shock do, volume control ventilation, or some variant thereof, is preferable, in the initial phases of resuscitation (in the latter phases, after the dust has settled, we usually use pressure modulated ventilation—see the section in this chapter on Treatment of Acute Pulmonary Failure). The tidal volume is set at 7 mL/kg ideal body weight (IBW); the inspiratory time, at 1 second; the respiratory rate, at 15 breaths/min; and the end expiratory pressure, at 0 cm H2O, with all of these settings designed to minimize the mean airway pressure. To maintain adequate arterial oxygen saturation, the inspired oxygen concentration is set at 1.00. (The oxygen concentrations can be decreased later, after blood gases come back and the patient is more stable.)
The quick-to-intubate-and-ventilate approach described above pertains to all patients in shock with one exception—patients who present immediately after injury with life-threatening torso hemorrhage. The bleeding can be into the abdomen or into the chest or into the pericardium. The diagnosis is usually made on the basis of the clinical setting or on sonographic imaging. Some of these patients have to be intubated in the emergency room. If possible, however, one should delay intubation until the patient is in the operating room (which is the immediate destination for all of these patients, once the problem of exsanguinating cavitary hemorrhage is recognized).
A patient in profound shock from bleeding into the torso can suddenly deteriorate, to the point of losing his vital signs, with intubation and initiation of positive pressure ventilation. Positive pressure ventilation has effects on the cardiovascular system. All of them are bad, and all are worsened in the face of hypovolemia. The positive pressure compresses the superior and inferior venae cavae, increasing the time needed to fill the right atrium and right ventricle during diastole. (Normal negative pressure ventilation, spontaneous ventilation, decreases the time needed.) Positive pressure squeezes the thin-walled chambers of the heart (the atria and the right ventricle), making it harder for the chambers to fill during diastole. (Negative pressure ventilation makes it easier for the chambers to fill.) Positive pressure squeezes the pulmonary artery, pulmonary microvasculature, and pulmonary veins, making it hard for the right ventricle to transmit its generated energy into the pulmonary artery. (Negative pressure makes it easier to transmit the energy.) Positive pressure ventilation also compresses the pulmonary veins, mandating longer times for the left atrium to fill during diastole. (Negative pressure allows for quicker filling.)
If the patient loses his vital signs in the operating room, with intubation, the surgeon and anesthesiologist will be ideally situated to deal definitively with the underlying problems of hemorrhage and airway management. In contrast, if the patient is intubated in the emergency department and loses his vital signs, the team will be at a major disadvantage in dealing with the underlying problems. An example is in the patient with a gunshot wound to the abdomen who losses vital signs shortly after intubation in the emergency department. Opening the chest will be done hastily, under suboptimal conditions and it is unlikely to be of help. The maneuver does not deal with the underlying problem-bleeding into the abdomen. The patient needs a celiotomy, which cannot be done in the emergency department.
Direct pressure should be the first maneuver in controlling external bleeding from any part of the body. Commercially available tourniquets or improvised pneumatic tourniquets can be used for bleeding from extremities. They are easy to apply and are usually safe for up to 2 hours, with the caveat that bleeding should be controlled quickly so as to minimize tourniquet time. Several commercially available, FDA-approved hemostatic agents are available for temporary control of external bleeding. They have been proven to be effective in prehospital and combat environments and can be effective in the hospital setting as well. Blood in the pleural cavities should be drained with a chest tube. Expansion of the lung will decrease further bleeding from the pulmonary parenchyma through apposition of the visceral and parietal pleurae and will reestablish ventilation through the compressed lung. The tube will also allow monitoring for ongoing bleeding, providing key information that can prompt early operative intervention. Bleeding from pelvic fractures may require temporary binder placement. More definitive control can come later, with angiographic embolization or surgical control. Major long bone fractures should be immobilized. Although it might not be necessary to say, patients with intra-abdominal or intractable intrathoracic bleeding should be prepared for the operating room.
Blind clamping, without direct visualization, in the emergency room, should not be attempted, in the initial control of external bleeding. It can result in target vessel injury or, worse, adjacent venous laceration with increased bleeding.
Vascular access is best obtained with percutaneously placed, large-bore (ideally 14-gauge or larger) venous catheters. The catheters can be placed in superficial veins in the upper extremities, in central veins at the thoracic outlet, or in the femoral veins; catheters can also be placed in the saphenous veins, by cutdown, or directly into interosseous sites (sternum, tibia, or humerus) using specially designed needle introducer systems (FAST-1, EZ IO), the major advantage of the latter devices being the minimal training required to achieve successful access. Choice of access depends on severity of the shock, pattern of injury, provider experience, and consequences of a complication with the access, should one occur. If veins in the lower extremities are to be used, they must be decannulated within 24 hours to minimize the risk of thrombosis and infection. Gaining central venous access can be dangerous as patients in hypovolemic shock will frequently have collapsed central veins. Urgency of placement predisposes to errors in technique. A pneumothorax or an unintentional arterial puncture in the unstable patient might prove fatal.
Initial fluid resuscitation begins with a warmed crystalloid solution. Either normal saline or lactated Ringer solution can be used. Use of lactate in the resuscitative fluid is reasonable if the shock seems to be severe and if the arterial pH is likely to be less than 7.20. The lactate will buffer the hydrogen ions that are released into the central circulation with the initiation of resuscitation. The resultant lactic acid is then oxidized in the liver to carbon dioxide and water, which are excreted by the lungs and kidneys.
If the arterial pH is not likely to be excessively low, normal saline can be used as the initial resuscitative fluid. A modest hyperchloremic acidemia in the immediate postresuscitative state might favorably change the conformation of albumin molecules, decreasing movement of plasma into the interstitium. The acidemia might also increase myocardial contractility.
Blood flow to the liver is not a factor in deciding on lactated Ringer versus normal saline. Even minimal flow, as in severe shock, will be enough to deliver the buffered hydrogen ion to the liver parenchyma. Lactated Ringer should not be used, however, if the patient has preexisting liver disease. Adequate oxidation requires functioning liver cells.
The rate at which the initial crystalloid resuscitation should be given depends on two factors: (1) the severity of the shock and the presence of uncontrolled bleeding. When bleeding has been controlled, resuscitation to normovolemia is the goal. (2) Two L is given as fast as possible, followed by a third liter infused over 10 minutes if necessary. This amount of fluid will resuscitate most patients in whom hemorrhage has been arrested.
If the patient is not resuscitated with this amount of fluid, one should renew the search for bleeding, which might be into the chest, abdomen, or retroperitoneum. In addition, one should begin to use blood products, while cutting back on asanguineous fluids.
Transfusion therapy can be life saving, but it is not without risk. Transfusion reactions, transmission of blood-borne pathogens, acute lung injury (ALI), and immunomodulation can all arise from the administration of blood products. In the acutely bleeding patient, allogeneic packed red cells should be used when the estimated blood loss exceeds 1.5 L (30% of the blood volume), and possibly earlier if there is the potential for ongoing bleeding or if the patient is at risk for having coronary artery disease (Table 12–1).
Table 12–1. Hematocrit triggers for transfusion: influence of coronary artery disease (CAD), environment in which the patient is being treated (emergency department vs. intensive care unit), and likelihood of bleeding.
In urgent settings, type-O blood should be given to restore circulating blood volume. Rh-positive blood can be given to men and women who are beyond childbearing age; Rh-negative blood has to be used in women of childbearing age. The patient’s blood type can be determined within 10 minutes, in most hospitals, and type-specific, uncrossed matched red cells should be used when they become available (except in the case of massive casualties, when type O, Rh-negative universal donor cells should be used, to minimize the chance of giving the wrong type of blood to a misidentified patient). Type specific cells should also be used in the setting of massive transfusion, when cross-matching becomes impossible because of the heterogeneous origin of the circulating cells following rapid blood volume replacement.
If resuscitation is ongoing and if it appears as though the total blood loss is likely to exceed one blood volume in 12 hours, plasma and platelets should be given in amounts sufficient to approximate a 1:1:1 ratio. This should be determined as early as possible to avoid dilutional coagulopathy. “Massive transfusion protocols” can maximize efficient use of blood products through the utilization of predetermined component ratios, bedside refrigeration, and in some cases, protocol-driven laboratory monitoring. Crystalloid infusion can be restricted in the case of massive transfusions—adequate amounts of crystalloids will be infused in conjunction with the blood products.
Giving excessive amounts of fluids in an effort to restore the blood pressure to normal or supranormal levels will create edema. Edema in the gut can create an abdominal compartment syndrome, with compression of the inferior vena cava, displacement of the diaphragm into the chest, and compression of the heart and lungs; edema in the liver can lead to compression of biliary ductules and inability to excrete bilirubin into the gut; edema in the lungs can hinder ventilation and oxygenation; and edema in wounded tissues can impede healing and the ability to fight off infection. Unnecessarily high blood pressures can also potentially exacerbate bleeding. On the other hand, inadequate resuscitation can leave the patient exposed to the many adverse late effects of prolonged shock, such as multiorgan failure.
The primary goal in fluid resuscitation for all forms of shock is the same: restoration of adequate end organ perfusion, the product of the mean pressure perfusing the organ and the blood flow to the organ. Resuscitating to a brachial systolic pressure of 80 mm Hg or a radial pulse in the bleeding patient is reasonable until hemorrhage has been controlled. (The treating physician will not know the cardiac output or organ blood flow in the early phases of resuscitation, but he or she can use clinical criteria, such as skin perfusion, urine output, and mental status, in managing the patient, along with the blood pressure.) After the bleeding is controlled, a systolic pressure of 90 mm Hg might be reasonable. In the very old, the blood pressure goal should be higher to ensure a cushion of perfusion for the brain, heart, and other viscera that might be supplied by arteries obstructed by atherosclerosis.
One must keep in mind during the resuscitation, however, that using the blood pressure to define severity of shock or to assess the adequacy of resuscitation can be hazardous. Most patients in hypovolemic shock will be able to constrict the arterioles in their skin, muscle, and visceral organs in response to the hypovolemia (the exception being inebriated patients). They can often maintain a normal pressure even in the face of continued shock. One must consider many variables in assessing adequacy of resuscitation, including peripheral perfusion, urine output, mental status, acid-base balance, and resolution of any signs of myocardial ischemia.
After severe trauma or major sepsis, many patients will demonstrate signs of intravascular coagulation, with prolonged clotting times, low platelet counts, decreased fibrinogen levels, and production of fibrin degradation products or fibrin monomers. Correction requires administration of plasma and platelets, especially to patients who continue to bleed and to those with severe head injuries, in whom intracranial bleeding could be devastating.
Traditional replacement of coagulation factors has been done with thawed frozen plasma. The advantages of frozen plasma are logistical; the disadvantage is that it has to be thawed prior to use, which may take from 30 to 60 minutes. Increasingly, trauma centers are using either prethawed plasma or “liquid” plasma that has never been frozen. The advantage of the former is that the product does not have to be thawed; the major disadvantage is the potential for waste. “Liquid” plasma has the potential advantage of increased factor activity with the disadvantage of waste. Finally, there has been interest in developing freeze dried plasma, particularly by the military. Although the Europeans have extensive experience with the product (it is approved for use in Europe), there is currently no FDA approved formulation in the United States.
Over the last decade, pharmacologic therapy for hemorrhage-related coagulopathy has become a standard adjunct in the setting of hemorrhagic shock. In the recent past, recombinant activated factor VII has been used routinely for severely injured patients with ongoing traumatic coagulopathy. Administration of doses between 80 and 100 mcg/kg is generally recommended for coagulopathy in trauma patients. Smaller doses may be useful for warfarin reversal in the setting of intracranial hemorrhage. Due to the mechanism of action, platelet and fibrinogen levels need to be adequate at the time of administration.
Tranexamic acid (TXA) is an antifibrinolytic agent that has recently been adopted for routine use by the military as a pharmacologic adjunct for hemorrhage control (REF). It is being used with increasing frequency in civilian settings. The impetus for use in trauma originated from a large prospective international trial (CRASH-2) as well as a large retrospective cohort of combat casualties. Although there is no universally recommended monitoring when using the product, it seems reasonable to think that it should be particularly useful in the presence of excessive fibrinolysis, which can be assessed with the use of the thromboelastogram (TEG), a test that is being used more and more often in diagnosing fibrinolysis in the bleeding patient.
Using pharmacologic agents to improve hemostasis can lead to procoagulant side effects. These have been well documented with activated factor VII but are less well known with antifibrinolytic agents such as TXA. If the patient is not bleeding and is not at risk for a devastating consequence of rebleeding, one should not give procoagulant factors—they will only fuel the fire of systemic inflammation and coagulation. As with any intervention, the benefit to risk ratio should be individualized.
Maintenance of normothermia is critical in the setting of hemorrhagic shock. Patients who have significant blood loss may lose the ability to increase metabolic heat production. In addition, initial fluid replacement is often done using room temperature or cold solutions such as crystalloid administered in the field by paramedics or unwarmed blood products in the hospital. The added stress of environmental or surgical exposure can make it difficult to maintain normothermia. The impact cannot be overstated. The adverse effects of hypothermia on coagulopathy can be profound.
For these reasons, hypothermia prevention and treatment should be an immediate and ongoing management priority during resuscitation from hemorrhagic shock. At the very least, one should keep the environment warm, infuse fluids through warmers, and keep the patient covered, as much as possible. These efforts should commence as soon as possible after the injury or after the onset of illness.
There is no role for using colloid solutions in the setting of hypovolemic shock except when size and weight of the crystalloid solutions limit their availability, as in treating mass casualties or under wartime conditions. Under these circumstances, solutions containing hetastarch or hypertonic saline and dextran can be used. Otherwise, colloids provide no benefit over crystalloid solutions, and they add to cost. Vasopressors should not be used in resuscitating neurologically intact hypovolemic patients, except in desperate situations for short periods while the vascular volume is reexpanded. The idea that vasopressors divert flow from nonessential organs to essential organs is ill-conceived. Although some organs can withstand ischemia for longer periods of time than others, there are very few parts of the body that are not essential. Patients given vasopressors in shock are at risk for ischemic gangrene of the limbs, gut necrosis, liver failure, and acute tubular necrosis. Vasopressors, however, are often indicated in patients in neurogenic shock, because those patients may have lost critical physiological compensatory responses (see section on Neurogenic Shock).
Elevation of the lower extremities above the level of the heart (Trendelenburg position) in a normovolemic subject shifts blood to the heart and increases ventricular end-diastolic volumes. In the hypovolemic patient, however, adrenergically mediated venoconstriction has likely already achieved this shift. Thus the position is of little value in treating hypovolemic shock, and its awkwardness can make evaluation and treatment of other problems more complicated. The position, however, is useful for the treatment of neurogenic shock.
In trauma patients, the pneumatic antishock garment can be useful for temporary compression of bleeding sites that cannot be controlled by other means, for temporary stabilization of pelvic fractures, and as a temporary expedient to increase the blood pressure during transport in patients in neurogenic shock. It has no other uses. It limits the physical examination. It precludes use of the veins in the lower part of the body as sites for venous access. It can hinder filling of the ventricles by compressing the inferior vena cava and the renal and hepatic veins. It can hinder left ventricular ejection by compressing the arterioles in the lower body. It can push the diaphragm into the chest and interfere with ventilation. It is of no use in displacing blood from the periphery to the heart in neurologically intact patients—discharge of the adrenergic system will already have achieved that goal.
CARDIAC COMPRESSIVE SHOCK
Diagnosis
Cardiac compressive shock can arise from any condition that compresses the heart or great veins, including pericardial tamponade, tension pneumothorax, massive hemothorax, rupture of the diaphragm with encroachment of abdominal viscera into the chest, and distention of the abdomen with compression of the intra-abdominal great veins and elevation of the diaphragm into the chest. All of these conditions are worsened if the patient has to be mechanically ventilated.
The signs of compressive shock are similar to those of hypovolemic shock—postural hypotension, poor cutaneous perfusion, oliguria, hypotension in the supine position, mental status changes, electrocardiographic signs of myocardial ischemia, metabolic acidemia, and hyperventilation—combined with distended neck veins. The only other type of shock that can produce the combination of poor perfusion associated with distended neck veins is cardiogenic shock, which rarely poses a problem in differential diagnosis. Cardiogenic shock usually develops against a background of evident disease that predisposes to primary myocardial dysfunction. Cardiac compression usually follows trauma or occurs in a setting where mechanical compromise of the heart or great veins can arise from imposition of external pressure (as in a possible pericardial tamponade).
The so-called paradoxic pulse is occasionally helpful in diagnosis. A spontaneous breath in a normovolemic subject without cardiac compression produces little effect on systemic blood pressure. If the heart is compressed, the systolic pressure can fall by more than 10 mm Hg. (In contrast, a fall in the blood pressure with positive pressure ventilation is common and nonspecific, especially in hypovolemic patients; the concept of a paradoxic pulse applies only to patients who are breathing on their own.)
The diagnosis of cardiac compression is facilitated if the patient can be monitored in an intensive care unit (ICU) with a pulmonary artery catheter, when small stroke volumes in the face of high filling pressures can be documented by direct measurement. In addition, the catheter can be used to compare pressures in the left and right atria. Under normal circumstances, the pressure in the left atrium is about 5 mm Hg higher than in the right. In tamponade, the pressures are the same.
Treatment
Infusion of fluid can transiently overcome some of the ill effects of cardiac compression, but the cause of shock in these patients is mechanical, and definitive treatment must correct the mechanical abnormality. Treatment of compressive shock caused by large-volume, high-pressure mechanical ventilation is discussed later in this chapter in the section on mechanical ventilation.
CARDIOGENIC SHOCK
Diagnosis
Cardiogenic shock can arise from several causes, including arrhythmias, ischemia-induced myocardial failure, valvular or septal defects, systemic or pulmonary hypertension, myocarditis, and myocardiopathies. Of all the forms of shock, it can be the most resistant to treatment. If the heart cannot pump, there may be nothing that can be done. On the other hand, in less severe cases, it is possible to improve the efficiency of the pumping capability that remains.
The diagnosis of cardiogenic shock usually depends on recognizing an underlying medical condition predisposing the heart to dysfunction in conjunction with an abnormal electrocardiogram. Given the relative oxygen demands of the left and right ventricles, shock caused by left ventricular failure is much more common in patients with ischemic heart disease and typically presents with chest pain, a third heart sound, rales, ST segment elevation on a 12-lead electrocardiogram, and, on chest film, an enlarged heart or pulmonary edema. Cardiogenic shock may be associated with distended neck veins if the right ventricle has failed, unless the patient is also hypovolemic, as in a bleeding patient with a recent myocardial infarction. In many cases, patients with recent shock or trauma may have mild to moderate forms of right ventricular dysfunction related primarily to the heart’s response to systemic inflammation or elevated ventilator pressures. Right-sided dysfunction can be associated with peripheral edema, an enlarged and tender liver, and, on chest film, an enlarged heart. The diagnosis is usually easy, but two common situations may pose a problem.
The first is a ruptured abdominal aortic aneurysm in a patient with coronary artery disease. The patient might have abdominal pain consistent with a myocardial infarction and electrocardiographic signs of ischemia—the ischemia being caused by hypovolemia and shock. The key is to observe the neck veins.
The second is to ascribe shock to myocardial contusion in a patient who has just suffered a blunt injury to the chest. Although blunt chest trauma can damage the heart, the damage is usually either fatal, with death at the scene of the injury, or, more often, of no clinical significance. A contusion that produces failure but not death is rare. Shock after blunt trauma in a patient who survives to reach the hospital is almost never caused by contusion—it is far more likely to be caused by hypovolemia or by a mechanical problem.
Treatment
In the initial treatment of acute dysrhythmias, we use the approach described by Ursic and Harken (ref in the ACS textbook). A bradydysrhythymia in a hypotensive patient with a heart rate less than 50 beats/min deserves treatment, even if the ventricular contractions are well coordinated. One should begin with the intravenous administration of atropine, at a dose of 0.5 mg, repeated at 2-minute intervals for a maximum dose of 2 mg. If the rate remains slow and if the patient is still unstable, the heart should be paced by transvenous or external means.
A tachydysrhythmia can put a patient at risk for myocardial ischemia regardless of origin (sinus vs nonsinus) or etiology (hypovolemic or cardiogenic shock). Thus one has to decide if the rate is so rapid that it threatens the patient’s myocardium. As a first approximation, the goal for most patients should be a ventricular rate between 50 and 100. But the goal can be different for different patients. The maximal ventricular rate, the rate that can be sustained for perhaps 5 minutes, but not longer, declines with age (220—age in years). The maximal aerobic rate, a rate that can be maintained indefinitely, but with strain, is 60%-90% of this value depending on the physical condition of the patient and the presence or absence of ischemic heart disease. For example, a healthy 20-year-old man in good condition should be able to tolerate and sustain a heart rate of 160 (80% of 200) without difficulty (although one should search for the cause of the tachycardia). On the other hand, a 65-year-old man with known coronary stenosis may have a myocardial aerobic threshold of 93 beats/min:
(220 − 65) × 0.6
Rates exceeding these limits should be treated.
A moribund patient with a tachydysrhythmia should undergo electrical cardioversion, an intervention that result in full cardiac function with normal blood supply to the brain in a matter of seconds. No other treatment has this potential. Electrical cardioversion is the treatment of choice for coarse ventricular fibrillation, ventricular tachycardia, and for supraventricular dysrhythmias with unsustainably rapid ventricular responses. It is not the treatment of choice for asystole or fine ventricular fibrillation, but no treatment for these dysrhythmias has a chance of achieving resuscitation with full neurological function. Nothing will be gained with cardioversion in the patient in asystole or fine fibrillation, but nothing will be lost.
One hundred joules (J) should be used initially, with rapid escalation to 360 J, as needed. The cardioversion takes precedence over securing the airway, and it takes precedence over obtaining vascular access; it even takes precedence over making a diagnosis of the arrhythmia. Once converted, the patient should be given a single 100-mg dose of lidocaine. Serum electrolytes should be measured and corrected, if needed. One to two grams of magnesium sulfate should be given intravenously over 15 minutes, regardless of initial plasma concentrations. More should be given later if the values are low.
Treatment of any non-moribund patient with a tachydysrhythmia begins with ensuring euvolemia and treating other possible extracardiac causes of a tachycardia (such as fever, stress, pain, and anxiety). Dangerously rapid tachydysrhythmias associated with abnormal ventricular conduction should be electrically cardioverted, followed with lidocaine, electrolyte correction, and administration of a single dose of magnesium. In the non-moribund patient with a dangerously rapid tachydysrhythmia and normal ventricular conduction, the initial goal is to slow the rate. Give up to 10 mg of verapamil intravenously over 10 minutes. This will slow the rate in the large majority of the patients. If the initial dose fails to slow the rate, an additional dose can be given 30 minutes after the initiation of the first dose. If the ventricular response is still too rapid, give digoxin. The digoxin is administered as a loading dose of 0.5 g intravenously, followed by 0.25 g every 6 hours for two additional doses (total of 1.0 g). More might be needed—the goal is to block the AV node enough so that the ventricular response is acceptable. Daily maintenance doses are usually needed, for long-term control, and the serum levels should be measured. Electrolytes should be corrected; magnesium should be supplemented.
For continued control of the rate, we favor digoxin. But one can also continue to use verapamil or add a beta-blocker, for long-term control. All three classes of drugs–calcium channel blockers, digoxin, and beta-blockers-slow AV nodal conduction, but, of the three, only digoxin increases myocardial contractility. Surgical patients need contractility to perfuse wounded or infected tissues.
If more than one drug has to be used, the patient will need to be in a monitored setting. Complete heart block is a potentially disastrous side effect with all of these drugs, especially when used in combination.
If ventricular conduction is normal and the patient is in atrial fibrillation, and if it is thought that the fibrillation is going to be of long duration, and if the physician is sure that the patient needs an “atrial kick,” the patient can be converted to a sinus rhythm with amiodarone. This set of conditions is rarely the case, however, in the noncardiac surgical patient. The “atrial kick” provides close to no added energy production from the heart in all but the most extreme cases of myocardial dysfunction. The atria in any reasonably functional heart serve only as reservoirs of energy, as capacitors, like other capacitance elements in the circulation, like the venules and small veins. The atria allow the ventricles to fill evenly under conditions of varying heart rates, but that goal is achieved with or without active contraction of the chambers.
Amiodarone frequently results in conversion of atrial fibrillation to a sinus rhythm, but the disadvantages of the drug, in the noncardiac patient, almost always outweigh the potential benefit. Conversion can lead to embolization of clot from the atrial appendage to the brain. The drug depresses myocardial contractility (potentially impeding wound healing and the ability to fight off infection). It has a long half-life. Its effects can last for weeks.
Opioids can be especially effective in treating cardiac failure after myocardial infarction. They relieve pain, provide sedation, block adrenergic discharge to the arterioles, block discharge to the venules and small veins, redistribute the blood from the atria and ventricles to the venous capacitance vessels in the periphery, and decrease myocardial oxygen requirements.
Diuretics are the keystone of therapy in congestive heart failure with large ventricular end-diastolic volumes. By decreasing vascular volume, diuretics decrease atrial pressures and mobilize peripheral and pulmonary edema. Pulmonary vascular pressures and volumes decrease; effectiveness of right ventricular contraction increases. Coronary blood flow increases as coronary sinus pressure drops. Decreasing pressures in the ventricles during diastole, when the ventricular muscle receives its nutrient blood flow, alleviates compression of the coronary vasculature in the endocardium. Decreasing pressures in the right atrium decreases the stiffness of the coronary vasculature, which decreases the stiffness of the ventricles during diastole (the garden hose effect). The ventricular end-diastolic volumes potentially can increase without much of an associated increase in the end-diastolic pressures.
Almost all patients in cardiac failure with ischemia and a rapid heart rate will benefit from a beta-adrenergic blocking agent (eg, esmolol or metoprolol). Decreasing the rate and reducing ventricular stiffness during systole decreases myocardial oxygen requirements. Increasing time in diastole and decreasing ventricular stiffness during diastole augments ventricular filling and increases efficiency of ventricular contraction. All of these effects reduce myocardial oxygen consumption and potentially salvage marginal myocardium. In many patients, the reduced oxygen requirements can be achieved with only minimal loss of energy output from the ventricles. The only contraindication to the use of beta-blockers, beyond the rare development of bronchospasm with administration of the drugs, is hypotension. This latter problem is easily monitored.
Hypertension is unusual but not unheard of in patients with cardiogenic shock. The hypertension is usually associated with inefficient delivery of energy into the aortic root. Treatment should begin with opioids, if the patient is in pain, and then diuresis, if the ventricular end-diastolic volumes are large. Nitroprusside and nitroglycerin are the most useful short-term vasodilators in surgical patients in heart failure (besides opioids). Both drugs act quickly and are easy to monitor; both dilate the systemic arterioles; nitroglycerin also dilates the systemic venules and small veins. For long-term control of pressure, angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers should be used in place of the nitrates. If the patient has a tachycardia or, as may well be the case, if the patient is at risk for having coronary artery disease or myocardial ischemia, beta-blockade can be used.
Beneficial consequences of controlling the pressure include mobilization of edema, both pulmonary and systemic; enhanced perfusion of the myocardium; reduction of ventricular work and oxygen requirements and, consequently, relief of myocardial ischemia. On the other hand, excessive venous dilation can decrease cardiac filling enough so that stroke volumes and blood pressures fall; excessive arteriolar dilation can make the pressures fall further.
Inotropic agents, such as dobutamine or milrinone, can increase cardiac output in some, but not all, patients in cardiogenic shock. Inotropic agents almost always result in increased myocardial oxygen requirements, but this is not usually a problem. Patients receiving the agents should be monitored in an ICU. Development of chest pain or ischemic electrocardiogram changes suggest that oxygen demand is exceeding supply. If it is necessary to use inotropic agents for more than 1 hour, a pulmonary artery catheter should be inserted. Systemic arterial pressures, atrial filling pressures, and cardiac output should be determined at different infusion rates. If any question remains about the adequacy of volume resuscitation, cardiovascular parameters should be measured before and after a fluid bolus is given.
Digitalis compounds should not be used in acute cardiac failure except to control ventricular rates in patients with supraventricular tachydysrhythmias. Toxicity may develop, especially when pH and electrolyte changes are unpredictable. The inotropic actions of digitalis are no different from those of dopamine and milrinone.
Although uncommon in the surgical setting, patients with cardiac failure and a low heart rate (< 70 beats/min) may temporarily benefit from the administration of a chronotropic agent, such as dopamine. (Isoproterenol is almost never used nowadays.) When using dopamine, the heart rate should be increased only to levels that can be tolerated comfortably. A 60-year-old patient with normal coronary arteries gains little with a heart rate that exceeds 120 beats/min; the limit is about 90 beats/min in the presence of coronary artery disease. In most cases, however, the price to be paid for using a chronotropic agent exceeds the potential benefit. Chronotropic agents increase myocardial work and oxygen requirements and shorten the time during diastole for coronary blood flow and ventricular filling. They should be used only as a temporary expedient. If they are used for more than 30 minutes, a pulmonary arterial catheter should be inserted. The goal of therapy is a normal or slightly supranormal cardiac output that provides adequate end-organ perfusion and reverses shock. Trying to achieve more than that only increases the risk of myocardial ischemia.
A vasoconstrictor is occasionally useful to increase coronary perfusion pressure in the setting of coronary stenoses. To be effective, the agent must increase aortic pressure enough so that the increased myocardial perfusion compensates for the increase in the myocardial oxygen requirements.
The major untoward effect of these agents is ischemic necrosis of noncardiac organs, such as the extremities or intestine. They will not increase perfusion to the brain in the setting of cardiogenic shock, assuming that the carotid arteries are open and that the patient has a functioning adrenergic nervous system. The endogenous adrenergic nervous system is ideally suited for ensuring adequate blood flow to the brain. Constrictors should be used only when absolutely necessary and for no more than 60 minutes unless a pulmonary arterial catheter is in place.
The transaortic balloon pump decreases the hindrance that the left ventricle faces when it ejects its blood into the aortic root and can be very effective in resuscitating selected patients with severe reversible left ventricular dysfunction (eg, after cardiopulmonary bypass or acute myocardial infarction). It should be used only if a pulmonary arterial catheter is in place.
Extracorporeal membrane oxygenation is most often used in conditions in which one can expect cardiac function to recover within a matter of a few days. Bleeding complications make it impractical for periods exceeding that time.
Although listed last, surgically correctable cardiac conditions should be identified and corrected early, prior to the development of irreversible organ dysfunction. Ruptured valves, occluded arteries, aneurysmal ventricular walls, and certain arrhythmias are examples of potentially correctable lesions. In these cases, early cardiac surgical consultation should be the rule.
NEUROGENIC SHOCK
Diagnosis
Shock caused by failure of the autonomic nervous system can arise from regional or general anesthetics, injuries to the spinal cord, or administration of autonomic blocking agents. The venules and small veins lose tone, worsened by paralysis of surrounding skeletal muscles. Blood pools in the periphery, ventricular end-diastolic volumes decrease, and stroke volumes and blood pressure fall. Loss of arteriolar tone in the denervated areas makes the pressure fall further. If the lesion is below the midthoracic sympathetic outflow (approximately T3), activation of the cardiac adrenergic nerves will increase the heart rate and augment ventricular systolic function; if the lesion is more cephalad, the heart will not be able to compensate. Cardiovascular decompensation in neurogenic shock can be profound.
The diagnosis rests on knowledge of the circumstances preceding the onset of shock and on the physical examination. The patient will always be hypotensive, and the skin will be warm and flushed in the denervated areas. The cause is usually obvious.
Nonfatal head injury—in contrast to spinal cord injury—does not produce neurogenic shock or any other kind of shock. In fact, increased intracranial pressure typically increases blood pressure and slows the heart rate (Cushing reflex). Hypotension and tachycardia should never be attributed to head injury—even severe head injury with cerebral dysfunction—until hypovolemia has been ruled out. It is a tragedy to ascribe shock to a head injury when the problem is bleeding from a ruptured spleen.
Treatment
Trendelenburg position, if it does not complicate other aspects of care, is useful. Intravenous fluids to fill the dilated venules and small veins should be given. Vasoconstrictors should be used if fluids and Trendelenburg position are not enough. Norepinephrine and phenylephrine are good choices if the heart rate is rapid. Dopamine is a good choice if the heart rate is slow.
The primary purpose of vasoconstricting agents in this setting is to restore tone in the venules and small veins; a secondary goal is to constrict dilated arterioles. The blood pressure should be increased to the point that coronary perfusion is sustained—as judged by normal ST–T segments on electrocardiography and absence of chest pain—and to the point that perfusion to the brain and spinal cord is supported. The pressure also has to be high enough to perfuse organs with preexisting obstructing proximal arterial lesions. These patients should be placed in the ICU for both neurologic and hemodynamic monitoring. If vasoconstrictors are used for more than several hours, or if the patient is at high risk for bleeding from multisystem trauma, central venous pressure monitoring or a pulmonary arterial catheter should be used to ensure adequate cardiac filling and function.
LOW-OUTPUT INFLAMMATORY SHOCK
Diagnosis
Bowel perforation, intestinal necrosis, abscesses, gangrene, and soft tissue infections can produce low-output inflammatory shock, as can ischemia-reperfusion and inadequate resuscitation of massive injuries or large burns. The cytokinemia arising from the systemic inflammation can disrupt the microvascular endothelium and prompt the loss of plasma into the interstitium. The shock mimics the clinical picture of severe hypovolemic shock, with signs of adrenergic discharge, oliguria, obtundation, and metabolic acidemia. The EKG may show signs of ischemia. Hyperthermia or hypothermia may be present. The diagnosis is usually clear from the clinical circumstances.
Treatment
Treatment consists of administration of intravenous fluids and antibiotics, correction of gastrointestinal leaks, debridement of dead tissue, and drainage of pus. The patient should be transferred to an ICU. Vasoconstrictors can be given for very short periods of time if the hypotension is so profound that it threatens the brain, the heart, or an organ with an obstructed arterial supply. Inotropes can be used more liberally, while the vascular volume is being replenished, but even then they should be used judiciously until additional physiologic data confirms a euvolemic state. This is easily obtained through the use of a central venous or pulmonary artery catheter. Alternatively, newer, noninvasive measurements of ventricular filling may prove useful. Successful volume expansion will convert the low-output inflammatory shock into a high-output state.
HIGH-OUTPUT INFLAMMATORY SHOCK
Diagnosis
High-output inflammatory shock can precede low-output inflammatory shock or can be the result of successful treatment of low-output shock. The shock usually, but not always, is associated with a fever. The patient is hypotensive with warm, well-perfused extremities, as the body attempts to control its core temperature by off-loading heat to the environment. If a pulmonary arterial catheter is placed, the cardiac output is found to be high, assuming that the ventricular end-diastolic volumes have been brought back to normal levels. The outputs will remain high, occasionally as high as twice normal, as long as the inflammatory state persists. The oxygen consumption may be increased by a factor of 1.5.
Treatment
Treatment consists of control of the underlying cause and fluid administration. Inotropes may be useful. If large amounts of fluids are necessary for the resuscitation and if inotropes are being considered, an assessment of ventricular end-diastolic volume should be made to ensure the heart is adequately filling and to assess the impact of the intervention. The most accurate means to accomplish this is through the use of a pulmonary artery catheter. As this is not always possible, other, less invasive monitoring techniques include the measurement of central venous pressure and serial echocardiography. All have advantages, disadvantages, and in some cases, complications. Regardless, the goal is to perfuse the inflamed tissues with adequate power so that the product of the cardiac output and the mean arterial pressure is normal. In many patients, the result will be a cardiac output that is increased by a factor of 1.5 with a blood pressure that is decreased to a value that is two-thirds of normal. As in other forms of shock, the pressure has to be high enough to perfuse the heart and brain and organs with potentially obstructed arteries, but it does not have to be normal. Vasoconstrictors can be dangerous, potentially leading to necrosis of the limbs, the gut, and the kidneys, especially if there is any degree of hypovolemia. They should not be used unless the clinician is positive that both the right and left ventricular end-diastolic volumes are normally expanded.
American College of Surgeons: ATLS: Advanced Trauma Life Support Student Manual. 9th ed. American College of Surgeons; 2012.
Chan PS et al, American Heart Association National Registry of Cardiopulmonary Resuscitation Investigators: Delayed time to defibrillation after in-hospital cardiac arrest. N Engl J Med. 2008;358:9.
CRASH-2 trial collaborators, Shakur H, Roberts I, et al: Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomized, placebo-controlled trial. Lancet. 2010;376:23-32.
Doyle, GS, Taillac PP: Tourniquets: a review of current use with proposals for expanded prehospital use. Prehosp Emerg Care. 2008;12:241.
Hess JR, Brohi K, Dutton RP, et al: The coagulopathy of trauma: a review of mechanisms. J Trauma. 2008;65:748-754.
Holcomb JB, de Junco DJ, Fox EE, et al: The prospective, observational, multicenter, major trauma transfusion (PROMMTT) study. JAMA Surg. 2013;148:127-136.
Holcomb JB, Minei KM, Scerbo ML, et al: Admission rapid thrombelastography can replace conventional coagulation tests in the emergency department. Ann Surg. 2012;256:476-486.
Holcomb JB, Wade CE, Michalek JE, et al: Increased plasma and platelet to red blood cell ratios improves outcome in 466 massively transfused civilian trauma patients. Ann Surg. 2008;248:447-458.
Martinaud C, Ausset S, Deshayes AV, et al: Use of freeze-dried plasma in French intensive care unit in Afghanistan. J Trauma. 2011;71:1761-1765.
Matijevic N, Wang Y, Cotton B, et al: Better hemostatic profiles of nevert-frozen liquid plasma compared with thawed fresh frozen plasma. J Trauma Acute Care Surg. 2013;74:84-91.
Nunez TC, Young PP, Holcomb JB, et al: Creation, implementation, and maturation of a massive transfusion protocol for the exsanguinating trauma patient. J Trauma. 2010;68:1498-1505.
Radwan ZA, Matijevic N, del Junco DJ, et al: An emergency department thawed plasma protocol for severely injury patients. JAMA Surg. 2013;148:170-175.
Shenkin HA et al: On the diagnosis of hemorrhage in man: a study of volunteers bled large amounts. Amer J Med. 1944;208:421.
Sperry JL, Ochao JB, Gunn SR, et al: An FFP:PRBC transfusion ratio >= 1:1.5 is associated with a lower risk of mortality after massive transfusion. J Trauma. 2008;65:986-993.
Spinella PC et al: The effect of recombinant activated factor VII on mortality in combat-related casualties with severe trauma and massive transfusion. J Trauma. 2008;64:286.
Tapia NM, Chang A, Norman M, et al: TEG-guided resuscitation is superior to standardized MTP resuscitation in massively transfused penetrating trauma patients. J Trauma Acute Care Surg.2013;74:378-386.
INITIAL TREATMENT OF ACUTE PULMONARY FAILURE
DIAGNOSIS OF PULMONARY FAILURE IN SURGICAL PATIENTS
Most causes of pulmonary failure in the surgical patient can be ascribed to one or more of nine causes: the pulmonary failure of shock, trauma, and sepsis; mechanical failure caused by deranged respiratory system mechanics; atelectasis; aspiration; pulmonary contusion; pneumonia; pulmonary embolism; cardiogenic pulmonary edema; and, rarely, neurogenic pulmonary edema.
The pulmonary failure of shock, trauma, and sepsis arises from extrapulmonary trauma, infection, or ischemia-reperfusion in the setting of shock. Products of coagulation and inflammation are washed out from the damaged tissues and carried to the lungs (or to the liver, in the case of the splanchnic circulation, and from there to the lungs), where they set up an acute inflammatory reaction. The extrapulmonary causes are many and range from necrotizing infections to noninfective inflammatory responses (such as pancreatitis) to reperfusion of ischemic limbs to soft tissue injury to broken bones (and embolism of fat and clot from the bone marrow—the so-called fat embolism syndrome, now an outdated term).
The concept of pulmonary failure secondary to extrapulmonary ischemia-reperfusion, coagulation, and inflammation, which is common in surgical patients, can be subsumed into a broader category of pulmonary failure, known as the acute respiratory distress syndrome (ARDS). ARDS is defined by the sudden onset of hypoxemia with bilateral infiltrates, a PaO2:Fio2 less than 200 and the absence of left atrial hypertension (a pulmonary arterial wedge pressure < 18 if measured). A less severe form, ALI requires a PaO2: Fio2 less than 300 with the other criteria.
The causes of ARDS include those that are responsible for the pulmonary failure of shock, trauma, and sepsis and also include severe pneumonia and aspiration. The end result in all of these conditions is activation of macrophages and other inflammatory cells in the lungs. The mediators disrupt the microvascular endothelium, increasing its permeability. Plasma extravasates into the interstitium and, in the case of the lungs, into the alveoli. The resultant pulmonary edema impairs both ventilation and oxygenation; the microembolization to the lungs impairs perfusion. Arterial oxygen saturation decreases and carbon dioxide content increases—assuming that no compensatory mechanisms come into play. Lastly, to make things worse, the inflammatory process in the lungs releases mediators into the systemic circulation that can lead to inflammation and dysfunction in the liver, gut, and kidneys.
A number of different mediators of coagulation and inflammation have been implicated as causes of the increased permeability. Proteases, kinins, complement, oxygen radicals, prostaglandins, thromboxanes, leukotrienes, lysosomal enzymes, and other mediators are released from aggregates of platelets and white cells or from the endothelium or plasma as a consequence of the interaction between the aggregates and the vessel wall. Some of these substances are chemoattractants of more platelets and white blood cells, and a vicious cycle of inflammation develops that worsens the disruption of the vascular endothelium.
Pathologically, ARDS (and the pulmonary failure of shock, trauma, and sepsis) is characterized by diffuse alveolar damage and a nonspecific inflammatory reaction, with the loss of alveolar epithelium and hyaline membrane formation. Monocytes and neutrophils invade the interstitium. Edema appears within a few hours, alveolar flooding is florid within 1 day, and fibrosis begins in 1-2 weeks. If the process is unchecked, the lungs become sodden and resemble liver tissue on gross inspection; scar tissue appears within a week, and function-limiting fibrosis begins to develop within 2 weeks. If early treatment is effective, the lungs return to normal, both grossly and microscopically.
Mechanical failure can arise from chest wall trauma, pain and weakness after surgery and anesthesia, debility caused by the catabolic metabolism of long-term illness, or bronchopleural fistula. Massive trauma to the chest with multiple fractures of multiple ribs or bilateral disruption of the costochondral junctions can result in a free-floating segment of chest wall known as a flail chest. Expansion and relaxation of the chest wall during spontaneous breathing results in paradoxic motion of the free segment in response to changes in intrathoracic pressure; ventilation becomes compromised; and the partial pressure of arterial carbon dioxide (Paco2) increases. In addition, hypoventilation leads to progressive atelectasis and hypoxemia. Lesser degrees of chest wall injury can lead to hypoventilation secondary to pain with similar results. Prolonged mechanical ventilation with loss of muscle mass and power in the diaphragm and the accessory muscles of respiration can require ventilatory support until muscle function returns to normal. A bronchopleural fistula—a communication from the airway to the pleural cavity to the atmosphere, either through a chest tube or through a hole in the chest wall—can develop after pulmonary surgery, trauma, or infection. Large air leaks can compromise ventilation to the uninvolved lung as well as to the diseased side because insufflated air preferentially goes to the side with the fistula.
Atelectasis—localized collapse of alveoli—can develop with prolonged immobilization, as during anesthesia or in association with bed rest. The problem is usually full-blown within a few hours after the initiating event. Only mechanical failure (to which it is related), aspiration, cardiogenic pulmonary edema, and pulmonary embolism can produce equivalent levels of hypoxemia so soon, and no other cause of hypoxemia can respond so quickly to therapy. The diagnosis is supported by auscultation of bronchial breath sounds at dependent portions of the lung and occasionally, if severe enough, by x-ray confirmation of plate-like collapse of pulmonary parenchyma. The most reliable confirmation of the diagnosis, however, comes with response to therapy, which can include pain control when necessary and encouragement of deep breathing, coughing, and ambulation when practical. When the hypoxia is severe and refractory to conservative measures, intubation and mechanical ventilation may be necessary, particularly if the underlying etiology (pain and immobility) cannot be reversed easily (eg, high spinal cord injury). Rarely, flexible bronchoscopy may be useful if the lung parenchymal volume loss is due to proximal bronchial obstruction. In general, most forms of atelectasis respond within a few hours to conservative therapy.
Aspiration of gastric contents or blood can occur in any patient who cannot protect the airway. Shock, severe brain injury, or pharmacologic depression (anesthesia, narcotics, or benzodiazepines) can result in a depressed level of consciousness and loss of airway protective reflexes. Gastric acid or particulate matter in the airways leads to disruption of the alveolar and microvascular membranes, causing interstitial and alveolar edema. The resultant hypoxemia is usually evident within a few hours and is associated with a localized infiltrate on x-ray. Recovery of gastric contents by suctioning from the endotracheal tree confirms the diagnosis.
Pulmonary contusion arises from direct trauma to the chest wall and the underlying lung parenchyma. Hypoxemia associated with a localized infiltrate on x-ray develops over 24 hours as the injured lung becomes edematous.
Pneumonia can arise primarily or may be superimposed on aspiration, pulmonary contusion, or the pulmonary failure of shock, trauma, and sepsis. The diagnosis is made by recovery of bacteria and purulent material from the endotracheal tree, hypoxemia, signs of systemic inflammation, and a localized infiltrate on x-ray. The Clinical Pulmonary Infection Score (CPIS), which is derived from these parameters, can be used to quantify the clinical, radiographic, and laboratory findings of pneumonia. It is useful both for diagnosis and for determining the length of treatment. Bronchoalveolar lavage and quantitative culture may occasionally be used to assist in distinguishing pneumonia from ARDS and other causes of pulmonary inflammation.
Pulmonary embolism typically presents with sudden deterioration of pulmonary function after an event—such as an operation, injury, or the beginning of immobilization—that can stimulate deposition of clot in a large systemic vein. Patients with cancer are at particularly high risk, and in any patient the greater the magnitude of operation or injury, the greater the chance of venous thrombosis and embolization. Clot emboli must be organized to be clinically significant; embolism to the lung of fresh soft clot rarely causes any difficulty. The pulmonary endothelium contains potent fibrinolysins that can break up any poorly organized embolus. Although uncommon in the initial 72 hours following an acquired risk factor (injury, surgery), early postinjury and postsurgical pulmonary embolism is well documented and has to be considered in the differential diagnosis of abrupt-onset hypoxemia.
The chest film is usually nonspecific. A definite diagnosis can be made by high-definition contrast enhanced computed tomograms of the pulmonary vasculature. Modern imaging is extremely sensitive. A negative study rules out an embolism. The CT can also identify atelectasis, infiltrates, and effusions that may not be readily apparent using a standard anterior-posterior radiograph done in the ICU. The major risk involves the physical movement of the patient to the radiology suite. The risk of contrast nephropathy is very low in a euvolemic patient, even in the setting of mild baseline renal disease.
Pulmonary arteriography, with right heart catheterization, can also be used to make the diagnosis of embolism but is seldom used nowadays, with one exception. The study can be very useful in hemodynamically unstable patients in whom a large “saddle embolus” is suspected. The catheter can be left in place, if an embolus is found, and used for catheter-directed thrombolysis.
Cardiogenic pulmonary edema arises from high left atrial and pulmonary microvascular hydrostatic pressures. Patients who have suffered an acute myocardial infarction can present this way, as can patients with underlying myocardial or coronary artery disease when faced with fluid shifts and surgical stress. Occasionally, the rapid administration of intravenous fluid—especially in elderly patients with poor myocardial performance—will outstrip the heart’s ability to pump, and pulmonary edema will result. Acute valvular disease, though rare after injury or cardiac surgery, is another possible cause of inability of the left heart to pump effectively.
The diagnosis is made on the basis of hypoxemia, rales, a third heart sound, perihilar infiltrates, Kerley lines, and cephalization of blood flow on x-ray along with elevated pulmonary arterial wedge pressures on pulmonary arterial catheterization. A wedge (or left atrial) pressure of 24 mm Hg can produce cardiogenic pulmonary edema even in the presence of an intact endothelium in the pulmonary microvasculature. Pulmonary arterial wedge pressures less than 24 mm Hg will generally not produce edema if the pulmonary vascular endothelium is intact; pressures exceeding 16 mm Hg can worsen the edema associated with increased permeability (such as ARDS). The goal for the wedge pressure in a patient with uncomplicated cardiogenic pulmonary edema in the absence of an inflammatory process in the lungs should be 20 mm Hg or less; the goal in a patient with an inflammatory process should be 12-16 mm Hg.
Neurogenic pulmonary edema is associated both experimentally and clinically with head injury and increased intracranial pressure. The exact mechanism by which this occurs is unknown, but it is probably related to sympathetic discharge with postmicrovascular vasoconstriction in the lungs and a resultant increase in pulmonary microvascular hydrostatic pressure. This form of pulmonary edema and oxygenation defect is rare. In the great majority of patients with a head injury and pulmonary edema, the edema will be caused by some other mechanism, such as ARDS.
INDICATIONS FOR INTUBATION & USE OF MECHANICAL VENTILATION
The indications for intubation and mechanical ventilation are related but often assessed separately. Patients who have primary airway compromise—caused by stridor, maxillofacial trauma, facial and airway burns with edema, or a depressed mental status—may need intubation to protect the airway. In these cases, early intervention is the rule as rapid clinical deterioration can convert a semiurgent procedure into an emergency. In some cases, intubation should be performed before the patient shows evidence of airway compromise. In severe cases, such as massive facial edema, early cricothyroidotomy should be performed.
Intubation of the airway is also indicated if mechanical ventilation is needed for the treatment of established pulmonary failure or for prophylaxis against potential failure or for pulmonary toilet in the face of aspiration. The decision to intubate and initiate mechanical ventilation should be made on the basis of clinical criteria. A respiratory rate exceeding 36 breaths/min, labored ventilation, use of accessory muscles of ventilation, and tachycardia are all indications for intervention. Finally, intubation and mechanical ventilation should be considered in anticipation of treatment that can compromise the airway or worsen the pulmonary status. These include the need for excessive sedation or narcotics, massive fluid resuscitation, and the manipulation of fractures.
Arterial blood gas (ABG) measurements are of no value in making decisions about intubation and mechanical ventilation in patients in extremis. These patients should be intubated regardless of the blood gas results. ABG measurements, however, can assist in the decision to intubate less severely stressed patients. In the setting of hypoxemia, intubation should be considered if the PaO2 is less than 60 mm Hg and the patient’s supplemental oxygen exceeds an O2 concentration of 50%. For hypercapneic patients, a Paco2 greater than 45 mm Hg in the setting of acidemia should prompt intubation, especially if serial measurements demonstrate a worsening respiratory acidosis. Regardless of the laboratory values, these guidelines should always be put in the clinical context. A Paco2 of 40 mm Hg in a patient breathing 40 breaths/min is as alarming as a Paco2 of 60 mm Hg in a patient with a respiratory rate of 10 breaths/min. A PaO2 of 60 mm Hg on room air in a patient with chronic lung disease may be acceptable; the same value in a patient who is tensing the sternocleidomastoid and intercostal muscles with each breath, making excessive or discoordinated use of the abdominal musculature, and who seems to be struggling to draw in enough air, mandates immediate intubation.
The indications for intubation should be more liberal for a surgical patient than for a medical patient. The medical patient with an exacerbation of chronic obstructive lung disease can be poorly served by placement of a foreign body in the trachea. Airway resistance increases, coughing becomes less effective, and opportunistic organisms obtain a foothold on and near the tube. The benefit from intubation may be minimal and noninvasive ventilation techniques, such as bilevel positive airway pressure (BiPAP), may be all that is needed. This support can be given simultaneously with other treatments—such as administration of bronchodilators, antibiotics, and diuretics—in order to avoid intubation and its potential complications.
Circumstances for the seriously ill surgical patient are usually different. The patient who has multiple injuries, for example, can temporarily tolerate the increased airway resistance, loss of cough, and increased likelihood of tracheobronchial infection. What cannot be tolerated is respiratory arrest during trauma resuscitation or during preparation for an operation.
The indications for intubation in the patient with a suspected or known injury to the cervical spine are the same as those in patients with no likelihood of injury. Under no circumstances should concern about the cervical spine lead to procrastination about securing the airway. The consequences of respiratory arrest and anoxic brain damage are as tragic as those of exacerbating a cervical spine injury.
Types of Intubation
The trachea can be intubated via the mouth, the nose, the cricothyroid membrane (cricothyroidotomy), or directly (tracheostomy). The tubes used for intubation used to come with either high pressure cuffs or low pressure cuffs. Because of problems with compromise of tracheal blood supply, and the subsequent problems of tracheomalacia, erosion into the innominate artery or the esophagus, and tracheal stenosis, the high pressure cuffs are no longer used. All modern tubes come with low pressure cuffs.
Of the four methods available for intubation, the orotracheal route is usually the easiest. Nasotracheal intubation requires the presence of spontaneous ventilation in order to guide tube placement; cricothyroidotomy and tracheotomy require surgical exposure. Orotracheal intubation allows for passage of a larger tube than the nasotracheal route and avoids the problems of sinusitis and necrosis of the nares, which can occur with nasotracheal intubation. On the other hand, nasotracheal intubation can be accomplished in the awake patient with minimal sedation, and some patients seem to find long-term presence of a nasotracheal tube more comfortable than that of an orotracheal tube. Neither nasotracheal nor orotracheal intubation requires neck flexion or axial rotation. Either approach can be used in patients with suspected injuries to the cervical spine, assuming that axial traction is maintained during the intubation.
Cricothyroidotomy is indicated when an urgent surgical airway is needed. Extensive maxillofacial trauma can make intubation by the orotracheal or nasotracheal route impossible. Translaryngeal intubation can also be difficult because of poor patient cooperation, altered anatomy, or airway or laryngeal swelling. If the patient is in extremis and respiratory collapse is imminent, attempts at orotracheal or nasotracheal intubation should not be prolonged. As a rule, if translaryngeal intubation is not successful after one or two attempts, cricothyroidotomy should be done. The cricothyroid membrane in the midline is bounded superiorly by the lower border of the thyroid cartilage. It is located by palpation and is incised by a stab incision. After the hole has been enlarged with the knife handle, a size 6 or 6.5 endotracheal tube should be inserted. After the airway is secured, the tube can be trimmed (without cutting the balloon tubing) to prevent accidental dislodgement. Alternatively a no. 4 or no. 6 tracheostomy tube can be used if available.
There are several advantages to using the endotracheal tube during an urgent cricothyroidotomy. These include increased tube compliance which facilitates insertion and, perhaps most importantly, universal availability. They are typically found in every airway kit or crash cart. A 6.5 tube will usually accommodate a bougie introducer which may facilitate insertion, particularly when the anatomy is difficult (obese or short neck) and the field is bloody. Larger endotracheal or tracheostomy tubes should not be used as they may not always pass easily through the cricothyroid space. In the short term, these smaller tubes are more than adequate as a rescue treatment and can easily be changed under more controlled circumstances.
Once the airway is secured and the patient stable, a more definitive airway can be planned as needed. The need to convert to a tracheotomy is not absolute. In some cases, the patient may no longer require airway protection. In others, endotracheal intubation may be a reasonable option. In the past, concerns over subglottic stenosis necessitated conversion of the cricothyroidotomy within several days. This has not been uniformly supported by the literature and should be individualized based on anticipated continued need for airway protection and mechanical ventilation.
Conversion of either an endotracheal airway or cricothyroidotomy to a tracheostomy should be done under controlled conditions. A transverse incision overlying the upper trachea is developed by separating the strap muscles of the neck in the midline. Often the thyroid isthmus must be either displaced or divided to allow for adequate exposure of the anterior surface of the trachea. The tracheostomy tube is placed through the second or third tracheal ring.
Tracheostomy placement is frequently performed for patients who require long-term mechanical ventilation. There are advantages and disadvantages to both the endotracheal tube and the tracheostomy. As a result, there are few absolute diagnostic or time standards for conversion beyond airway control.
One of the theoretical advantages of continued endotracheal intubation is the ease of tube repositioning, which allows distributing pressure on the tracheal mucosa over a larger area, compared with the balloon on the end of a tracheostomy tube, which is fixed in place. The result is a much lower incidence of late tracheal stenosis and tracheoinnominate artery and tracheoesophageal fistulas, compared with a tracheostomy. In addition, because the opening of a translaryngeal tube is well away from the neck and chest, intravenous catheters in these areas can be kept sterile. Finally, the cuffs on translaryngeal tubes usually lie in a more axial position in the trachea than those on a tracheostomy tube and are better able to maintain a seal in patients with poor pulmonary compliance and high inspiratory pressures.
On the other hand, for long-term care, airway resistance with a tracheostomy is lower, nursing care is simpler, suctioning is more direct, and the tubes do not damage the vocal cords or larynx. In addition and perhaps most importantly, accidental extubation is less serious. A well-established tracheostomy tract can be easily reintubated while the patient continues to breathe through the stoma. Tracheostomy is also of benefit when weaning from mechanical ventilation is slow and the patient has failed extubation on multiple occasions. The presence of a tracheostomy allows for prolonged periods off the ventilator without the need for reintubation. If the patient develops respiratory distress off the ventilator and a tracheostomy is present, the ventilator can simply be reconnected to the tracheostomy tube.
The timing of conversion from a translaryngeal intubation to a tracheostomy is controversial. Recommendations as short as 3 days have been made, but large numbers of patients have been intubated for months by the orotracheal or nasotracheal route without serious sequelae. Patients should be converted when airway protection, pulmonary toilet, or any of the other indications outlined above are present. If, in addition, the need for more than 2-3 weeks of intubation is obvious, the threshold for performing tracheostomy should be lowered.
Modes of Mechanical Ventilation
Once the airway is controlled, the ventilator should be set up beginning with the mode of ventilation. There are three primary variables used to describe the mode of mechanical ventilation: trigger, limit, and cycle (Table 12–2). The trigger can be patient or time triggered with the latter often referred to as “machine triggered.” This is the variable that determines when a patient receives a breath (starts inspiration). The second is the limit variable and refers to the setting that, when reached, is maintained constant throughout the inspiratory cycle (ie, the “upper limit”). Limit variables are either pressure or flow. When flow is the limit variable, the ventilator is said to be in volume control or volume limited because of the relationship flow × time = volume. Finally, the cycle variable is that which, once reached, terminates the inspiratory cycle and allows passive expiration. Using these three variables, different modes of ventilation have been created. Some are mostly of historical interest, and others are newer, combination modes designed to maximize patient physiology, safety, and comfort.
Table 12–2. Characteristics of five commonly used modes of mechanical ventilation.
Machine triggers are time functions based on the set rate, inspiratory time, and inspiratory to expiratory ratio (I:E ratio). Two of the three can be set, and the third is determined. A rate of 20 breaths/min and an inspiratory time of 1 second results in an I:E ratio of 1:2 (1 s inspiration + 2 s expiration = 3 s for a complete cycle; 20 cycles/min).
Patient triggers for delivery of an assisted breath can be either pressure-based or “flow by” depending on the ventilator model. A pressure trigger requires the patient to generate negative pressure at the onset of inspiration—the pressure in the ventilator tubing falls below a preset value and the ventilator detects this fall in pressure and responds by delivering a breath. The time involved in generating and delivering the breath to the patient, however, can make this form of breathing uncomfortable for the patient. Modern ventilators avoid this problem of triggering by using a flow-by circuit. The ventilator delivers a constant flow of air through the ventilator tubing during expiration, usually at a low level of approximately 5 L/min. The ventilator compares the expiratory and inspiratory flow rates. If the patient is making no inspiratory effort, the flow rates will be the same. If the patient begins to take a breath, the expiratory rate will fall below the inspiratory rate. The ventilator is programmed to trigger a breath when the difference in the flow rates reaches a preset value, usually around 2 L/min, or when the expiratory flow rate falls to 3 L/min. The patient is rewarded with the free flow of at least some air as soon as the effort is initiated. The great majority of patients prefer flow-by over pressure triggering.
Volume control ventilation is most often used today in situations in which the ventilation needs to be kept simple and the efforts made by the patient need to be minimized, as in the acutely injured or ill patient. The assist-control mode is the most commonly used mode of volume ventilation. It is designed to assist any ventilatory effort made by the patient by delivering a machine breath. Whenever the patient begins to inspire, the ventilator is triggered and the preset machine tidal volume is given. A machine backup rate is also set to ensure a minimal number of machine breaths in the absence of spontaneous ventilatory efforts.
In pressure control ventilation, the inspiratory pressure, inspiratory time, and I:E ratio are selected, and the ventilator automatically adjusts the gas flow rate to maintain a constant pressure during inspiration. The main advantage of this over volume control is that gas flow more closely matches the change in lung compliance that occurs during inspiration. This has the theoretical benefit of a more even distribution of inspired gas and possibly a lower risk of regional alveolar overdistention. It is also more comfortable for the awake patient. Although this can be achieved through manipulating the flow pattern in more advanced volume control ventilators, it is automatic in pressure control ventilation. Physiologic inspiratory times and I:E ratios are usually chosen to improve patient comfort. An inspiratory time of 1 second with an expiratory time of 2-3 seconds is typical. Longer inspiratory times with shorter expiratory times (inverse ratio ventilation) can be used if the physiologic times prove inadequate to provide enough support. The long inspiratory times, along with the short expiratory times, result in air trapping and increase the mean airway pressure. The net result is an increase in functional residual capacity (FRC), similar to that accomplished with high positive end-expiratory pressure (PEEP) levels.
Pressure support ventilation is also a pressure-limited form of ventilation and in most cases, can be considered a distinct mode of ventilation (Table 12–2). It differs from pressure control in that it is always patient triggered and the inspiratory time is determined by the patient and not set by the ventilator. As in pressure control ventilation, the ventilator adjusts the flow to maintain a constant pressure during inspiration. The inspiratory time, however, is determined by the interaction of the gas flow with the patient’s inspiratory effort. To do this, the ventilator measures the peak inspiratory flow rate during inspiration. The flow rate usually reaches a maximum value early in the inspiration and then tapers off as the patient’s inspiratory effort decreases. When the flow rate decreases to a predetermined fraction of the maximal flow (generally 25% of maximum), gas flow is terminated, and the patient is allowed to exhale. Pressure support can also be used in conjunction with the intermittent mandatory ventilation (IMV) mode (see next section).
The level of the pressure support is set so that the patient breathes comfortably at a reasonable rate, usually less than 24 breaths/min. The goal of the support is to ensure adequate oxygenation and a pH greater than 7.30. The tidal volume generated under these circumstances is generally unimportant.
The mode has many advantages. It is usually comfortable for the patient. It overcomes resistance to inspiratory flow in the endotracheal tube and in the ventilatory apparatus and decreases the work of breathing. It makes it impossible for the ventilator to deliver excessively high pressures. The flow is maintained for as long as the patient continues to make an inspiratory effort, so the patient can sigh at will. This minimizes the development of atelectasis. It is also ideally suited for preparing the patient for weaning and extubation.
With IMV, all aspects of breathing are controlled including the rate, inspiratory time, and expiratory time (and as a result, I:E ratio). The limit variable can be either pressure (PC IMV) or volume (VC IMV). The breaths are generally synchronized (SIMV) if the patient has spontaneous respiratory effort. In this mode, any attempt to breathe at a greater frequency than the set rate is unsupported unless additional pressure support is added. In this case, the patient receives two different modes during mechanical ventilation. The first is the mandatory, machine-triggered breath at the set rate and inspiratory time. The second is a spontaneous, patient-triggered breath at a rate equal to the total minus the set rate with an inspiratory time determined by the patient (see previous discussion of pressure support ventilation). These two breaths will have different waveform characteristics on the ventilator display.
Assist control mode was originally set up to “assist” the patient’s spontaneous effort with a completely supported mechanical breath. It can be used with a volume or pressure limit (VC or PC) and set up with a backup rate when spontaneous effort is minimal or absent. The main distinction from SIMV is that all of the patient’s inspiratory efforts are completely supported (not just those at the set rate). This has the small disadvantage of air trapping when the patient’s respiratory rate is excessively high (> 30-35 breaths per minute) and should be used with caution in patients at risk for hyperinflation (severe emphysema). There is no role for pressure support ventilation in this mode as all breaths are completely assisted.
Over the past 15 years, it has become possible to ventilate patients with even more sophisticated hybrid modes. Some ventilators can be set up to deliver constant pressure during the inspiration in such a way that the tidal volume delivered falls in a preset range (pressure-limited volume control, PRVC). Some ventilators can be set up to deliver a preset tidal volume but without exceeding a preset pressure. Some ventilators can be set up with gradually decreasing ventilatory support with algorithms built into the system to minimize the need for physician adjustment of the ventilator during weaning.
Setting Up the Ventilator
After choosing the mode (AC, SIMV, or PS; PC or VC), five parameters remain to be determined: the backup ventilatory rate, the goal tidal volume of the machine-delivered breaths, the inspiratory time, the inspired oxygen concentration (Fio2), and the PEEP level. The first two of these parameters determine ventilation; the latter three are important in determining oxygenation.
Ventilation has three components: minute ventilation (VE), alveolar ventilation (VA), and dead space ventilation (VD). Although VA is most closely related to Paco2, at steady state, the relationship with VEand VD is roughly constant, and therefore, VE, which is easily quantified, can be used as a surrogate. In patients with uncomplicated pulmonary failure, the respiratory rate can be set at 12-15 breaths/min and the tidal volume set to 7 mL/kg IBW. This produces a VE of 6-7.5 L/min and a VA of 4-5 L/min (assuming VD of 33% in a 70 kg patient). In the absence of significant pulmonary dysfunction, this will result in a Paco2 of approximately 40 mm Hg and is a good starting point from which adjustments can be made.
If the Paco2 is elevated, increases in the respiratory rate will often correct the problem. Although this is less efficient than increasing the tidal volume (due to the increased dead space ventilation that occurs with higher respiratory rates), it is a reasonable first step when the respiratory rate is less than 25 breaths/min. Excessively high respiratory rates (> 30 breaths/min) can result in air trapping, especially in patients with expiratory air flow obstruction (chronic obstructive pulmonary disease or severe asthma). On the other hand, excessively high volumes may be associated with elevated airway pressures and can result in barotrauma (pneumothorax), volutrauma (alveolar overdistention), or both. Except in certain circumstances (intracranial hypertension), it is better to accept a mild respiratory acidosis than to ventilate the patient using excessively large tidal volumes (> 10 mL/kg IBW) or excessively high airway pressures (plateau pressure > 30 cm H2O). When the pH is less than 7.20, very high rates or volumes may be necessary until the pH can be brought into the normal range either through renal compensatory mechanisms or administered bicarbonate. Very high rates or volumes may also be necessary when a bronchopleural fistula is present, to compensate for the volume lost through the fistula.
The inspired oxygen concentration should be kept high enough so that, in most cases, the oxygen saturation of arterial blood exceeds 92%. Patients with chronic obstructive pulmonary disease and long-standing CO2 retention are an exception. Such patients have lost the ability to increase their respiratory drive in response to increases in Paco2 and rely instead on their response to hypoxemia. Increasing the arterial oxygen saturation by adding exogenous oxygen takes away this hypoxic ventilatory stimulus and makes weaning from ventilatory support more difficult.
All of the nonoxygen volume of ventilator gas is made up of nitrogen, which, unlike oxygen, is not absorbed from alveoli. Nitrogen can be of great value in stenting open the alveoli. When it is replaced by increasing concentrations of oxygen, increased atelectasis caused by oxygen absorption can occur. In addition, high concentrations of oxygen can cause chronic pulmonary fibrosis. Ideally, the inspired oxygen concentration should be kept at 0.50 or less.
Keeping the inspired oxygen levels at acceptably low levels is frequently facilitated by the use of PEEP. The pressure is generated by closure of a valve in the expiratory circuit of the ventilator to keep the airway pressure above a preset level during expiration and to minimize alveolar collapse. Placement of an endotracheal tube bypasses the normal physiologic PEEP present during spontaneous ventilation from closure of the glottis at the end of expiration. In addition, supine patients may have a lower FRC due to increased intra-abdominal pressure and cephalad displacement of the diaphragm into the chest. This can be overcome through the use of low levels of “physiologic” PEEP (5 cm H2O). Increasing the PEEP should be considered when the respiratory system compliance is low or when adequate oxygenation requires an Fio2 that exceeds 0.50.
Low levels of PEEP (< 10 cm H2O) are well tolerated by most patients. The consequences of excessive PEEP are barotrauma and decreased cardiac output. First, the high pressure can compress the superior and inferior vena cava and the pulmonary veins, compromising diastolic filling of the ventricles (in contrast with a spontaneous inspiration, which augments filling). Second, the high pressures can compress the thin-walled atria and right ventricle, further compromising end-diastolic volumes (also in contrast with a spontaneous inspiration). Finally, the high pressures can compress the pulmonary microvasculature, making it difficult for the right ventricle to push blood through the pulmonary vasculature. The remedy for the decreased cardiac output is usually fluid infusion. The potential problem with this remedy is worsening of the pulmonary failure that prompted the use of the PEEP in the first place. Accounting for all of these factors, PEEP levels greater than 10-12 cm H2O should generally be used with a pulmonary arterial catheter in place. Titrating to the optimal oxygen delivery, and not arterial PaO2, will ensure a balance between the risks and benefits of high PEEP levels. Monitoring the mixed venous oxygen saturation serves as a reasonable method to achieve this goal. Even with invasive monitoring, PEEP levels greater than 15-20 cm H2O are rarely of benefit.
Ventilator Safety & Alarms
As can be inferred, modern ventilators are complex, and they should, in general, be used only in the setting of continuous cardiopulmonary monitoring to include electrocardiography and pulse oximetry. In addition, the ventilators themselves have alarms for early warning of apnea, changes in tidal volume or minute ventilation, and excessive inspiratory pressures. These should be individualized to each patient so that nurses, respiratory therapists, and physicians are notified early in the course of the physiologic derangement. In many cases, the ventilator alarm will precede changes in the pulse oximeter or electrocardiogram. All personnel taking care of the patient should be knowledgeable with both the equipment and the mode of ventilation.
Discontinuing Mechanical Ventilation
Patients who seem to be doing well and who have required mechanical ventilation for less than 24 hours can frequently be extubated quickly after undergoing a trial of spontaneous ventilation. Patients must be able to maintain their own airway, and their acute illness should be resolving. They should be able to maintain adequate oxygenation with an inspired oxygen concentration of 0.40 or less and with a PEEP of 8 cm water or less.
The majority of ventilated patients are most effectively weaned with daily spontaneous breathing trials. The breathing trial can be given with T-piece ventilation in which the endotracheal tube is attached to a length of tubing connected to a blow-by oxygen source. Alternatively, the trial can be accomplished with a low level (typically 5 cm of water) of pressure support with PEEP or with PEEP alone. In either case, the patient is asked to support his or her own breathing for 30 minutes. If the patient is breathing comfortably at the end of the trial, the patient can be extubated. If a question arises as to the degree of comfort, arterial blood should be drawn for gases, and the patient should be put back on the ventilator while waiting for the results of the blood gas analysis. If the patient was reasonably comfortable at the end of the 30-minute trial and if the pH comes back at a normal value, the patient can be extubated. Note that at the conclusion of the 30-minute trial, full ventilator support should be resumed pending the laboratory results. The patient needs to be well rested when the endotracheal tube is removed. If the patient fails the 30 minute trial, full support is resumed for the remainder of the day, and the trial is repeated the following day. In some cases, the duration of the breathing trial can be extended to up to 2 hours. Although the ability to predict successful extubation is not significantly different, the increased duration may be appropriate for patients who have already required reintubation following completion of a 30 minute SBT. There is generally no role for breathing trials of longer duration when the patient is endotracheally intubated. In fact, this may serve to unnecessarily fatigue the patient making successful extubation, less likely.
Weaning from mechanical ventilation can also be achieved with IMV. Although generally inferior to the once-daily spontaneous breathing trial, patients who are severely debilitated and have required mechanical ventilation for prolonged periods (> 2-3 weeks) can be successfully weaned using this technique when combined with a gradual reduction in pressure support. The IMV rate is gradually decreased, requiring the patient to contribute increasingly to the maintenance of adequate minute ventilation. The patient’s overall clinical status, respiratory rate, and arterial Pco2 are used as guidelines to determine the rate of weaning. When an IMV of 4/min or less is well tolerated for long periods, the patient is placed on pressure support, which is weaned daily until mechanical support is no longer needed. As noted above, patients with an endotracheal tube in place (vs tracheostomy) should only undergo brief periods where the pressure support is less than 5-8 cm H2O (30-120 minutes). This amount of PS is required to mitigate the increased resistance of the endotracheal tube. Patients who repeatedly fail extubation or are severely deconditioned benefit from a more deliberate and gradual weaning of the ventilator. Frequently, these patients benefit from tracheostomy and optimization of nutritional status as adjuncts to weaning. Factors that increase the work of breathing such as reactive airway disease, large pleural effusions, and chest wall or visceral edema should be treated and minimized.
Extubation
The decision to extubate the patient depends both on the assessment for the need for airway protection as well as the need for mechanical ventilation. As mentioned previously, the latter can be determined based on the result of a 30-minute trial of spontaneous breathing. The former should be based on several factors, including the patient’s level of consciousness, the presence of airway injury or edema, the need for ongoing endotracheal suctioning, and the possible need for further operative procedures within the next 24 hours. Finally, a subjective determination of a patient’s ability to tolerate extubation and spontaneous ventilation should be made. An alert and communicative patient who can lift her head off the pillow is a good candidate for extubation; a lethargic, diaphoretic patient is not. For patients who require continued airway protection but no longer require mechanical ventilatory support, a tracheostomy should be considered.
ADJUVANT DIAGNOSTIC & THERAPEUTIC MEASURES
Chest Radiographs
Chest x-rays should be obtained daily in patients being treated with mechanical ventilation. A review of the film should confirm the placement of all lines and tubes, including the endotracheal tube, central venous catheters, pleural tubes (thoracostomies), and nas/orogastric or nas/oroenteric tubes. A search for specific pulmonary and pleural processes should be performed. Local infiltrates such as pneumonia or patchy/diffuse processes such as the ARDS should be identified.
In addition to a daily chest radiograph, a stat chest x-ray should be obtained whenever a patient’s cardiopulmonary status rapidly deteriorates. Tubes or lines might be displaced; new problems with a reversible etiology such a pneumothorax, a lobar collapse, or a new infiltrate suggesting aspiration might be identified.
Sedation & Muscle Relaxants
Mechanically ventilated patients frequently require sedatives and/or analgesia to ameliorate the agitation and pain associated with their disease and treatment. Narcotic analgesia in the form of intermittent or continuous opiate infusion may be sufficient. Narcotics, however, should not be used to treat agitation and anxiety that is thought to be caused by the ventilator. Sedating agents, including propofol and benzodiazepines, should be used instead. In addition, haloperidol and risperidone may be useful adjuncts, either alone or in combination with benzodiazepines. As a general rule, intermittent dosing is preferred to continuous infusions. When the latter is used, the agent should be stopped at least once daily—giving the patient a so-called sedation holiday—to assess neurologic status and determine the need for continuing sedation.
Neuromuscular blocking agents add an additional level of patient control and can greatly simplify ventilatory management in patients with severe pulmonary insufficiency. These agents should be reserved for severe patient-ventilator dyssynchrony, a situation in which the patient’s spontaneous respiratory efforts result in discoordinated and inadequate ventilation by the mechanical ventilator. This may have the untoward effect of life-threatening hypoxemia in a patient with little physiologic reserve.
Nonphysiologic ventilatory methods, such as inverse ratio or high-frequency oscillatory ventilation, may also require the use of neuromuscular blocking agents. Major side effects include a potential increased risk of ventilator-associated pneumonia (VAP), through loss of cough mechanism, and an association with late polyneuromyopathy of critical illness. As a result, they should be used only when absolutely necessary and for the shortest possible time.
Antibiotics
Ventilator-associated pneumonia is the most common nosocomial infection in the ICU. The risk of acquiring VAP is directly related to the duration of mechanical ventilation. There is no gold standard for VAP diagnosis. Possible criteria include a new or progressive infiltrate on chest radiograph, worsening hypoxemia, increased sputum quantity, new onset of purulent sputum associated with abundant white cells and organisms on Gram-stained smears, or positive sputum cultures with known pathogenic organisms. Signs of systemic sepsis with increased temperature, leukocytosis, increasing fluid requirements, and glucose intolerance are also common findings in VAP.
If all of these are present, antibiotics should be started. If only one or two are present, antibiotics are probably best withheld to avoid overgrowth of resistant organisms that could later cause fatal pneumonia. Exceptions to this approach include older, severely debilitated patients, immunocompromised patients, and those who are critically ill in whom delayed antibiotic therapy might result in irretrievable deterioration. Thus, an 80-year-old patient with flail chest and a new infiltrate should probably be given antibiotics early; a 20-year-old patient who was hospitalized for a gunshot wound involving the colon and who develops questionable pneumonia 2 weeks later is more likely to tolerate a delay in the initiation of antibiotics until the diagnosis is more definite. In addition, the latter patient may have an alternative explanation for his fever and leukocytosis, such as an intra-abdominal abscess. In this case, the wrong diagnosis might delay appropriate source control (abscess drainage). The CPIS can be useful to guide the diagnosis. The goal is to avoid overtreatment with the risk of antimicrobial resistance and superinfection. Antibiotics can safely be discontinued in patients empirically started on antibiotics for suspected pneumonia who have a CPIS value of 6 or less at 72 hours.
King DR: Emergent cricothyroidotomy in the morbidly obese: a safe, no-visualization technique. J Trauma. 2011;71:1873-1874.
Graham DB, Eastman AL, Aldy KN, et al: Outcomes and long-term follow up after emergent cricothyroidotomy: is routine conversion to tracheostomy necessary? Am Surg. 2011;77: 1707-1711.
Barr J, Fraser GL, Puntillo K, et al: Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med. 2013;41: 263-306.
Schweickert WD, Pohlman MC, Pohlman AS, et al: Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomized controlled trial. Lancet. 2009;373:1874-1882.
TREATMENT OF THE MORE CHALLENGING PATIENT
This discussion of shock and pulmonary failure in the surgical patient has concentrated on making a clinical diagnosis and directing treatment on the basis of that diagnosis. This approach works well in many patients, but in some it is not sufficient. Effective treatment in the more seriously ill patient frequently has to take into account the underlying physiological abnormalities if the treatment is to work. With this approach, the clinical diagnosis becomes less important. Dealing with the underlying physiological problem becomes paramount.
COMMON PHYSIOLOGICAL RESPONSES TO SEVERE SHOCK
The body responds to the shock state with compensatory responses. These responses help the patient deal with the initial abnormalities of the shock but can contribute to the later consequences of cardiac and pulmonary failure. Understanding these responses can help the physician in managing the consequences.
Neurohumoral Responses
The neurohumoral responses to shock include discharge of the cardiovascular nerves and release of vasoactive, metabolically active, and volume-conserving hormones. The responses can be lifesaving before therapy begins and serve to maintain homeostasis once therapy has started.
Adrenergic discharge constricts the arterioles, venules, and small veins in all parts of the body except the brain and heart and augments myocardial systolic function. The result is increased cardiac output and blood pressure and diversion of flow to the brain and heart.
The vasoactive hormones angiotensin II and vasopressin act in concert with discharge of the cardiovascular adrenergic nerves. Angiotensin II constricts the vasculature in the skin, kidneys, and splanchnic organs and diverts blood flow to the heart and brain. It also stimulates the adrenal medulla to release aldosterone, resulting in reabsorption of sodium ions from the glomerular filtrate. Vasopressin, like adrenergic discharge and angiotensin II, constricts the vascular sphincters in the skin and splanchnic organs (it does not constrict the renal vasculature) and diverts blood flow to the heart and brain. It also stimulates reabsorption of water from the distal tubules.
Metabolic Responses
In all severe shock states, intracellular hydrogen ion concentrations increase. To compensate, extracellular sodium flows down its electrochemical gradient into the cells, along with chloride and water, in exchange for intracellular hydrogen ion. Intracellular pH increases back toward normal, but the cells swell, with perhaps an increase of 3 L in the intracellular volume.
Hypovolemia, hypotension, pain, and other stresses of critical illness stimulate the release of cortisol, glucagon, and epinephrine—all of which increase extracellular glucose concentrations. Thus, glucose should not be used in the initial fluid resuscitation of the patient in shock—it is not necessary and can even induce an osmotic diuresis, worsening hypovolemia and confusing the clinical picture. Glucose-containing solutions should be reserved for those patients who might be in insulin shock.
On the other hand, the endogenously produced glucose generated by the physiological release of the counter- regulatory hormones provides fuel for nervous system function, metabolism of blood cells, and wound healing. The modest increase in extracellular osmolality also helps replenish vascular volume by drawing water out of the cells and by increasing the interstitial hydrostatic pressure. The increased pressure drives interstitial protein into the lymphatics and from there into the vascular space. Interstitial oncotic pressure falls, and plasma oncotic pressure rises. The augmented oncotic gradient between the vascular and interstitial spaces draws water, sodium, and chloride into the vascular space from the interstitial space. This replenishment of vascular volume will continue as long as interstitial hydrostatic pressures are maintained and as long as interstitial protein stores, which constitute more than half of the total extracellular protein content, can be recruited. A certain degree of hyperglycemia might be beneficial in the postresuscitative phase. Once the patient has recovered, however, it appears that it is best to aggressively keep the blood glucose levels low, at 120 mg/dL or less.
Other hormones with potential metabolic actions, including insulin and growth hormone, are also released during critical illnesses. They have little effect, however, compared with cortisol, glucagon, and epinephrine. Indeed, infusion of cortisol, glucagon, and epinephrine in normal subjects can produce most of the metabolic changes of critical illness.
Microvascular Responses
In severely ill patients, three responses—dilation of systemic arterioles, failure of cell membrane function, and disruption of the vascular endothelium—serve to worsen the patient’s condition. In decompensated shock, the systemic arterioles lose their ability to constrict, while the postcapillary sphincters remain constricted. Microvascular hydrostatic pressure rises. Water, sodium, and chloride are driven out of the vascular space and into the interstitium. The process is limited, however, because the oncotic gradient, which increases as fluid is lost from plasma, prevents further fluid losses.
Trauma and sepsis activate coagulation and inflammation, which can disrupt microvascular endothelial integrity in severely ill patients. Platelet and white cell microaggregates that form in injured or infected tissues embolize to the lungs or liver, where they lodge in the microvasculature. The microaggregates, endothelium, and plasma in the regions of embolization release kinins, platelet-activating factors, fibrin degradation products, thromboxanes, prostacyclin, prostaglandins, complement, leukotrienes, lysosomal enzymes, oxygen radicals, and other toxic factors, which damage the endothelium and dilate the vasculature in the region of the emboli and distally. Protein, water, sodium, and chloride extravasate into the interstitium. The amount of extravasation is limited by the increases in interstitial hydrostatic pressure that arise from interstitial flooding and by dilution of interstitial protein concentrations. The edema that results can be massive and can involve any tissue in the body.
PULMONARY ARTERY CATHETER (SWAN-GANZ CATHETER)
The pulmonary arterial catheter can be useful in evaluating the cardiovascular consequences associated with the physiological responses described above, and it can be invaluable in directing treatment in selected, seriously ill patients. The modern pulmonary arterial catheter is equipped with a thermistor and an oximeter on its tip. It permits measurement of the cardiac output; right atrial, pulmonary arterial, and pulmonary arterial wedge pressures; and mixed venous oxygen contents. Knowledge of the cardiac output and filling pressures can be used to assess ventricular function as fluid is administered or withheld. The mixed venous oxygen saturation reflects the adequacy of oxygen delivery to the periphery; a value less than 60% indicates inadequate peripheral oxygenation and can be used to evaluate adequacy of the cardiac output and of systemic arterial oxygen content. It can also be used to determine oxygen consumption, which is calculated as the cardiac output multiplied by the difference of the oxygen contents of blood in the systemic and pulmonary arteries. Oxygen consumption can fall in severely ill patients, and measurements of consumption can help assess the patient’s response to resuscitation. All of this information can help in dealing with the physiological abnormalities of the shock state and the pulmonary failure that can arise from the shock.
The catheter is particularly useful when treatment of one organ system might harm another. For example, fluid administration might be needed to treat septic shock, but excess fluid might contribute to pulmonary failure; a diuretic might be indicated in an oliguric patient in congestive heart failure, but excessive diuresis might decrease the cardiac output to the point that the kidneys fail; and fluid might be needed for cardiovascular resuscitation in a patient with multiple injuries, but too much fluid might exacerbate cerebral edema. The pulmonary arterial catheter can be extremely helpful in these situations.
Data obtained from the Swan-Ganz catheter can be misleading, however, if mistakes are made in performing the measurements. The cardiac output, as measured by thermodilution, is obtained by creating a temperature differential in the blood in the right atrium and analyzing the change in temperature in the blood over time as it flows past a thermistor on the end of the pulmonary arterial catheter. The greater the area under the temperature curve, the smaller the flow through the right heart. If injections of cold saline are used to create the temperature differential, they should be made at random times during the respiratory cycle to give the best indication of the output available to the patient, but some prefer to make the injections at a consistent time in the cycle to minimize variability in the cardiac output–associated heart-lung interactions. If a heater coil in the catheter is used to create the temperature differential, the changes are made randomly by a program in the equipment used with the catheter. All calculations are made by a computer in the equipment.
When one is obtaining pulmonary arterial or mixed venous blood, the balloon on the end of the catheter should be deflated, and the blood should be withdrawn slowly. If the blood is withdrawn too quickly, the walls of the pulmonary artery will collapse around the end of the catheter, and the specimen will be contaminated by blood that is pulled back, in a retrograde manner, past ventilated and nonperfused alveoli. The oximeter on the tip of the catheter has to be calibrated frequently by comparing the oxygen saturations of blood obtained from the pulmonary artery with the saturations readout by the oximeter. One must be certain that the blood that is to be used for calibration is truly representative.
The pressures measured with the pulmonary arterial catheter are displayed on an oscilloscope and include a mean pressure that is calculated by computer circuitry in the monitoring equipment. These mean pressures can be used in patient management. They have the advantage that they represent the pressures throughout the respiratory cycle and thus average in the variability associated with heart-lung interactions. Some clinicians prefer to read the end-expiratory pressures from the oscilloscope screen and use those values in patient management. Those pressures are relatively independent of heart-lung interactions, but they can be difficult to interpret, even by the most experienced ICU nurse or physician.
Of the five pressures obtained from the catheter, only two—the right atrial and the mean pulmonary arterial pressures—can be taken at face value; the other three—the pulmonary arterial systolic, diastolic, and wedge pressures—are subject to errors of measurement and interpretation. The pulmonary arterial wedge pressure usually is the same as the left atrial pressure. The wedge pressure will not reflect left atrial pressure; however, if the catheter is in a portion of the vasculature occluded by inflated alveoli. If the wedge pressure varies by more than 10 mm Hg with cycles of mechanical ventilation, one should assume that the tip of the catheter is facing the pressure in the alveoli rather than the pressure in the left atrium.
To account for variations in size of the patient, the cardiac output can be indexed to the calculated body surface area. Alternatively, however, one can use the patient’s desirable body weight, calculated on the assumption that a desirable weight is one that is associated with longevity and freedom from diabetes. A body mass index (BMI) of 21 is convenient to use for both men and women. Making a rough approximation of the patient’s height, to the nearest half-foot, the desirable weights associated with that height, assuming a BMI of 21, are indicated in Table 12–3. The cardiac outputs associated with that weight are also indicated, assuming that the subjects are supine, nonstressed, resting, fasting, and in a thermoneutral environment. The resting oxygen consumptions under these conditions are
Table 12–3. Approximate desirable weight, cardiac output, and oxygen consumption in young resting, supine, fasting individuals of varying heights, in a thermoneutral environment.
3.5 mL × weight (−1) × min (−1)
The outputs and the consumptions for patients older than 50 years are adjusted with the assumption that metabolic activity decreases by 10% per decade after age 50. Thus, for a 70-year-old person who is 6 feet tall, a normal cardiac output is 7 L/min multiplied by 0.8, or 5.6 L/min. The oxygen consumption is 245 mL/min multiplied by 0.8 or 195 mL/min.
OXYHEMOGLOBIN DISSOCIATION
The amount of oxygen contained in the blood and the amount of oxygen available to be delivered to the tissues can be expressed as a concentration, a saturation, or a partial pressure. All three have their value. Understanding their relationships can help in understanding the cardiac and pulmonary pathophysiology of the critically ill surgical patient.
The concentration of oxygen in the blood, or oxygen content, is expressed as milliliters of O2/dL of blood, or vol%. The oxygen content can be measured directly, but the measurement is time consuming, and the content is usually calculated on the basis of the other two measures of blood oxygenation, the oxygen saturation (So2) and the Po2. The oxygen content is related to these other quantities by the following formula:
where [Hb] is expressed as g/dL and the Po2 as mm Hg.
Thus, for example, the oxygen content of a blood specimen with a [Hb] of 12 g/dL, an So2 of 90%, and a Po2 of 60 mm Hg is 14.7 vol%.
The first term in the equation represents the O2 carried by the hemoglobin molecule; the second, the O2 dissolved in the blood water. This second term is small compared with the first as long as the [Hb] is greater than, say, 7 g/dL and the Po2 is less than, say, 100 mm Hg. Omitting the second term then simplifies the formula to read as follows:
For the previous set of blood gases, this would give a Co2 of 14.5 vol%.
The formula can be made even simpler by substituting the fraction 4/3 for the decimal 1.34:
Because [Hb] and the So2 can usually be approximated by integers with little loss of accuracy, the calculation frequently allows cancellation of the three and can be done mentally. For the previous example, the oxygen content would be 14.4 vol%.
Calculation of the oxygen content requires knowledge of the So2. Many pulmonary arterial catheters are now equipped with sensors mounted on their tips that directly measure the saturation of the blood in the pulmonary artery. Alternatively, blood can be withdrawn from the tip of the catheter and sent to the laboratory, where the So2 can be easily measured by an instrument known as a co-oximeter. Most laboratories will make this measurement by specific request, but some will calculate the So2 from the Po2. This calculation is frequently inaccurate for mixed venous specimens but is usually accurate for arterial blood. The calculation is made from equations that are based on the oxyhemoglobin dissociation curve (Figure 12–1), an empirically derived relationship between the So2 of nonfetal human blood and its Po2. The saturation for a given Po2 depends on blood temperature, [H+], and Pco2 and on the red cell concentration of 2,3-diphosphoglycerate (2,3-DPG). The laboratory should be told the temperature, and it will measure the [H+] and Pco2. It will then calculate the So2 from the Po2 with the assumption that the 2,3-DPG concentration is normal.
Figure 12–1. Oxyhemoglobin dissociation curve for human blood at 37°C with a Pco2 of 40 mm Hg, a pH of 7.40, and a normal 2,3-DPG red cell concentration. Approximate values from Table 12–4 fall close to the idealized curve.
Table 12–4. Approximate correlations for partial pressures of oxygen and oxygen saturation in blood at 37°C with a pH of 7.4, a Pco2 of 40 mm Hg, and a normal 2,3-DPG red cell concentration.
It is helpful, however, to have some guidelines for converting back and forth between So2 and Po2. Five approximations for points on the dissociation curve for a patient with normal temperature, [H+], Pco2, and 2,3-DPG levels are given in Table 12–4. The P50 of human hemoglobin—the Po2 at which the molecule is half-saturated—is 27 mm Hg (approximated as 25 mm Hg in the table). The Po2 and So2for mixed venous blood in a person with a [Hb] of 15 g/dL and a normal O2 consumption and cardiac output are 40 mm Hg and 75%, respectively. A Po2 of 60 mm Hg—a value that should be exceeded by most patients in an ICU—corresponds to a So2 of 90%. A Po2 of 80 mm Hg corresponds to a So2 of 95%. Remembering the values in the table allows construction of a dissociation curve and facilitates conversion from one measure of oxygenation to the other. For example, in a patient with a normal temperature, [H+], Pco2, and 2,3-DPG, and a [Hb] of 10 g/dL, a Po2 of 60 mm Hg in the systemic arterial blood would create an oxygen content of 12 vol% (from Equation 1), a value that would be adequate if the patient had normal coronary arteries and a good heart. Such a value would be inadequate, however, in the face of underlying heart disease.
CAUSES OF ELEVATED PaCO2
The patient in pulmonary failure will frequently have an elevated arterial carbon dioxide tension. The arterial Pco2 is proportionate to CO2 production divided by alveolar ventilation—defined as the volume of air exchanged per unit time in functioning alveoli. Since CO2 production is usually fairly constant in adequately perfused patients, the Paco2 comes to be inversely proportionate to alveolar ventilation. An elevated Paco2 in the presence of normal CO2 production means inadequate alveolar ventilation. Ventilation should be assessed with respect to how much work is required to generate the Paco2. In the case of spontaneous ventilation, this assessment involves the frequency and depth of breathing; in the case of mechanical ventilation, the frequency of the machine-generated breaths and the tidal volume of those breaths.
The Paco2 also gives an indication of dead space ventilation—the ventilation of nonperfused airways. Since minute or total ventilation is dead space ventilation plus alveolar ventilation, a normal Paco2combined with a normal minute ventilation implies a normal dead space ventilation. A normal Paco2 that must be generated by a supranormal minute ventilation implies increased dead space ventilation. Normal dead space ventilation is one-third of total ventilation, but many critically ill surgical patients will have dead space ventilation that is up to two-thirds of total ventilation. Increased dead space ventilation can be caused by hypovolemia with poor perfusion of nondependent alveoli, ARDS, pulmonary emboli, pulmonary vasoconstriction, and mechanical ventilation-induced compression of the pulmonary vasculature. Hypovolemia should be treated by expansion of the vascular volume. Emboli should be treated by anticoagulation or by elimination of their source. Dead space generated by mechanical ventilation should be minimized by adjustment of the ventilator, usually by decreasing tidal volumes or end-expiratory pressures, while at the same time maintaining enough mechanical support to generate a normal Pco2 and alveolar ventilation.
CAUSES OF LOW PaO2
Almost all surgical patients with pulmonary failure will have systemic arterial hypoxemia. There are five physiological causes: low inspired O2 concentration, diffusion block between alveolar gas and capillary blood, subnormal alveolar ventilation, shunting of blood through completely nonventilated portions of the lung or bypassing of blood past the lung, and perfusion of parts of the lung that have low ventilation/perfusion ratios. In addition, any process that decreases the mixed venous oxygen content in the presence of any of the above can lower the arterial Po2 even further. Low mixed venous oxygen content can be caused by a low arterial oxygen content, low cardiac output, or high O2 consumption.
Arterial hypoxemia in the surgical patient is usually caused by shunting, low ventilation/perfusion ratios, low mixed venous oxygen content, or a combination of these factors. Low inspired O2concentrations at sea level are impossible so long as the ventilator is functioning properly. (This must be checked, however, as the first step in diagnosing and correcting the cause of a low PaO2.) Diffusion block is exceedingly rare in surgical patients. Subnormal alveolar ventilation can be ruled out with a normal arterial Pco2 assuming CO2 production is not depressed. Thus, shunting and areas of low ventilation/perfusion ratios, along with low mixed venous oxygen content, remain as causes for almost all cases of hypoxemia in the surgical patient. Shunting and low ventilation/perfusion ratios do not need to be distinguished from each other very often, but the distinction can be made by increasing the inspired O2 concentration to 100%: Hypoxemia caused by areas of low ventilation/perfusion ratios will be at least partially corrected by 100% O2; hypoxemia caused by shunting will not. The mixed venous oxygen content can be measured with the pulmonary arterial catheter.
ACID-BASE BALANCE
Acid-base abnormalities can arise from the hypoventilation of pulmonary insufficiency or from the metabolic abnormalities of shock. The former has already been discussed. The latter can become more involved.
The hydrogen ion, carbon dioxide gas, and bicarbonate equilibrate with one another in the plasma water, and if two of the quantities are known, the third can be calculated. In practice, the Pco2 and [H+], which are measured directly with the blood gas apparatus, will be known. The [HCo3−] can then be calculated by the Henderson-Hasselbalch equation, which can be written in the following form:
where [HCo3−] is expressed as mmol/L, Pco2 as mm Hg, and [H+] as nmol/L. This form of the equation requires conversion of pH, the more common expression of [H+], into nmol/L, the more logical expression, but the conversion is not difficult (Table 12–5). The values in the table are easy to remember if one notes that each value in the column under [H+] is 80% of the value immediately above, with the exception of 80 and 63, which are off by 1. Thus, by Equation 4, if the Pco2 is 60 mm Hg and the pH is 7.30, the [HCO3−] is 29 mmol/L.
Table 12–5. Conversion of pH to hydrogen ion concentration.
The [HCO3−] calculated by this equation is the amount of bicarbonate ion dissolved in the plasma water and can be obtained only from a specimen of blood that is obtained and processed without exposure to the atmosphere. The “CO2 combining power” that is typically measured along with electrolyte concentrations in blood that is not processed anaerobically includes not only the [HCO3−] but any CO2 gas and carbonic acid that is dissolved in the plasma as well. The CO2 combining power is usually about 2 mmol/L greater than the calculated (and actual) [HCO3−].
The base deficit or excess is determined by comparing the calculated [HCO3−] with the [HCO3−] that might be expected in a patient with a given Pco2 and [H+]. These expected values have been determined by analyzing blood obtained from patients with a wide variety of pulmonary disorders. For example, the kidneys in a patient with chronic respiratory acidemia can usually compensate to the extent that a chronic elevation in Pco2 of 10 mm Hg will generate an increase in [HCO3−] of 3 mmol/L. A patient with chronic obstructive lung disease and a chronically elevated Pco2 of 60 mm Hg would be expected to have a [HCO3−] of 30 mmol/L—6 mmol/L more than a normal value of 24. If such a patient had a pH of 7.30, the actual [HCO3−] would be 29 mmol/L (from Equation 4; see the example in the preceding paragraph). That is, the observed value would be 1 mmol/L less than predicted, and the patient would be said to have a base deficit of 1 mmol/L.
The difficulty with the concept of base deficit and excess is that it rests on historically determined values, which may not be applicable to the patient at hand. For example, if a surgical patient with previously normal lungs lost his or her airway after an operation and began to hypoventilate, one would expect the [HCO3−] to be normal—24 mmol/L—because the kidneys would not have had time to compensate for the hypercapnia. If the Pco2 was 60 mm Hg and the pH 7.30, the physician should be concerned because the [HCO3−] is 29 mmol/L (these values are the same as in the preceding paragraphs). A value of 29 mmol/L should alert the physician to the fact that the [HCO3−] is too high, perhaps because NaHco3 had been given unnecessarily. The base deficit, however, would be 1 mmol/L, suggesting that the patient’s [HCO3−] was appropriate. The base deficit would be misleading.
The use of base deficit and excess is ensconced in the literature, and the terms are used in this chapter. However, the concept of [HCO3−] may be preferable. Errors in patient evaluation are more likely to be minimized if the physician interprets that value in the light of a particular patient’s situation. If a chronically ill patient in the ICU has severe ARDS and a Pco2 of 60 mm Hg with a pH of 7.30, no attempt should be made to change the accompanying [HCO3−] of 29 mmol/L—that value represents the expected renal compensation for such a chronic hypercapnia (though the impaired alveolar ventilation should be of concern). Alternatively, if the patient’s Pco2 is 60 mm Hg and the pH is 7.45, the patient has an inappropriately high [HCO3−] of approximately 40 mmol/L (calculated from Equation 4), perhaps because of unreplaced losses of hydrogen ion from the stomach, chronic use of a loop diuretic, or administration of excessive amounts of acetate in the patient’s parenteral nutrition. In this situation, the [HCO3−] should be brought down into the low 30s. The excessively high [HCO3−] and its resultant alkalemia may be blunting the patient’s ventilatory drive.
Thus, in dealing with acid-base disorders, the calculation of the bicarbonate concentration in arterial plasma can be taken from the blood gas laboratory or calculated by the clinician. In the case of a metabolic acidemia, the underlying abnormality should be corrected and then, if the pH remains less than 7.20, sodium bicarbonate can be used, but only after resuscitation has been initiated and only with the intent of bringing the pH up to a modestly higher level, such as a pH of 7.30. The bicarbonate produces carbon dioxide and water locally, in the interstitial fluid at the sites where the hydrogen ions are being produced. In the absence of resuscitation, the locally generated carbon dioxide can cross back into the cell, worsening intracellular acidosis. There is no problem with bicarbonate if it is given after some local flow has been achieved. The generated carbon dioxide will be washed centrally into the pulmonary vasculature, where it will be eliminated by the lungs.
Metabolic alkalemia in the surgical patient is usually easy to recognize and treat. Contraction alkalemia is treated with fluid expansion. Hypokalemic, hypochloremic metabolic alkalemia caused by unreplaced loss of gastric fluid (continuous nasogastric suction or protracted vomiting), is treated with normal saline supplemented with potassium chloride. Hypokalemic hypochloremic alkalemia caused by use of loop diuretics is treated by withholding diuresis. In situations where continued diuresis is warranted, the addition of acetazolamide to the diuretic regimen is helpful. Although the administration of 0.1 N hydrochloric acid can reverse severe alkalemia, it is rarely necessary and should only be given as a slow central intravenous drip over a period of 48 hours. The amount of acid to be given is calculated on the basis of the presumed extracellular chloride deficit, with the assumption that the interstitial chloride concentration is the same as the plasma concentration, that is, with the assumption that the Donnan factor for chloride is 1.
RISK ASSESSMENT
Predicting the likelihood of survival in critically ill surgical patients is best accomplished by evaluating clinical and laboratory findings. Computation of a severity of illness score is usually unnecessary. Nonetheless, several scoring systems have been developed with the intention of increasing the precision of the estimate. All such systems assign a mathematical probability for survival in groups of patients, and many are useful for research purposes because they allow comparisons of patients among different institutions. None of them, however, are accurate enough to predict survival for an individual patient, though some are still clinically useful for assessing the effects of therapy.
The APACHE II score, in which clinical data and 14 measured variables are entered into a formula to assess the probability of survival, takes about 30 minutes to calculate by hand—less by computer. The score can predict survival in critically ill medical patients; it has not been found to be of value in the usual surgical patient, and in any case, it is too cumbersome unless one has a particular interest in this kind of methodology.
Methods for predicting survival in trauma patients are well established, though most trauma systems are designed to evaluate all trauma patients and not the specific subset of critically ill trauma patients. The Injury Severity Score, the Revised Trauma Score, and the ASCOT score have proved to be most reliable. The Glasgow Coma Score is quite accurate for predicting survival in patients with head injuries. Combining the Glasgow Coma Score with a simple measurement of fluid requirement has also proved to be accurate in critically injured trauma patients.
MULTIPLE CHOICE QUESTIONS