Care of the Patient With a Critical Illness Wally Gordon, MD, FRCS (Edin.), FRCS (Eng.) Norfolk, Virginia
A method of care applicable to all forms of critical illness is presented. A patient is considered to be critically ill when he is threatened with hypoxia. According to this concept, procedures to understand and solve problems of critical care are coordinated and unified. The relevant physiology and monitoring of the components of the oxygenating system are described. The treatment of patients with impaired function of these components is described. Scheme Care of the patient with a lifethreatening illness may be complicated and is frequently urgent. Without procedural guidelines for understanding and solving problems, chaos and confusion, detrimental to the patient, can result. Most critically ill patients are hypoxic, or are suffering from the effects of hypoxia not necessarily still present, or are threatened with hypoxia. Restoration of oxygenation of the brain within a few minutes is the top priority in critical care; but all steps in the management of a patient's serious illness are taken in order to restore or maintain oxygenation of tissue cells. To obtain this objective, the components of the oxygenation mechanism must be appreciated and the adequacy of their function assessed.1 They load, contain, deliver, and unload oxygen. Each of these four functions will be considered under the headings Physiology, Monitors, and Treatment (of deranged physiology). This scheme is summarized in Figure 1. The monitoring of the oxygenating system, and the actions which such monitoring provokes, constitute critical care.
Load Physiology Nerve and muscle actions suck gases through the conduction zone into the diffusion zone. There the inhaled gases and the blood gases are tranferred, respectively, to and from the blood, according to the simple physical laws of gases. The exhalation of alveolar gas may be either passive or forcible. Requests for reprints should be addressed to Dr. Wally Gordon, Department of Surgery, United States Public Health Service Hospital, 6500 Hampton Boulevard, Norfolk, Va 23508
Monitors Clinical and x-ray signs may reveal a flail chest wall, depressed neuromuscular activity, or an obstructed airway. The concentration of inhaled oxygen (FIO2) is obviously an important factor determining the pressure of oxygen in the alveoli (PAO2). The pressure of carbon dioxide in the arterial blood (PaCO2) indicates the adequacy of ventilation. The pressure of oxygen in the arterial blood (PaO2) reflects the PAO2 and the fraction of the cardiac output which is by-passing normally functioning alveoli (the shunt). The difference between PAO2 and PaO2 is the alveolar arterial oxygen gradient (A-aO2 gradient, normal 4 to 10 torr with FIG2 0.2, 80 to 100 torr with FIO2 1.0).
Treatment Any airway obstruction must be relieved immediately. It may be necessary to perform cricothyroidostomy or tracheostomy. Ventilate the apneic patient artifically. If the patient is unconscious, insert a cuffed endotracheal tube to diminish the chance of inhaling oropharyngeal secretions or vomitus. The administration of antispasmodics, antibiotics, and removal of secretions via bronchoscope or tracheostome may improve ventilation. If PaCO2 is less than 50 torr, but PaO2 is inadequate (see Unload, Treat-
ment), deliver 60 percent oxygen (FIO2 0.6), through a well-fitting mask. When PaO2 remains inadequate on FIG2 0.6, start mechanical ventilation with a volume-controlled ventilator. If PaCO2 is more than 50 torr, begin mechanical ventilation, unless
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 69, NO. 3, 1977
the patient has chronic lung disease with persistently high PaCO2 and adequate PaO2. Ventilate an adult at ten strokes per minute with tidal or stroke volume at 12 ml/kg body weight. Provide an infant with the required volume of oxygen by ventilating 20 times per minute. Doubling the stroke volume in an infant would cause unwanted high intrathoracic pressures. Begin ventilation with the FIO2 level at least 0.4, and adjust the stroke volume and FIG2, in the following manner. Increase the stroke volume by 100 ml of gas and measure PaO2, 30 minutes after each increment. When PaO2 shows no further improvement, no advantage is gained from further increases in stroke volume. At this point, FIO2 must be increased or decreased, until PaO2 is adequate. This can be done by trial and error. Alternatively, following the measurement of PaO2, the shunt value can be obtained from a nomogram which will also show the FIO2 level required to attain the desired PaO2 with that particular shunt.2 With resting oxygen consumption, normal cardiac output, FIO2 at 1.0 and PaO2 at more than 150 torr, a shunt of one percent, in addition to the normal four percent, may be assumed for every 20 torr below a PaO2 of 600 torr. Shunting may be improved by positive-end expiratory pressure (PEEP), applied in increments of 5 cm up to 15 cm H2G. Since oxygen inhaled at a pressure of more than 400 torr (FIG2 0.6 at a pressure of 1 atmosphere) may damage the lungs3 consider applying PEEP, when an FIO2 of 0.6 at sea level does not maintain adequate PaO2. At higher altitudes, proportionately higher concentrations of oxygen are safe. PEEP may aggravate shunting and may reduce cardiac output. If the necessarily large stroke volumes produce hypocarbia, the PaCO2 level may be raised by slowing the ventilator or increasing dead space with a tube inserted between the Y-piece of the ventilator and the endo-
tracheal tube. Perform mechanical ventilation of 155
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Contain Physiology Almost all of the oxygen of the blood is loosely combined with hemoglobin within the red blood cells. Only 0.3 ml oxygen is dissolved in each 100 ml plasma when the tension is 100
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of ventilation. When it is not required for mechanical ventilation or airway toilet, remove the endotracheal tube, as 40 percent oxygen can be easily delivered by mask.
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Oxygen content of blood can be calculated from a well-known equation: (SaO2 x Hb x 1.39) +PO2 x 0.0031 Study of blood coagulation factors may reveal the derangement causing bleeding.
...................
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OXYSEIATING SYSTEM
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. COMPONENTS OF THE :OXY6ENNING SYSTEM s
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PNYSIELOGY
Figure 1. Summary of the Scheme on Care of the Critically Ill Patient
the lungs via a translaryngeal tube, unless a primary tracheostomy has been made because the translaryngeal tube cannot be passed. The inability to cope with secretions via the translaryngeal tube (a situation which is unusual in units with expert nursing personnel) is the only clear indication for tracheostomy. An arbitrary time period, during which the translaryngeal tube is in position, is not an indication to change to a tracheostomy tube. The author has retained translaryngeal nasotracheal or orotracheal tubes in patients for 30 days and laryngoscopic, bronchoscopic, and necropsy studies did not show significant lesions due to the tube. Unless the patient is apneic, assist the ventilation rather than control it. With proper adjustment, the machine is well-tolerated and muscle 156
Treatmen t Bleeding must be stopped ......... ._ by..direct
relaxants are rarely necessary. When the concentration of oxygen in the ventilating gas has been reduced to 40 percent, disconnect the patient from the ventilator and maintain the desired FIO2 through a T-piece attached to the endotracheal tube. If the patient's spontaneous ventilation rate is more than 30 breaths per minute, at any time during the next four hours, reconnect the ventilator to prevent exhausting the patient. Exhaustion is unlikely to develop later, in a patient who has been comfortable for four hours. This test should not be made in a patient who is under the influence of sedative or analgesic drugs. In the unconscious patient, measurement of tidal and minute volume may be a better indication of the need for continued mechanical ventilation. A rising PaCO2 level confirms the inadequacy
ligation. Treat the hypovolemia following hemorrhage by infusion of liquid (see Deliver, Treatment). Regulate the amount of red cells transfused, by serial estimations of hematocrit reading. Maintain the hematocrit value at 33 or higher if hemoglobin saturation is less than 70 percent (see Unload, Treatment). Replace the hemoglobin with cross-matched red cells, so-that the components of the unnecessary plasma can be stored for use in patients who need specific factors. Transfuse platelets when their count is less than 20,000/ml blood. In disseminated intravascular coagulation, treat the primary cause which may be obstetric, bacterial, toxic, or hemolytic. Administer heparin (700 units/kg body weight during the first 24 hours) by continuous intravenous infusion, following a loading dose of 7,000 units, and continue until the levels of fibrin-split products are normal.4 If the patient requires red cells, transfuse with fresh whole blood, which will supply coagulation components.
Deliver Physiology Heart: The stroke volume depends on preload, which is a stretching force,
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 69, NO. 3, 1977
afterload, which is a force resisting shortening, and contractility, which is the capacity of heart muscle fibers to shorten in response to an adequate stimulus. Plasma: Stroke volume falls when vasoconstriction, compensating for a reduced circulating blood volume, reaches its limit. Heart rate must increase to maintain blood flow. Plasma albumin maintains an osmotic pressure gradient between the intravascular and extravascular spaces. Sodium is a most important factor in regulating the volume and distribution of body water. Blood vessels: Reduction in cardiac output, circulating blood volume, or oxygen content causes constriction of small blood vessels which may lead to irreversible tissue damage.
Monitors Heart: Pulmonary wedge pressure or pulmonary artery diastolic pressure, as measured with a balloon-tipped catheter,5 reflects the mean left atrial pressure representing the preload of the left ventricle. The mean right atrial or central venous pressure reflects the
preload of the right ventricle. Usually, measurement of myocardial contractility is difficult. Afterload is estimated by dividing the systemic or pulmonary arterial pressure, by the cardiac output. Cardiac output may be measured by invasive and non-invasive methods. The heart may fail as a pump because of myocardial infarction, tamponade, dysrhythmia, or severe non-cardiogenic shock; conditions which are revealed by electrocardiograph, chest x-rays, and clinical signs. Plasma: In order to guide maintenance and the replacement of extracellular liquid, measure the intake and output of water and electrolytes. Plasma or serum osmolality (normal 285 mOsm/kg H2 0) reflects changes in the solute or solvent in the extravascular space. Urine osmolality (normally greater than serum osmolality) reflects the urine concentration and dilution which are the functions of renal tubules. Blood vessels: Blood vessel caliber is not measured directly, but blood flow can be measured in some organs by methods often considered impractical and may be judged clinically in the brain, heart, kidney, and skin.
Table 1. Laboratory Results in Oliguria Low Perfusion
Intrinsic Lesion
U/P osmolality
more than 2/1
less than 1.1/1
U/P creatinine conc.
more than 40/1
less than 10/1
U/P urea nitrogen conc.
more than 20/1
less than 10/1
Urinary sodium conc.
less than 20mEq/liter
more than 40mEq/liter
U/P = urine/plasma ratio
Whole body oxygen consumption is a good indication of perfusion in general.
Treatment Heart: If the circulation is arrested, start conventional cardiopulmonary maneuvers for resuscitation.6 If the electrocardiogram shows cardiac arrest, inject 1 mg of epinephrine in 10 ml of saline, intravenously, or directly into the heart every five minutes. Defibrillate immediately when ventricular fibrillation is present, when it is uncertain if fibrillation or standstill exists, and when ventricular tachycardia is present without a pulse. If external cardiac compression is ineffective, or if pneumothorax, or cardiac tamponade is present, perform thoracotomy and internal cardiac compression immediately. Treat cardiac tamponade by immediate aspiration of the pericardial effusion. This is likely to be followed by surgery especially in traumatic cases. Manage dysrhythmia by correction of the blood gas abnormality, and with drugs, or electrically.7 Plasma: To increase the preload, administer an intravenous, isotonic, crystalloid solution. Add 25 percent human serum albumin to maintain adequate plasma osmotic pressure for better retention of liquid within the intravascular space. Continue this treatment of hypovolemia until the pulmonary wedge pressure or the pulmonary artery diastolic pressure is 15 torr, or the central venous pressure (which does not correlate with left atrial pressure) is 15 torr, or 20 cm saline. Lower pressures are acceptable, if the urine flow rate is more than 30 ml per hour. Pressures above these levels do not seem to produce any further increase in stroke volume.8 If there is concern over the ability of the
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 69, NO. 3, 1977
heart to handle the increased preload, this capacity can be checked by a challenge of 200 ml of liquid given intravenously in ten minutes, with further challenges controlled by the level of intravascular pressures.9 The burned patient loses liquid and protein into the interstitial space and from the burn surface. Give colloid solution (1 ml/kg body weight x % body surface burn), and the same volume of balanced electrolyte solution and five percent dextrose in water (30 ml/kg of body weight), in the first 24 hours following the burn. Give half this volume intravenously in the first eight hours, and the remainder in the next 16 hours. Subsequent management should be according to the parameters described above. Calculate the area of body surface burned from a chart which considers the patient's
age.10 The crystalloid or colloid solutions which are used in the replacement and maintenance of plasma volume should contain the 150 gm of glucose required daily by the brain. If the patient cannot take an oral diet after five days, more carbohydrates, amino acids, fats, minerals, and vitamins should be added to the intravenous solutions. Control the nutrition therapy, by using an easily calculated nitrogen balance. Blood vessels: The undesirable effects of vasoconstriction may be diminished by maintaining adequate circulating blood volume, as described above. When angiography shows reduced intracranial perfusion, surgical relief of vascular occlusion should be considered, especially in a patient with a head injury. In myocardial infarction, with reduced cardiac output, expect little improvement from further stimulation of undamaged muscle, but some bene157
fit may be obtained from reduction in preload and afterload by diuretic and vasodilator drugs. Direct coronary artery surgery may be indicated. Perfusion of lung vessels may be reduced by embolism, disseminated intravascular coagulation, and left ventricular failure. Treat pulmonary embolism with heparin, 500 units/kg of body weight, spread over 24 hours and given intravenously for ten days. Heparin therapy should be preceded and controlled by tests of the coagulation and partial thromboplastin times. Maintain the coagulation time at about 30 minutes.1 1 Hypoxemia may require that oxygen and mechanical ventilation be used. Surgical occlusion of the inferior vena cava should be considered, when embolism continues in the presence of adequate anticoagulation or bleeding. Treatment of disseminated intravascular coagulation and of left ventricular failure are described above. Maintain urine flow at more than 30 ml per hour by increasing the preload. Oliguria may be due to poor perfusion or to an intrinsic lesion of the kidney. Table 1 indicates how one may be distinguished from the other. Elevation of blood urea nitrogen and creatinine, which may be present with polyuria or oliguria, confirms the inability of the kidney to excrete waste products. Assuming that plasma volume and albumin concentration are normal and diuretics have failed, treat the oliguric stage of intrinsic renal failure by restricting water intake to 6 ml/kg of body weight per 24 hours (plus water equal in volume to other losses) and by reducing daily protein intake to 0.5 gm/kg of body weight. If it is available, dialysis can be started early, without any restrictions in diet.12 In the presence of hypercatabolism (blood urea rising by more than 60 mg percent per day), dialysis is urgently required. The problem of providing adequate nourishment in a small volume might be solved by intravenous
feeding. In addition to being caused by poor perfusion and intrinsic lesions of the kidney, cessation of urine flow may be due to obstruction of the urinary tract. Such a cause of "renal" failure can be revealed by excretion urography, cystoscopy, and by retrograde catheterization of the ureters and radiography. 158
Unload Physiology Increased temperature, hydrogen ion concentration of the blood, and concentration of 2,3,DPG in red blood cells all assist in the unloading of oxygen. A pressure gradient drives oxygen, released from hemoglobin, through the plasma and extracellular space into the mitochondria of the tissue cells. The minimal effective PaO2 level is about 26 torr, a pressure at which hemoglobin is 50 percent saturated. Since the normal average volume of oxygen extracted from 100 ml of blood is 5 ml, the oxygen content of each 100 ml blood flowing at the normal rate should be at least 10 ml.
Monitors The PO2 of a tissue and the PO2 of plasma at the venous end of the related capillary are in equilibrium, The tension of oxygen in mixed venous blood (mixed PvO2, normal 40 torr) is usually a valuable indication of the degree of tissue oxygenation in general. When oxygenation is inadequate, lactate is present in the blood in excess of that expected from the pyruvate concentration. The usual cause of a non-respiratory acidemia is hypoxia, which excess lactate (XL) would confirm.
Treatment Adjust ventilation with the appropriate concentration of oxygen to produce a PaO2 level sufficient to load and unload the required volume of oxygen. If the hematocrit value is 45, a PaO2 of 26 torr will provide an adequate volume of oxygen. If the hematocrit is 30, a PaO2 of 40 torr is necessary. If the hematocrit reading is 24, sufficient oxygen will be available to the tissues only when PaO2 level is 100. At normal flow rates, the myocardium extracts 11.5 ml of oxygen, more than any other organ, from each 100 ml of blood. If oxygen content is inadequate, the oxygen demand is met by an increase in coronary blood flow. As this might be difficult in a seriously ill patient, especially in one with coronary artery lesions, it is safer to maintain hematocrit at 33, if PaO2 is more than 90 torr, or at proportionally more than 33, depending on the PaO2.
If oxygen content is dangerously low, use only fresh blood which has a high concentration of 2,3,DPG, and will release oxygen easily. In an emergency, it is probably best not to lower the concentration of hydrogen ions because acidemia facilitates the release of oxygen. An increased concentration of hydrogen ions may prevent production of 2,3,DPG, but improved oxygenation reduces acidemia and fresh erythrocytes may become available. To increase the volume of available oxygen through improved tissue perfusion, maintain heart contractility and preload (adequate circulating blood volume) and reduce the afterload
(vasodilatation). In cases of septic shock and in the newborn, oxygen is prevented from reaching cells and mixed PvO2 is high. The cause of this derangement is uncertain, but the hypoxia of septic shock may be diminished by massive antibiotic therapy, drainage of collections of pus, and hysterectomy. When unloading cannot be increased to provide an adequate volume of oxygen, consider reducing oxygen demand by hypothermia. For coma, following arrest of the circulation, induce hypothermia immediately to reduce brain damage, brain edema, and hyperpyrexia. Literature Cited 1. Finch CA, Lenfant C: Oxygen transport in man. N Engl J Med 286:407-415, 1972 2. Bednarek J, Matsumoto T: Diagnosing and treating shock lung. Hospital Physician, September:66-73, 1974 3. Hedley-Whyte J, Winter PM: Oxygen therapy. Clin Pharmacol Ther
8:696-737, 1967 4. Bull BS: Disseminated intravascular coagulation. In Weil MH, Shubin H (eds): Critical Care Medicine Handbook. New York, 1974, p 351 5. Swan AJC, Ganz W, Forrester J, et al: Catheterization of the heart in man with the use of a flow-directed balloon-tipped catheter. N EngI J Med 283:447-451, 1970 6. Gordon AS: Standards for cardiopulmonary resuscitation and emergency cardiac care. JAMA 227(suppl):833-868, 1974 7. Escher DJW, Furman S: Emergency treatment of cardiac arrhythmias. JAMA 214:2028-2034, 1970 8. Kirklin JW, Archie JP: The cardiovascular subsystem in surgical patients. Surg Gynecol Obstet 139:17-23, 1974 9. Starchuk E, Weil MH, Shubin H: Fluid challenge. In Weil MH, Shubin H (eds): Critical Care Medicine Handbook. New York, 1974 10. Artz CP, Warbrough DR: Burns. In Sabiston DC (ed): Textbook of Surgery. Philadelphia, WB Saunders, 1972, p 272 11. Winsor T: Pulmonary embolism. In Weil MH, Shubin H (eds): Critical Care Medicine Handbook. New York, 1974, p 152 12. Lewi:i AJ, Maxwell MH: Diagnosis and treatment of acute renal failure. In Weil MH, Shubin H (eds): Critical Care Medicine Handbook. New York, 1974, p 225
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 69, NO. 3, 1977
A method of care applicable to all forms of critical illness is presented. A patient is considered to be critically ill when he is threatened with hypoxia. According to this concept, procedures to understand and solve problems of critical care are coordinated and unified. The relevant physiology and monitoring of the components of the oxygenating system are described. The treatment of patients with impaired function of these components is described. Scheme Care of the patient with a lifethreatening illness may be complicated and is frequently urgent. Without procedural guidelines for understanding and solving problems, chaos and confusion, detrimental to the patient, can result. Most critically ill patients are hypoxic, or are suffering from the effects of hypoxia not necessarily still present, or are threatened with hypoxia. Restoration of oxygenation of the brain within a few minutes is the top priority in critical care; but all steps in the management of a patient's serious illness are taken in order to restore or maintain oxygenation of tissue cells. To obtain this objective, the components of the oxygenation mechanism must be appreciated and the adequacy of their function assessed.1 They load, contain, deliver, and unload oxygen. Each of these four functions will be considered under the headings Physiology, Monitors, and Treatment (of deranged physiology). This scheme is summarized in Figure 1. The monitoring of the oxygenating system, and the actions which such monitoring provokes, constitute critical care.
Load Physiology Nerve and muscle actions suck gases through the conduction zone into the diffusion zone. There the inhaled gases and the blood gases are tranferred, respectively, to and from the blood, according to the simple physical laws of gases. The exhalation of alveolar gas may be either passive or forcible. Requests for reprints should be addressed to Dr. Wally Gordon, Department of Surgery, United States Public Health Service Hospital, 6500 Hampton Boulevard, Norfolk, Va 23508
Monitors Clinical and x-ray signs may reveal a flail chest wall, depressed neuromuscular activity, or an obstructed airway. The concentration of inhaled oxygen (FIO2) is obviously an important factor determining the pressure of oxygen in the alveoli (PAO2). The pressure of carbon dioxide in the arterial blood (PaCO2) indicates the adequacy of ventilation. The pressure of oxygen in the arterial blood (PaO2) reflects the PAO2 and the fraction of the cardiac output which is by-passing normally functioning alveoli (the shunt). The difference between PAO2 and PaO2 is the alveolar arterial oxygen gradient (A-aO2 gradient, normal 4 to 10 torr with FIG2 0.2, 80 to 100 torr with FIO2 1.0).
Treatment Any airway obstruction must be relieved immediately. It may be necessary to perform cricothyroidostomy or tracheostomy. Ventilate the apneic patient artifically. If the patient is unconscious, insert a cuffed endotracheal tube to diminish the chance of inhaling oropharyngeal secretions or vomitus. The administration of antispasmodics, antibiotics, and removal of secretions via bronchoscope or tracheostome may improve ventilation. If PaCO2 is less than 50 torr, but PaO2 is inadequate (see Unload, Treat-
ment), deliver 60 percent oxygen (FIO2 0.6), through a well-fitting mask. When PaO2 remains inadequate on FIG2 0.6, start mechanical ventilation with a volume-controlled ventilator. If PaCO2 is more than 50 torr, begin mechanical ventilation, unless
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 69, NO. 3, 1977
the patient has chronic lung disease with persistently high PaCO2 and adequate PaO2. Ventilate an adult at ten strokes per minute with tidal or stroke volume at 12 ml/kg body weight. Provide an infant with the required volume of oxygen by ventilating 20 times per minute. Doubling the stroke volume in an infant would cause unwanted high intrathoracic pressures. Begin ventilation with the FIO2 level at least 0.4, and adjust the stroke volume and FIG2, in the following manner. Increase the stroke volume by 100 ml of gas and measure PaO2, 30 minutes after each increment. When PaO2 shows no further improvement, no advantage is gained from further increases in stroke volume. At this point, FIO2 must be increased or decreased, until PaO2 is adequate. This can be done by trial and error. Alternatively, following the measurement of PaO2, the shunt value can be obtained from a nomogram which will also show the FIO2 level required to attain the desired PaO2 with that particular shunt.2 With resting oxygen consumption, normal cardiac output, FIO2 at 1.0 and PaO2 at more than 150 torr, a shunt of one percent, in addition to the normal four percent, may be assumed for every 20 torr below a PaO2 of 600 torr. Shunting may be improved by positive-end expiratory pressure (PEEP), applied in increments of 5 cm up to 15 cm H2G. Since oxygen inhaled at a pressure of more than 400 torr (FIG2 0.6 at a pressure of 1 atmosphere) may damage the lungs3 consider applying PEEP, when an FIO2 of 0.6 at sea level does not maintain adequate PaO2. At higher altitudes, proportionately higher concentrations of oxygen are safe. PEEP may aggravate shunting and may reduce cardiac output. If the necessarily large stroke volumes produce hypocarbia, the PaCO2 level may be raised by slowing the ventilator or increasing dead space with a tube inserted between the Y-piece of the ventilator and the endo-
tracheal tube. Perform mechanical ventilation of 155
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Contain Physiology Almost all of the oxygen of the blood is loosely combined with hemoglobin within the red blood cells. Only 0.3 ml oxygen is dissolved in each 100 ml plasma when the tension is 100
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of ventilation. When it is not required for mechanical ventilation or airway toilet, remove the endotracheal tube, as 40 percent oxygen can be easily delivered by mask.
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Oxygen content of blood can be calculated from a well-known equation: (SaO2 x Hb x 1.39) +PO2 x 0.0031 Study of blood coagulation factors may reveal the derangement causing bleeding.
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PNYSIELOGY
Figure 1. Summary of the Scheme on Care of the Critically Ill Patient
the lungs via a translaryngeal tube, unless a primary tracheostomy has been made because the translaryngeal tube cannot be passed. The inability to cope with secretions via the translaryngeal tube (a situation which is unusual in units with expert nursing personnel) is the only clear indication for tracheostomy. An arbitrary time period, during which the translaryngeal tube is in position, is not an indication to change to a tracheostomy tube. The author has retained translaryngeal nasotracheal or orotracheal tubes in patients for 30 days and laryngoscopic, bronchoscopic, and necropsy studies did not show significant lesions due to the tube. Unless the patient is apneic, assist the ventilation rather than control it. With proper adjustment, the machine is well-tolerated and muscle 156
Treatmen t Bleeding must be stopped ......... ._ by..direct
relaxants are rarely necessary. When the concentration of oxygen in the ventilating gas has been reduced to 40 percent, disconnect the patient from the ventilator and maintain the desired FIO2 through a T-piece attached to the endotracheal tube. If the patient's spontaneous ventilation rate is more than 30 breaths per minute, at any time during the next four hours, reconnect the ventilator to prevent exhausting the patient. Exhaustion is unlikely to develop later, in a patient who has been comfortable for four hours. This test should not be made in a patient who is under the influence of sedative or analgesic drugs. In the unconscious patient, measurement of tidal and minute volume may be a better indication of the need for continued mechanical ventilation. A rising PaCO2 level confirms the inadequacy
ligation. Treat the hypovolemia following hemorrhage by infusion of liquid (see Deliver, Treatment). Regulate the amount of red cells transfused, by serial estimations of hematocrit reading. Maintain the hematocrit value at 33 or higher if hemoglobin saturation is less than 70 percent (see Unload, Treatment). Replace the hemoglobin with cross-matched red cells, so-that the components of the unnecessary plasma can be stored for use in patients who need specific factors. Transfuse platelets when their count is less than 20,000/ml blood. In disseminated intravascular coagulation, treat the primary cause which may be obstetric, bacterial, toxic, or hemolytic. Administer heparin (700 units/kg body weight during the first 24 hours) by continuous intravenous infusion, following a loading dose of 7,000 units, and continue until the levels of fibrin-split products are normal.4 If the patient requires red cells, transfuse with fresh whole blood, which will supply coagulation components.
Deliver Physiology Heart: The stroke volume depends on preload, which is a stretching force,
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 69, NO. 3, 1977
afterload, which is a force resisting shortening, and contractility, which is the capacity of heart muscle fibers to shorten in response to an adequate stimulus. Plasma: Stroke volume falls when vasoconstriction, compensating for a reduced circulating blood volume, reaches its limit. Heart rate must increase to maintain blood flow. Plasma albumin maintains an osmotic pressure gradient between the intravascular and extravascular spaces. Sodium is a most important factor in regulating the volume and distribution of body water. Blood vessels: Reduction in cardiac output, circulating blood volume, or oxygen content causes constriction of small blood vessels which may lead to irreversible tissue damage.
Monitors Heart: Pulmonary wedge pressure or pulmonary artery diastolic pressure, as measured with a balloon-tipped catheter,5 reflects the mean left atrial pressure representing the preload of the left ventricle. The mean right atrial or central venous pressure reflects the
preload of the right ventricle. Usually, measurement of myocardial contractility is difficult. Afterload is estimated by dividing the systemic or pulmonary arterial pressure, by the cardiac output. Cardiac output may be measured by invasive and non-invasive methods. The heart may fail as a pump because of myocardial infarction, tamponade, dysrhythmia, or severe non-cardiogenic shock; conditions which are revealed by electrocardiograph, chest x-rays, and clinical signs. Plasma: In order to guide maintenance and the replacement of extracellular liquid, measure the intake and output of water and electrolytes. Plasma or serum osmolality (normal 285 mOsm/kg H2 0) reflects changes in the solute or solvent in the extravascular space. Urine osmolality (normally greater than serum osmolality) reflects the urine concentration and dilution which are the functions of renal tubules. Blood vessels: Blood vessel caliber is not measured directly, but blood flow can be measured in some organs by methods often considered impractical and may be judged clinically in the brain, heart, kidney, and skin.
Table 1. Laboratory Results in Oliguria Low Perfusion
Intrinsic Lesion
U/P osmolality
more than 2/1
less than 1.1/1
U/P creatinine conc.
more than 40/1
less than 10/1
U/P urea nitrogen conc.
more than 20/1
less than 10/1
Urinary sodium conc.
less than 20mEq/liter
more than 40mEq/liter
U/P = urine/plasma ratio
Whole body oxygen consumption is a good indication of perfusion in general.
Treatment Heart: If the circulation is arrested, start conventional cardiopulmonary maneuvers for resuscitation.6 If the electrocardiogram shows cardiac arrest, inject 1 mg of epinephrine in 10 ml of saline, intravenously, or directly into the heart every five minutes. Defibrillate immediately when ventricular fibrillation is present, when it is uncertain if fibrillation or standstill exists, and when ventricular tachycardia is present without a pulse. If external cardiac compression is ineffective, or if pneumothorax, or cardiac tamponade is present, perform thoracotomy and internal cardiac compression immediately. Treat cardiac tamponade by immediate aspiration of the pericardial effusion. This is likely to be followed by surgery especially in traumatic cases. Manage dysrhythmia by correction of the blood gas abnormality, and with drugs, or electrically.7 Plasma: To increase the preload, administer an intravenous, isotonic, crystalloid solution. Add 25 percent human serum albumin to maintain adequate plasma osmotic pressure for better retention of liquid within the intravascular space. Continue this treatment of hypovolemia until the pulmonary wedge pressure or the pulmonary artery diastolic pressure is 15 torr, or the central venous pressure (which does not correlate with left atrial pressure) is 15 torr, or 20 cm saline. Lower pressures are acceptable, if the urine flow rate is more than 30 ml per hour. Pressures above these levels do not seem to produce any further increase in stroke volume.8 If there is concern over the ability of the
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heart to handle the increased preload, this capacity can be checked by a challenge of 200 ml of liquid given intravenously in ten minutes, with further challenges controlled by the level of intravascular pressures.9 The burned patient loses liquid and protein into the interstitial space and from the burn surface. Give colloid solution (1 ml/kg body weight x % body surface burn), and the same volume of balanced electrolyte solution and five percent dextrose in water (30 ml/kg of body weight), in the first 24 hours following the burn. Give half this volume intravenously in the first eight hours, and the remainder in the next 16 hours. Subsequent management should be according to the parameters described above. Calculate the area of body surface burned from a chart which considers the patient's
age.10 The crystalloid or colloid solutions which are used in the replacement and maintenance of plasma volume should contain the 150 gm of glucose required daily by the brain. If the patient cannot take an oral diet after five days, more carbohydrates, amino acids, fats, minerals, and vitamins should be added to the intravenous solutions. Control the nutrition therapy, by using an easily calculated nitrogen balance. Blood vessels: The undesirable effects of vasoconstriction may be diminished by maintaining adequate circulating blood volume, as described above. When angiography shows reduced intracranial perfusion, surgical relief of vascular occlusion should be considered, especially in a patient with a head injury. In myocardial infarction, with reduced cardiac output, expect little improvement from further stimulation of undamaged muscle, but some bene157
fit may be obtained from reduction in preload and afterload by diuretic and vasodilator drugs. Direct coronary artery surgery may be indicated. Perfusion of lung vessels may be reduced by embolism, disseminated intravascular coagulation, and left ventricular failure. Treat pulmonary embolism with heparin, 500 units/kg of body weight, spread over 24 hours and given intravenously for ten days. Heparin therapy should be preceded and controlled by tests of the coagulation and partial thromboplastin times. Maintain the coagulation time at about 30 minutes.1 1 Hypoxemia may require that oxygen and mechanical ventilation be used. Surgical occlusion of the inferior vena cava should be considered, when embolism continues in the presence of adequate anticoagulation or bleeding. Treatment of disseminated intravascular coagulation and of left ventricular failure are described above. Maintain urine flow at more than 30 ml per hour by increasing the preload. Oliguria may be due to poor perfusion or to an intrinsic lesion of the kidney. Table 1 indicates how one may be distinguished from the other. Elevation of blood urea nitrogen and creatinine, which may be present with polyuria or oliguria, confirms the inability of the kidney to excrete waste products. Assuming that plasma volume and albumin concentration are normal and diuretics have failed, treat the oliguric stage of intrinsic renal failure by restricting water intake to 6 ml/kg of body weight per 24 hours (plus water equal in volume to other losses) and by reducing daily protein intake to 0.5 gm/kg of body weight. If it is available, dialysis can be started early, without any restrictions in diet.12 In the presence of hypercatabolism (blood urea rising by more than 60 mg percent per day), dialysis is urgently required. The problem of providing adequate nourishment in a small volume might be solved by intravenous
feeding. In addition to being caused by poor perfusion and intrinsic lesions of the kidney, cessation of urine flow may be due to obstruction of the urinary tract. Such a cause of "renal" failure can be revealed by excretion urography, cystoscopy, and by retrograde catheterization of the ureters and radiography. 158
Unload Physiology Increased temperature, hydrogen ion concentration of the blood, and concentration of 2,3,DPG in red blood cells all assist in the unloading of oxygen. A pressure gradient drives oxygen, released from hemoglobin, through the plasma and extracellular space into the mitochondria of the tissue cells. The minimal effective PaO2 level is about 26 torr, a pressure at which hemoglobin is 50 percent saturated. Since the normal average volume of oxygen extracted from 100 ml of blood is 5 ml, the oxygen content of each 100 ml blood flowing at the normal rate should be at least 10 ml.
Monitors The PO2 of a tissue and the PO2 of plasma at the venous end of the related capillary are in equilibrium, The tension of oxygen in mixed venous blood (mixed PvO2, normal 40 torr) is usually a valuable indication of the degree of tissue oxygenation in general. When oxygenation is inadequate, lactate is present in the blood in excess of that expected from the pyruvate concentration. The usual cause of a non-respiratory acidemia is hypoxia, which excess lactate (XL) would confirm.
Treatment Adjust ventilation with the appropriate concentration of oxygen to produce a PaO2 level sufficient to load and unload the required volume of oxygen. If the hematocrit value is 45, a PaO2 of 26 torr will provide an adequate volume of oxygen. If the hematocrit is 30, a PaO2 of 40 torr is necessary. If the hematocrit reading is 24, sufficient oxygen will be available to the tissues only when PaO2 level is 100. At normal flow rates, the myocardium extracts 11.5 ml of oxygen, more than any other organ, from each 100 ml of blood. If oxygen content is inadequate, the oxygen demand is met by an increase in coronary blood flow. As this might be difficult in a seriously ill patient, especially in one with coronary artery lesions, it is safer to maintain hematocrit at 33, if PaO2 is more than 90 torr, or at proportionally more than 33, depending on the PaO2.
If oxygen content is dangerously low, use only fresh blood which has a high concentration of 2,3,DPG, and will release oxygen easily. In an emergency, it is probably best not to lower the concentration of hydrogen ions because acidemia facilitates the release of oxygen. An increased concentration of hydrogen ions may prevent production of 2,3,DPG, but improved oxygenation reduces acidemia and fresh erythrocytes may become available. To increase the volume of available oxygen through improved tissue perfusion, maintain heart contractility and preload (adequate circulating blood volume) and reduce the afterload
(vasodilatation). In cases of septic shock and in the newborn, oxygen is prevented from reaching cells and mixed PvO2 is high. The cause of this derangement is uncertain, but the hypoxia of septic shock may be diminished by massive antibiotic therapy, drainage of collections of pus, and hysterectomy. When unloading cannot be increased to provide an adequate volume of oxygen, consider reducing oxygen demand by hypothermia. For coma, following arrest of the circulation, induce hypothermia immediately to reduce brain damage, brain edema, and hyperpyrexia. Literature Cited 1. Finch CA, Lenfant C: Oxygen transport in man. N Engl J Med 286:407-415, 1972 2. Bednarek J, Matsumoto T: Diagnosing and treating shock lung. Hospital Physician, September:66-73, 1974 3. Hedley-Whyte J, Winter PM: Oxygen therapy. Clin Pharmacol Ther
8:696-737, 1967 4. Bull BS: Disseminated intravascular coagulation. In Weil MH, Shubin H (eds): Critical Care Medicine Handbook. New York, 1974, p 351 5. Swan AJC, Ganz W, Forrester J, et al: Catheterization of the heart in man with the use of a flow-directed balloon-tipped catheter. N EngI J Med 283:447-451, 1970 6. Gordon AS: Standards for cardiopulmonary resuscitation and emergency cardiac care. JAMA 227(suppl):833-868, 1974 7. Escher DJW, Furman S: Emergency treatment of cardiac arrhythmias. JAMA 214:2028-2034, 1970 8. Kirklin JW, Archie JP: The cardiovascular subsystem in surgical patients. Surg Gynecol Obstet 139:17-23, 1974 9. Starchuk E, Weil MH, Shubin H: Fluid challenge. In Weil MH, Shubin H (eds): Critical Care Medicine Handbook. New York, 1974 10. Artz CP, Warbrough DR: Burns. In Sabiston DC (ed): Textbook of Surgery. Philadelphia, WB Saunders, 1972, p 272 11. Winsor T: Pulmonary embolism. In Weil MH, Shubin H (eds): Critical Care Medicine Handbook. New York, 1974, p 152 12. Lewi:i AJ, Maxwell MH: Diagnosis and treatment of acute renal failure. In Weil MH, Shubin H (eds): Critical Care Medicine Handbook. New York, 1974, p 225
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