Extreme Hypercapnia in a Fully Alert Patient* Horst-H. Meissner, M.D.; and Cory Franklin, M.D.
A patient is described with decompensated chronic obstructive lung disease (COLD) and extreme hypercapnia. Despite an arterial COs level of 160 mm Hg, the patient remained awake and alert. This indicates that COs narcosis is not an invariable finding in severe hypercapnia. (Chest 1992; 102:1298-99)
I
t has been reported that the degree of encephalopathy or "narcosis" known to be associated with carbon dioxide retention can be roughly correlated with the level of arterial PC02 • 1 We present a patient who developed extremely high For editorial comment see page 986
levels of arterial Pco2 after low-flow oxygen administration but nevertheless remained alert and oriented despite the severe hypercapnia. CASE REpORT
A 70-year-old man with a history of severe chronic obstructive lung disease (COLD) and home oxygen use for the last ten years presented to the emergency department at Cook County Hospital, Chicago. He reported a two-week history of yellowish, productive cough associated with wheezing and increased shortness of breath that was unresponsive to oral antibiotics. Medical history included a 120 pack-year smoking history, mild hypertension, and congestive heart failure. Medications at the time of hospital admission were digoxin, furosemide, theophylline, terbutaline, and ipratropium bromide (Atrovent). On arrival to the emergency department, the patient was alert and oriented to person, place, and time. Blood pressure was 110/60 mm Hg, pulse rate was 130 beats per minute, respiratory rate was 321min, and temperature was 37°C. Physical examination was remarkable for decreased breath sounds and scattered rhonchi bilaterally. The chest roentgenogram showed signs of COLD, old tuberculous changes in the left upper lobe, emphysematous blebs in the left lower lobe, and an infiltrate in the right lower lobe. The patienfs arterial blood gas (ABG) values can be seen in Table 1. Serum sodium, serum urea nitrogen, and serum creatinine were within normal limits. The ECG showed a first degree AV block and changes compatible with ischemia in the lateral leads. Digoxin level was reported at 3.0 mgIL. The patient was treated with low-Row oxygen, antibiotics, bronchodilators, and methylprednisolone, and exhibited initially some clinical improvement. He continued to have persistent arterial *From the Division of Critical Care Medicine and Department of Medicine, Cook County Hospital, and University of Health Sciences/fhe Chicago Medical School, North Chicago. Reprint requests: Dr. Franklin, Cook County Hospital, Bldg A/Wd 15, 1835 W Harrison, Chicago 60612
hypoxemia, however, and si~nificant CO 2 retention (ABG 2). The patient's oxygen therapy was sli~htly increased without significant improvement (ABG 3). During this time, the patient remained fully alert and oriented despite an arterial Pco2 of 112 mm Hg now. It was decided to transfer him to the medical intensive care unit (MICU) for intra-arterial blood gas monitoring. Several hours after admission to the MICU, the patient's breathing became increasingly labored (ABG 4). He experienced difficulty speaking due to shortness of breath but was still alert and oriented and able to answer questions appropriately despite an arterial Pco2 of 160 mm Hg. He became tachycardic and hypotensive at this point and was intubated, then sedated and rested for three days on mechanical ventilation. He was extubated on the sixth day (ABG 5) and discharged from the MICU one day later (ABG 6). DISCUSSION
Previous reports in the medical literature describe patients with similar levels of CO2 retention. However, in all those cases, the patients were either stuporous or exhibited frank coma. 2-4 It has been suggested that the presence and degree of cerebral symptoms depend on a number of variables, including hypoxemia, coexistent infection, and length of time the patient has had an elevated PaC0 2 • s The issue of how and when to administer oxygen to patients with COLD and hypercapnic respiratory failure remains a point of contention. Despite the fact that current literature suggests that the controlled administration of oxygen to prevent severe hypoxemia during hypercapnia appears safe,2.3.6 some physicians, nurses, and paramedics still withhold oxygen or administer it too sparingly, fearing that patients will develop life-threatening CO2 narcosis. Aubier and colleagues7 documented that in patients with COLD and acute respiratory failure, 100 percent oxygen administration raised arterial Pco2 by an average of 23 mm Hg over 15 min. They suggested this was a more complex problem than simply oxygen-induced loss of central chemoreceptor drive. Other authors have attributed the CO2 retention to a loss of chemoreceptor drive, diaphragmatic muscle fatigue, hypophosphatemia, and relief of pulmonary vasoconstriction. M-ll Decreases in minute ventilation, hereditary hypercapnia, and the Haldane effect have also been implicated. 12-14 In our review of the literature, this case is the first to document that even in the face of extreme hypercapnia, a patient may retain not only consciousness but also the ability to answer questions appropriately. This supports the theory that the narcosis attributed to CO 2 retention is not entirely a function of the absolute level of arterial PC02 • 7 ACKNOWLEDGMENT: We would like to thank Dr. Yaakov Friedman, Medical Intensive Care Unit, Cook County Hospital, for reviewing the manuscript.
Table I-Patients Arterial Blood Gas (ABC) Values ABG
Hospital Day
FIo2 *
pH
Pa0 2 , mm Hg
PaC02 , mm Hg
HC03- , mEqIL
O 2 Saturation
1 2 3 4 5 6
1 6 7 8 14 15
2LNC 2LNC 3LNC 6LNC 35%FM 3LNC
7.41 7.38 7.32 7.14 7.41 7.39
47 51
64 96
45 58
0.89 0.83 0.74 0.89 0.94 0.93
48
82 73 72
112 160 61 62
59 56
39 38
*NC = nasal cannula; FM = face mask.
1298
Extreme Hypercapnia in Fully Alert Patient (Meissner, Franklin)
REFERENCES
Sieker HO, Hickam JB. Carbon dioxide intoxication: the clinical syndrome, its etiology and management with particular reference to the use of mechanical respirators. Medicine 1956; 35:389-423
2 Posner JB, Swanson AG, Plum F. Acid-base balance in cerebrospinal Ruid. Arch Neuroll965; 12:479-96 3 Comroe JH Jr, Coates EO Jr. Mental changes occurring in chronically anoxemic patients during oxygen therapy. JAMA 1950; 143:1044-48 4 Goldstein B, Shannon DC, Todres ID. Supercarbia in children: clinical course and outcome. Crit Care Med 1990; 18:166-68
5 Westlake EK, Simpson T, Kaye M. Carbon dioxide narcosis in emphysema. Q J Med 1955; 94:155-73 6 Campbell EJM. The J Burns Amberson Lecture: the management of acute respiratory failure in chronic bronchitis and emphysema. Am Rev Respir Dis 1967; 96:626-39 7 Aubier M, Murciano D, Milic-Emili J, Touaty E, Daghfous J, Pariente R, et al. Effects ofthe administration ofO, on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure. Am Rev Respir Dis 1980; 122:747-54
8 Stradling JR. Hypercapnia during oxygen therapy in airways obstruction: a reappraisal, Thorax 1986; 41:897-902 9 Juan G, Calverley P, Talamo C, Schnader J, Roussos C, Effect of carbon dioxide on diaphragmatic function in human beings, N Engl J Med 1984; 310:874-79 10 Aubier M, Murciano D, Lecocguic Y, Viires N, Jacquens Y, Squara P, et aI. Effect of hypophosphatemia on diaphragmatic contractility in patients with acute respiratory failure. N Eng! J Med 1985; 313:420-24 II Lee J, Read J. Effect of oxygen breathing on distribution of pulmonary blood Row in chronic obstructive lung disease, Am Rev Respir Dis 1967; 96:II73-80 12 Parot S, SaunierC, Gautier H, Milic-Emili J, Sadoul P. Breathing pattern and hypercapnia in patients with obstructive pulmonary disease. Am Rev Respir Dis 1980; 121:985-91 13 Collins DD, S(,'Oggin CH, Zwillich C\v, Weil Jv. Hereditary aspects of decreased hypoxic response. J Clin Invest 1978; 62:105-10 14 Lenfant C. Arteriolar-alveolar difference in Peo, during air and oxygen breathing. J Appl Physioll966; 21:1356-62
Periaortic Hematoma Formation Leading to Aortic Valve Failure*
the homograft valve was caused by compression and distortion by blood transmitted directly from the left ventricle into a space between the homograft and an external cavity fonned by a Dacron wrap. The latter had been placed to help control suture-line bleeding. This case presentation demonstrates an unusual cause of homograft failure and suggests that wrapping of a homograft conduit by native aorta or an external Dacron wrap is not a substitute for meticulous surgical technique to assure a (Che.t 1992; 102:1299-1301) hemostatic suture line.
E
xperience with aortic valve homografts began nearly 35 years ago and advances in graft preservation and storage procedures have stimulated more widespread use of this prosthesis. I The aortic valve homograft has been particularly valuable in the treatment of native and prosthetic aortic valve endocarditis complicated by valvular insufficiency or perivalvular abscess formation .... These prostheses do have the potential for failure principally related to gradual valve wear leading to aortic insufficiency and rarely calcific stenosis. '.' Meticulous surgical technique is an essential component to placement of the homograft valve, but this may prove extremely difficult even for the experienced surgeon in the presence of extensive tissue destruction associated with complicated aortic valve endocarditis. We present a patient who developed relatively early aortic homograft stenosis and insufficiency due to external compression and distortion of the homograft conduit by an external Dacron wrap that had been placed to assist with hemostasis. CASE REPORT
A 45-year-old man initially presented eight years prior to the current hospital admission with enterococcal endocarditis complicated by acute aortic insufficiency and left ventricular failure. Aortic valve replacement was uneventfully performed with a No. 27 BjorkShiley prosthesis. Seven years later, he presented with signi6cant prosthetic aortic valvular insufficiency. Evaluation revealed a subvalvular abscess cavity, partial dehiscence of the prosthetic valve, and aortic annular destruction. Considering the extensive destruction of the aortic annulus in the face of prosthetic valve infection, the aortic root was replaced with a 24-mm aortic valve homograft conduit into which the left and right coronary arteries were ,I
A Complication of Homograft Placement for second Valve Surgery William T. Pochis, M.D.; Michael P. Cinquegrani, M.D.; Robert P. McManus, M.D., FC.C.P.; and G. Hossein Almassi, M.D., FC.C.P.
The aortic homograft has become the replacement valve of choice in the treatment of complicated endocarditis involving native and prosthetic aortic valves. Complications are rare, typically involving chronic leaflet degeneration causing valvular insufficiency or rarely chronic calcific stenosis. We present a case in which functional stenosis of *From the Divisions of Cardiology (Drs. Pochis and Cinquegrani) and Cardiothoracic Surgery (Drs. McManus and Almassi), Medical College of Wis(,'Onsin, Milwaukee. Reprint requests: Dr. Cinquegrani, Division ofCardiology, Medical College of Wisconsin, Milwaukee 53226
FIGURE 1. Simultaneous pressure tracings from the left ventricle (LV), central aorta (Ao), and pulmonary artery (PA) demonstrate a 100 mm Hg peak-to-peak pressure gradient across the stenotic homograft aortic valve, CHEST 1102 I 4 I OCTOBER, 1992
1299
A patient is described with decompensated chronic obstructive lung disease (COLD) and extreme hypercapnia. Despite an arterial COs level of 160 mm Hg, the patient remained awake and alert. This indicates that COs narcosis is not an invariable finding in severe hypercapnia. (Chest 1992; 102:1298-99)
I
t has been reported that the degree of encephalopathy or "narcosis" known to be associated with carbon dioxide retention can be roughly correlated with the level of arterial PC02 • 1 We present a patient who developed extremely high For editorial comment see page 986
levels of arterial Pco2 after low-flow oxygen administration but nevertheless remained alert and oriented despite the severe hypercapnia. CASE REpORT
A 70-year-old man with a history of severe chronic obstructive lung disease (COLD) and home oxygen use for the last ten years presented to the emergency department at Cook County Hospital, Chicago. He reported a two-week history of yellowish, productive cough associated with wheezing and increased shortness of breath that was unresponsive to oral antibiotics. Medical history included a 120 pack-year smoking history, mild hypertension, and congestive heart failure. Medications at the time of hospital admission were digoxin, furosemide, theophylline, terbutaline, and ipratropium bromide (Atrovent). On arrival to the emergency department, the patient was alert and oriented to person, place, and time. Blood pressure was 110/60 mm Hg, pulse rate was 130 beats per minute, respiratory rate was 321min, and temperature was 37°C. Physical examination was remarkable for decreased breath sounds and scattered rhonchi bilaterally. The chest roentgenogram showed signs of COLD, old tuberculous changes in the left upper lobe, emphysematous blebs in the left lower lobe, and an infiltrate in the right lower lobe. The patienfs arterial blood gas (ABG) values can be seen in Table 1. Serum sodium, serum urea nitrogen, and serum creatinine were within normal limits. The ECG showed a first degree AV block and changes compatible with ischemia in the lateral leads. Digoxin level was reported at 3.0 mgIL. The patient was treated with low-Row oxygen, antibiotics, bronchodilators, and methylprednisolone, and exhibited initially some clinical improvement. He continued to have persistent arterial *From the Division of Critical Care Medicine and Department of Medicine, Cook County Hospital, and University of Health Sciences/fhe Chicago Medical School, North Chicago. Reprint requests: Dr. Franklin, Cook County Hospital, Bldg A/Wd 15, 1835 W Harrison, Chicago 60612
hypoxemia, however, and si~nificant CO 2 retention (ABG 2). The patient's oxygen therapy was sli~htly increased without significant improvement (ABG 3). During this time, the patient remained fully alert and oriented despite an arterial Pco2 of 112 mm Hg now. It was decided to transfer him to the medical intensive care unit (MICU) for intra-arterial blood gas monitoring. Several hours after admission to the MICU, the patient's breathing became increasingly labored (ABG 4). He experienced difficulty speaking due to shortness of breath but was still alert and oriented and able to answer questions appropriately despite an arterial Pco2 of 160 mm Hg. He became tachycardic and hypotensive at this point and was intubated, then sedated and rested for three days on mechanical ventilation. He was extubated on the sixth day (ABG 5) and discharged from the MICU one day later (ABG 6). DISCUSSION
Previous reports in the medical literature describe patients with similar levels of CO2 retention. However, in all those cases, the patients were either stuporous or exhibited frank coma. 2-4 It has been suggested that the presence and degree of cerebral symptoms depend on a number of variables, including hypoxemia, coexistent infection, and length of time the patient has had an elevated PaC0 2 • s The issue of how and when to administer oxygen to patients with COLD and hypercapnic respiratory failure remains a point of contention. Despite the fact that current literature suggests that the controlled administration of oxygen to prevent severe hypoxemia during hypercapnia appears safe,2.3.6 some physicians, nurses, and paramedics still withhold oxygen or administer it too sparingly, fearing that patients will develop life-threatening CO2 narcosis. Aubier and colleagues7 documented that in patients with COLD and acute respiratory failure, 100 percent oxygen administration raised arterial Pco2 by an average of 23 mm Hg over 15 min. They suggested this was a more complex problem than simply oxygen-induced loss of central chemoreceptor drive. Other authors have attributed the CO2 retention to a loss of chemoreceptor drive, diaphragmatic muscle fatigue, hypophosphatemia, and relief of pulmonary vasoconstriction. M-ll Decreases in minute ventilation, hereditary hypercapnia, and the Haldane effect have also been implicated. 12-14 In our review of the literature, this case is the first to document that even in the face of extreme hypercapnia, a patient may retain not only consciousness but also the ability to answer questions appropriately. This supports the theory that the narcosis attributed to CO 2 retention is not entirely a function of the absolute level of arterial PC02 • 7 ACKNOWLEDGMENT: We would like to thank Dr. Yaakov Friedman, Medical Intensive Care Unit, Cook County Hospital, for reviewing the manuscript.
Table I-Patients Arterial Blood Gas (ABC) Values ABG
Hospital Day
FIo2 *
pH
Pa0 2 , mm Hg
PaC02 , mm Hg
HC03- , mEqIL
O 2 Saturation
1 2 3 4 5 6
1 6 7 8 14 15
2LNC 2LNC 3LNC 6LNC 35%FM 3LNC
7.41 7.38 7.32 7.14 7.41 7.39
47 51
64 96
45 58
0.89 0.83 0.74 0.89 0.94 0.93
48
82 73 72
112 160 61 62
59 56
39 38
*NC = nasal cannula; FM = face mask.
1298
Extreme Hypercapnia in Fully Alert Patient (Meissner, Franklin)
REFERENCES
Sieker HO, Hickam JB. Carbon dioxide intoxication: the clinical syndrome, its etiology and management with particular reference to the use of mechanical respirators. Medicine 1956; 35:389-423
2 Posner JB, Swanson AG, Plum F. Acid-base balance in cerebrospinal Ruid. Arch Neuroll965; 12:479-96 3 Comroe JH Jr, Coates EO Jr. Mental changes occurring in chronically anoxemic patients during oxygen therapy. JAMA 1950; 143:1044-48 4 Goldstein B, Shannon DC, Todres ID. Supercarbia in children: clinical course and outcome. Crit Care Med 1990; 18:166-68
5 Westlake EK, Simpson T, Kaye M. Carbon dioxide narcosis in emphysema. Q J Med 1955; 94:155-73 6 Campbell EJM. The J Burns Amberson Lecture: the management of acute respiratory failure in chronic bronchitis and emphysema. Am Rev Respir Dis 1967; 96:626-39 7 Aubier M, Murciano D, Milic-Emili J, Touaty E, Daghfous J, Pariente R, et al. Effects ofthe administration ofO, on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure. Am Rev Respir Dis 1980; 122:747-54
8 Stradling JR. Hypercapnia during oxygen therapy in airways obstruction: a reappraisal, Thorax 1986; 41:897-902 9 Juan G, Calverley P, Talamo C, Schnader J, Roussos C, Effect of carbon dioxide on diaphragmatic function in human beings, N Engl J Med 1984; 310:874-79 10 Aubier M, Murciano D, Lecocguic Y, Viires N, Jacquens Y, Squara P, et aI. Effect of hypophosphatemia on diaphragmatic contractility in patients with acute respiratory failure. N Eng! J Med 1985; 313:420-24 II Lee J, Read J. Effect of oxygen breathing on distribution of pulmonary blood Row in chronic obstructive lung disease, Am Rev Respir Dis 1967; 96:II73-80 12 Parot S, SaunierC, Gautier H, Milic-Emili J, Sadoul P. Breathing pattern and hypercapnia in patients with obstructive pulmonary disease. Am Rev Respir Dis 1980; 121:985-91 13 Collins DD, S(,'Oggin CH, Zwillich C\v, Weil Jv. Hereditary aspects of decreased hypoxic response. J Clin Invest 1978; 62:105-10 14 Lenfant C. Arteriolar-alveolar difference in Peo, during air and oxygen breathing. J Appl Physioll966; 21:1356-62
Periaortic Hematoma Formation Leading to Aortic Valve Failure*
the homograft valve was caused by compression and distortion by blood transmitted directly from the left ventricle into a space between the homograft and an external cavity fonned by a Dacron wrap. The latter had been placed to help control suture-line bleeding. This case presentation demonstrates an unusual cause of homograft failure and suggests that wrapping of a homograft conduit by native aorta or an external Dacron wrap is not a substitute for meticulous surgical technique to assure a (Che.t 1992; 102:1299-1301) hemostatic suture line.
E
xperience with aortic valve homografts began nearly 35 years ago and advances in graft preservation and storage procedures have stimulated more widespread use of this prosthesis. I The aortic valve homograft has been particularly valuable in the treatment of native and prosthetic aortic valve endocarditis complicated by valvular insufficiency or perivalvular abscess formation .... These prostheses do have the potential for failure principally related to gradual valve wear leading to aortic insufficiency and rarely calcific stenosis. '.' Meticulous surgical technique is an essential component to placement of the homograft valve, but this may prove extremely difficult even for the experienced surgeon in the presence of extensive tissue destruction associated with complicated aortic valve endocarditis. We present a patient who developed relatively early aortic homograft stenosis and insufficiency due to external compression and distortion of the homograft conduit by an external Dacron wrap that had been placed to assist with hemostasis. CASE REPORT
A 45-year-old man initially presented eight years prior to the current hospital admission with enterococcal endocarditis complicated by acute aortic insufficiency and left ventricular failure. Aortic valve replacement was uneventfully performed with a No. 27 BjorkShiley prosthesis. Seven years later, he presented with signi6cant prosthetic aortic valvular insufficiency. Evaluation revealed a subvalvular abscess cavity, partial dehiscence of the prosthetic valve, and aortic annular destruction. Considering the extensive destruction of the aortic annulus in the face of prosthetic valve infection, the aortic root was replaced with a 24-mm aortic valve homograft conduit into which the left and right coronary arteries were ,I
A Complication of Homograft Placement for second Valve Surgery William T. Pochis, M.D.; Michael P. Cinquegrani, M.D.; Robert P. McManus, M.D., FC.C.P.; and G. Hossein Almassi, M.D., FC.C.P.
The aortic homograft has become the replacement valve of choice in the treatment of complicated endocarditis involving native and prosthetic aortic valves. Complications are rare, typically involving chronic leaflet degeneration causing valvular insufficiency or rarely chronic calcific stenosis. We present a case in which functional stenosis of *From the Divisions of Cardiology (Drs. Pochis and Cinquegrani) and Cardiothoracic Surgery (Drs. McManus and Almassi), Medical College of Wis(,'Onsin, Milwaukee. Reprint requests: Dr. Cinquegrani, Division ofCardiology, Medical College of Wisconsin, Milwaukee 53226
FIGURE 1. Simultaneous pressure tracings from the left ventricle (LV), central aorta (Ao), and pulmonary artery (PA) demonstrate a 100 mm Hg peak-to-peak pressure gradient across the stenotic homograft aortic valve, CHEST 1102 I 4 I OCTOBER, 1992
1299
