Hemorrhagic cardiac tamponade: a clinicopathologic correlation. Mayo Clin Proc 1984; 59:785-90 4 CD-ROM:Medline, USA, National Library of Medicine 5 Walvogel FA. Staphylococcus aureus. In: GL Mandell, RG Douglas, JE Bennett, eds. Principles and practice of infectious diseases. 3th ed. New York: Churchill Livingstone 1990; 1:489-510
Hyperventilation in Sepsis and Acidosis What is the Limit? To the Editor: A well-recognized compensatory response to metabolic acidosis and sepsis is an increased alveolar ventilation resulting in a lowered arterial C02 tension, usually to a range between 10 to 15 mm Hg. 1•2 We recently observed an elderly acidotic and septic patient with an arterial PaC02 of 7.2 mm Hg, which we believe represents the lowest reported arterial PaC02 in a patient who eventually survived. A 78-year-old man, nonsmoker, previously in good health with no known medical problems, was admitted to the hospital with shortness of breath and general weakness for 2-weeks. He also described dysuria but no other symptoms. On examination the patient was alert and oriented, BP was 130/ 80 mm Hg, pulse rate was 100/ min, temperature was 96° F and respiratory rate was 28/min (Kussmaul pattern). The rest of the examination was unremarkable. Laboratory values included arterial blood gas analysis while receiving supplemental oxygen revealing pH 6.97, PaC02 7.2 mm Hg, and Pa02 270 mm Hg. Chemistry included Na+ 134 mEq/ L, K+7.4 mEq/L, Cl-94 mEq/L, HC03-5 mEq/ L, glucose 103 mg/dl, BUN 242 mg/dl, and creatinine 18.8 mg/ dl. Lactic acid level was 5.4 mEq/ L (normal 0.5-2.2). He was given sodium bicarbonate and a repeat arterial blood sample while breathing oxygen 4 L/min revealed pH 7.22, PaC02 8.2 mm Hg, and Pa02 193 mm Hg. The patient underwent urgent hemodialysis. Blood and urine cultures grew Klebsiella pneumoniae and the appropriate antibiotics were started. The patient's condition improved and a few days later, a repeat arterial blood sample while breathing room air revealed pH 7.34, PaC02 21 mm Hg, and Pa02 108 mm Hg. Renal sonogram showed bilateral hydronephrosis; this was followed by cystoscopy that showed multiple bladder stones, and cystolithotomy was done. The patient was discharged with BUN 79 mg/ dl and creatinine 7.7 mg/ dl. This, to our knowledge, is the lowest level of PaC02 documented in the English language literature. The only similar low value was shown on top of Mount Everest, where a young healthy man was able to hyperventilate to a PaC02 of 7.5 mm Hg in response to extreme hypoxia. 3 Our case shows the extreme limits to which an individual can hyperventilate in response to sepsis and acidosis. This response seems to be independent of age.
Ayman 0. Soubani, M.D., New England Medical Center, Boston , Massachusetts; and Faroque A. Khan, M .B., F.C.C.P., SUNY at Stony Brook, Stony Brook, New York REFERENCES
Albert MD, Dell RB, Winter RW. Quantitative displacement of acid-base equilibrium in metabolic acidosis. Ann Intern Med 1967; 66:312-22 2 Fulop M. The ventilatory response in severe metabolic acidosis. Clin Sci Mol Med 1976; 50:367-73
3 West JB. Science on top. In: Everest: the testing place. New York: McGraw-Hill Book Co, 1985; 111-25
Pronus Angina To the Editor: Among the valuable data presented by Klein and colleagues on pronus angina, they reported blood pressure responses to squatting as well as other challenges (stooping, knee-chest position) but somehow omitted the systolic time interval (STI) response only to squatting.1 We studied the responses to both prompt and sustained (2 min) squatting, prompt squatting having more marked effects. 2 Squatting decreased heart rate, isovolumic contraction time, pre-ejection period, and pulse transmission time (usually omitted by most calculations for systolic time intervals); squatting increased the time from onset of depolarization (Q wave) to the first heart sound, left ventricular ejection time, and ejection time index.2 We considered the changes in STI to be consistent with bradycardia and increased ventricular filling induced by squatting. These comments are meant only to supplement a very nice study.
David H. Spodick, M.D ., D.Sc. , F.C.C.P., Cardiology Division, Saint Vincent Hospital, Worcester, Massachusetts REFERENCES
Klein HO, Nuriel H, Levi A, Kaplinski E, DeSegni E. Pronus angina (angina pectoris induced by stooping or crouching): a proposed mechanism. Chest 1993; 104:65-70 2 Lance VQ, Spodick DH. Physiological responses to prompt and sustained squatting. Br Heart J 1977; 39:559-62
Selecting a Vena Caval Device To the Editor: Black et aP have appropriately highlighted the risk of pulmonary thromboembolism from upper extremity deep venous thrombosis. The indication for filter insertion in the superior vena cava was clearly established but their preference for the Venatech device is subject to question. Published follow-up data on this device show a migration rate of 14 percent and an occlusion rate of 22 percent. 2 In contrast, published data on the Greenfield filter show an occlusion rate of 4 percent3 and no significant proximal migration. This is also the only device that has been used successfully in the suprarenal position, where it has 100 percent patency at long-term follow-up.4 Selection of a vena caval device for permanent insertion should be based on its long-term consequences rather than the convenience of insertion.
Lazar]. Greenfield, M.D., F .C.C.P., Department of Surgery, University of Michigan, Ann Arbor, Michigan REFERENCES
Black MD, French GJ, Rasuli P, Bouchard AC. Upper extremity deep venous thrombosis: underdiagnosed and potentially lethal. Chest 1993; 103:1887-90 2 Millward SF, Marsh Jl, Peterson RA, Rasuli P, French G, Wilson C, eta!. LGM (Vena Tech) vena cava filter: clinical experience in 64 patients. J Vase Intervent Radiol1991; 2:429-33 3 Greenfield LJ, Michna BA. Twelve year clinical experience with the Greenfield vena cava filter. Surgery 1988; 104:706-12 4 Greenfield LJ, Cho KJ, Proctor MC, Sobel M, ShahS, Wingo J. Late results of suprarenal Greenfield vena cava filter placement. Arch Surg 1992; 127:969-73 Communications to the Editor