Ventillatory stimulus suppression in intrinsic peep ...

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arterial blood gas analysis, PetCO 2 and PaCO2-PetCO 2 gradient were similar to those obtained without PEEP. Case 2. A 54-year-old woman with a history of ...
Correspondence We would like to recommend that should m e a n expired PCO 2 be measured, with the IL 1312, the response of the PCO 2 electrode should be checked at P C O 2 levels lower than 30 m m H g and an appropriate correction should be used if the electrode fails to respond exactly within _+1 m m H g . Yours sincerely, D. J. M. Raurich and J. Ibafiez

References 1. Severinghaus JW, Beadley AF (1958) Electrodes for blood PO 2 and P C O 2 determinations. J Appl Physiol 13:515 Dr. J.M. Raurich, Intensive Care Unit, Hospital Son Dureta, E-07014 Palma de Mallorca, Spain

Haemorrhagic shock with paradoxical bradycardia Dear Sir, We read with interest the article by Barriot and Riou [1] on paradoxical bradycardia in haemorrhagic shock. They c o m m e n t that it is related to an extreme and rapid blood loss with hypovolaemia. Our experience with the case described below would suggest that blood loss need not necessarily be rapid and that paradoxical bradycardia m a y occur with hypovolaemia resulting from m u c h lower rates of blood loss. A 50-year-old w o m a n with widespread pelvic endometrial carcinoma and recurrent deep venous thrombosis with pulmonary eraboll complicated by heparin induced thrombocytopenia (HITS) had a filter inserted into the inferior vena cava via a right femoral vein puncture. Initial haemostasis was good. Warfarin was commenced the following day and at 48 h bruising and swelling were noted in the right thigh, consistent with a haematoma. At this stage the haemoglobin was stable at 12 g/dl, the prothrombin index was 50°70 and the platelet count was 6 4 x 109/1. The Warfarin, which was her only regular medication, was ceased and overnight 4 units of FFP were given to correct the prothrombin index. During this 12-h period the patient gradually deteriorated and her blood pressure fell from 110/70 to 100/50 with a tachycardia increasing from 100 to 130. She also became mildly hypothermic with evidence of peripheral shutdown. The following day the patient became shocked and had no recordable blood pressure. Auscultation of the heart revealed a heart rate of approximately 40 beats/rain, with loud heart sounds. Inspire of these findings the patient was fully conscious and breathing spontaneously. The h a e m a t o m a on the right thigh was by now m u c h more extensive. She was resuscitated with 3 units of SPPS and the haemoglobin was found to be 5.9 g/dl. A n E C G during the second unit of SPPS showed the heart rate had increased but there was still a relative sinus bradycardia of 100 beats/min with a systolic blood pressure of 50 m m H g . She was transferred to the Intensive Care Unit where resuscitation was continued with fluids and blood transfusion. The patient was successfully resuscitated from her haemorrhagic shock with volume replacement alone. This patient demonstrates that paradoxical bradycardia m a y occur from haemorrhagic shock that evolves over a m u c h longer period of time than that cited by Barriot and Riou [1]. The realisation of this p h e n o m e n o n is important as massive blood loss may occur insidiously into the retroperitoneal space or into a large area of soft tissue before it is detected and a paradoxical bradycardia would make rapid clinical assessment especially difficult. Yours sincerely, B.R. Wylie, N.A. Singh, D. McWilliam and K.A. Rickard

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References 1. Barriot P, Riou B (1987) Haemorrhagic shock with paradoxical bradycardia. Intensive Care Med 13:203 B.R. Wylie, Blood Transfusion Service, 153 Clarence Street, Sydney NSW 2000, Australia

Ventilatory stimulus suppression in intrinsic peep patients Dear Sir, It has been shown that the addition of external P E E P in similar a m o u n t s to the pre-existing levels of intrinsic P E E P may decrease the work of breathing in assisted mechanical ventilation. There are some controversies about the possible change of lung volume due to such a m o u n t s of PEEP [1-3]. We report two mechanically ventilated patients with COPD in w h o m the application of PEEPe to counterbalance PEEPi resulted in an immediate decrease so far as the complete abolition of inspiratory efforts. Case 1. A 71-year-old m a n with an acute exacerbation of C O P D developed hypoxemia and hypercapnia, he was intubated and mechanically ventilated in the assist-control mode (AMV). Four days later, whilst he was ventilated with FiO2: 0.3, V v 550 ml, RR:15x', I/E: 1/2.7, Inspiratory flow rate: 501/min (Servo Ventilator 900 C Siemens-Elema), he triggered the ventilator continously with a frequency of 17 breaths/min in AMV, Arterial blood gas analysis showed: p H = 7 . 4 7 , P O 2 = 1 0 4 m m H g , P C O 2 = 34 m m H g , St Bic = 26 mEq/1. P E E P measured (as Pepe et al. previously described) was 10cm H20. End-tidal CO 2 pressure was 31 m m H g . We applied increasing a m o u n t s of PEEPe, until 10 cm H 2 0 P E E P were reached. At this level the intensity of inspiratory efforts to trigger the ventilation suddenly decreased until they disappeared, remaining at ventilator back-up frequency; at this m o m e n t the arterial blood gas analysis, PetCO 2 and PaCO2-PetCO 2 gradient were similar to those obtained without PEEP. Case 2. A 54-year-old w o m a n with a history of bronchial asthma was admitted to the hospital for acute attack of asthma that needed mechanical ventilation. Six days later, when the bronchospasm improved, A M V was established with FiO2: 0.3, VT: 500 ml, RR: 20x', I/E: 1/2.7, inspiratory flow rate: 501/min; the patient remained calm while she triggered the ventilator at a rate of 22 × ', maintaining the arterial blood gases values at pH = 7.45, PO 2 - 8I, P C O 2 = 41, St Bic = 28, SaO 2 = 96070. We found a 5 cm H 2 0 PEEPi, and a PEEP trial was begun in an attempt to diminish the work of breathing. A n initial 5 cm H 2 0 PEEPe level showed no changes either in arterial blood gas analysis or hemodynamic measurements. After that a 10 cm H 2 0 PEEP level was instituted and the patient showed a rapidly progressive decrease in her inspiratory efforts to trigger the ventilator until they disappeared, remaining at the ventilator back-up frequency, then the arterial blood gas analysis showed pH: 7.46, PO 2 = 107, P C O 2 = 38, St Bic = 28, SaO 2 = 98°70, without changes in PetCO 2. Intrinsic P E E P represents an undesirable p h e n o m e n o n occasioning hemodynamic instability in patients with airflow obstruction when mechanical ventilation is instituted [4]. Recently, it was studied as an inspiratory threshold load for the respiratory muscles [1], and it was investigated the usefulness of added PEEP in an attempt to diminish the gradient between alveolar and m o u t h pressures in the beginning of inspiration [2, 3].

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When we added PEEPe in similar or higher amounts than PEEPi, both patients showed a rapidly progressive decrease in their respiratory efforts enabling complete abolishing the triggered assisted ventilation. The clinically unchanged P(A-a)O 2 and PaCO2-PetCO2 suggest that the alleviation of the inspiratory threshold load with PEEP was probably the most important factor in diminishing the respiratory center output. However, this remains to be demonstrated on a large scale. Yours sincerely, R. Fermindez and S. Benito

References 1. Smith TC, Marini J, Lamb V (1987) The inspiratory threshold load resulting from air-trapping during mechanical ventilation. Am Rev Respir Dis 135:A 52 2. Gay P, Rodarte J, Hubmayr R (1987) The effect of extrinsic PEEP on lung volume, isovolume flow and respiratory work in dynamically hyperinflated patients. A m Rev Respir Dis 135:A 52 3. Simkovitz P, Brown K, Goldberg P, Milic-Emili J, Gottfried S (1987) Interaction between intrinsic and externally applied PEEP during mechanical ventilation. Am Rev Respir Dis 135:A 202 4. Pepe P, Marini J (1982) Occult positive end-expiratory pressure in mechanically ventilated patients with airflow obstruction. A m Rev Respir Dis 126:166-170 Dr. R. Fermindez, Servicio de Medicina Intensiva, Hospital de la Santa Creu i Sant Pau, Avda. St. Antoni M a Claret 167, E-08025 Barcelona, Spain

The use of continuous arteriovenous hemodialysis in the management of patients with oliguria associated with multiple organ failure Dear Sir, The management of multiple organ failure (MOF) is one of the most difficult and demanding challenges in Intensive Care. The association of acute respiratory failure with acute renal failure is very common, and when this occurs, causes an alarming increase in the mortality rate [1]. The addition of sequential hemofiltration (SHF) followed by standard acetate hemodialysis to conventional therapy (ventilatory support, inotropes, colloids, crystalloids, antibiotics,

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etc.), has been successfully used in NON OLIGURIC septic patients [2]. Nevertheless, these measures alone have not improved mortality rates in patients with MOF and oliguria, which has led us to change to Continuous Arterio Venous Hemofiltration (CAVH) [3]. One of our problems has been the very high catabolic states occurring in these patients, associated with oliguria and acute renal failure, transforming this often serious condition into an uncontrollable one.

We have treated 6 patients who fulfilled the classic criteria of MOF [41 (3 males and 3 females with a mean age of 44+_ 15.5 years) with CAVH, but after 48 h azotemia had worsened, the serum creatinine and K had increased and we could not control the high urea generation rates. For this reason a continuous infusion of 500 ml/h of 1.5% peritoneal dialysis solution into the filter chamber was started, thus performing continuous arterio-venous hemodialysis (CAVHD) [5] (Fig. 1). With this technique we were able to add a diffusive mechanism to the convection achieved by CAVH. The association of CAVHD to conventional therapy markedly improved the urea clearence and laboratory data (Tables 1 and 2), and reduced to 50% the high mortality rate normally seen in this group of patients [6]. In the past we have suggested that the most important role of hemofiltration in septic-induced MOF is the elimination of middle molecular weight vasoactive peptides (MW 500-8000) which may play a crucial role in the development and progression of the abnormally high microvascular permeability (Capillary Leak Syndrome) [7]. Today we see that the main purpose of hemofiltration is to allow adequate fluid and nutritional therapy without restriction in order to control the hypercatabolic state, despite the acute oliguric renal failure. Yours sincerely, E. Barzilay, N. Weksler, D. Kessler and J. Prego

References 1. Miller SB, Anderson RJ (1986) The kidney in acute respiratory failure. J Crit Care 2:45 2. Gotloib L, Barzilay E, Shustak A, Lev A (1984) Sequential hemoflltration in non oliguric high permeability pulmonary edema of severe sepsis: preliminary report. Crit Care Med 100:358 3. Kramer P, Kaufhold G, Grone H J, Wigger W, Rieger J, Matthaei D, Stokke T, Burchardi H, Scheler F (1980) Management of anuric intensive-care patients with arteriovenous hemofiltration. Int J Artif Organs 3:225 4. Goris JA, Boekhorst te TPA, Nuytinck JKS, Gimbrere JSF (1985) Multiple-Organ Failure. Generalized autodestructive inflammation? Arch Surg 120:1109

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Fig. 1, Continuous arteriovenous natural hemofiltration/dialysis (CAVNHD) without pumps