Henning Pontoppidan

Pulmonary Complications and Water Retention in Prolonged Mechanical Ventilation

Abstract In a retrospective study of 100 patients treated with prolonged mechanical ventilation, water retention without evidence of cardiac failure developed in 19. This was associated with radiologic evidence of pulmonary edema and with the following significant changes: a mean gain in weight of 2.6 kg; a mean increase in the alveolar-arterial oxygen tension gradient of 127 mm of mercury; a decrease in vital capacity of 29 per cent; a reduction in estimated compliance of 31 per cent; a fall in hematocrit of.13 percent; and a decrease in serum sodium of 5.80 mEq per liter. These changes were reversed after the institution of a negative water balance by restriction of water intake and by diuretic therapy. Radiologic improvement was usually prompt. The appearance of pulmonary edema may be related to a relative water overload, a rise in antidiuretic hormone production or subclinical cardiac failure.

Pulmonary barotrauma during mechanical ventilation

In the treatment of acute respiratory failure, pulmonary barotrauma (subcutaneous emphysema, pneumothorax, and pneumomediastinum) developed in ten patients (10%) receiving IPPV without PEEP and in seven patients (11%) receiving IPPV with PEEP. Pre-existing chronic obstructive pulmonary disease seemed to predispose to the development of pulmonary barotrauma. Necropsy findings revealed the presence of pneumonitis and pulmonary edema in the majority of patients, in addition to pulmonary emphysema in some. Available information fails to demonstrate a correlation between the incidence of pulmonary barotrauma and the magnitude of air-way pressure required for adequate mechanical ventilation. The addition of PEEP to IPPV during therapy for acute respiratory failure does not in-crease the incidence of pulmonary barotrauma.

Effect of mechanical ventilation with end-inspiratory pause on blood-gas exchange.

The effects of end-inspiratory pause (EIP) on gas exchange were measured in 10 adult patients with acute respiratory insufficiency while maintained on mechanical ventilation. Four inspiratory patterns were studied with a constant tidal volume (10 to 15 ml/kg body weight), respiratory rate (9 to 12 breaths/ min), FIO2 (0.5) and end-expiratory pressure. Inspiratory flow rate (&OV0312;insp) and EIP time were varied to produce a control pattern (&OV0312;insp = 60 L/min, EIP = 0), 2 EIP patterns of 0.6 and 1.2 seconds with a similar &OV0312;insp and a “slow” flow pattern (&OV0312;insp = 30 L/min) without EIP. The control pattern was applied before and after each study period.Arterial oxygenation was unchanged with both EIP and “slow” flow patterns when compared to control. Dead-space ventilation (VD/VT) and Paco2 were significantly decreased (p<0.01) as EIP was increased from 0 to 1.2 seconds, but remained unchanged with slow inspiratory flow. Thus, EIP improved the efficiency of ventilation with no apparent improvement in oxygenation in patients with acute respiratory insufficiency.

Inappropriate response to increased plasma ADH during mechanical ventilation in acute respiratory failure.

The effect of mechanical ventilation (IPPV) and positive end-expiratory pressure (PEEP) on plasma ADH was studied in eight patients with acute respiratory failure. The study was divided into two 60-minute periods, PEEP of 10 cm H2O being added to IPPV during first or second hour in random order. Mean decreases in urinary flow from 1.11 to 0.78 ml/min (P < 8.05) and cardiac index (determined in six patients) from 4.3 to 3.4 1/min/m2 (P < 0.01) were observed with PEEP. Although a twofold increase in plasma ADH (mean 8.1 to 18.8 μU/ml, P < 0.05) following PEEP was associated with a decrease in urinary flow, inconsistent changes in free-water and osmolal clearance and urinary osmolality point to an inappropriate response to increased ADH. The decrease in urinary flow and concurrent reduction in urinary sodium excretion suggest an overriding influence of the decrease in cardiac index on renal function.

Pathophysiologic Pathways of the Adult Respiratory Distress Syndrome

To achieve a better understanding of the pathogenesis of acute lung injury and effective prevention and therapy, the intensive care physician must recognize that most hospitalized patients with acute lung disease fall into two broad categories: n n1) n nA large group has ‘classic’ pulmonary complications. These often develop after surgery and are due to small airway closure, atelectasis, and/or pulmonary edema resulting from an elevated left atrial pressure without abnormally increased microcirculatory permeability. This type of acute respiratory failure (ARF) is characterized by preservation of basic pulmonary architecture, and as a rule it is preventable and reversible provided effective treatment is instituted early [43]. n n n n n2) n nA smaller population in which diffuse alveolar capillary membrane injury is commonly diagnosed as the adult respiratory distress syndrome (ARDS) [23, 40, 41]. Table 18.1 lists some of the diverse conditions which can produce this type of severe lung injury; each injury is characterized by an increased permeability to plasma proteins by the alveolar capillary membrane. Table 18.2 suggests possible pathophysiologic mechanisms leading to the acute lung injury.

Pathogenesis and therapy of acute lung injury

The purpose of this chapter is to review recent research in the pathogenesis and treatment of acute hypoxemic respiratory failure in man. For a more detailed review, the reader is referred to contemporary reviews and reports listed in References 27 and 55.

Case 21-1975

Presentation of Case A 20-year-old woman was admitted to the hospital because of pneumonia. She was in excellent health until one week previously, when she awoke with a headache and a mild sore thr...

From continuous positive-pressure breathing to ventilator-induced lung injury.

Continuous positive-pressure ventilation in acute respiratory failure. By Kumar A, Falke KJ, Geffin B, Aldredge CF, Laver MB, Lowentein E, Pontoppidan H. N Engl J Med 1970; 283:1430-6. Reprinted with permission. Continuous positive-pressure ventilation was used in eight patients with severe acute respiratory failure. Cardiac output and lung function were studied during continuous positive-pressure ventilation (mean end-expiratory pressure, 13 cm H2O) and a 30-min interval of intermittent positive-pressure ventilation. Although the mean cardiac index increased from 3.6 to 4.5 l/min per square meter of body surface area, the mean intrapulmonary shunt increased by 9% with changeover to intermittent positive-pressure ventilation. Satisfactory oxygenation was maintained in all patients during continuous positive-pressure ventilation with 50% inspired oxygen or less. With intermittent positive-pressure ventilation, arterial oxygen tension promptly fell by 161 mm of mercury, 79% occurring within 1 min. Prevention of air-space collapse during expiration and an increase in functional residual capacity probably explain improved oxygenation with continuous positive-pressure ventilation. In four patients, subcutaneous emphysema or pneumothorax developed. Weighed against the effects of prolonged hypoxemia, these complications were not severe enough to warrant cessation of continuous positive-pressure ventilation.

PROLONGED ARTIFICIAL VENTILATION: A QUANTITATIVE APPROACH.

A special five bed unit for the care of patients requiring tracheostomy and prolonged artificial ventilation was established at the Massachusetts General Hospital in 1961. More than 300 patients have been treated in this unit. This experience is the background for a discussion of the complex problems of choosing the type and pattern of ventilation, insuring adequate oxygenation and carbon dioxide elimination, and preventing and treating complications.

Weaning from Mechanical Ventilation

Weaning from mechanical ventilation is a poorly understood and often frustrating phase of management of acute respiratory failure (ARF) [6]. With the exception of diseases known to require prolonged, uninterrupted, mechanical ventilation (MV)—i.e., severe tetanus, polyneuritis, and massive chest trauma with severe flailing—consideration should be given to weaning from MV as soon as certain simple criteria are met. These criteria are as follows: (a) vital capacity > 4–5 ml/kg, (b) inspiratory force > 10 cm H2O, ( left( c right),,A - a{rm{ }}{P_{{O_2}}}; < ;350;torr, ) (d) positive end-expiratory pressure requirement < 10 cm H2O, (e) stable cardiovascular system, (f) chest-wall flailing not severe, and (g) close supervision by experienced physicians.