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Biomedical subjects

J J Marini

Publications and source records attributed to J J Marini.

At least 19 recordsLinked to original sources
PubMed1992

Round table conference on ventilatory failure, Brussels, Belgium, March 16-18, 1991.

It was possible to reach agreement on several important issues relating to VF. First, the phenomenon of CO2 retention may have both pathophysiologic and compensatory components. There is increased awareness of the nature, intensity, and significance of the cross-talk between the ventilatory control center and the pump itself, as expressed in breathing pattern and indices of ventilatory drive. We are learning to interpret that information more effectively to assess functional reserve. Second, knowledge concerning the relative importance of various muscle groups is still incomplete, and the impact of disease on muscle function, lung mechanics, and ventilatory control is not fully understood. Dynamic hyperinflation and sleep disturbances provide two clear examples of conditions whose wide-ranging influence on drive, workload, and muscle function was, until quite recently, under appreciated. Finally, there was a general consensus that our therapeutic approaches to VF should be modified to reflect improved understanding of the pathogenesis of CO2 retention and iatrogenic lung injury. In the acute setting, measures to limit alveolar distention, such as controlling airway pressure, revising blood gas targets, and/or using adjunctive methods for blood gas exchange may avoid barotraumatic edema and rupture. The potential for non-invasive ventilation to avert intubation, facilitate ventilator withdrawal, and help patients with chronic VF to achieve compensation without machine dependence is now being actively investigated. This two day conference proved a stimulating forum for interchange of ideas regarding the state of the field, and allowed many opportunities for scientific interaction, both during outside the formal program.(ABSTRACT TRUNCATED AT 250 WORDS)

Europe↗
PubMed1992

Principles of mechanical ventilator use in respiratory failure.

Recent advances in our knowledge of the pathophysiology of acute and chronic respiratory failure have significantly revised our strategies for ventilatory support. Gas exchange, muscle function, barotrauma, and the course and prognosis of the mechanically ventilated patient are now better understood. Furthermore, impressive technological innovations have enabled the clinician to monitor patient-ventilator interactions closely and to undertake ventilatory approaches unthought of only a short time ago. The purpose of this review is to highlight key management principles and therapeutic options that derive from our improved understanding of respiratory failure and its treatment.

Humans↗
PubMed1992

Lung mechanics and gas exchange during pressure-control ventilation in dogs. Augmentation of CO2 elimination by an intratracheal catheter.

Increased awareness of pressure-related injury to the alveolar-capillary interface has renewed interest in modes of ventilation that limit alveolar distention such as pressure-controlled ventilation (PCV). We examined respiratory system mechanics and gas exchange during PCV in six dogs. Our data conformed to the predictions of our single-compartment mathematical model of respiratory dynamics during PCV (J Appl Physiol 1989; 67:1081-92). For a fixed pressure (Pset) and inspiratory time fraction (Tl/Ttot) (15 cm H2O and 0.3, respectively), minute ventilation (VE) reached a well-defined plateau as frequency (f) increased from 10 to 50 breaths/min and tidal volume (VT) fell progressively. Concomitantly, the physiologic dead-space fraction (VD/VT) increased from 0.50 +/- 0.04 to 0.85 +/- 0.04, and arterial PCO2 (PaCO2) rose from 39 +/- 4 to 76 +/- 12 mm Hg. At a fixed combination of frequency, applied pressure, and Tl/Ttot (40 breaths/min, 15 cm H2O, and 0.3), VE did not change when we introduced fresh gas continuously from an intratracheal catheter. However, PaCO2 and VD/VT fell progressively as catheter flow increased from zero to 14 L/min (60 +/- 12 to 40 +/- 12 mm Hg and 0.83 +/- 0.03 to 0.25 +/- 0.14 mm Hg, respectively). We conclude that during PCV at a fixed Pset and Tl/Ttot increasing frequency caused VT to fall and VE to reach a plateau. Declining VT was associated with a rise in PaCO2 because of a subsequent fall in alveolar ventilation. Insufflating fresh gas by an intratracheal catheter increased alveolar ventilation and improved CO2 elimination by washing out the anatomic dead space.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Tracheal gas insufflation during pressure-control ventilation. Effect of catheter position, diameter, and flow rate.

In the setting of acute lung injury, ventilatory strategies that adjust minute ventilation (VE) to achieve eucapnia often lead to alveolar rupture or damage. Tracheal gas insufflation (TGI) reduces the VE requirements of conventional mechanical ventilation by decreasing the effective dead-space fraction (VD/VT) of each breath. We studied the effect of catheter flow rate (Vcath) and position as well as catheter tip diameter and configuration on CO2 elimination during TGI-augmented pressure-controlled ventilation (PCV) in normal dogs. We studied three catheter positions (1, 5, and 10 cm above the carina) at Vcath of 2, 5, and 10 L/min (n = 6). When the catheter tip was positioned 1 cm above the carina, PaCO2 decreased significantly from a baseline (PCV alone) of 67 +/- 10 mm Hg to 52 +/- 11, 43 +/- 9, and 32 +/- 7 mm Hg (p < 0.05) at Vcath of 2, 5, and 10 L/min, respectively. For the same Vcath values, positioning the catheter tip 10 cm above the carina increased PaCO2 to 54 +/- 15, 46 +/- 12, and 40 +/- 11 mm Hg. Advancing the catheter tip 2 cm below the carina did not improve PaCO2 significantly (n = 3). At a catheter position of 1 cm above the carina and a Vcath of 10 L/min, changing the luminal inner diameter (1.5 versus 3.0 mm) or tip configuration (open tip versus occluded tip with two side holes) of the catheter did not change PaCO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Volume-cycled decelerating flow. An alternative form of mechanical ventilation.

The linearly decelerating flow waveform for volume-cycled mechanical ventilation is an option on many modern ventilators. We have developed mathematical models for two available forms of volume-cycled decelerating-flow ventilation (VCDF). These equations use clinician-chosen ventilator settings as inputs (frequency, tidal volume, peak inspiratory flow or inspiratory time fraction, and end-inspiratory pause), and patient-determined inputs which describe the patient's ventilatory impedance (inspiratory [RI] and expiratory [RE] resistance and respiratory system compliance [C]. The equations predict key outcome variables: mean airway pressure; and peak, mean, and end-expiratory alveolar pressures. The mathematical expressions were validated in a mechanical lung analog. Values observed in the test lung were compared to values predicted by the mathematical models for a wide range of ventilator settings and impedance combinations (RI and RE, 5 to 40 cm H2O.s/L; C, 0.02 to 0.10 L/cm H2O). The correspondence between observed and predicted values was generally excellent across the broad range of inputs tested (r greater than or equal to 0.98). Outcome variables were quite sensitive to clinician-chosen inputs over certain critical ranges. Carefully applied, VCDF offers several theoretic advantages for the clinical setting; however, appropriate caution must be exercised to avoid the application of tissue-injuring pressure.

Humans↗
PubMed1992

Validation of a technique to assess maximal inspiratory pressure in poorly cooperative patients.

The maximal pressure that can be generated during an inspiratory effort against an occluded airway serves as an index of respiratory muscle strength. We devised a method that permits accurate measurement of MIP, with near maximal values, and does not require patient cooperation. Twenty-two critically ill intubated patients performed MIP maneuvers before and after coaching. For the initial 11 patients, MIP was measured after the airway was occluded in 20 s with a one-way valve that permitted only exhalation. In the latter 11 patients, DS (approximately 1/3 VT) was added in an effort to increase respiratory drive before the noncoached MIP maneuver. We found no significant difference between coached and noncoached MIP maneuvers when P0.1 during the first 100 ms of inspiratory efforts prior to the noncoached MIP maneuver was greater than 2 cm H2O. Thus, MIP can be reliably measured in critically ill patients with or without coaching.

Adult↗
PubMed1992

Mean airway pressure: physiologic determinants and clinical importance--Part 1: Physiologic determinants and measurements.

PURPOSES: To discuss the theoretical relationship of mean alveolar pressure to its most easily measured analog, the mean airway pressure, and to describe the key determinants, measurement considerations, and clinical implications of this index. DATA SOURCES: Relevant articles from the medical and physiologic literature, as well as mathematical arguments developed in this article from first principles. STUDY SELECTION: Theoretical, experimental, and clinical information that elucidates the physiologic importance, measurement, or adverse consequences of mean airway pressure. DATA EXTRACTION: Mathematical models were used in conjunction with data from the published literature to develop a unified description of the physiological and clinical relevance of mean airway pressure. SYNTHESIS: Geometrical and mathematical analyses demonstrate that shared elements comprise mean airway pressure and mean alveolar pressure, two variables that are related by the formula: mean alveolar pressure = mean airway pressure + (VE/60) x (RE-RI), where VE, RE, and RI are minute ventilation and expiratory and inspiratory resistances, respectively. Clear guidelines can be developed for selecting the site of mean airway pressure determination, for specifying technical requirements for mean airway pressure measurement, and for delineating clinical options to adjust the level of mean airway pressure. Problems in viewing mean airway pressure as a reflection of mean alveolar pressure can be interpreted against the theoretical basis of their interrelationship. In certain settings, mean airway pressure closely relates to levels of ventilation, arterial oxygenation, cardiovascular function, and barotrauma. Because mean airway pressure is associated with both beneficial and adverse effects, a thorough understanding of its theoretical and practical basis is integral to formulating an effective pressure-targeted strategy of ventilatory support. CONCLUSIONS: Mean airway pressure closely reflects mean alveolar pressure, except when flow-resistive pressure losses differ greatly for the inspiratory and expiratory phases of the ventilatory cycle. Under conditions of passive inflation, mean airway pressure correlates with alveolar ventilation, arterial oxygenation, hemodynamic performance, and barotrauma. We encourage wider use of this index, appropriately measured and interpreted, as well as its incorporation into rational strategies for the ventilatory management of critical illness.

Airway Resistance↗
PubMed1992

Mean airway pressure: physiologic determinants and clinical importance--Part 2: Clinical implications.

PURPOSES: To discuss the theoretical relationship of mean alveolar pressure to its most easily measured analog, mean airway pressure, and to describe the key determinants, measurement considerations, and clinical implications of this index. DATA SOURCES: Relevant articles from the medical and physiological literature, as well as mathematical arguments developed in this article from first principles. STUDY SELECTION: Theoretical, experimental, and clinical information that elucidates the physiologic importance, measurement, or adverse consequences of mean airway pressure. DATA EXTRACTION: Mathematical models were used in conjunction with data from the published literature to develop a unified description of the physiological and clinical relevance of mean airway pressure. SYNTHESIS: Geometrical and mathematical analyses demonstrate that shared elements comprise mean airway pressure and mean alveolar pressure, two variables that are related by the formula: mean alveolar pressure = mean airway pressure + (VE/60) x (RE - RI), where VE, RE, and RI are minute ventilation and expiratory and inspiratory resistances, respectively. Clear guidelines can be developed for selecting the site of mean airway pressure determination, for specifying technical requirements for mean airway pressure measurement, and for delineating clinical options to adjust the level of mean airway pressure. Problems in viewing mean airway pressure as a reflection of mean alveolar pressure can be interpreted against the theoretical basis of their interrelationship. In certain settings, mean airway pressure closely relates to levels of ventilation, arterial oxygenation, cardiovascular function, and barotrauma. Because mean airway pressure is associated with both beneficial and adverse actions, a thorough understanding of its theoretical and practical basis is integral to formulating an effective pressure-targeted strategy of ventilatory support. CONCLUSIONS: Mean airway pressure closely reflects mean alveolar pressure, except when flow-resistive pressure losses differ greatly for the inspiratory and expiratory phases of the ventilatory cycle. Under conditions of passive inflation, mean airway pressure correlates with alveolar ventilation, arterial oxygenation, hemodynamic performance, and barotrauma. We encourage wider use of this index, appropriately measured and interpreted, as well as its incorporation into rational strategies for the ventilatory management of critical illness.

Adolescent↗
PubMed1991

Inverse ratio ventilation in ARDS. Rationale and implementation.

Conventional ventilatory support of patients with the adult respiratory distress syndrome (ARDS) consists of volume-cycled ventilation with applied positive end-expiratory pressure (PEEP). Unfortunately, recent evidence suggests that this strategy, as currently implemented, may perpetuate lung damage by overinflating and injuring distensible alveolar tissues. An alternative strategy--termed inverse ratio ventilation (IRV)--extends the inspiratory time, and, in concept, maintains or improves gas exchange at lower levels of PEEP and peak distending pressures. There are two methods to administer IRV: (1) volume-cycled ventilation with an end-inspiratory pause, or with a slow or decelerating inspiratory flow rate; or (2) pressure-controlled ventilation applied with a long inspiratory time. There are several real or theoretical problems common to both forms of IRV: excessive gas-trapping; adverse hemodynamic effects; and the need for sedation in most patients. Although there are many anecdotal reports of IRV, there are no controlled studies that compare outcome in ARDS patients treated with IRV as opposed to conventional ventilation. Nonetheless, clinicians are using IRV with increasing frequency. In the absence of well-designed clinical trials, we present interim guidelines for a ventilatory strategy in patients with ARDS based on the literature and our own clinical experience.

Humans↗
PubMed1990

Breath-stacking increases the depth and duration of chest expansion by incentive spirometry.

Although the objective of incentive spirometry is to achieve and hold high lung volumes, many patients with pain or weakness are unable to sustain the effort needed to perform effective exercises. We questioned whether using a one-way valve to prevent exhalation would allow rest between inspiratory efforts and cause volume to cumulate during successive tidal efforts, improving both the depth and duration of the inspiratory maneuver. We studied 26 cooperative but naive patients recovering from surgery, trauma, or critical illness whose pain or weakness impaired ability to achieve and sustain deep inspiration. All subjects breathed via mouthpiece from a spirometer prefilled with 100% oxygen. Three different maneuvers were performed in random order by all subjects: (1) standard inspiratory capacity without valve or inspiratory hold, (2) inspiratory capacity (IC) with breathholding aided by a one-way valve, and (3) uncoached breath-stacking, during which successive tidal breaths were cumulated by one-way valving. A fourth maneuver was added in the last 13 subjects studied: an initial coached IC effort with subsequent valved stacking of tidal efforts. When compared with IC, "breath stacking" (valved) maneuvers increased inspired volume by an average of 15 to 20% (p less than 0.05). More importantly, there was a severalfold increase in the time over which high lung volume was sustained (p less than 0.001). Our results indicate that one-way valving helps to achieve and sustain deep inspiration, even in uncoached patients.

Humans↗
PubMed1990

Strategies to minimize breathing effort during mechanical ventilation.

A primary objective of mechanical ventilation is to alleviate the intolerable effort of breathing while allowing the patient to perform enough work to prevent atrophy. By assuming the workload associated with breathing, mechanical support averts ventilatory failure, prevents respiratory arrest, assures CO2 removal and pH homeostasis, while permitting the overtaxed respiratory muscles to replenish energy reserves as the primary process is addressed. Skillful manipulation of the breathing workload can often facilitate the ventilator withdrawal process. The objectives of this article are to characterize the magnitude of ventilatory work performed by the machine and patient during mechanical ventilation and to formulate a strategy for minimizing the breathing workload.

Humans↗
PubMed1990

Lung mechanics in the adult respiratory distress syndrome. Recent conceptual advances and implications for management.

Since the earliest description of the adult respiratory distress syndrome (ARDS), impaired lung compliance has been a key diagnostic feature. Newer data suggest that a clear understanding of the mechanisms of acute lung injury may be needed to select the ventilatory pressures and patterns of flow delivery required for optimal gas exchange, adequate oxygen supply to tissue, and avoidance of barotrauma. This discussion briefly reviews the ARDS-specific derangements of lung mechanisms, describes measurement techniques applicable to the clinical setting, and suggests ways in which such information can be used in patient management.

Airway Resistance↗
PubMed1989

Systemic gas embolism complicating mechanical ventilation in the adult respiratory distress syndrome.

Most forms of barotrauma related to mechanical ventilation are known to occur in both adult and pediatric patients. The pressure-driven transfer of gas from the alveolar compartment to the systemic circulation, a devastating complication of ventilatory support in infants, is not generally recognized as a consequence of ventilatory support in adults. Two young adult patients who received ventilatory support with high levels of positive pressure for pneumonia and the adult respiratory distress syndrome developed massive sub-pleural air cysts, interstitial emphysema, and tension pneumothoraces. Despite receiving appropriate treatment for these problems, the patients had recurrent episodes of cerebral infarction, myocardial injury, and a characteristic pattern of livedo reticularis. This distinctive triad of findings, otherwise unexplained and occurring in the setting of cystic barotrauma, is highly suggestive of systemic gas embolism. Although our patients presented with dramatic clinical features, we believe that patients with ventilator-related gas embolism may present more commonly with subtler signs, such as puzzling disturbances in heart rhythm or mental status, seizure activity, hypotension, localized pain, or other embolic manifestations readily ascribed to other causes in critically ill patients.

Adult↗
PubMed1989

Determinants and limits of pressure-preset ventilation: a mathematical model of pressure control.

In recent years, four square-wave modes of pressure-preset mechanical ventilation (PPV)--pressure control, pressure support, inverse ratio, and airway pressure release ventilation--have been introduced to clinical practice. Conceptually, they share important features. Yet, because there remains widespread uncertainty regarding their ventilatory characteristics, efficacy, and appropriate use, the potential range of application is only now being investigated. To construct a unifying mathematical model of PPV, we developed a system of equations for prediction of the major "outcome" variables of PPV--tidal volume, minute ventilation, auto-positive end-expiratory pressure, mean alveolar pressure, and mechanical work--from the primary clinical "inputs" from patient (resistance, compliance) and clinician (applied pressure, frequency, inspiratory time fraction). Our analysis revealed distinct bounding limits for the outcome variables of ventilation and pressure and important implications for their clinical determinants. Although simplifying assumptions were required to enable construction of this mathematical analogue of respiratory system behavior, this model provides a firm conceptual framework for understanding the physiological interactions between PPV and the patients they are intended to help.

Humans↗