Limitations of volumetric indices obtained by trans-thoracic thermodilution.

Transthoracic thermodilution (TTT) measures cardiac output without the need for right heart catheterization. In addition, two volumetric hemodynamic indices have been derived from the mathematical analysis of the TTT curve: the global end diastolic volume (a quantitative measure of cardiac preload) and the extravascular lung water volume (a quantitative measure of pulmonary edema). Despite the undeniable appeal of these two novel parameters, uncertainty exists regarding both the validity of their mathematical derivation and their physiological significance. This concise review attempts to discuss such concerns.

Prolonged mechanical ventilation after critical illness.

A significant number of patients that have been critically ill require mechanical ventilation for extended periods of time as they progress towards recovery. Many of these patients can be cared for outside of the Intensive Care Unit in facilities focused on stabilizing the underlying medical problems, managing ventilatory support, and planning for rehabilitation and home care. Although these units have varied administrative structures, they have reported similar encouraging rates of weaning and survival. In a recent study about such a ward at a large academic hospital, it was observed that, although the majority of patients were liberated from the ventilator and returned home with a satisfactory activity level, a significant number of patients did not; these patients eventually died after a protracted hospital stay, mostly after a consensual withdrawal of life support. In the present article, a relevant literature review is presented concerning the outcome of patients undergoing prolonged mechanical ventilation. The main focus of the research was to address how to alleviate the burden of prolonged critical illness on mechanically ventilated patients who may eventually die after a great deal of suffering, and to identify the tangible emotional and financial costs to these patients, their families, and society.

Acute lung injury after pulmonary resection.

Primary Acute Lung Injury (ALI) after lung resection (or "post-pneumonectomy pulmonary edema") is a rare form of acute respiratory failure characterized by dyspnea, hypoxemia, diffuse infiltrates on chest radiogram, and rapid evolution often unresponsive to therapy. ALI occurs almost exclusively following pneumonectomy, within 3 days from surgery and without a preceding cause. Factors implicated in its pathogenesis may include excessive fluid administration, alveolar injury during one-lung ventilation, pulmonary hypertension, and impaired lymph drainage. There is no specific therapy. Suggested measures in the perioperative care include the meticulous maintenance of physiological stability, judicious fluid restriction, and the limitation of ventilatory volumes and pressures.

Pathophysiology and management of the flail chest.

Flail chest occurs when a series of adjacent ribs are fractured in at least 2 places, anteriorly and posteriorly. This section of the chest wall becomes unstable and it moves inwards during spontaneous inspiration. The physiological impact of a flail chest depends on multiple factors, including the size of the flail segment, the intrathoracic pressure generated during spontaneous ventilation, and the associated damage to the lung and chest wall. Treatment varies with the severity of the physiologic impairment attributable to the flail segment itself. Immediate surgical fixation may decrease morbidity, but conservative treatment with positive pressure ventilation is preferred when multiple injuries to the intrathoracic organs are present.

Different modes of assisted ventilation in patients with acute respiratory failure.

The aim of the present study was to verify that the patient/ventilator interaction is similar, regardless of the mode of assisted mechanical ventilation (i.e. pressure- or volume-limited) used, if tidal volume (VT) and peak inspiratory flow (PIF) are matched. Therefore, the authors compared the effects of three different modes of assisted ventilation on the work of breathing (WOB) and gas exchange in patients with acute respiratory failure. For Protocol 1, in seven patients, the authors compared pressure support, assist pressure control and assist control (with square and decelerating wave inspiratory flow pattern) set to deliver the same VT and PIF. For Protocol 2, in another 10 patients, the authors compared pressure support and assist control with high (0.8 L x s(-1)) and low (0.6 L x s(-1)) PIFs set to deliver the same VT. In Protocol 1, there was no difference in WOB and gas exchange between the three modes of assisted ventilation tested. In Protocol 2, the decrease of PIFs during assist control significantly increased WOB. In conclusion, different modes of assisted ventilation similarly reduce work of breathing and provide adequate gas exchange at fixed tidal volume and peak inspiratory flow only. During assist control, tidal volume and peak inspiratory flow (set by the physician) are the main determinants of the patient/ventilator interaction.

Hemodynamic monitoring.

The goal of hemodynamic monitoring is to maintain adequate tissue perfusion. Classical hemodynamic monitoring is based on the invasive measurement of systemic, pulmonary arterial and venous pressures, and of cardiac output. Since organ blood flow cannot be directly measured in clinical practice, arterial blood pressure is used, despite limitations, as estimate of adequacy of tissue perfusion. A mean arterial pressure (MAP) of 70 mm Hg may be considered a reasonable target, associated with sign of adequate organ perfusion, in most patients. In the approach to hypotension, which is the most common cause of hemodynamic instability in critical ill patients, increasing levels of monitoring may be used. Assuming that central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP) are adequate estimates of the volume of the systemic and pulmonary circulation respectively, the following decision tree is suggested: 1) make a working diagnosis based on the relationship between pressure (CVP and PAOP) and cardiac output or stroke volume (CO or SV); 2) consider conditions that may alter reliability of CVP and PAOP in estimate adequately circulating volumes such as abnormal pressure/volume relationship (compliance) of the RV or LV, increased intrathoracic pressure (PEEP, autoPEEP, intra-abdominal pressure), valvular heart disease (mitral stenosis); 3) look at the history; 4) separating RV and LV by reciprocal variations of CVP, PAOP and SV. CVP is often used as sole parameter to monitor hemodynamic. However CVP alone may not differentiate between changes in volume (different venous return curve) or changes in contractility (different starling curve). Finally, other techniques such as echocardiography, transesophageal Doppler and volume-based monitoring system are now available.

The effects of pressurization rate on breathing pattern, work of breathing, gas exchange and patient comfort in pressure support ventilation.

The aim of this study was to investigate the effects of different pressurization rates during pressure support ventilation on breathing pattern, work of breathing, gas exchange and patient comfort in patients with acute lung injury. The pressurization rate modifies the initial pressure ramp by changing the initial peak flow rate: the increase in pressurization rate is associated with a decrease in the time to reach the level of pressure support ventilation by increasing the peak flow rate. Ten intubated patients (age 64+/-17 yrs, body mass index 24+/-17 Kg x m(-2), arterial oxygen tension/inspired oxygen fraction 214+/-59) were studied in random order varying the pressurization rate at 5 and 15 cmH2O of pressure support ventilation. Breathing comfort was evaluated by a visual analogue scale. Increasing the pressurization rate caused an increase of peak flow rate from 473+/-141 mL x s(-1) to 758+/-302 mL x s(-1) at pressure support ventilation 5 (p<0.05) and from 481+/-126 mL x s(-1) to 1,121+/-175 mL x s(-1) at pressure support ventilation 15 (p<0.05). At the lowest pressurization rate the tidal volume was the lowest, the respiratory rate and the work of breathing were the highest (p<0.05) compared with other pressurization rates. Excluding the lowest pressurization rate, in all the other pressurization rates tested the breathing pattern and the work of breathing did not change. The lowest and the highest pressurization rates caused the worst patient comfort (p<0.05). The gas exchange was stable throughout the study. The presented results suggest: 1) the lowest pressurization rate caused the lowest tidal volume, highest respiratory rate and highest work of breathing; 2) at the other pressurization rates no differences in breathing pattern and work of breathing were observed; and 3) the patient's comfort was worse at the lowest and highest pressurization rates.

Permissive hypercapnia.

The term permissive hypercapnia defines a ventilatory strategy for acute respiratory failure in which the lungs are ventilated with a low inspiratory volume and pressure. The aim of permissive hypercapnia is to minimize lung damage during mechanical ventilation; its limitation is the resulting hypoventilation and carbon dioxide (CO2) retention. In this article we discuss the rationale, physiologic implications, and implementation of permissive hypercapnia. We then review recent clinical studies that tested the effect of various approaches to permissive hypercapnia on the outcome of patients with acute respiratory failure.

Intraoperative monitoring of myocardial ischemia.

Cardiovascular complications are commonly observed in surgical patients, and myocardial ischemia is the most important determinant of perioperative morbidity. The clinical criteria defining a patient population at increased risk for cardiovascular events are presented. The authors review the principles of monitoring and diagnosing myocardial ischemia, focusing on eletrocardiography and TransEsophageal Echocardiography. These patients must be closely followed long after the end of surgery, since the risk for cardiac morbidity is high for several hours postoperatively.

Comparison of the effects of nitric oxide, nitroprusside, and nifedipine on hemodynamics and right ventricular contractility in patients with chronic pulmonary hypertension.

STUDY OBJECTIVES: The effects of inhaled nitric oxide (NO) on hemodynamics and right ventricular (RV) contractility were compared with those of nitroprusside and nifedipine in 14 patients with severe chronic pulmonary hypertension. STUDY DESIGN: Micromanometer and balloon-tipped right heart catheterization were performed. Inhaled NO, IV nitroprusside, and sublingual nifedipine were administered sequentially while patients breathed > 90% oxygen. SETTING: Cardiac catheterization laboratory in a tertiary care teaching hospital. PATIENTS: Fourteen patients with severe pulmonary hypertension unrelated to left ventricular dysfunction. MEASUREMENTS AND RESULTS: During NO inhalation, mean systemic arterial pressure (MAP) was unchanged, but pulmonary artery (PA) pressure ([mean +/- SEM] 49 +/- 2 mm Hg vs 44 +/- 2 mm Hg; p < 0.01), pulmonary vascular resistance (PVR; 829 +/- 68 vs 669 +/- 64 dyne x s x cm(-5); p < 0.01) and RV end-diastolic pressure (RVEDP; 12 +/- 1 vs 10 +/- 1 mm Hg; p < 0.01) decreased. Stroke volume index (SVI; 31 +/- 2 vs 35 +/- 3 mL/m(2); p < 0.05) increased, and the first derivative of RV pressure at 15 mm Hg developed pressure (RV +dP/dt at DP15) was unchanged. During nitroprusside administration, MAP decreased (105 +/- 5 vs 76 +/- 5 mm Hg; p < 0.01), PA was unchanged (48 +/- 2 vs 45 +/- 3 mm Hg; p = not significant), and PVR decreased (791 +/- 53 vs 665 +/- 53 dyne x s x cm(-5); p < 0.01). RV +dP/dt at DP15 increased (425 +/- 22 vs 465 +/- 29 mm Hg/s; p < 0.05), but SVI was unchanged. Nifedipine decreased MAP (103 +/- 5 vs 94 +/- 5 mm Hg; p < 0.01), PA and PVR were unchanged, RVEDP increased (12 +/- 1 vs 14 +/- 2 mm Hg; p < 0.01), and RV +dP/dt at DP15 decreased (432 +/- 90 vs 389 +/- 21 mm Hg/s; p < 0.05). CONCLUSIONS: Inhaled NO is a selective pulmonary vasodilator in patients with chronic pulmonary hypertension that improves cardiac performance without altering RV contractility. Nitroprusside caused a similar degree of pulmonary vasodilation. In contrast to inhaled NO, nitroprusside caused systemic hypotension associated with an increase in RV contractility. Acute administration of nifedipine did not cause pulmonary vasodilation, but RVEDP increased and RV contractility decreased.

Nitric oxide: modulation of the pulmonary circulation.

Nitric oxide (NO) is synthetized throughout the body by the enzyme NO synthase (NOS), cyclic GMP transduction pathway causes pulmonary vasodilatation anti-platelets aggregation and inhibition of leukocyte adhesion. Inducible NOS is expressed in leukocytes in response to a variety of inflammatory stimuli and can be inhibited by corticosteroids. Inhaled NO is a selective pulmonary vasodilator. In USA inhaled NO was approved by FDA for hypoxemic respiratory failure in infants and children. In adults it may be useful in various clinical therapy: pulmonary hypertension, lung transplantation, ARDS but new clinical investigations are necessary.

Inhaled nitric oxide delivery by anesthesia machines.

UNLABELLED: Inhaled nitric oxide (NO) is a selective pulmonary vasodilator used to treat intraoperative pulmonary hypertension and hypoxemia. In contrast to NO delivered by critical care ventilators, NO delivered by anesthesia machines can be complicated by rebreathing. We evaluated two methods of administering NO intraoperatively: via the nitrous oxide (N(2)O) flowmeter and via the INOvent (Datex-Ohmeda, Madison, WI). We hypothesized that both systems would deliver NO accurately when the fresh gas flow (FGF) rate was higher than the minute ventilation (VE). Each system was set to deliver NO to a lung model. Rebreathing of NO was obtained by decreasing FGF and by simulating partial NO uptake by the lung. At FGF > or = VE (6 L/min), both systems delivered an inspired NO concentration ([NO]) within approximately 10% of the [NO] set. At FGF < VE and complete NO uptake, the N(2)O flowmeter delivered a lower [NO] (70 and 40% of the [NO] set at 4 and 2 L/min, respectively) and the INOvent delivered a higher [NO] (10 and 23% higher than the [NO] set at 4 and 2 L/min, respectively). Decreasing the NO uptake increased the inspired [NO] similarly with both systems. At 4 L/min FGF, [NO] increased by 10%-20% with 60% uptake and by 18%-23% with 30% uptake. At 2 L/min, [NO] increased by 30%-33% with 60% uptake and by 60%-69% with 30% uptake. We conclude that intraoperative NO inhalation is accurate when administered either by the N(2)O flowmeter of an anesthesia machine or by the INOvent when FGF > or = VE. IMPLICATIONS: Inhaled nitric oxide (NO) is a selective pulmonary vasodilator. In a lung model, we demonstrated that NO can be delivered accurately by a N(2)O flowmeter or by a commercial device. We provide guidelines for intraoperative NO delivery.

Use of inhaled nitric oxide for ARDS.

Inhalation of low inspired concentration of nitric oxide reduces pulmonary hypertension and increases arterial oxygen tension in patients with acute respiratory distress syndrome (ARDS), and appears to be safe. Research on the physiologic mechanisms regulating the action of inhaled nitric oxide may provide clinicians with ways to further potentiate and prolong its beneficial effects.

Physiologic determinants of the response to inhaled nitric oxide in patients with acute respiratory distress syndrome.

BACKGROUND: The response to inhaled nitric oxide (NO) in patients with acute respiratory distress syndrome (ARDS) varies. It is unclear which patients will respond favorably and whether the initial response persists over time. The authors defined a clinically useful response to inhaled NO as an increase of more than 20% of the ratio of the partial pressure of oxygen (Pa(O2)) to the inspiratory fraction of oxygen (FIO2), a decrease of more than 20% of pulmonary vascular resistance, or both. The authors hypothesized that patients who initially respond favorably are likely to show persistent improvements of gas exchange and hemodynamics after 48 h of NO inhalation. METHODS: The medical records and collected research data of 88 patients with ARDS who received 92 trials of NO inhalation between March 1991 and February 1996 were reviewed. RESULTS: Fifty-three of the 92 trials (58%) produced a clinically significant response to NO. In the responding patients who continued to receive NO therapy (n = 43), the Pa(O2)/FiO2 ratio remained higher (120 +/- 46 vs. 89 +/- 32 mmHg before NO; P < 0.01) and the mean pulmonary artery pressure remained lower (35 +/- 8 vs. 40 +/- 12 mmHg before NO; P < 0.01) at 48 h. Only 33% of the patients with septic shock responded to inhaled NO compared with 64% of those without septic shock (P < 0.02). CONCLUSIONS: Most patients with ARDS had clinically useful responses to NO inhalation. Patients with an initial favorable response maintained the improvement at 48 h. Patients with septic shock were less likely to respond favorably.