A decade of progress in critical care echocardiography: a narrative review.

INTRODUCTION: This narrative review focusing on critical care echocardiography (CCE) has been written by a group of experts in the field, with the aim of outlining the state of the art in CCE in the 10 years after its official recognition and definition. RESULTS: In the last 10 years, CCE has become an essential branch of critical care ultrasonography and has gained general acceptance. Its use, both as a diagnostic tool and for hemodynamic monitoring, has increased markedly, influencing contemporary cardiorespiratory management. Recent studies suggest that the use of CCE may have a positive impact on outcomes. CCE may be used in critically ill patients in many different clinical situations, both in their early evaluation of in the emergency department and during intensive care unit (ICU) admission and stay. CCE has also proven its utility in perioperative settings, as well as in the management of mechanical circulatory support. CCE may be performed with very simple diagnostic objectives. This application, referred to as basic CCE, does not require a high level of training. Advanced CCE, on the other hand, uses ultrasonography for full evaluation of cardiac function and hemodynamics, and requires extensive training, with formal certification now available. Indeed, recent years have seen the creation of worldwide certification in advanced CCE. While transthoracic CCE remains the most commonly used method, the transesophageal route has gained importance, particularly for intubated and ventilated patients. CONCLUSION: CCE is now widely accepted by the critical care community as a valuable tool in the ICU and emergency department, and in perioperative settings.

Correction to: A decade of progress in critical care echocardiography: a narrative review.

The original version of this article unfortunately contained a mistake.

Fluid and volume monitoring.

BACKGROUND: Fluid resuscitation is not only used to prevent acute kidney injury (AKI) but fluid management is also a cornerstone of treatment for patients with established AKI and renal failure. Ultrafiltration removes volume initially from the intravascular compartment inducing a relative degree of hypovolemia. Normal reflex mechanisms attempt to sustain blood pressure constant despite marked changes in blood volume and cardiac output. Thus, compensated shock with a normal blood pressure is a major cause of AKI or exacerbations of AKI during ultrafiltration. METHODS: We undertook a systematic review of the literature using MEDLINE, Google Scholar and PubMed searches. We determined a list of key questions and convened a 2-day consensus conference to develop summary statements via a series of alternating breakout and plenary sessions. In these sessions, we identified supporting evidence and generated clinical practice recommendations and/or directions for future research. RESULTS: We defined three aspects of fluid monitoring: i) normal and pathophysiological cardiovascular mechanisms; ii) measures of volume responsiveness and impending cardiovascular collapse during volume removal, and; iii) measured indices of each using non-invasive and minimally invasive continuous and intermittent monitoring techniques. The evidence documents that AKI can occur in the setting of normotensive hypovolemia and that under-resuscitation represents a major cause of both AKI and mortality ion critically ill patients. Traditional measures of intravascular volume and ventricular filling do not predict volume responsiveness whereas dynamic functional hemodynamic markers, such as pulse pressure or stroke volume variation during positive pressure breathing or mean flow changes with passive leg raising are highly predictive of volume responsiveness. Numerous commercially-available devices exist that can acquire these signals. CONCLUSIONS: Prospective clinical trials using functional hemodynamic markers in the diagnosis and management of AKI and volume status during ultrafiltration need to be performed. More traditional measure of preload be abandoned as marked of volume responsiveness though still useful to assess overall volume status.

Diagnostic workup, etiologies and management of acute right ventricle failure : A state-of-the-art paper.

INTRODUCTION: This is a state-of-the-art article of the diagnostic process, etiologies and management of acute right ventricular (RV) failure in critically ill patients. It is based on a large review of previously published articles in the field, as well as the expertise of the authors. RESULTS: The authors propose the ten key points and directions for future research in the field. RV failure (RVF) is frequent in the ICU, magnified by the frequent need for positive pressure ventilation. While no universal definition of RVF is accepted, we propose that RVF may be defined as a state in which the right ventricle is unable to meet the demands for blood flow without excessive use of the Frank-Starling mechanism (i.e. increase in stroke volume associated with increased preload). Both echocardiography and hemodynamic monitoring play a central role in the evaluation of RVF in the ICU. Management of RVF includes treatment of the causes, respiratory optimization and hemodynamic support. The administration of fluids is potentially deleterious and unlikely to lead to improvement in cardiac output in the majority of cases. Vasopressors are needed in the setting of shock to restore the systemic pressure and avoid RV ischemia; inotropic drug or inodilator therapies may also be needed. In the most severe cases, recent mechanical circulatory support devices are proposed to unload the RV and improve organ perfusion CONCLUSION: RV function evaluation is key in the critically-ill patients for hemodynamic management, as fluid optimization, vasopressor strategy and respiratory support. RV failure may be diagnosed by the association of different devices and parameters, while echocardiography is crucial.

Assessment of left ventricular contractile state by preload-adjusted maximal power using echocardiographic automated border detection.

OBJECTIVES: We sought to assess the ability of preload-adjusted maximal power measured by echocardiographic automated border detection (ABD) to quantify left ventricular (LV) contractility by determining the effects of alterations in preload, afterload and contractile state. BACKGROUND: Preload-adjusted maximal power can reflect LV contractile state relatively independent of changes in loading conditions. METHODS: Eight anesthetized dogs had placement of aortic electromagnetic flow probes, LV and arterial pressure catheters and inferior vena caval (IVC) occluders; four had placement of thoracic aortic balloon occluders. Echocardiographic ABD measures of cross-sectional area were used as a surrogate for LV volume, and flow was estimated as the first derivative of area with respect to time. Power was calculated as the product of flow and pressure. RESULTS: Preload independence during vena caval occlusions was achieved by preload adjustment (1/[end-diastolic area]3/2). Afterload independence was demonstrated by preload-adjusted maximal power being unaffected by acute increases in LV systolic pressure induced by aortic occlusion. ABD preload-adjusted maximal power reflected changes in contractile state: increasing with dobutamine infusion from 36+/-14 to 70+/-15 mW/cm4 (p < 0.05 vs. control) and decreasing with propranolol infusion from 35+/-13 to 17+/-7 mW/cm4 (p < 0.05 vs. control). These changes were significantly correlated with calculations of preload-adjusted maximal power using aortic flow (r = 0.90, SEE 10.5 mW/cm4) and load-independent measures of end-systolic elastance from pressure-area loops (r = 0.90, SEE 10.6 mW/cm4). Calculations of normalized preload-adjusted maximal power using arterial pressure were also closely correlated with similar calculations using LV pressure (r = 0.99, SEE 3%). CONCLUSIONS: Preload-adjusted maximal power using echocardiographic ABD can predict LV contractile state relatively independent of loading conditions and has potential for clinical application.

Assessment of left ventricular performance by on-line pressure-area relations using echocardiographic automated border detection.

OBJECTIVES: The purpose of this study was to evaluate left ventricular performance by on-line pressure-area relations using echocardiographic automated border detection in the in situ canine heart in a manner similar to pressure-volume analyses. BACKGROUND: Echocardiographic automated border detection can measure ventricular cavity area as an index of volume and may be interfaced with pressure to construct pressure-area loops on-line. METHODS: Eight anesthetized open chest dogs had simultaneous measurement of ventricular pressure, aortic flow and midventricular short-axis area. Pressure-area loops were constructed by a computer workstation interfaced with the ultrasound system. Stroke area (Maximal area--Minimal area) and stroke force (integral of P dA [P = pressure; A = area]) values during inferior vena cava (n = 8) and aortic (n = 4) occlusions were compared with stroke volume and estimates of stroke work, respectively. Inotropic modulation was induced with dobutamine infusion (2 to 5 micrograms/kg body weight per min), followed by propranolol infusion (2 to 5 mg). End-systolic and maximal elastance and preload recruitable stroke force (stroke force versus end-diastolic area) were derived for each period. RESULTS: Changes in stroke area and stroke force were significantly correlated with changes in stroke volume and estimates of stroke work during caval occlusion (n = 8) (r = 0.87 +/- 0.02, SEE = 8 +/- 1% and r = 0.90 +/- 0.03, SEE = 8 +/- 2%, respectively). In dogs with aortic occlusion (n = 4), changes in stroke area significantly correlated with changes in stroke volume for pooled data (r = 0.84, SEE = 8%, y = 1.0x + 3). Ventricular performance increased with dobutamine infusion (n = 7): end-systolic elastance 30 +/- 11 to 67 +/- 24 mm Hg/cm2 (p < 0.02 vs. control values); maximal elastance 37 +/- 11 to 82 +/- 26 mm Hg/cm2 (p < 0.02 vs. control values); preload recruitable stroke force 81 +/- 24 to 197 +/- 92 mm Hg (p < 0.02 vs. control values). Decreases occurred with propranolol infusion (n = 5) end-systolic elastance 20 +/- 4 to 13 +/- 4 mm Hg/cm2 (p < 0.002 vs. control values); maximal elastance 29 +/- 8 to 15 +/- 5 mm Hg/cm2 (p < 0.002 vs. control values); preload recruitable stroke force 66 +/- 14 to 40 +/- 9 mm Hg (p < 0.002 vs. control values). CONCLUSIONS: On-line pressure-area relations are a potentially useful means to assess left ventricular performance in a manner that is quantitatively similar to the predicted responses of pressure-volume relations.

Suppression of cytokine-mediated beta2-integrin activation on circulating neutrophils in critically ill patients.

The beta2 integrin CD11b plays a central role in inflammation and the systemic inflammatory response syndrome (SIRS). The CD11b molecule activates in two ways: the density of membrane-bound CD11b up-regulates and the molecule undergoes a conformational change that confers adhesiveness to counter-receptors. We studied the kinetics of CD11b activation in patients with SIRS. We found a significantly diminished CD11b activation in response to tumor necrosis factor alpha (TNF-alpha). This affected all circulating polymorphonuclear neutrophils (PMN) and was an intrinsic property of the cells and not due to antagonism by soluble TNF-alpha receptors or loss of cellular receptors for TNF-alpha. Diminished responsiveness correlated with the severity of organ failure and lasted for months in some patients but had no impact on mortality. We speculate that reduced CD11b responsiveness in SIRS contributes to the high risk of recurrent infection, but that it may also be protective against excessive PMN activation within the vascular space.

Therapeutic advances in the treatment of Peyronie's disease.

Peyronie's disease (PD) is an under-diagnosed condition with prevalence in the male population as high as 9%. It is a localized connective tissue disorder of the penis characterized by scarring of the tunica albuginea. Its pathophysiology, however, remains incompletely elucidated. For the management of the acute phase of PD, there are currently numerous available oral drugs, but the scientific evidence for their use is weak. In terms of intralesional injections, collagenase clostridium histolyticum is currently the only Food and Drug Administration-approved drug for the management of patients with PD and a palpable plaque with dorsal or dorsolateral curvature >30°. Other available intralesional injectable drugs include verapamil and interferon-alpha-2B, however, their use is considered off-label. Iontophoresis, shockwave therapy, and radiation therapy have also been described with unconvincing results, and as such, their use is currently not recommended. Traction therapy, as part of a multimodal approach, is an underused additional tool for the prevention of PD-associated loss of penile length, but its efficacy is dependent on patient compliance. Surgical therapy remains the gold standard for patients in the chronic phase of the disease. In patients with adequate erectile function, tunical plication and/or incision/partial excision and grafting can be offered, depending on degree of curvature and/or presence of destabilizing deformity. In patients with erectile dysfunction non-responsive to oral therapy, insertion of an inflatable penile prosthesis with or without straightening procedures should be offered.

On-line estimation of changes in left ventricular stroke volume by transesophageal echocardiographic automated border detection in patients undergoing coronary artery bypass grafting.

Echocardiographic automated border detection can determine the interface between blood and myocardial tissue and calculate left ventricular (LV) cavity area in real-time. The objective was to determine if on-line measurements of LV cavity area by transesophageal automated border detection could be used to determine beat-to-beat changes in stroke volume in humans. Studies were attempted on 9 consecutive patients, aged 66 +/- 8 years, undergoing coronary bypass surgery. Stroke volume was measured by electromagnetic flow from the ascending aorta, and LV cavity area was measured at the midventricular short-axis level. Simultaneous area and flow data were recorded on a computer workstation through a customized interface with the ultrasound system. Recordings were performed during baseline apnea and rapid alterations induced by inferior vena caval occlusions before and after cardiopulmonary bypass. Measurements of stroke area (maximal area-minimal area) were correlated with stroke volume for matched beats. Data were available for analysis on 8 of 9 patients before and on 5 patients after cardiopulmonary bypass for 644 beats. Stroke area was closely correlated with stroke volume both before (mean R = 0.94 +/- 0.03, SEE = 0.33 +/- 0.12 cm2) and after (mean R = 0.92 +/- 0.05, SEE = 0.59 +/- 0.81 cm2) cardiopulmonary bypass. The slopes of these stroke area-stroke volume relations were quite reproducible from before to after cardiopulmonary bypass in the same patient but varied between individual patients. Transesophageal automated border detection has potential for on-line estimation of changes in stroke volume in selected patients.

Changes in electrocardiographic morphology reflect instantaneous changes in left ventricular volume and output in cardiac surgery patients.

We examined the relation between changes in R-to-T wave amplitude ratios (R:T) and left ventricular (LV) performance as cardiac output was rapidly varied by inferior vena caval occlusion in 6 subjects prior to cardiopulmonary bypass. To assess the influence of contractility, paired studies before and after bypass were performed in 4 subjects. Stroke volume and cardiac output were assessed by aortic flow probe, and transesophageal echocardiographic LV area measures using the automated border-detection method were used to give LV stroke area, stroke force, maximal LV area, fractional area change, end-systolic elastance, and preload recruitable stroke force. Data were collected on computer and analyzed by linear regression. Significant changes in R:T and measured LV variables during the inferior vena caval occlusion were stroke volume (r = 0.81), LV stroke area (r = 0.77), LV stroke force (r = 0.81), maximal LV area (r = 0.78), and cardiac output (r = 0.80). However, R:T varied inconsistently in relation to fractional area change. After cardiopulmonary bypass, the linear relation between R:T with LV stroke force, LV stroke volume, and maximal LV area persisted, but at a lesser slope. Although absolute pre-inferior vena caval occlusion R:T did not correlate with end-systolic elastance or preload recruitable stroke force, the change in the slope of these linear relations correlated well with the change in end-systolic elastance after surgery (r = 0.92). Instantaneous changes in electrocardiographic morphology reflect changes in LV preload-dependent variables, whereas long-term changes in electrocardiographic morphology may also reflect changes in contractile state.

Etiology of metabolic acidosis during saline resuscitation in endotoxemia.

We sought to understand the mechanism of metabolic acidosis that results in acute resuscitated endotoxic shock. In six pentobarbital-anesthetized dogs, shock was induced by Escherichia coli endotoxin infusion (1 mg/kg) and was treated with saline infusion to maintain mean arterial pressure > 80 mmHg. Blood gases and strong ions were measured during control conditions and at 15, 45, 90, and 180 min after endotoxin infusion. The mean saline requirement was 1833+/-523 mL over a 3 h period. The total acid load from each source was calculated using the standard base deficit. The mean arterial pH decreased from 7.32 to 7.11 (p < .01); pCO2 and lactate were unchanged. Saline accounted for 42% of the total acid load. However, 52% of the total acid load was unexplained. Although serum Na+ did not change, serum Cl-increased (127.7+/-5.1 mmol/L vs. 137.0+/-6.1 mmol/L; p=.016). We conclude that saline resuscitation alone accounts for more than one-third of the acidosis seen in this canine model of acute endotoxemia, whereas lactate accounts for less than 10%. A large amount of the acid load can be attributed to differential Na+ and Cl- shifts from extravascular to vascular spaces.

Cardiac augmentation by phasic high intrathoracic pressure support in man.

Left ventricular performance can be significantly influenced by changes in intrathoracic pressure. In man, sustained increases in intrathoracic pressure unload the left ventricle, but since venous return decreases, increased intrathoracic pressure is associated with a decreased cardiac output. In a canine model of acute ventricular failure, it has been shown that phasic increases in intrathoracic pressure, which do not decrease venous return, improve steady-state cardiac output. We thus studied the cardiovascular effects of phasic high intrathoracic pressure support (PHIPS) in seven patients with shock in our intensive care unit whose condition was not responsive to conventional types of therapy. The PHIPS was generated by abdominal and chest wall binding during positive-pressure ventilation. As compared to the state before PHIPS, the PHIPS was associated with an increase in esophageal pressure (6.6 +/- 1.1 mm Hg; p less than 0.01) and in mean arterial pressure (43.0 +/- 6.1 to 51.0 +/- 7.7 mm Hg; p less than 0.01) while not changing arterial pressure relative to esophageal pressure. Cardiac output also increased from 3.6 +/- 0.5 to 4.2 +/- 0.6 L/min (p less than 0.05), while left ventricular filling pressures remained constant. In one subject a gated cardiac blood pool scan demonstrated a PHIPS-associated increase in ejection fraction and decreased end-diastolic volume. These results are consistent with the hypothesis that PHIPS, by increasing intrathoracic pressure, augments left ventricular performance by reducing left ventricular afterload. This appears to be a promising area for future research.

Cardiopulmonary effects of positive pressure ventilation during acute lung injury.

STUDY OBJECTIVES: To assess the gas exchange and hemodynamic effects of pressure-limited ventilation (PLV) strategies in acute lung injury (ALI). We hypothesized that in ALI, the reduction of plateau airway pressure (Paw) would be associated with less alveolar overdistention and thus have better hemodynamic and gas exchange characteristics than larger tidal volume (Vr) ventilation. SETTING: Laboratory. DESIGN: Prospective time-controlled sequential animal study. MEASUREMENTS: Right atrial, pulmonary artery, left atrial, arterial, lateral pleural (Ppl), and pericardial (Ppc) pressures, Paw, ventricular stroke volume, mean expired CO2, and arterial and mixed venous oxygen contents. Airway resistance and static lung compliance were also measured. INTERVENTIONS: Intermittent positive pressure ventilation (IPPV) given before (control) and after induction of ALI by oleic acid infusion (0.1 mL/kg). IPPV at FIO2 of 1, VT of 12 mL/kg, and frequency adjusted to maintain normocarbia. ALI PLV was given during ALI and defined as that VT which gave a similar plateau Paw to that of control IPPV. High-frequency jet ventilation (HFJV) and ALI HFJV were also given and defined as frequency within 10% of heart rate and mean Paw similar to that during control IPPV. RESULTS: After ALI, static lung compliance, PaO2, and pH decreased, whereas airway resistance and PaCO2 increased. For a constant lung volume, Ppl and Ppc were not different between control and ALI. Both absolute dead space (VD) and intrapulmonary shunt fraction increased after ALI, but absolute VD was lower with ALI PLV and ALI HFJV when compared with ALI IPPV. Ventilation did not alter hemodynamics during ALI. CONCLUSIONS: Changes in lung volume determine Ppc and Ppl. PLV strategies do not alter hemodynamics but result in less of an increase in VD/VT than would be predicted from the obligatory decrease in VT.

Transvisceral lactate fluxes during early endotoxemia.

The pathogenesis of hyperlacticemia during sepsis is poorly understood. We investigated the role of lung, kidney, gut, liver, and muscle in endogenous lactate uptake and release during early endotoxemia in an intact, pentobarbital-anesthetized dog model (n = 14). Ultrasonic flow probes were placed around the portal vein and hepatic, renal, and femoral arteries. After splenectomy, catheters were inserted into the pulmonary artery, aorta, and hepatic, left renal, and femoral veins. Whole blood lactate and blood gases from all catheters, organ flows, and cardiac output were measured before and 30 to 45 min after a bolus infusion of Eacherichia coli endotoxin (1 mg/kg). After endotoxin infusion, mean arterial blood lactate level increased from 0.92 +/- 0.11 to 1.60 +/- 0.15 mmol/L (p < 0.0001). Lung lactate flux changed from uptake to release of lactate adding a mean of 9.97 +/- 16.23 mmol/h (p < 0.05) to the systemic circulation. Liver and muscle lactate fluxes remained neutral at all times, while kidney and gut took up lactate from the circulation both before and after endotoxin infusion (mean renal uptake, 2.73 +/- 3.85 mmol/L; p < 0.001; mean gut uptake, 2.46 +/- 2.31 mmol/h; p < 0.002). Except for the kidney, where a decrease in blood flow correlated with diminished uptake, there was no correlation between changes in transvisceral lactate fluxes and organ or systemic oxygen delivery during endotoxemia. A positive correlation between lactate uptake and oxygen consumption during endotoxemia was seen for both gut (p < 0.0001) and kidney (p < 0.002). We conclude that, in the dog, the pathogenesis of endotoxin-induced hyperlacticemia is complex. The lung may be responsible for significant lactate release, and other viscera that normally take up lactate are unable to adequately clear this increased lactate.

Measurements of right ventricular volumes during fluid challenge.

The effects of fluid loading on RV function were studied in 41 acutely ill patients monitored with a modified pulmonary artery catheter equipped for measuring RVef. Hemodynamic evaluation was performed before and after infusion of 300 ml of 4.5 percent albumin solution in 30 min. Changes in SI did not correlate with Pra or Ppao but did with RVEDVI. For the entire group, RVef was unchanged (27 +/- 9 vs 27 +/- 9 percent). In the eight patients with an initial RVEDVI greater than 140 ml/m2, the fluid challenge increased Pra and Ppao and reduced LVSWI without any other significant effect. There was no significant correlation between RVEDVI and Pra and only a weak correlation between RVESVI and Ppa. However, there was a highly linear correlation between both RVEDVI and RVESVI and changes in RVEDVI and in RVESVI, suggesting that in the absence of severe pulmonary hypertension RV output is primarily dependent on RV preload.

Monitoring the effect of CPAP on left ventricular function using continuous mixed-blood saturation.

The hypothetic benefit of CPAP on cardiac performance and on a reduction in VO2 was tested in a patient before heart transplantation after acute myocardial infarction using continuous SvO2 monitoring. The CPAP added to inotropic support (enoximone plus dobutamine) and intraaortic balloon pumping dramatically increased SvO2 in relation to both an increase in cardiac output and a decrease in VO2 secondary to respiratory work reduction, validating the initial hypotheses.