Increase In Intrathoracic Pressure Research Articles

Spontaneous Hemomediastinum Complicating Steroid-Induced Mediastinal Lipomatosis

Spontaneous hemomediastinum is a rare event, occurring in association with bleeding disorders, intratumoral bleeding, or following an abrupt increase in intrathoracic pressure. We report the case of a patient with systemic lupus erythematosus, nephrotic syndrome, and renal failure, in whom mediastinal lipomatosis (ML) developed following increased corticosteroid therapy. Anticoagulant therapy likely precipitated a massive spontaneous hemomediastinum secondary to diffuse hemorrhage of mediastinal fat, which required emergency decompressive surgery. Steroid-induced ML is common and usually well tolerated, but clinicians should be aware of its potential risk of bleeding when associated with anticoagulant therapy. This case further emphasizes the bleeding complications of treatment with low-molecular-weight heparin in patients with renal failure.

Effects of hypoxia on diaphragm activity in anesthetized rats

Hypoxia is one of the most common conditions observed by PACU nurses after surgery. It may be caused by a reduced functional residual capacity, hypoventilation, and/or ventilation-perfusion mismatch. Hypoxia can also affect diaphragm contractility, making it difficult to wean postoperative patients from mechanical ventilation. Clinically, however, there is no method to directly measure diaphragm contractility; therefore, indicators of intrathoracic pressure such as tidal volume are used. The purpose of this study was to directly measure the effects of diaphragm shortening in 12 anesthetized Sprague-Dawley rats before, during, and after induced hypoxia. A miniaturized ultrasonic sensor was used to measure changes in diaphragm thickness as an index of diaphragm shortening. A stainless steel electrode was attached adjacent to the ultrasonic sensor and used to measure the electromyogram (EMG) of the diaphragm. After normoxic measurements were recorded, hypoxia was initiated by connecting the tracheal cannula to a latex balloon containing 7.4% oxygen in nitrogen. During the first 5 minutes of hypoxia, diaphragm shortening, EMG, and intrathoracic pressure increased. Over the next 30 to 100 minutes, EMG and intrathoracic pressure remained elevated, whereas diaphragm shortening decreased to 50% of control, which was defined as diaphragm fatigue. The mean time for hypoxia-induced diaphragm fatigue to occur was 63 minutes. These results indicate that hypoxia-induced decline in diaphragm shortening was not caused by a decrease in muscle excitation as measured by EMG. These data suggest that impairment in mechanical-chemical coupling (diaphragm shortening) could be a result of decreased oxygen availability associated with the lower arterial blood oxygen content. Thus, the increase in intrathoracic pressure throughout hypoxia suggests that intrathoracic pressure is not always a consistent index of the contractile state of the diaphragm. © 2001 by American Society of PeriAnesthesia Nurses.

High-frequency jet ventilation in life-threatening bilateral pulmonary contusion.

TRAUMA is the leading cause of death among young people in developed countries. 1 Because up to 80% of trauma deaths occur during the first 24 h after trauma, 1 early resuscitation and rapid assessment of trauma lesions are of paramount importance to improving the prognosis. Among traumatic lesions, pulmonary contusion is frequent but has not been recognized as an independent prognosis factor. 2-4 In very few cases, pulmonary contusion may lead to severe hypoxia and hypercarbia, which cannot be adequately controlled using conventional mechanical ventilation. Hypoxia and hypercarbia may have deleterious effects, such as enhancement of brain injury and development of circulatory shock. 5 In the most severe cases, aggressive therapeutic methods, such as extracorporeal membrane oxygenation (ECMO), have been reported. 6 At our institution, high-frequency jet ventilation (HFJV) has been used routinely for many years for the treatment of severe acute respiratory distress syndrome. 7,8 We report a series of severe trauma patients with life-threatening pulmonary contusion successfully treated with HFJV when the conventional mechanical ventilation approach failed to provide appropriate gas exchange. The current data suggest that HFJV can be a life-saving technique in severely hypoxemic patients with bilateral pulmonary contusion.

A Case of Fatal Paradoxical Fat Embolism Syndrome Detected by Intraoperative Transesophageal Echocardiography

We report a case of paradoxical fat embolism syndrome (PFES) detected by intraoperative transesophageal echocardiography (TEE). Case Report A 30-yr-old male truck driver with no history of cardiac or cerebral disease was admitted to the intensive care unit after his truck was struck by another truck from behind, and the dashboard trapped him. On arrival, he had no apparent neurological deficit, with normal findings on brain computed tomography (CT). Tachypnea (36 breaths/min), tachycardia (81 bpm), and hypercapnia (Paco2: 55.0 mm Hg) with normal oxygenation and normal arterial blood pressure were observed. Surgery was performed to fixate the closed fractures of the right femoral shaft fracture with intramedullary nails (with 12-mm diameter and 38-cm length) during general anesthesia. Approximately 90 min after starting the operation, a decreased end-tidal CO2 and oxygen saturation (Spo2) occurred followed by hypercapnia, hypoxia, tachycardia, hypotension, and pulmonary hypertension (pulmonary artery pressure was 46/29 mm Hg). TEE revealed multiple small vesicles in all four heart chambers (Fig. 1), marked pulmonary artery dilation, and depression of contraction of the right ventricle. PFES was strongly suspected, and the operation was completed as quickly as possible.Figure 1: Transesophageal echocardiographic four-chambers’ view, showing massive fat emboli in the left atrium (LA), left ventricle (LV), and Aorta (Ao). Shown are multiple small echogenic vesicles in the LA, LV, and Ao. Contraction of the right ventricle (RV) was decreased, and ventricular septum was overhung toward the LV.Postoperatively, the patient remained in a coma. Brain CT findings were almost the same as those of preoperative examination both immediately after, and 3 h after, the operation. However, there was severe global edema in both cerebral hemispheres at 8 h after the operation. After hypothermic therapy with a blood temperature of 34°C for 3 days, the patient remained in a coma; cerebral edema was observed on brain CT, which did not improve. Contrast TEE using plasma protein fraction revealed the appearance of microbubbles in both atria almost simultaneously. However, the location of the shunt was not identified by color Doppler echocardiography. Phagocytosis of fat vesicles by macrophages was also demonstrated in both pulmonary and arterial blood samples (Fig. 2) and a bronchoalveolar lavage fluid sample. The patient died on the ninth hospital day of severe hypotension caused by brain herniation. The request to perform an autopsy was denied by his family.Figure 2: Phagocytosis of fat vesicles by macrophages was demonstrated in arterial blood samples on the second hospital day. The triangle shows macrophages, including fat vesicles with Sudan stain.Discussion Intraoperative TEE yields real-time information on the frequency of embolic events during intramedullary procedures (1–3). In our case, the appearance of fat vesicles was observed continuously independently of surgical manipulations. However, it was difficult to distinguish between fat particles and microbubbles. No definitive treatment for PFES has been established. It has generally been reported that early stabilization of fracture sites decreases the incidence of fat embolism (4). When PFES is suspected, intramedullary procedures should be discontinued and other treatment options for long-bone fracture considered (5,6). We selected general anesthesia for the patient, because massive intraoperative bleeding was anticipated. However, mechanical positive-pressure ventilation would increase both intrathoracic pressure and right atrial pressure, possibly causing functional right-to-left shunt. One possible option to prevent an increase in intrathoracic pressure would be the use of other anesthetic techniques, such as continuous epidural or spinal anesthesia.

Heart rate variability and hemodynamic alterations in canines with normal cardiac function during exposure to pressure support, continuous positive airway pressure, and a combination of pressure support and continuous positive airway pressure.

Variations in intrathoracic pressure generated by different ventilator weaning modes may significantly affect intrathoracic hemodynamics and cardiovascular stability. Although several investigators have attributed cardiovascular alterations during ventilator weaning to augmented sympathetic tone, there is limited investigation of changes in autonomic tone during ventilator weaning. Heart rate variability (HRV), the analysis of beat-to-beat changes in heart rate, is a noninvasive indicator of autonomic tone that might be useful in the identification of patients who are at risk for weaning difficulty due to underlying cardiac dysfunction. The authors describe HRV and hemodynamics in response to 3 ventilatory conditions: pressure support (PS) 10 cmH2O, continuous positive airway pressure (CPAP) 10 cmH2O, and a combination of PS 10 cmH2O and CPAP 10 cmH2O (PS + CPAP) in a group of canines with normal ventricular function. Six canines were studied in the laboratory. Continuous 3-lead electrocardiographic data were collected during baseline (controlled mechanical ventilation) and following transition to each of the ventilatory conditions (PS, CPAP, PS + CPAP) for analysis of HRV. HRV was evaluated using power spectral analysis to define the power under the curve in a very low frequency range (0.0033 to < 0.04 Hz, sympathetic tone), a low frequency range (0.04 to < 0.15 Hz, primarily sympathetic tone), and a high frequency range (0.15 to < 0.40 Hz, parasympathetic tone). A thermodilution pulmonary artery catheter measured cardiac output and right ventricular end-diastolic volume to describe global hemodynamics. There were significant increases in very low frequency power (sympathetic tone) with a concomitant significant reduction in high-frequency power (parasympathetic tone) with exposure to PS + CPAP. These alterations in HRV were associated with significantly increased heart rate and reduced right ventricular end-diastolic volume. Although there was a small but significant increase in cardiac output with exposure to PS, HRV was unchanged. These data indicate that there was a relative shift in autonomic balance to increased sympathetic and decreased parasympathetic tone with exposure to PS + CPAP. The increase in intrathoracic pressure reduced right ventricular end-diastolic volume (preload). This hemodynamic alteration generated a change in autonomic tone, so that cardiac output could be maintained. Individuals with autonomic and/or cardiovascular dysfunction may not be capable of this type of response and may fail to successfully wean from mechanical ventilation.

Cardiorespiratory interactions during resistive load breathing.

The addition to the respiratory system of a resistive load results in breathing pattern changes and in negative intrathoracic pressure increases. The aim of this study was to use resistive load breathing as a stimulus to the cardiorespiratory interaction and to examine the extent of the changes in heart rate variability (HRV) and respiratory sinus arrhythmia (RSA) in relation to the breathing pattern changes. HRV and RSA were studied in seven healthy subjects where four resistive loads were applied in a random order during the breath and 8-min recording made in each condition. The HRV spectral power components were computed from the R-R interval sequences, and the RSA amplitude and phase were computed from the sinusoid fitting the instantaneous heart rate within each breath. Adding resistive loads resulted in 1) increasing respiratory period, 2) unchanging heart rate, and 3) increasing HRV and changing RSA characteristics. HRV and RSA characteristics are linearly correlated to the respiratory period. These modifications appear to be linked to load-induced changes in the respiratory period in each individual, because HRV and RSA characteristics are similar at a respiratory period obtained either by loading or by imposed frequency breathing. The present results are discussed with regard to the importance of the breathing cycle duration in these cardiorespiratory interactions, suggesting that these interactions may depend on the time necessary for activation and dissipation of neurotransmitters involved in RSA.

Localized airway anesthesia with lidocaine partially suppresses cardiovascular responses To lung inflation.

Lung inflation causes cardiovascular suppression via an increase in intrathoracic pressure and neural mechanisms. To examine the mechanisms involved, we mea-sured the heart rate (HR) and arterial blood pressure (AP) responses to lung inflation before and after spraying the bronchi with lidocaine to suppress airway reflex. Thirty women participated in the study. One group (n = 20, Group BT) had their tracheas intubated by using double-lumen tubes. The other group (n = 10, Group TT) received an ordinary endotracheal tube. They were all studied under general anesthesia by using nitrous oxide, isoflurane, and muscle relaxation after a thiopental induction. In each patient, airway pressure was increased for 3 s, and changes in HR and AP were measured. Lung inflation was repeated after 5 mL of 4% lidocaine had been sprayed into the main bronchi unilaterally in Group BT or bilaterally in Group TT. There were no significant differences in cardiovascular responses between left and right lung inflation with the pressure at 20 and 30 cm H(2)O. Both lungs inflated at 20 cm H(2)O caused an increase in HR with a significantly greater decrease in AP than with unilateral inflation. Anesthesia of the bronchi abolished the HR increase, but not the AP decrease. Lung inflation at 30 cm H(2)O caused significant decreases in HR and AP which were not affected with topical anesthesia. These results indicate that the cardiovascular responses elicited by lung inflation in anesthetized humans are predominantly the direct effect of the increase in intrathoracic pressure, although sympathetic afferent activity induced via stimulation of mechanoreceptors in the airways contributes. Localized airway anesthesia with lidocaine is unlikely to suppress the cardiovascular responses to lung inflation. This suggests that a limited number of neurogenic mechanisms are involved in the cardiovascular responses to lung inflation in anesthetized humans.

A new method of predicting pulmonary capillary wedge pressure: the arterial pressure ratio.

The response of arterial blood pressure to an increase in intrathoracic pressure has been shown to be predictive of pulmonary capillary wedge pressure. We devised a new method, which we termed the arterial pressure ratio. We defined arterial pressure ratio as the ratio of systolic blood pressure of the final beat during the strain phase of the Valsalva manoeuvre to that during apnoea before the manoeuvre, and tested the accuracy of arterial pressure ratio in predicting pulmonary capillary wedge pressure. In 30 patients scheduled for elective abdominal aortic reconstruction, following induction of general anaesthesia and tracheal intubation, a 20-G catheter and pulmonary artery catheter were inserted through the radial artery and right internal jugular vein, respectively. Pulmonary capillary wedge pressure was then measured during a brief period of apnoea and the Valsalva manoeuvre was performed by application of pressure to the reservoir bag. Airway pressure was maintained at 30 cmH2O for 10 s and then released. Radial arterial pressure and airway pressure were recorded simultaneously, and arterial pressure ratio was calculated. There was a close linear correlation between arterial pressure ratio and pulmonary capillary wedge pressure (r = 0.88, p < 0.0001).

Demonstration of venous return abnormalities induced by coughing during Tc-99m MAA lung perfusion imaging.

Lung perfusion imaging with Tc-99m MAA was performed in a patient thought to have pulmonary embolism. The dynamic flow images obtained before static lung perfusion imaging showed delayed drainage of the tracer into the right brachiocephalic vein and superior vena cava, and unusual demonstration of the right lateral thoracic and intercostal veins as collateral pathways. It was thought that coughing at the time of bolus injection of the tracer into a right antecubital vein caused an increase of intrathoracic pressure and consequently disturbed the venous return to the thorax.

Cardiovascular effects of mechanical ventilation.

The heart and lungs work closely to meet the tissues’ oxygen demands. If the balance between oxygen demand and supply becomes disturbed in critical illness, tissue hypoxia and cell death can rapidly result. An essential part of critical care is to maintain cardiopulmonary function with the help of pharmacotherapy, fluid management, and respiratory support. Paradoxically, interventions aimed at improving the function of one system can sometimes have undesirable effects on the other and, although the pulmonary consequences of cardiac disease are well recognised, the influences of changes in pulmonary physiology on cardiac function are less well appreciated. Cardiopulmonary interactions (the effects of spontaneous and mechanical ventilation on the circulation) were first documented in 1733, when Stephen Hales showed that the blood pressure of healthy people fell during spontaneous inspiration.1 Over a century later Kussmaul described pulsus paradoxus (the inspiratory absence of the radial pulse) in patients with tuberculous pericarditis.2 Cardiopulmonary interactions are present in health, and can be exaggerated or abnormal in the presence of disease. This article will provide an overview of this broad topic. By emphasising the underlying physiological principles and the influence of disease states upon these, we hope that respiratory support will then be tailored to the individual patient. Spontaneous and mechanical ventilation induce changes in intrapleural or intrathoracic pressure and lung volume, which can independently affect the key determinants of cardiovascular performance: atrial filling or preload; the impedance to ventricular emptying or afterload; heart rate and myocardial contractility. Changes in intrathoracic pressure are transmitted to the intrathoracic structures: namely the heart and pericardium, and the great arteries and veins. Spontaneous inspiration produces a negative pleural pressure, and the reduction in intrathoracic pressure is transmitted to the right atrium. In contrast, intermittent positive pressure ventilation (IPPV) produces inspiratory increases in intrathoracic pressure and therefore …

Effects of extrathoracic airway obstruction on intrathoracic pressure and pulmonary artery pressure in exercising horses

Abstract Objective To determine whether dorsal displacesment of the soft palate (DDSP) results in pulmonary artery hypertension and leads to increases in transmural pulmonary artery pressure (TPAP); to determine whether pulmonary hypertension can be prevented by prior administration of furosemide; and to determine whether tracheostomy reduces pulmonary hypertension. Animals 7 healthy horses. Procedure Horses were subjected to 3 conditions (control conditions, conditions after induction of DDSP, and conditions after tracheostomy). Horses were evaluated during exercise after being given saline (0.9% NaCI) solution or furosemide. Results Controlling for drug, horse, and speed of treadmill, DDSP-induced increase in intrathoracic pressure was associated with a significant increase in minimum (36 mm Hg), mean (82 mm Hg), and maximum (141 mm Hg) pulmonary artery pressure, compared with values for control horses (30, 75, and 132 mm Hg, respectively). Increases in pulmonary artery pressure did not induce concomitant increases in TPAP. Tracheostomy led to a significant reduction of minimum (53 mm Hg), and mean (79 mm Hg) TPAP pressure, compared with values for control horses (56 and 83 mm Hg, respectively). When adjusted for horse, speed of treadmill, and type of obstruction, all aspects of the pulmonary artery and TPAP curves were significantly decreased after administration of furosemide, compared with those for horses given saline (0.9% NaCI) solution. Conclusions DDSP was associated with increases in pulmonary artery pressure but not with increases in TPAP. Clinical Relevance Expiratory obstructions such as DDSP are likely to result in pulmonary hypertension during strenuous exercise, but may not have a role in the pathogenesis of exercise-induced pulmonary hemorrhage. (Am J Vet Res 1999;60:485-494).

Acute Transient Sialadenopathy Associated with Laryngeal Mask Airway

Acute Transient Sialadenopathy Associated with Laryngeal Mask Airway

Effects of mechanical ventilation on the kidney

Mechanical ventilation with positive airway pressure has an inhibitory effect on the kidney, which results in a decrease of renal water and sodium excretion. Physical, hormonal, and nervous factors are involved in this process. The increase of intrathoracic pressure results in a decrease of atrial transmural pressures, cardiac output, and mean arterial pressure. Low-pressure and high-pressure baroreceptors are unloaded, and plasma vasopressin concentrations and sympathetic activity increase. The decrease of renal perfusion and the increase of renal nerve sympathetic activity stimulate the renin-angiotensin system. Angiotensin II formation stimulates aldosterone production. Whether a decrease of atrial natriuretic peptide plays a major role is not yet clear. The resulting (physiologic) reaction of the kidney is an increased reabsorption of water and sodium. The effects are directly related to the increase of intrathoracic pressure (which also depends on the level of positive end-expiratory pressure). They can be partially attenuated by extracellular volume loading.

Forward blood flow during cardiopulmonary resuscitation in patients with severe accidental hypothermia. An echocardiographic study.

The mechanism responsible for the forward blood flow associated with external chest compression is still controversial. Evidence for both blood flow caused by direct cardiac compression and blood flow generated by a general increase in intrathoracic pressure has been found in experimental as well as clinical studies. No data are available concerning the mechanism causing forward blood flow in hypothermic patients undergoing cardiopulmonary resuscitation. Therefore, echocardiographic findings during external chest compression in seven hypothermic arrest victims are reported. All transesophageal echocardiographic studies performed at the Anaesthesia department between 1994 and 1997 were reviewed and seven hypothermic patients with transesophageal echocardiography performed during cardiopulmonary resuscitation were identified. An open mitral valve or a circumferential reduction in aortic diameter during the compression phase was found in four of seven patients, indicating that primarily an increase in intrathoracic pressure (thoracic pump mechanism) generated forward blood flow. In three patients, mitral valve closure during external chest compression indicated that direct cardiac compression (cardiac pump mechanism) contributed to forward blood flow. Two patients studied during active compression-decompression cardiopulmonary resuscitation demonstrated enhanced right ventricular filling and aortic valve opening during active decompression of the thorax. In contrast to normothermic arrest victims, an open mitral valve during external chest compression is a common finding during hypothermia, indicating that thoracic pump mechanism is important for forward blood flow during cardiopulmonary resuscitation in hypothermic arrest victims. Aortic valve opening in two hypothermic arrest victims suggests forward blood flow also during active decompression of the thorax with the Cardiopump.

Sustained activation of muscle sympathetic outflow during static lung inflation depends on a high intrathoracic pressure

Muscle sympathetic nerve activity is strongly activated during a static inflation of the lungs in awake human subjects. The purpose of the present study was to test the hypothesis that this sustained activation is due to the associated increase in intrathoracic pressure. In ten subjects microneurographic techniques were used to record muscle sympathetic activity from the peroneal nerve and arterial pressure was monitored continuously by finger-pulse photoplethysmography. Holding the breath at inspiratory capacity with the glottis closed and inspiratory muscles relaxed caused a sustained activation of muscle sympathetic nerve activity but not of skin sympathetic activity. Conversely, when subjects held the lungs maximally inflated by a constant inspiratory effort and an open glottis there was no sympathetic activation despite a similar initial fall in mean arterial pressure. Because intrathoracic pressure was below or close to atmospheric in the latter condition, it is concluded that a high intrathoracic pressure is required for the sympathetic response. Furthermore, the present results provide further support for the idea that unloading of cardiopulmonary baroreceptors is responsible for the sustained activation of muscle sympathetic nerve activity during static lung inflations in human subjects.

Effects of Positive End-Expiratory Pressure on Hepatic Venous Oxygenation in Dogs

Background : Positive end-expiratory pressure(PEEP) ventilation causes reduction in cardiac output and increase of intra-thoracic pressure, hence reduction of hepatic blood flow. The purpose of this study is to evaluate the changes of hepatic venous oxygen saturation, tension and content during increase and removal of PEEP and to evaluate hemodynamic variable which has the greatest effect on hepatic oxygenation. Method : Eight dogs were anethetised with 1.0 vol% isoflurane and 100% oxygen. After 30 minutes of stabilization of vital signs, PEEP were increased from 0 cmH2O to 5 cmH2O and 10 cmH2O and lowered to 0 cmH2O again, and hemodynamic data (heart rate, arterial blood pressure, central venous pressure(CVP), pulmonary arterial pressure, pulmonary arterial occlusion pressure and cardiac output(CO)) and hepatic venous oxygenation data (hepatic venous oxygen saturation(ShvO2), tension(PhvO2) and content(ChvO2)) were measured at each step. Results : CO, ShvO2, PhvO2 and ChvO2 decreased significantly at 10 cmH2O PEEP compared to the baseline and 5 cmH2O PEEP and CO, ShvO2 and ChvO2 increased signicantly with removal of PEEP. CVP increased significantly at 10 cmH2O PEEP and decreased significantly with PEEP removal. PEEP showed close correlationship with CO and CVP considering all steps of PEEP and PEEP removal. ShvO2 and PhvO2 showed most close correlationship with CO considering all steps of PEEP and PEEP removal. Conclusion : ShvO2 with PEEP therapy is dependent upon CO. Therefore cardiac output maintenance is essential during PEEP therapy. For exact evaluation of hepatic oxygenation, it is valuable to monitor ShvO2. (Korean J Anesthesiol 1998; 35: 861∼869)

Divergence of Intracranial and Central Venous Pressures in Lightly Anesthetized, Tracheally Intubated Dogs That Move in Response to a Noxious Stimulus

BACKGROUND Intracranial pressure (ICP) may increase in tracheally intubated subjects during periods of movement (e.g, bucking and coughing). Recent research has suggested that factors other than passive congestion of the cerebral vessels, resulting from increases in central venous pressure, may contribute to the ICP response. The current study evaluated this issue in a canine model of intracranial hypertension and additionally evaluated the relationship between ICP and static increases in superior vena caval pressure. METHODS Six dogs were lightly anesthetized with 0.65% end-expired halothane in oxygen and nitrogen, and ventilation was mechanically controlled. Intracranial pressure was increased to a stable baseline of 15-20 mmHg using a subarachnoid infusion of warm 0.9% saline solution. The following variables were quantified before, and for 6 min after, initiating a 1-min noxious stimulus to the trachea and skin: ICP, central venous pressure, electromyograms (masseter, deltoid, and intercostal muscles), intrathoracic pressure, and cerebral perfusion pressure (defined as mean arterial pressure -- ICP). Later, the protocol was repeated in the presence of neuromuscular block with pancuronium. Finally, in the same dogs, occlusion of the superior vena cava at its junction with the right atrium was used to increase superior vena caval pressure in 5-mmHg increments, from 5 to 30 mmHG, so that the resulting increases in ICP could be quantified. RESULTS In unparalyzed dogs whose heads were maintained at the level of the right atrium, there was a 22-mmHg increase in ICP at 1 min after initiating the noxious stimulus (P<0.05). The ICP increase was related to electromyogram activation and a 6-mmHg increase in central venous pressure; however, it was not associated with significant increases in intrathoracic pressure or cerebral perfusion pressure. Treatment with pancuronium abolished the electromyographic, ICP, and central venous pressure responses to noxious stimulus. When superior vena caval pressure was statically manipulated, the resulting ICP increase was only one half the magnitude of the superior vena caval pressure increase. After elevating the head 14 cm, the ratio of ICP to superior vena pressure increases was reduced to one third. CONCLUSIONS If these results apply to humans, it was concluded that increases in ICP that accompany movement in tracheally intubated patients may arise from two complementary factors: (1) cerebrovascular dilation that correlates with electromyographic activity and is mediated by ascending neural pathways that transmit proprioreceptive information, and (2) passive venous congestion that results from any increase in central venous pressure. The influence of the latter factor can be reduced by elevating the head. (Key words: Blood pressure, venous pressure; mean arterial pressure. Muscle: afferent activity; electromyograms, skeletal. Neuromuscular relaxants: pancuronium.)

Transoesophageal echocardiographic assessment of mitral and aortic valve function during cardiopulmonary resuscitation

There has been controversy over whether forward blood flow during closed-chest cardiopulmonary resuscitation (CPR) is generated by a general increase in intrathoracic pressure (chest-pump theory) or by creating atrioventricular gradients that close the mitral valve and open the aortic valve during thoracic compression (cardiac pump theory). The crucial issue is the position of the mitral valve during the downstroke of chest movement. Questions remain over the actual mechanics of mitral and aortic valve function. This report describes an intraoperative cardiac arrest followed by CPR during which routinely instituted two-dimensional transoesophageal Doppler echocardiography enabled study of the motion of the valves of the left heart and the transmitral blood flow.

Mechanical ventilation and the cardiovascular system

AB Ventilation has profound effects on the cardiovascular system through almost every aspect of its control. Four concepts determine most acute aspects of mechanical ventilation and its withdrawal. First, ventilation is exercise. A cardiovascular system unable to meet the increased metabolic demand of breathing will prevent successful weaning. Second, hyperinflation and increasing lung volume per se, and not the increase in airway pressure, determine the hemodynamic effect of ventilation. However, in a given patient, if ventilatory modes are matched for similar tidal volumes and mean airway pressures, then the hemodynamic effects of these modes of ventilation will also be similar. Third, although decreases in intrathoracic pressure increase left ventricular afterload, of more clinical relevance is the transition from spontaneous ventilatory efforts to positive pressure ventilation because the fall in venous return is much less, whereas the decrease in left ventricular afterload is identical for the same relative increase in intrathoracic pressure. Fourth, the decrease in venous return seen during positive pressure ventilation probably reflects an impairment in left ventricular filling rather than a reduction in the pressure gradient for venous return because of the associated increase in intra-abdominal pressure during inspiration.

Blunt traumatic rupture of a mitral papillary muscle head

Severe mitral regurgitation developed in a patient after a lateral-impact motor vehicle accident. The papillary muscle head was disrupted without evidence of other myocardial injury. We hypothesize that a dramatic and sudden increase in intrathoracic pressure may have produced the injury. The patient experienced progressive heart failure and underwent successful mitral valve repair 9 days after the accident.