Rise In Intrathoracic Pressure Research Articles

Heart-Lung Interactions.

The pulmonary and cardiovascular systems have profound effects on each other. Overall cardiac function is determined by heart rate, preload, contractility, and afterload. Changes in lung volume, intrathoracic pressure (ITP), and hypoxemia can simultaneously change all of these four hemodynamic determinants for both ventricles and can even lead to cardiovascular collapse. Intubation using sedation depresses vasomotor tone. Also, the interdependence between right and left ventricles can be affected by lung volume-induced changes in pulmonary vascular resistance and the rise in ITP. An increase in venous return due to negative ITP during spontaneous inspiration can shift the septum to the left and cause a decrease in left ventricle compliance. During positive pressure ventilation, the increase in ITP causes a decrease in venous return (preload), minimizing ventricular interdependence and will decrease left ventricle afterload augmenting cardiac output. Thus, positive pressure ventilation is beneficial in acute heart failure patients and detrimental in hypovolemic patients where it can cause a significant decrease in venous return and cardiac output. Recently, this phenomenon has been used to assess patient's volume responsiveness to fluid by measuring pulse pressure variation and stroke volume variation. Heart-lung interaction is very dynamic and changes in lung volume, ITP, and oxygen level can have various effects on the cardiovascular system depending on preexisting cardiovascular function and volume status. Heart failure and either hypo or hypervolemia predispose to greater effects of ventilation of cardiovascular function and gas exchange. This review is an overview of the basics of heart-lung interaction.

Long-standing Valsalva retinopathy

Valsalva retinopathy occurs due to a sudden rise in intrathoracic pressure (Valsalva maneuver) which is transmitted to the superficial retinal vessels resulting in their rupture. It is often encountered in...

Forward blood flow provoked by changing intravascular pressure using an extracorporeal circulation during cardiopulmonary resuscitation

Since both “cardiac pump” and “thoracic pump” theories have been proved during cardiopulmonary resuscitation (CPR), the mechanism of forward blood flow during closed chest compression still remains open to question. The cardiac pump seems to work by the direct compression of the cardiac ventricles between the sternum and vertebral column. A pressure gradient created between the ventricle and aorta generates systemic blood flow. However, the thoracic pump mechanism presumes chest compression causes a rise in intrathoracic pressure which generates a blood flow from the thoracic cavity to the systemic circulation. Retrograde blood flow from the right heart into the systemic veins is prevented by a concomitant collapse of veins at the thoracic inlet. We hypothesize that the intrinsic decrease of vascular resistance from the aorta to peripheral arteries and the existence of competent venous valves enable blood to flow unidirectionally by the fluctuation of intravascular pressures during closed chest compression. The purpose of this study is to prove an antegrade arterial blood flow without cardiac compression and intrathoracic pressure changes in an animal cardiac arrest model. We demonstrate that arterial pulses can be developed by using an extracorporeal circuit, resulting in forward blood flow from the aorta through the systemic vasculature. It can be suggested that changes in intravascular pressure provoked by either cardiac or thoracic pump generate systemic blood flow during closed chest compression, while systemic vascular patency and valve function may be required for successful CPR.

Designing a video laryngoscope imaging system with a 7mm blade for neonatal patients

When a newborn infant has been pushed from the birth canal due to ventilation failure while using a resuscitation mask, the doctor must implement infant intubation and other emergency steps to keep the baby alive. However, due to the excessively small mouth area of a newborn or premature infant, the doctors are unable to view the glottis entrance, which can lead to either a failed intubation or longer intubation time, thereby resulting in either a drop in oxygen levels or a rise in intrathoracic pressure. Although the normal video laryngoscope with a 12mm metal blade certainly improves this type of difficult intubation, nevertheless, doctors often complain that the depth of field (DOF) is insufficient and the width of the blade is too wide when performing intubation on neonatal patients. Therefore, this study aims to develop two modules of infant’s video laryngoscope, an ultra-thin 7mm metal blade and an optical imaging system, the core technology of which includes an optical design of a 2.5mm lens and verifications of imaging quality. In order to allow physicians to determine the infant’s airway position immediately and to avoid the binocular disparity from a physician while giving intubation, this study has simulated the optical properties of monolithic lenses while designing the imaging system, allowing the doctor to have a clearer and undistorted image within the field of view.

Syndrome de Perthes secondaire à une crise d’asthme : à propos d’un cas chez un enfant de 15 ans

Perthes syndrome, or traumatic asphyxia syndrome, is a rare clinical entity, associating cyanosis, cervicofacial petechiae and subconjunctival hemorrhage. It is usually secondary to chest trauma, but can occur in any situation of abrupt rise in intrathoracic pressure with closed glottis. In this paper, we present a case of Perthes syndrome that triggered an asthma attack for a child during surgery.

Obstructive sleep apnea and cardiovascular comorbidities: a large epidemiologic study.

Obstructive sleep apnea (OSA) is a common disorder, characterized by cyclic cessation of airflow for 10 seconds or more. There is growing awareness that OSA is related to the development and progression of cardiovascular disease. However, only a few studies have associated OSA directly to major cardiovascular events. The aim of this study was to evaluate the relationship between OSA and cardiovascular morbidity in a well defined population of patients.The electronic database of the central district of a major health management organization was searched for all patients diagnosed with OSA in 2002–2010. For each patient identified, an age- and sex-matched patient was randomly selected from the members of the same health management organization who did not have OSA. Data on demographics, socioeconomic status, and relevant medical parameters were collected as well.The study population included 2797 patients, average age 58.1, in which 76.6% were males. There was a significant correlation between OSA and the presence of ischemic heart disease (P < 0.001), pulmonary hypertension (P < 0.001), congestive heart failure (P < 0.001), cardiomyopathy (P = 0.003), and arrhythmia (P < 0.001). OSA was also significantly correlated with low socioeconomic status (P < 0.001).OSA and cardiovascular disease were strongly correlated. As such, early diagnosis and treatment of OSA may change the course of both diseases. We suggest that sleep disordered breathing should be routinely assessed in patients with cardiovascular problems. An ear–nose–throat evaluation may also be important to rule out anatomic disorders that cause upper airway obstruction.

Positive End-Expiratory Pressure as a Factor Influencing Cerebral Perfusion Pressure (an experimental study)

Objective: to evaluate the effect of positive end-expiratory pressure (PEEP) on cerebral perfusion pressure (CPP) in intracranial hypertension in an experiment using a biological model. Materials and methods. The experiment was carried out on 10 pigs aged 2 months and weighing 17—20 kg. The experimental animals were anesthetized. The authors monitored the following parameters: invasive arterial and central venous pressures, intracranial pressure (ICP), and peak inspiratory pressure. ICP was simulated with a subdurally placed balloon. During mechanical ventilation (MV), PEEP was gradually increased up to 5, 10, 15, and 20 cm H2O. Results. PEEP elevation during MV was accompanied by a progressive rise in intrathoracic pressure and a reduction in mean blood pressure. When PEEP was increased, there was a significant rise in ICP in the intact brain and basic subcompensated intracranial hypertension; no statistically significant change in ICP was observed in decompensated intracranial hypertension. The safe PEEP with regard to CPP was determined by the severity of basic intracranial distention (it was 15 cm H2O in the intact brain and 10 cm H2O in subcompensated hypertension); PEEP exerted no significant effect on CPP in decompensated intracranial hypertension. Conclusion. The effect of PEEP on CPP is determined by not only the value of PEEP, but also by the severity of brain damage. Key words: positive end-expiratory pressure, intracranial pressure, cerebral perfusion pressure.

Atrial Fibrillation Complicating Left Pneumothorax After Malpositioning of a Double-Lumen Tube

A 66-year-old woman (weight 133.3 lbs, height 158 cm) was scheduled for atrial septal defect (ASD) repair through a thoracotomy. Preoperative chest radiography was normal, and an electrocardiogram showed an incomplete right bundle-branch block. Transesophageal echocardiography revealed moderate right atrium and ventricle dilation, a pulmonary arterial pressure of 52 mmHg, and an ASD-associated left-to-right shunt. In the operating room, her blood pressure was 125/75 mmHg, her heart rate was 94 beats/min, and the SpO2 was 97% on room air. The patient was intubated with a 35F left-sided double-lumen tube (DLT) under direct laryngoscopy to a depth of 31 cm at the incisors. The DLT placement was checked by auscultation. During manual ventilation, increased airway resistance was noted, and no breath sounds were heard over either lung fields. The tube was pulled back 2 cm, and bilateral breath sounds were again documented. The end-tidal carbon dioxide waveform was present on the monitor. At that time, rapid-rate atrial fibrillation of 130 beats/min occurred with a blood pressure of 63/40 mmHg. Phenylephrine boluses were given to maintain hemodynamic stability. Correct positioning of the DLT was confirmed by fiberoptic bronchoscopy. Meanwhile, SpO2 remained within the normal range. Soon thereafter, a median sternotomy was performed instead of a thoracotomy, and a left pneumothorax was diagnosed and released by pleural opening. This was followed by rapid conversion of the atrial fibrillation into sinus rhythm and restoration of normal blood pressure. During one-lung ventilation, barotrauma from excessive tidal volume and high airway pressure may occur if a left-sided DLT is positioned distally such that the entire tidal volume is directed to only one lobe.1Silvalingam P. Tio R. Tension pneumothorax, pneumomediastinum, pneumoperitoneum, and subcutaneous emphysema in a 15-year-old Chinese girl after a double-lumen tube intubation and one-lung ventilation.J Cardiothorac Vasc Anesth. 1999; 13: 312-315Abstract Full Text PDF PubMed Scopus (34) Google Scholar, 2Malik S. Shapiro W.A. Jablons D. et al.Contralateral tension pneumothorax during one-lung ventilation for lobectomy: Diagnosis aided by fiberoptic bronchoscopy.Anesth Analg. 2002; 95: 570-572PubMed Google Scholar In our patient, high peak airway pressure may have been generated during manual ventilation to check the DLT position, which was placed too distal. The average depth of insertion for patients 170 cm tall was 29 cm, and for each 10-cm increase or decrease in height, the average placement depth was increased or decreased 1 cm.3Brodsky J.B. Benumof J.L. Ehrenwerth J. et al.Depth of placement of left double-lumen endobronchial tubes.Anesth Analg. 1991; 73: 570-572Crossref PubMed Scopus (95) Google Scholar A pneumothorax presents as increased airway pressure, decreased tidal volume, decreased SpO, and hypotension. Sudden-onset atrial fibrillation may occur for a variety of reasons during anesthesia. Our patient developed rapid-rate atrial fibrillation with hypotension, probably as a complication of the pneumothorax, which was diagnosed only after sternotomy. Had we initiated one-lung ventilation, cardiovascular collapse would have developed. Previous reports showed that a pneumothorax may be associated with numerous electrocardiographic changes.4Price J.W. Novel electrocardiographic changes associated with iatrogenic pneumothorax.Am J Crit Care. 2006; 15: 415-419PubMed Google Scholar, 5Strizik B. Forman R. New ECG changes associated with a tension pneumothorax.Chest. 1999; 115: 1742-1744Crossref PubMed Scopus (37) Google Scholar The sudden rise in intrathoracic pressure and rotation around the longitudinal axis of the heart has been suggested as a cause of these changes. A proposed mechanism for PR-segment changes is atrial ischemia caused by compression of air on the collapsed lung and subsequently on the heart. In our patient, a shift in heart position secondary to the pneumothorax in addition to the atrial enlargement may have predisposed to this mechanical irritation and subsequent atrial fibrillation. In conclusion, we report a case of atrial fibrillation complicating a left pneumothorax that was caused by barotrauma after malpositioning of a DLT in the presence of an ASD. Atrial fibrillation was reverted by releasing the pneumothorax. The diagnosis of a pneumothorax should be considered during DLT insertion whenever a patient develops cardiovascular instability.

A structural model of perfusion and oxygenation in low-flow states

Background Recent investigations underscore the critical importance of ventilation strategies on resuscitation outcomes. In low perfusion states, such as cardiac arrest and traumatic shock, the rise in intrathoracic pressure that accompanies positive-pressure ventilation can significantly impede venous return and lead to a decrease in cardiac output. The optimal ventilation strategy in these “low-flow” states remains unclear. Objective To create a mathematical model of perfusion and oxygenation to predict the effects of PPV with both normotension and hypotension. Methods The lung pressure–volume relationship was modeled using a novel formula allowing manipulation of various lung characteristics. A separate formula was then derived to predict mean intrathoracic pressure (MITP) for specific minute ventilation values using the pressure–volume formula. The addition of positive end-expiratory pressure was also modeled. Finally, a formula was derived to model oxygen absorbance as a function of alveolar surface area and flow based on ventilation rate and MITP. Results Mathematical models of the lung pressure–volume relationship, MITP, and absorbance were successfully derived. Manipulation of total lung capacity, compliance, upper and lower inflection points, positive end-expiratory pressure, and minute ventilation allowed prediction of optimal ventilation rate and tidal volume for a normal lung and with various abnormal characteristics to simulate particular disease states, such as acute respiratory distress syndrome (ARDS). For a normal lung, ventilation rates of 4–6 breaths/min with higher tidal volumes (15–20 mL/kg) resulted in the lowest predicted MITP values (5 cm H 2O) and the highest absorbance. The input of lung parameters that would simulate ARDS resulted in optimal ventilation rates of 10–12 breaths/min with lower tidal volumes (8–10 mL/kg) and higher predicted MITP values (10–15 cm H 2O). Conclusions A mathematical model of ventilation was successfully derived allowing manipulation of multiple pulmonary physiological variables to predict MITP and potentially identify optimal ventilation strategies. This model suggests the use of lower ventilation rates and larger tidal volumes to minimize the hemodynamic effects of positive pressure ventilation in patients with hypoperfusion but normal lung characteristics.

The effect of the transient rise in intrathoracic pressure on cardio-pulmonary dynamics (author's transl)

The effect of the transient rise in intrathoracic pressure on cardio-pulmonary dynamics (author's transl)

Managing the pneumonectomy space after extrapleural pneumonectomy: postoperative intrathoracic pressure monitoring☆☆☆

Rapid fluid evacuation of the pneumonectomy space can cause ipsilateral mediastinal shift, contralateral lung hyperexpansion, compromised caval blood return and a precipitous drop in cardiac output. Conversely, rapid fluid accumulation can cause contralateral mediastinal shift with compression of the remaining lung and respiratory insufficiency. In this retrospective analysis, we evaluate the efficacy of intrathoracic pressure monitoring and intermittent fluid aspiration to manage the pneumonectomy space in the early postoperative period following extrapleural pneumonectomy. Prior to chest closure, a 14 F Rob-Nel catheter was placed in the pneumonectomy space and connected to pressure tubing to monitor ipsilateral intrathoracic pressure continuously. Central venous pressure monitoring and serial chest X-rays were performed according to usual intensive care routine. Pneumonectomy space fluid was aspirated intermittently when there was increase in intrathoracic pressure, refractory hypotension, mediastinal shift on chest X-ray, or clinical decline. Postoperative imaging was re-evaluated retrospectively for confirmation of mediastinal shift by a senior radiologist. From January to December 2008, 47 patients underwent extrapleural pneumonectomy for pleural mesothelioma (median age 65 years with range 34-79 years, 77% male). Twenty (43%) patients had left-sided disease and 32 (68%) received local heated intra-operative cisplatin-based chemotherapy. The median baseline pneumonectomy space pressure was 3 cm H(2)O (range: -6 to +12). The median amount of fluid withdrawn over the first 2 days postoperatively was 300 cc (range: 0-1980 cc). Thirty-one (69%) patients had minimal, if any, change in mediastinal position during the first 2 postoperative days with intermittent drainage performed when the pneumonectomy space pressure rose. Eleven (25%) patients had increasing contralateral shift, four of whom had return of the mediastinum to baseline during this time period. The median fluid drained from the four patients whose contralateral shift resolved was 290 cc (range: 220-800 cc) compared to 200 cc (range: 150-480 cc) from the seven patients whose contralateral shift remained, but this difference did not reach significance (p=0.365). Intrathoracic pressure monitoring may be used as a guide for intermittent fluid evacuation of the pneumonectomy space prior to onset of clinical signs or symptoms, to avoid the cardiopulmonary risks of rapid fluid removal. Contralateral mediastinal shift should be treated with incremental drainage when there is a rise in intrathoracic pressure to prevent cardiovascular complications.

Abstract 45: A Mathematical Model of Ventilation, Perfusion, and Oxygenation in Low-Flow States

Background: Recent investigations underscore the critical importance of ventilation strategies on resuscitation outcomes. In low perfusion states, such as cardiac arrest and traumatic shock, the rise in intrathoracic pressure that accompanies positive-pressure ventilation (PPV) can significantly impede venous return and lead to a decrease in cardiac output. The optimal ventilation strategy in these “low-flow” states remains unclear. Objectives: To create a mathematical model of perfusion and oxygenation to predict the effects of PPV with both normotension and hypotension. Methods: The lung pressure-volume relationship was modeled using a novel formula allowing manipulation of various lung characteristics, including vital capacity, compliance, and the upper and lower inflection points. A separate formula was then derived to predict mean intrathoracic pressure for a given minute ventilation using the pressure-volume formula. The addition of positive end-expiratory pressure was also modeled. Finally, a formula was derived to model oxygen absorbance as a function of alveolar surface area and flow based on ventilation rate and mean intrathoracic pressure. Results: Mathematical models of the lung pressure-volume relationship, mean intrathoracic pressure, and absorbance were successfully derived. Manipulation of vital capacity, compliance, upper and lower inflection points, positive end-expiratory pressure, and minute ventilation allowed prediction of optimal ventilation rate and tidal volume for a normal and an ARDS lung. For a normal lung, optimal values for both mean intrathoracic pressure and absorption were achieved with a ventilation rate of 4 breaths/min. A decrease in the upper inflection point or increase in minute ventilation resulted in faster optimal ventilation rates, although none exceeded 14 breaths/min. Conclusions: A mathematical model of ventilation was successfully created allowing manipulation of multiple variables related to lung compliance and ventilation strategy. This model suggests the use of lower ventilation rates with larger tidal volumes to minimize the hemodynamic effects of PPV and maximize oxygen absorbance.

Paroxysmal coughing, subdural and retinal bleeding: a computer modelling approach

Unexplained subdural and retinal haemorrhages in an infant are commonly attributed to 'shaking', the mechanism of which is believed to be traumatic venous rupture. However, the haemorrhagic retinopathy reported as a result of Valsalva manoeuvres and the subdural bleeding that is a rare complication of pertussis together demonstrate that if a sustained rise in intrathoracic pressure is transmitted to cerebral and retinal vessels, it may result in bleeding, similar to that reported in inflicted injury. Such haemorrhages would be expected to occur whenever severe paroxysmal coughing were induced, whatever the cause. This study used a computer modelling approach to investigate feeding accidents as the trigger for bleeding. A dynamic circulatory model of a 3-month-old infant was induced to 'cough', and the response to changes in physiological variables monitored. It showed that coughing causes intracranial pressures to build up exponentially to approach a maximum, proportional to the amount of pressure the musculature of the thorax can produce, as venous return is impeded. They do not have time to become dangerous during individual coughs, as blood quickly returns after the cough is over, reestablishing normal pressures. Paroxysmal coughing, however, does not allow blood to return between coughs, with the result that very high luminal pressures may be generated, sufficient to damage veins. A history of coughing, vomiting or choking is not uncommon in otherwise normal infants with retinal and subdural bleeding. Our findings suggest that paroxysmal coughing could account for such bleeding in some cases.

Effect of incremental positive end-expiratory pressure ventilation on right ventricular function in anesthetized pigs: A thermodilution study

The effects of positive end-expiratory pressure (PEEP) ventilation on right ventricular preload, after-load, and contractility under physiologic circumstances are controversial. We studied hemodynamics and right ventricular volumes (thermodilution) in 12 anesthetized pigs in which PEEP was increased by steps of 5 cm H 2O at 15 minute intervals (0 to 20 cm H 2O). At 20 cm H 2O PEEP, cardiac output decreased by 2.0 ± 0.7 (mean ± SD) L/min, and mean arterial blood pressure by 50 ± 14 mm Hg. Heart rate increased by 39 ± 24 b/min. At 20 cm H 2O PEEP, right ventricular stroke volume fell by 25 ± 7 mL, end-diastolic volume by 50 ± 21 mL, end-systolic volume by 25 ± 17 mL, and ejection fraction by 17% ±0 10% (all p <.005). For mean values during PEEP, end-diastolic volume linearly and inversely related to central venous pressure. Stroke volume, ejection fraction, and end-systolic volume linearly and positively related to end-diastolic volume; relations did not differ from those without PEEP. Transmural mean pulmonary artery pressure linearly and positively related to cardiac output. Transmural systolic pulmonary artery pressure and central venous pressure linearly and positively related to endsystolic and end-diastolic volumes, respectively. We conclude that, during incremental PEEP ventilation up to 20 cm H 2O in anesthetized pigs with an intact baroreceptor reflex, a rise in intrathoracic pressure induces a linear fall in right ventricular preload and stroke volume at an unaltered pump function. Right ventricular ejection fraction and afterload diminish as a normal response to decreased preload. There are no effects on pulmonary vascular resistance, and right ventricular compliance and contractility, in spite of coronary hypotension and tachycardia.

Cough in Tetraplegic Subjects: An Active Process

To determine the role of the clavicular portion of the pectoralis major during cough in tetraplegic subjects. Eight patients with longstanding traumatic transection of the lower cervical cord. The electromyographic activity of the pectoralis major and abdominal external oblique muscles and the changes in the anteroposterior diameter of the lower rib cage, the upper rib cage, and the abdomen were measured during voluntary coughing efforts in the seated posture. When coughing, all subjects showed a large amount of electrical activity in the pectoralis major with no activity in the external oblique. Simultaneously, they had a clear-cut decrease in the anteroposterior diameter of the upper rib cage together with an increase in the anteroposterior diameter of the abdomen. In five subjects, the anteroposterior diameter of the lower rib cage also showed an initial increase. These changes were seen when cough was initiated at functional residual capacity or at a higher lung volume; they were also seen during a fit of coughing. In tetraplegic subjects the clavicular portion of the pectoralis major plays a major role during coughing. Its contraction causes a reduction in the size of the upper part of the rib cage and a rise in intrathoracic pressure; this pressure rise results secondarily in an outward (paradoxical) motion of the abdomen and the lower rib cage. Cough in tetraplegic subjects is thus an active, rather than a passive, process, and its effectiveness might be improved by a combination of specific muscle training and abdominal binding.

Cyclic elevation of intrathoracic pressure can close the mitral valve during cardiac arrest in dogs.

Mitral valve closure during cardiopulmonary resuscitation may result from direct cardiac compression. An alternative hypothesis is that with a rise in intrathoracic pressure, mitral valve closure can occur but may be influenced by whether the lungs are inflated or deflated. To test this hypothesis, we placed a large-bore cannula into the thoraces of 11 dogs. Intrathoracic pressure was changed by inflating and deflating the thorax through the cannula while the airway was open, as well as by inflating and deflating the lungs with the thoracic cannula clamped. Mitral valve motion was observed with two-dimensional echocardiography from the right chest wall or esophagus in eight of the dogs. With a rise in intrathoracic pressure from thoracic inflation, all eight dogs showed closure of the mitral valve, while with thoracic deflation, all showed mitral valve opening. With lung inflation and deflation alone, however, the mitral valve remained open throughout the cycle. In seven dogs, with thoracic inflation, the peak gradient from the left ventricle to the left atrium was (mean +/- SEM) 18 +/- 4 mm Hg and the average gradient was 7 +/- 3 mm Hg, while with lung inflation alone, the average gradient was -1 +/- 1 mm Hg (p less than 0.01 vs. thoracic inflation). Thus, mitral valve closure, with concomitant retrograde pressure gradients, can be produced by intrathoracic pressure changes with accompanying lung deflation. With lung inflation alone, however, the mitral valve remains open, and there are no significant transmitral pressure gradients. We conclude that intrathoracic pressure changes can cause the mitral valve to close or to remain open, depending on how intrathoracic pressure is generated.

Augmentation of carotid flow during cardiopulmonary resuscitation by ventilation at high airway pressure simultaneous with chest compression

Prior studies in dogs indicate that (1) blood flow during cardiopulmonary resuscitation results from the induced rise in intrathoracic pressure rather than from direct cardiac compression, and (2) maneuvers that increase intrathoracic pressure lead to increased carotid blood flow. Therefore, a system was devised for administering cyclical increases in intrathoracic pressure without lung overinflation for use during cardiac arrest. Ventilation at high airway pressure (60 to 100 mm Hg) was performed simultaneously with chest compression at a rate of 40/min in seven dogs with cardiac arrest. Airway pressure returned to the atmospheric level between compression-ventilation periods to allow venous return. This new technique was compared with conventional cardiopulmonary resuscitation both with and without sustained abdominal compression by binding. Peak chest compression force was held constant during all forms of resuscitation. Carotid blood flow was higher during simultaneous compression-ventilation resuscitation than with conventional resuscitation both without abdominal binding (mean ± standard error of the mean 18.7 ± 4.7 versus 5.1 ± 1.08 ml/min, p < 0.05) and with abdominal binding (28.6 ± 3.5 versus 13.8 ± 3.4 ml/min, p < 0.001). Carotid blood flow before cardiac arrest was 142 ± 26 ml/min. Carotid flow could be further increased over that during simultaneous compression-ventilation resuscitation with abdominal binding by interposing 20 mm Hg negative airway pressure between compression-ventilation periods. Similar results were obtained in six pigs and one baboon with cardiac arrest. Oxygenation and removal of carbon dioxide were adequate after 10 min of simultaneous compression-ventilation resuscitation. Although coronary blood flow was low with both techniques, left circumflex coronary flow was significantly greater with simultaneous compression-ventilation resuscitation (3.7 ±0.5 ml/min) than with conventional resuscitation (1.1 ± 0.5 ml/min, p < 0.01). Thus, in animals with cardiac arrest simultaneous compression-ventilation resuscitation can substantially increase carotid blood flow over that obtained with conventional cardiopulmonary resuscitation. Negative airway pressure added between compression-ventilation periods and abdominal binding can further augment carotid flow.

New Developments in Cardiopulmonary Resuscitation

The traditional concept of cardiopulmonary resuscitation (CPR) is that the heart is squeezed between the sternum and the spine during external cardiac massage to create a pressure gradient that forces blood from the heart to the periphery. Although the heart may actually be squeezed in some persons by this maneuver, a newer view of CPR holds that closed-chest compression produces a generalized rise in intrathoracic pressure that is applied to the pulmonary vascular bed as well as the heart. Thus, the heart does not serve primarily as a pump during external cardiac massage but instead acts as a conduit for blood from the lungs. Furthermore, flow into extrathoracic vessels depends on their tendency to remain open or to collapse: forward flow occurs across the head during CPR because a pressure gradient is developed between the carotid artery and the more compressible jugular vein. These ideas have potential clinical implications and greatly increase our understanding of the physiology of CPR.

Cough-CPR: documentation of systemic perfusion in man and in an experimental model: a "window" to the mechanism of blood flow in external CPR.

Maintenance of arterial pressure and consciousness by vigorous coughing during ventricular fibrillation has been previously documented. Observations in 4 additional patients with unstable rhythms and in fibrillating dogs confirm that coughing: (1) produces an arterial pulse; (2) produces opening of the aortic valve; (3) generates forward blood flow; and (4) can maintain consciousness during circulatory arrest. The authors speculate that cough-induced systemic perfusion results from compression of the pulmonary vascular beds by a rise in intrathoracic pressure, the left heart acting only as a one-way conduit to the lower pressure extrathoracic vascular outlets. Recent data suggest that conventional CPR likewise produces blood flow by compression of the pulmonary vascular blood pool, and not by cardiac compression as previously thought.

SIMULTANEOUS CHEST COMPRESSION AND VENTILATION AT HIGH AIRWAY PRESSURE DURING CARDIOPULMONARY RESUSCITATION

In most patients blood flow during cardiopulmonary resuscitation (CPR) results from a rise in intrathoracic pressure rather than from direct heart compression. Intrathoracic pressure was increased by the use of positive-pressure ventilation synchronous with sternal compression in eleven arrested patients who were intubated. A computer system allowed 15-30 s periods of alternation between conventional CPR and "new CPR" (rate of 40/min, 60% compression duration, and simultaneous ventilation at airway pressures from 60 to 110 cm H 2O). Compression force was identical with the two methods. New CPR increased mean systolic radial artery pressure significantly from 40·6±4·4 to 53·1±3·9 mm Hg for 14 runs in nine patients. In 15 runs in ten patients an index of carotid flow increased with new CPR to 252% (range 113-643%) of control values. Lowering airway pressure during new CPR lowered flow index and arterial pressure, confirming that these increases with new CPR were due to higher intrathoracic pressure. Thus, increased airway pressure synchronous with sternal compression increases arterial pressure and likely blood flow during CPR in man. However, further studies of potential complications and long-term effects of new CPR, particularly on adequacy of ventilation, are needed before clinical implementation is undertaken.