Acute Ventricular Failure Research Articles

OMI/NOMI: Time for a New Classification of Acute Myocardial Infarction.

Forty percent of patients with acute coronary occlusion myocardial infarction (OMI) do not present with STEMI criteria, which delays their treatment and increases morbidity and mortality. The need to identify these patients promptly is crucial, and this sets the stage for the proposed reclassification. Many of these patients can be identified by other ECG and clinical features. Background/Objectives: We sought to evaluate cases of STEMI and NSTEMI that result in OMI. Additionally, we focused on the consequences of delayed revascularization in NSTEMI patients with acute coronary occlusion (NSTEMI-OMI). Methods: The study is a retrospective analysis conducted on 334 patients who underwent coronary angiography for acute coronary syndrome at UHC "Mother Teresa", Tirana, Albania, during January-May 2023. "OMI was defined as an acute culprit lesion with TIMI 0-2 flow, or an acute culprit lesion with TIMI 3 flow intervened upon and with highly elevated troponin (cTnI > 10.0 ng/mL, hs-cTnI > 5000 ng/L)". The presence or absence of STEMI criteria were determined in the final diagnosis written on the chart by a cardiologist using the third universal definition of MI. Ejection fraction (EF), total ischemia time, length of stay, and complications were compared between groups. Mechanical complications include acute ventricular failure, cardiogenic shock, rupture of the interventricular septum, rupture of the free wall, rupture of the papillary muscle, and pericarditis. Electrical complications include ventricular arrhythmias, supraventricular arrhythmias, and atrioventricular and interventricular blocks. Results: There were 334 patients included, 98 (29.3%) of whom were NSTEMI-OMI patients. Ninety-six patients (40%) of OMI patients did not fulfill the STEMI criteria. Only 11 patients (11%) of STEMI(-)OMI had PCI performed within the first 12 h vs. 76 patients (77%) with STEMI(+)OMI, p < 0.001. There was no difference in the percent of patients requiring PCI between the STEMI(+)OMI 98 patients (93%) and STEMI(-)OMI 87 patients (89%) (p = 0.496). The overall in-hospital mortality was 19 patients (5.7%), with subgroup mortality of 14 patients (4.2%) with STEMI(+)OMI, 2 patients (0.6%) with STEMI(+) NOMI, and 3 patients (0.9%) with STEMI(-)OMI, 0% STEMI(-)NOMI, (p = 0.013). Patients with mechanical complications included 67 patients (46.8%) with STEMI(+)OMI and 45 patients (46.4%) with STEMI(-)OMI. In addition, 26 patients (18.5%) with STEMI(+)OMI and 13 patients (13.1%) with STEMI(-)OMI developed electrical complications. Conclusions: STEMI(-)OMI patients had significant delays in catheterization, yet had angiographic findings, rates of PCI, and complications similar to STEMI(+)OMI. These data add further support to refocusing the paradigm of acute MI to improve recognition and rapid reperfusion of all OMIs, rather than only those with STEMI criteria.

Anatomy-physiology considerations for cardiogenic shock with right ventricular involvement

Since the discovery of right ventricular infarction, interest in the characteristics of the right ventricle has been increasing. Right ventricular function is now known to be a predictor of mortality in different settings. The right ventricle is a low-pressure, high-compliance, high-volume chamber. To carry out its normal function, it is coupled to the pulmonary circulation and the left ventricle. In the face of acute changes in pressure, volume overload and ischemia, it dilates to adapt to its new load. Its manifestation may be ventricular dysfunction and/or failure that will progress to cardiogenic shock due to right ventricular involvement. Various entities may be the cause of acute dysfunction: right ventricular infarction (alterations in contractility due to ischemia) and high-risk pulmonary thromboembolism (increased afterload). Both share a similar ventricular pathophysiology and high mortality without treatment. Understanding anatomy and physiology, dysfunction and acute ventricular failure are important to define a convenient diagnosis and treatment oriented towards pathophysiology. In this first part, the anatomy and physiology, acute right ventricular dysfunction/failure and cardiogenic shock are taken into consideration, from the perspective of these two entities. In another paper, treatment aimed at cardiogenic shock due to right ventricular involvement will be reviewed.

DoxoDB: A Database for the Expression Analysis of Doxorubicin-Induced lncRNA Genes.

Cancer and cardiovascular disease are the leading causes of death worldwide. Recent evidence suggests that these two life-threatening diseases share several features in disease progression, such as angiogenesis, fibrosis, and immune responses. This has led to the emergence of a new field called cardio-oncology. Doxorubicin is a chemotherapy drug widely used to treat cancer, such as bladder and breast cancer. However, this drug causes serious side effects, including acute ventricular dysfunction, cardiomyopathy, and heart failure. Based on this evidence, we hypothesize that comparing the expression profiles of cells and tissues treated with doxorubicin may yield new insights into the adverse effects of the drug on cellular activities. To test this hypothesis, we analyzed published RNA sequencing (RNA-seq) data from doxorubicin-treated cells to identify commonly differentially expressed genes, including long non-coding RNAs (lncRNAs) as they are known to be dysregulated in diseased tissues and cells. From our systematic analysis, we identified several doxorubicin-induced genes. To confirm these findings, we treated human cardiac fibroblasts with doxorubicin to record expression changes in the selected doxorubicin-induced genes and performed a loss-of-function experiment of the lncRNA MAP3K4-AS1. To further disseminate the analyzed data, we built the web database DoxoDB.

Post Ligation Cardiac Syndrome: an Educational Presentation.

Although technically simple, surgical correction of patent ductus arteriosus can have serious complications. In this context, acute ventricular failure must be remembered, as its prompt diagnosis and proper management can change clinical outcomes.

Infective Endocarditis and COVID 19: A Systematic Review

Coronavirus Disease-19 (COVID-19) is a pandemic caused by severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). COVID-19 is known to cause a wide variety of cardiovascular manifestations, including myocarditis, pericarditis, myocardial infarction, stroke, thrombus, pulmonary embolism and acute ventricular failure In this paper, we explore cases of infective endocarditis (IE) that occurred in patients who were concurrently (not sure if they were concurrently infected but if so, makes the sentence smoother and easier to understand) infected with COVID-19 and discuss its association in contributing to factors that can ultimately lead to the development of infective endocarditis. Some of these factors that contribute to IE in COVID-19 include severe inflammatory response, endothelial damage and dysfunction and immunosuppression caused by medications that are used to treat COVID-19. In this systematic review, 12 papers detailing 15 pertinent cases of IE following an infection with COVID-19 were identified. Data from these cases were tabulated and analyzed. The ages of the patients ranged from 20-70 years, with 73% of the patients developing IE of native heart valves and the remaining 27% developing IE of mechanical and bioprosthetic valves. The three most common organism implicated were Enterococcus faecalis (28.57%), Methicillin Resistant Staphylococcus aureus (MRSA) (14.28%), and Methicillin Sensitive Staphylococcus aureus (MSSA) (14.28%). Medical management of these cases involved antibiotic therapy and was reported in 80% of the cases, while only one patient (6.67%) underwent surgical valve replacement. The mortality rate of the patients in this review was quite high at 38%, and other major complications included cardioembolic stroke (20%) and septic embolization to the extremities (6.67%). COVID-19 infection results in a severe inflammatory response caused by a variety of mechanisms. This severe degree of widespread inflammation may result in damage to the endocardium, thus creating an environment to which microorganisms can adhere to and colonize. Additionally, the immunosuppressive medications used in a COVID-19 infection can result in an increased risk of developing infections that have the potential to spread to the endocardium via a hematogenous route. Physicians should be aware of occurrences of IE in COVID-19, as delay in diagnosis and management may cause significant morbidity and mortality.

Salvage Coronary Artery Bypass Predicts Increased Mortality During Aortic Root Operation

Aortic root replacement (ROOT) has been an established therapy, yet the impact of adding coronary artery bypass grafting (CABG) to ROOT (CABG-R) is unknown. The purpose of this research was to investigate the impact of CABG on the outcomes of ROOT. A retrospective review from 2004 to 2016 of patients undergoing nonemergent ROOT surgical procedure was performed. Cohorts were established based on the presence or absence of added CABG. A propensity-score weighted comparison of outcomes was then conducted. A total of 867 patients met inclusion criteria and were analyzed (711 ROOT [72.0%], 156 CABG-R [18.0%]). CABG-R patients were older and had higher proportions of previous valve operation, hypertension, endocarditis, immunosuppressive therapy, renal insufficiency, and redo operation (all p < 0.01). Indications for CABG included anatomy (n= 48, 30.8%), coronary artery disease (80, 51.3%), and ventricular failure (28, 17.9%). The permanent stroke rate was not significantly increased with the addition of CABG-R (p= 0.06). Thirty-day mortality was 5.5% for the entire cohort but was substantially higher in patients who underwent concomitant CABG (3.4% ROOT, 15.4% CABG-R). Mortality rates were highest among patients with acute ventricular failure and CABG (28.8%) compared with patients who underwent CABG for coronary artery disease (6.3%) or patients for anatomy (22.9%; p= 0.003). CABG-R results in increased postoperative morbidity or mortality compared with isolated ROOT. Outcomes, however, are influenced by the specific clinical indication. CABG for coronary artery disease was associated with similar outcomes compared with isolated ROOT. Patients undergoing unplanned CABG for acute ventricular failure had the worst outcomes, thus underscoring the importance of technical success during coronary reimplantation.

Cardiac surgery in sub-Saharan Africa: a report of 3-year experience at the Douala General Hospital

Background: Cardiac surgery was started at the Douala General Hospital since 2012 as a result of a North-South collaboration between Cameroon and Belgium. Five cardiac surgery missions have been carried out since then. This work aimed at assessing three years of this initial experience. Methods: We carried out a cross-sectional descriptive study between November 2012 and March 2016. We reviewed the case records of all patients with heart disease, and with an indication for surgery. Results: A total of 45 patients with heart diseases who had an indication for surgery were retained for this study. There were 23 women and 22 men. Of these, 27 patients benefited from surgical intervention. Their mean age was 41±18 years (range, 14 to 85 years). The most common physical sign was heart murmur in 29 (64.4%) patients. Valvular Heart diseases were the most frequent in 32 (71.1%) patients, which were predominantly rheumatic heart diseases (RHD) in 25 (55.6%) patients. The most frequent surgical procedures were valve replacement with prosthesis, followed by repairs of congenital abnormalities. Mechanical prosthesis were mostly used (8/12 cases). Short-term intra-hospital mortality was 7.4%. The main cause of death was acute ventricular failure. Conclusions: The pilot phase of the cardiac surgery program at the General Hospital of Douala (DGH) was successful. Patients could be operated at a lower cost locally. Efforts must be made for the creation of an autonomous local team.

Effect of tidal volume, intrathoracic pressure, and cardiac contractility on variations in pulse pressure, stroke volume, and intrathoracic blood volume

We evaluated the impact of increasing tidal volume (V (t)), decreased chest wall compliance, and left ventricular (LV) contractility during intermittent positive-pressure ventilation (IPPV) on the relation between pulse pressure (PP) and LV stroke volume (SV(LV)) variation (PPV and SVV, respectively), and intrathoracic blood volume (ITBV) changes. Sixteen pentobarbital-anesthetized thoracotomized mongrel dogs were studied both before and after propranolol-induced acute ventricular failure (AVF) (n=4), with and without chest and abdominal pneumatic binders to decrease chest wall compliance (n=6), and during V (t) of 5, 10, 15, and 25ml/kg (n=6). SV(LV) and right ventricular stroke volume (SV(RV)) were derived from electromagnetic flow probes around aortic and pulmonary artery roots. Arterial pressure was measured in the aorta using a fluid-filled catheter. Arterial PPV and SVV were calculated over three breaths as (max-min)/[(max+min)/2]. ITBV changes during ventilation were inferred from the beat-to-beat volume differences between SV(RV) and SV(LV). Arterial PP and SV(LV) were tightly correlated during IPPV under all conditions (r (2)=0.85). Both PPV and SVV increased progressively as V (t) increased and with thoraco-abdominal binding, and tended to decrease during AVF. SV(RV) phasically decreased during inspiration, whereas SV(LV) phasically decreased 2-3 beats later, such that ITBV decreased during inspiration and returned to apneic values during expiration. ITBV decrements increased with increasing V (t) or with thoraco-abdominal binding, and decreased during AVF owing to variations in SV(RV), such that both PPV and SVV tightly correlated with inspiration-associated changes in SV(RV) and ITBV. Arterial PP and SV(LV) are tightly correlated during IPPV and their relation is not altered by selective changes in LV contractility, intrathoracic pressure, or V (t). However, contractility, intrathoracic pressure, and V (t) directly alter the magnitude of PPV and SVV primarily by altering the inspiration-associated decreases in SV(RV) and ITBV.

Early activation of apoptotic pathways in experimental acute afterload-induced right ventricular failure

Early activation of apoptotic pathways in experimental acute afterload-induced right ventricular failure

Effect of spinal cord injury upon prostate: adenocarcinoma of prostate in a spinal cord injury patient - a case report

IntroductionFollowing spinal cord injury, prostate undergoes atrophy probably due to interruption of neuro-hormonal pathways. The incidence of carcinoma of prostate is lower in patients with spinal cord injury above T-10 than in those with lesion below T-10.Case presentationA Caucasian male sustained T-4 paraplegia in 1991 at the age of 59-years. He had long-term indwelling urethral catheter. In May 1995, routine blood test showed prostate-specific antigen to be 17.7 mg/ml. Prostate biopsy revealed moderately differentiated primary adenocarcinoma of prostate; Gleason score was 3+3. Bone scans showed no evidence of metastatic bone disease. Bilateral orchidectomy was performed in September 1995. MRI of pelvis revealed no evidence of spread beyond prostatic capsule. There was no pelvic lymphadenopathy. In October 1996, this patient got chest infection and recovered fully after taking amoxicillin. In February 2001, he developed pneumonia and was prescribed cefuroxime intravenously. In March 2001, cystoscopy and electrohydraulic lithotripsy of vesical calculi were carried out. In August 2001, this patient was admitted to spinal unit for management of pressure sores. He expired on 28 June 2002 in local hospital. Cause of death was recorded as acute ventricular failure, congestive heart failure, chronic respiratory failure and spinal cord injury.ConclusionAlthough prostate gland undergoes atrophy in men who sustained spinal cord injury in early age, physicians should be vigilant and look for prostatic diseases particularly in men, who have sustained spinal cord injury during later period of life. Patients with cervical and upper dorsal lesions are at risk of developing potentially life-threatening chest complications after major surgical procedures including radical prostatectomy. Therefore, it may be advisable to consider chemoprevention of prostate cancer with Finasteride, especially in men, who sustained cervical and upper dorsal spinal cord injury during later part of their life.

Simultaneous variation of ventricular pacing site and timing with biventricular pacing in acute ventricular failure improves function by interventricular assist

The goal of this work was to investigate the hemodynamic effects of simultaneous left ventricular (LV) pacing site (LVPS) and interventricular pacing delay (VVD) variation with biventricular pacing (BiVP) during acute LV failure. Simultaneously varying LVPS and VVD with BiVP has been shown to improve hemodynamics during acute right ventricular (RV) failure. However, effects during acute LV failure have not been reported. In six open-chest pigs, acute LV volume overload was induced by regurgitant flow via an aortic-LV conduit. Epicardial BiVP was implemented with right atrial and ventricular leads and a custom LV pacing array. Fifty-four LVPS-VVD combinations were tested in random order. Cardiac output was evaluated by aortic flow probe, ventricular systolic function by maximum rate of ventricular pressure change, and mechanical interventricular synchrony by normalized RV-LV pressure diagram area. Simultaneous LVPS-VVD variation improved all measures of cardiac function. The observed effect was different for each functional index, with evidence of LVPS-VVD interaction. Compared with effects of LVPS-VVD variation in a model of acute RV failure, hemodynamic changes were markedly different. However, in both models, maximum rate of ventricular pressure change of the failing ventricle was improved with synchronous interventricular contraction, suggesting that, in acute ventricular failure, BiVP can recruit the unstressed ventricle to support systolic function of the failing one. Thus simultaneously varying LVPS and VVD with BiVP during acute ventricular failure can improve cardiac function by "interventricular assist", with hemodynamic effects dependent on the type of failure. This supports the potential utility of temporary BiVP for the treatment of acute ventricular failure commonly seen after cardiac surgery.

Yin and Yang of cGMP signalling in hydrostatic lung edema

Background Hydrostatic lung edema is a characteristic complication of acute left-sided ventricular or valvular heart failure that if untreated has a high mortality due to the resulting respiratory failure. Traditionally, formation of hydrostatic lung edema has been attributed to an imbalance of Starling forces, i.e. transcapillary hydrostatic and oncotic pressure in the pulmonary circulation resulting in interstitial and finally, alveolar edema. Yet, mechanosensitive cell responses may play a critical regulatory role in this scenario.

Dekompensierte Pulmonale Hypertonie

Right ventricular failure may result from an newly developed disease (e.g. as a consequence of acute respiratory distress syndrome [ARDS] or of severe pulmonary embolism) or of already present pulmonary hypertension (PHT). There is as yet no generally recognized definition of acute or chronic right ventricular failure. The particular clinical picture and the associated hemodynamics determine this condition. Right ventricular failure in the course of PHT represents a great challenge in clinical and intensive care practice. Once the vicious circle of right heart failure is reached an optimal balance has to be found between preload and afterload. In addition to optimizing blood volume, positive inotropic drugs (e.g. dobutamine) are available to maintain systemic blood pressure. Furthermore an increase in right ventricular contractility by inodilators is aimed at. The central goal in the treatment of right heart failure as part of PHT is to lower pulmonary vascular resistance and thus decrease right ventricular afterload. However, it is very difficult to break the vicious circle involved in the acute right heart syndrome, it must be the primary aim of treatment to recognize as early as possible any worsening of PHT and prevent acute right heart failure. Lung transplantation or surgical atrioseptostomy may represent possible ultimate therapeutic options for patients with PHT.

Marfan syndrome as a predisposing factor for traumatic aortic insufficiency

Despite the increase in car accidents, aortic valve injury from blunt trauma remains rare. In one case, a 30-year-old Marfan male, who was under observation at our outpatient clinic, suffered from aortic regurgitation due to a tear in the left coronary cusp of a previously echocardiographically normal valve. Acute ventricular failure demanded surgical management within 3 days after an automobile accident. The case was successfully treated by replacement of the aortic valve with a no. 23 Sorin Bicarbon prosthesis. The patient fully recovered and experienced an uneventful 6 months of follow-up.

Dynamic effects of positive-pressure ventilation on canine left ventricular pressure-volume relations.

Positive-pressure ventilation (PPV) may affect left ventricular (LV) performance by altering both LV diastolic compliance and pericardial pressure (Ppc). We measured the effect of PPV on LV intraluminal pressure, Ppc, LV volume, and LV cross-sectional area in 17 acute anesthetized dogs. To account for changes in lung volume independent of changes in Ppc and differences in contractility, measures were made during both open- and closed-chest conditions, during closed chest with and without chest wall binding, and after propranolol-induced acute ventricular failure (AVF). Apneic end-systolic pressure-volume relations (ESPVR) were generated by inferior vena caval occlusions. With the open chest, PPV had no effects. With the chest closed, PPV inspiration decreased LV end-diastolic volume (EDV) along its diastolic compliance curve and decreased end-systolic volume (ESV) such that the end-systolic pressure-volume domain was shifted to a point left of the LV ESPVR, even when referenced to Ppc. The decrease in EDV was greater in control than in AVF conditions, whereas the shift of the ESV to the left of the ESPVR was greater with AVF than in control conditions. We conclude that the hemodynamic effects of PPV inspiration are due primarily to changes in intrathoracic pressure and that the inspiration-induced decreases of LV EDV reflect direct effects of intrathoracic pressure on LV filling. The decreases in LV ESV exceed the amount explained solely by a reduction in LV ejection pressure.

Technique for commissural alignment of the arterial trunks during orthotopic heart transplantation

Twisting, buckling, and stretching of the pulmonary artery due to faulty alignment or disproportionately long arterial trunks are known technical complications during orthotopic heart transplantation. Failure to recognize these potentially lethal problems intraoperatively may lead to acute ventricular distention and failure. We describe a technique for alignment of the arterial trunks during orthotopic heart transplantation based on the constant commissural orientation of the aortic and pulmonary valves.

The effects of positive end-expiratory pressure on heart-lung interactions

Pulmonary artery occlusion pressure (Ppao) may not reflect left ventricular (LV) filling pressure during mechanical ventilation with positive end-expiratory pressure (PEEP) either because the catheter tip is not in zone III conditions or because pericardial pressure (Ppc) is also elevated. Ppc can be estimated from pleural pressure (Ppl) or, when right ventricular (RV) function is normal, from right atria[ pressure (Pra) (Am Heart J 108:603–605,1984). If the pericardium limits LV diastolic filling or RV diastolic compliance changes, then these estimates of Ppc may be inaccurate. We previously showed that nadir Ppao, immediately after abrupt PEEP removal, reflects on-PEEP LV filling pressure (Am J Physiol 249:H770–H776, 1985). We performed this study to determine if (1) the pericardium limits LV filling pressure during PEEP and (2) on-PEEP LV filling pressure can be estimated by on-PEEP Ppao minus Pra or nadir Ppao. We compared these relations when RV performance was normal (control), after induction of acute ventricular failure (AVF) with propranolol, and after subsequent induction of acute lung injury (AVF-OA) with oleic acid in an acute, anesthetized, closed-chest intact canine model (n = 7). PEEP was increased from 0 to 15 cm H2O in 5-cm H 2O increments. Nadir Ppao was measured on termination of 15 cm H 2O PEEP. Juxtacardiac Ppl and Ppc increased parallel to increasing PEEP in all conditions except at 0 and 5 cm H 2O PEEP in two dogs during AVF, when Ppc exceeded Ppl by as much as 4 mm Hg. Pre and Ppc covaried linearly in all conditions and at all levels of PEEP, although Pre was greater than Ppc (by 5.5 + 1.2 mm Hg [x + SE] in control, 7.1 + 2.1 mm Hg in AVF, and 6.6 + 1.5 in AVF-OA; P < .01). As PEEP increased, Ppao increased more than left atrial pressure (Pla) ( P < .01). Nadir Ppao reflected the difference between Pla and Ppc during PEEP ( P < .01). Error in Pra and Ppao relative to Ppc and Pla, respectively, confounded the estimate of LV filling pressure, such that Ppao-Pra showed no relation to Pla-Ppc at greater than 10 cm H 2O PEEP in control or at any level of PEEP in AVF and AVF-OA conditions. We conclude that the pericardium does not usually limit diastolic filling during PEEP. Also, Ppao-Pra may inaccurately estimate LV filling pressure when either RV performance or PEEP changes.

The arterial pressure waveform during acute ventricular failure and synchronized external chest compression.

Methods for mechanical cardiac support by intermittent increases in the intrathoracic pressure have recently been described. In the present study the responses of the arterial pressure waveform to mechanical ventilation with and without synchronized external chest compression (SEC) in the presence of acute ventricular failure (AVF) were evaluated by measuring the systolic pressure variation (SPV). SPV, the difference between the maximal and minimal values of systolic blood during a single positive pressure breath, consists of delta up and delta down components when systolic blood pressure during a short apnea is used as reference value. During intermittent positive pressure ventilation (IPPV) alone, AVF caused SPV to decrease significantly from 8.8 +/- 4.0 to 5.7 +/- 1.9 mm Hg, and further to 3.1 +/- 1.1 mm Hg after volume loading (P less than 0.02). The decrease in SPV was due to a significant decrease in the delta down component, whereas the delta up became the major component of the reduced SPV. The application of SEC caused significant increases in the delta down, delta up, and overall SPV during AVF without volume loading. However, during AVF with volume loading, SEC increased only the delta up component of the SPV, signifying a transient increase in the left ventricular stroke output. It is concluded that the disappearance of the delta down component of the SPV is characteristic of congestive heart failure. Analysis of the arterial waveform offers a readily available monitoring tool for the differentiation of the possible effects on increased intrathoracic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary effects of oleic acid-induced pulmonary edema and mechanical ventilation: Henning RJ, Heyman V, Alcover I, et al. Anesth Analg 65:925, 1986

Changes in intrathoracic pressure can influence cardiac performance by altering ventricular loading conditions. Since ventricular loading, both from systemic venous return (preload) and from left ventricular wall stress (afterload), varies during the cardiac cycle, we reasoned that appropriately placed, phasic, cardiac cycle-specific (synchronous) increases in intrathoracic pressure might augment ventricular ejection in acute ventricular failure. Recent studies in animals suggest that synchronous increases in intrathoracic pressure during systole increase ejection. We compared the hemodynamic effect of synchronous increases in intrathoracic pressure with similar increases delivered at random in the cardiac cycle in patients with congestive cardiomyopathy (n = 9). Intrathoracic pressure was estimated by measuring esophageal pressure. High-frequency jet ventilation (HFJV) synchronized with the electrocardiogram (synchronous HFJV) was compared with HFJV at a fixed frequency within 15 percent of the heart rate (asynchronous HFJV) and with intermittent positive-pressure breathing (IPPB) (tidal volume = 10 ml/kg; f = 15). All forms of ventilation resulted in the same mean airway pressure and esophageal pressure. Mean pulmonary arterial occlusion pressure and arterial pressure were constant in all conditions. Cardiac output was greater with synchronous HFJV than with either IPPB or asynchronous HFJV (4.5±0.7 L/min compared with 3.5±0.7 and 3.4±0.6 L/min [mean±SE], respectively; p<0.05). Mixed venous oxygen saturation covaried with cardiac output (p<0.05), such that calculated oxygen consumption remained constant for all conditions. We conclude that synchronous HFJV augments cardiac output more efficiently than do similar increases in intrathoracic pressure delivered randomly in the cardiac cycle.

Ventricular Assist by Cardiac Cycle-Specific Increases in Intrathoracic Pressure

Changes in intrathoracic pressure can influence cardiac performance by altering ventricular loading conditions. Since ventricular loading, both from systemic venous return (preload) and from left ventricular wall stress (afterload), varies during the cardiac cycle, we reasoned that appropriately placed, phasic, cardiac cycle-specific (synchronous) increases in intrathoracic pressure might augment ventricular ejection in acute ventricular failure. Recent studies in animals suggest that synchronous increases in intrathoracic pressure during systole increase ejection. We compared the hemodynamic effect of synchronous increases in intrathoracic pressure with similar increases delivered at random in the cardiac cycle in patients with congestive cardiomyopathy (n = 9). Intrathoracic pressure was estimated by measuring esophageal pressure. High-frequency jet ventilation (HFJV) synchronized with the electrocardiogram (synchronous HFJV) was compared with HFJV at a fixed frequency within 15 percent of the heart rate (asynchronous HFJV) and with intermittent positive-pressure breathing (IPPB) (tidal volume = 10 ml/kg; f = 15). All forms of ventilation resulted in the same mean airway pressure and esophageal pressure. Mean pulmonary arterial occlusion pressure and arterial pressure were constant in all conditions. Cardiac output was greater with synchronous HFJV than with either IPPB or asynchronous HFJV (4.5 +/- 0.7 L/min compared with 3.5 +/- 0.7 and 3.4 +/- 0.6 L/min [mean +/- SE], respectively; p less than 0.05). Mixed venous oxygen saturation covaried with cardiac output (p less than 0.05), such that calculated oxygen consumption remained constant for all conditions. We conclude that synchronous HFJV augments cardiac output more efficiently than do similar increases in intrathoracic pressure delivered randomly in the cardiac cycle.