Cardiac tamponade as an initial presentation of papillary carcinoma with psammoma bodies and intranuclear grooves-A diagnostic dilemma.

Involvement of body fluids by adenocarcinoma is a common phenomenon. However, metastasis to the pericardial fluid by adenocarcinoma is a rare occurrence. The most common malignancies associated with malignant pericardial effusion are carcinoma of the lung, breast, esophagus, melanoma, lymphoma, and leukemia. Here, we discuss a case of a 36-year-old female with hemorrhagic pericardial effusion presenting with cardiac tamponade and psammoma bodies which was suspected and reported as metastatic papillary carcinoma of thyroid on cytomorphology; however, the immunocytochemical and radiological features confirmed metastatic papillary adenocarcinoma of lung contrary to the thyroid which is more common and expected.

Sost Haploinsufficiency Provokes Peracute Lethal Cardiac Tamponade without Rescuing the Osteopenia in a Mouse Model of Excess Glucocorticoids.

Glucocorticoid-induced secondary osteoporosis is the most predictable side effect of this anti-inflammatory. One of the main mechanisms by which glucocorticoids achieve such deleterious outcome in bone is by antagonizing Wnt/ß-catenin signaling. Sclerostin, encoded by Sost gene, is the main negative regulator of the proformative and antiresorptive role of the Wnt signaling pathway in the skeleton. It was hypothesized that the partial inactivation of sclerostin function by genetic manipulation will rescue the osteopenia induced by high endogenous glucocorticoid levels. Sost-deficient mice were crossed with an established mouse model of excess glucocorticoids, and the effects on bone mass and structure were evaluated. Sost haploinsufficiency did not rescue the low bone mass induced by high glucocorticoids. Intriguingly, the critical manifestation of Sost deficiency combined with glucocorticoid excess was sporadic, sudden, unprovoked, and nonconvulsive death. Detailed histopathologic analysis in a wide range of tissues identified peracute hemopericardium and cardiac tamponade to be the cause. These preclinical studies reveal outcomes with direct relevance to ongoing clinical trials that explore the use of antisclerostin antibodies as a treatment for osteoporosis. They particularly highlight a potential for increased cardiovascular risk and may inform improved stratification of patients who might otherwise benefit from antisclerostin antibody treatment.

Varón de 89 años con dolor abdominal. Manifestación atípica de taponamiento cardiaco / An 89-year old male with abdominal pain. An atypical manifestation of cardiac amponade

El taponamiento cardiaco consiste la acumulación dentro de la cavidad pericárdica de líquido en cantidad y rapidez suficiente como para comprometer el llenado ventricular. Las formas agudas suelen deberse a rotura cardiaca o disección aórtica, las formas subagudas son numerosas, pero entre otras entidades frecuentes encontramos las neoplasias, la uremia y aquellas entidades consideradas de origen idiopático. El taponamiento cardiaco es siempre una emergencia médica (AU)

Cardiac tamponade is the rapid accumulation of a large amount of fluid in the pericardial cavity that impairs ventricular filling. Acute forms are often due to cardiac rupture or aortic dissection. Subacute forms are numerous, however, the most frequent entities are neoplasms, uremias and idiopathic. Cardiac tamponade is always a medical emergency (AU)

Chylous pericardial effusion after aortic valve replacement.

Chylous pericardial effusion after open-heart surgery is a rare complication. We report a case of chylous pericardial effusion following aortic valve replacement, which presented as cardiac tamponade, and its subsequent management.

Jejunal luminal microdialysate lactate in cardiac tamponade--effect of low systemic blood flow on gut mucosa.

OBJECTIVE: To assess gut mucosal metabolic response and susceptibility to dysoxia during low systemic blood flow induced by cardiac tamponade. DESIGN: A randomized, controlled animal experiment. SETTING: National laboratory animal center. INTERVENTIONS: Cardiac tamponade was induced in six pigs, while six additional pigs served as controls. In the tamponade group, fluid was injected into the pericardial space to reduce aortic flow, aiming first at a flow of 50 ml/kg per min and then at 30 ml/kg per min. Each step lasted for 60 min. MEASUREMENTS AND RESULTS: We measured luminal lactate by microdialysis and mucosal PCO(2) by tonometry in the mid-jejunum. Aortic and superior mesenteric artery blood flow, arterial and mesenteric venous lactate, pyruvate and ketone bodies and regional lactate exchange were measured. The distribution of aortic blood flow to superior mesenteric artery remained unchanged (baseline 14 (12-16)%; median (interquartile range), stepwise flow reduction 11 (10-17)% and 13 (12-19)%, NS) during reduction of aortic blood flow from 81 (61-95) ml/kg per min to 49 (47-49) ml/kg per min and 23 (21-27) ml/kg per min. Systemic hyperlactatemia developed early, whereas gut luminal lactate increased only after 60 min of hypoperfusion and could be largely explained by arterial hyperlactatemia. Mesenteric venous lactate-to-pyruvate (L/P) ratio increased after 30 min of tamponade, but both venous-arterial lactate and pyruvate gradients turned negative (gut lactate and pyruvate uptake). Mesenteric venous ss-hydroxybutyrate to acetoacetate ratio increased after 60 min. No changes were observed in the controls. CONCLUSIONS: Jejunal mucosal dysoxia and anaerobic metabolism occurs late during low systemic blood flow induced by experimental cardiac tamponade.

Mild hypothermia alters the oxygen consumption/delivery relationship by decreasing the slope of the supply-dependent line.

OBJECTIVE: To evaluate the effect of mild hypothermia on the relationship between systemic oxygen consumption and oxygen delivery. DESIGN: Prospective animal study. SETTING: University research laboratory. SUBJECTS: Anesthetized and ventilated rabbits. INTERVENTIONS: Rabbits were subjected to stepwise cardiac tamponade to reduce oxygen delivery while body temperature was maintained at 34 degrees C (group H, n = 8) or 39 degrees C (group N, n = 8). MEASUREMENTS AND MAIN RESULTS: The oxygen consumption/oxygen delivery relationship was analyzed by the dual-line method. The slope of the supply-dependent line was significantly decreased in group H (y = 0.57x + 1.3) compared with that in group N (y = 0.72x + 1.7), indicating that the ability of tissues to extract oxygen was impaired during hypothermia. Consequently, the proportion of the supply-independent area over the entire range of oxygen delivery was decreased in response to hypothermia. CONCLUSION: The potential for tissue hypoxia is likely to be increased during hypothermia when the circulation becomes unstable and oxygen delivery decreases.

Controlling malignant pericardial effusion by intrapericardial carboplatin administration in patients with primary non-small-cell lung cancer.

Malignant pericarditis, when associated with massive pericardial effusion, presents a critical condition in lung cancer patients. Because this condition often arises in terminally ill patients, intensive therapy such as multi-drug combination chemotherapy is rarely appropriate. This study evaluated the clinical relevance of intrapericardial administration of carboplatin for controlling malignant pericardial effusions associated with non-small-cell lung carcinoma (NSCLC). The method used for 10 eligible patients consisted of draining the pericardial effusion and infusing 300 mg/body of carboplatin in 50 ml of saline through an in-place catheter into the pericardial space and clamping the catheter for 40 min. Nine of the 10 patients showed satisfactory results, and 8 experienced complete regression of the effusion. No major or minor adverse effects were observed. Pharmacokinetics analysis revealed that the concentration of free platinum in the pericardial fluid was very high while that of total platinum in the circulating plasma was very low, assuring the usefulness of the intrapericardial instillation of carboplatin in terminally ill patients for controlling malignant pericardial effusion when the systemic delivery of cytotoxic agents is inappropriate.

Interleukin-1beta alters the oxygen delivery-oxygen consumption relationship in rabbits by increasing the slope of the supply-independent line.

When systemic oxygen delivery (DO2) is reduced, oxygen consumption (VO2) is maintained until a critical level is reached (DO2crit). Sepsis is thought to shift DO2crit to the right and lengthen the supply-dependent portion. We tested the effect of interleukin (IL)-1beta, which is one of the key cytokines related to sepsis, on the DO2-VO2 relationship. Fifteen rabbits were subjected to stepwise cardiac tamponade to reduce DO2 to 10% by inflating a handmade balloon placed into the pericardial sac. Seven rabbits were given 10 microg/kg of IL-1beta intravenously (IL-1beta group) prior to the graded cardiac tamponade. The remainder received saline alone (control group). The DO2-VO2 relationship was analyzed by the dual-line method. IL-1beta significantly decreased mean arterial pressure (65 +/- 11 mmHg from baseline 85 +/- 7 mmHg) without altering cardiac output. The IL-1beta group showed significantly steeper supply-independent line slopes than did the control group (0.19 +/- 0.02 vs. 0.11 +/- 0.02, respectively), which resulted in a DO2crit shift to the left (IL-1beta group, 8.7 +/- 1.7 ml/kg x min vs. control, 11.7 +/- 0.7 ml/kg x min). The IL-1beta group also showed greater PO2 and plasma lactate levels in the portal vein than did the control group. These results indicate that IL-1beta impairs systemic oxygen uptake even before VO2 becomes supply-dependent, presumably due to maldistribution of the blood flow including the splanchnic circulation.

Jejunal mucosal nitric oxide production and substrate dependency during acute mesenteric hypoperfusion in pigs.

OBJECTIVE: Jejunal nitric oxide (NO) formation is impaired during mucosal hypoperfusion. This study was undertaken to investigate whether this phenomenon could result from a restricted mucosal availability of NO-synthase substrates, ie, oxygen and/or L-arginine. DESIGN: Controlled study using laboratory animals. SETTING: University animal research laboratory. SUBJECTS: Eighteen chloralose-anesthetized, ventilated, juvenile Landrace domestic pigs. INTERVENTIONS: Mesenteric hypoperfusion was induced by intrapericardial infusion of Ringer's solution to achieve decreased cardiac output by creation of cardiac tamponade. MEASUREMENTS AND MAIN RESULTS: Animals were prepared for jejunal intraluminal perfusion with 150 mM NaCl or 3 mM L-arginine solution in an isolated intestinal segment and then subjected to cardiac tamponade. Jejunal mucosal NO formation was measured with a tonometric technique. Mesenteric blood flow was measured as portal blood flow, and mucosal perfusion was measured by laser Doppler flowmetry. Regional oxygen consumption and delivery were calculated from arterial and portal blood samples. Cardiac tamponade reduced jejunal NO formation (-52%), mesenteric oxygen delivery (-75%), oxygen consumption (-39%), and mucosal perfusion (-43%). Oxygenation of the jejunal intraluminal perfusate completely restored the intestinal NO levels within 30 mins, whereas presence of L-arginine was without effect. CONCLUSIONS: The study indicates that oxygen rather than L-arginine is the rate-limiting factor for mucosal NO production during acute reduced splanchnic perfusion.

Detecting gastrointestinal hypoperfusion during cardiac tamponade in pigs: a role for nitric oxide tonometry?

OBJECTIVE: To evaluate different techniques and regional approaches for detecting critical reductions in gastrointestinal (GI) perfusion. DESIGN: Laboratory, animal, controlled study. SETTING: University animal research laboratory. SUBJECTS: Thirteen anesthetized, ventilated, juvenile domestic pigs. INTERVENTIONS: Dextran was infused into the pericardial sac to achieve cardiac tamponade that reduced cardiac output to 25% of baseline value. Hemodynamics were invasively monitored, and blood gases were sampled in the systemic and portal circulations. Tonometers were placed in the corpus of the stomach and in the jejunum, 50 cm aboral to the ligament of Treitz. MEASUREMENTS AND MAIN RESULTS: We measured cardiac output, portal venous blood flow, mesenteric oxygen delivery and consumption, systemic and portal venous blood gases and acid-base balance, stomach and jejunal transepithelial potential difference, stomach and jejunal intramucosal pH, arterial plasma concentrations of asymmetric dimethylarginine, and jejunal, intraluminal nitric oxide. One hour of cardiac tamponade decreased mesenteric oxygen delivery and consumption in a linear fashion and resulted in mesenteric acidosis, as evidenced by decreases in pH, standard bicarbonate, oxygen saturation, and PO2 and increases in PCO2. The potential difference in the jejunum decreased earlier than in the stomach, whereas stomach intramucosal pH decreased before jejunal intramucosal pH. Intraluminal nitric oxide in the jejunum was markedly reduced soon after cardiac tamponade. This reduction was accompanied by an increase in arterial plasma concentrations of the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine. Investigated variables were unchanged in control animals. CONCLUSIONS: Both intramucosal pH and potential difference measurements may be used to detect critical reduction in GI perfusion. Regional and temporal differences may reduce the accuracy of these methods. Jejunal tonometry can yield an early nitric oxide measurement that indicates mesenteric low-flow conditions. Jejunal tonometry also yields quantitative information about this modulator of hemodynamic and mucosal barrier function, information that is relevant to GI failure during shock.

Effects of nitric oxide on blood flow distribution and O2 extraction capabilities during endotoxic shock.

The effects of the nitric oxide (NO) synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) and the NO donor 3-morpholinosydnonimine (SIN-1) were tested in 18 endotoxic dogs. L-NMMA infusion (10 mg . kg-1 . h-1) increased arterial and pulmonary artery pressures and systemic and pulmonary vascular resistances but decreased cardiac index, left ventricular stroke work index, and blood flow to the hepatic, portal, mesenteric, and renal beds. SIN-1 infusion (2 microg . kg-1 . min-1) increased cardiac index; left ventricular stroke work index; and hepatic, portal, and mesenteric blood flow. It did not significantly influence arterial and pulmonary artery pressures but decreased renal blood flow. The critical O2 delivery was similar in the L-NMMA group and in the control group (13.3 +/- 1.6 vs. 12.8 +/- 3.3 ml . kg-1 . min-1) but lower in the SIN-1 group (9.1 +/- 1.8 ml . kg-1 . min-1, both P < 0.05). The critical O2 extraction ratio was also higher in the SIN-1 group than in the other groups (58.7 +/- 10.6 vs. 42.2 +/- 7.6% in controls, P < 0.05; 43.0 +/- 15.5% in L-NMMA group, P = not significant). We conclude that NO is not implicated in the alterations in O2 extraction capabilities observed early after endotoxin administration.

Sodium nitroprusside does not influence tissue oxygen extraction capabilities during a critical reduction in oxygen delivery.

By its regulating effects on blood vessel tone, nitric oxide (NO) may play an important role in the coupling of oxygen delivery (DO2) to metabolic rate. We reasoned that if endogenous NO synthesis is an important modulator of oxygen extraction ratio (O2ER), then administration of a NO donor will alter oxygen extraction capabilities during a fall in blood flow. We studied the effects of the NO donor, nitroprusside, on the relationship between DO2 and oxygen uptake (VO2) during an acute reduction in DO2 induced by cardiac tamponade. Twenty-one healthy, anaesthetised, mechanically ventilated dogs were randomly divided into 3 groups. Group 1 (n = 7) served as control; Groups 2 and 3 were given sodium nitroprusside at 1.0 microgram/kg.min (n = 7), and 2.5 micrograms/kg.min intravenously (n = 7), respectively. All animals were given normal saline i.v. at a rate of 20 ml/kg.h throughout the study. Cardiac tamponade was induced by bolus injections of normal saline into the pericardial space. In the control animals the critical DO2 (DO2crit) was found at 10.1 +/- 1.5 ml/kg.min and critical O2ER (O2ERcrit) at 63.3 +/- 10.9%. Nitroprusside at the lower dose decreased systemic vascular resistance but did not significantly influence arterial pressure, cardiac output, DO2 or VO2; neither DO2crit nor O2ERcrit was altered (9.3 +/- 2.9 ml/kg.min and 70.4 +/- 20.9%). Nitroprusside at the higher dose induced significant decreases in mean arterial pressure and systemic vascular resistance, but had no significant effect on cardiac output. DO2crit (9.2 +/- 2.0 ml/kg.min) and O2ERcrit (59.8 +/- 13.2%) were similar to the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Prostaglandin E1 increases oxygen extraction capabilities in experimental sepsis.

By its microvascular and anti-inflammatory actions, prostaglandin E1 (PGE1) has been suggested both in animal models and in humans to have a therapeutic value in sepsis. To investigate whether PGE1 could improve the oxygen extraction capabilities in severe sepsis, our study focused on the relationship between oxygen uptake (VO2) and oxygen delivery (DO2) during an acute reduction in blood flow induced by cardiac tamponade in endotoxic dogs. Thirty anesthetized, ventilated dogs were divided into three groups. A first group (N = 10) served as a control receiving 20 ml/kg/hr of saline intravenously. A second group (N = 10) received PGE1 at 100 ng/kg/min along with the same saline infusion. A third group (N = 10) received the same dose of PGE1 with only 1 ml/kg/hr of saline. Thirty minutes after the initiation of this therapy, Escherichia coli endotoxin (2 mg/kg) was injected in each dog. In each group, the administration of PGE1, fluids, or both was continued throughout the study. Tamponade was then induced by repeated bolus injections of warm saline into the pericardial space. Steady-state measurements of VO2 (derived from the expired gases) and DO2 (the product of cardiac index and oxygen content) were obtained sequentially after each saline injection. The administration of PGE1 + fluids resulted in significant increases in stroke volume, cardiac index, and DO2 and reductions in systemic and pulmonary vascular resistance. Stroke volume and cardiac index were lower in the PGE1 alone than in the PGE1 + fluids group. The VO2 levels at critical DO2 (DO2crit) were identical. However, DO2crit, which was 12.2 +/- 2.8 ml/kg/min in the control group, was significantly decreased to 9.8 +/- 2.0 ml/kg/min in the PGE1 + fluids and to 9.3 +/- 2.7 ml/kg/min in the PGE1 alone group (both P < 0.05). Critical oxygen extraction ratio (O2ERcrit) which was 47 +/- 14% in the control group, was increased to 63 +/- 16% in the PGE1 + fluids group and to 61 +/- 17% in the PGE1 alone group (both P < 0.05). To investigate whether PGE1 also improves oxygen extraction capabilities in the absence of endotoxin, a second series of experiments was performed in 14 dogs, receiving saline alone (Control, N = 7) or plus PGE1 at 100 ng/kg/min (PGE1, N = 7). DO2crit was 10.7 +/- 2.9 ml/kg/min in the PGE1 group vs 10.1 +/- 1.8 ml/kg/min in the control group (NS). O2ERcrit tended to be higher in the PGE1 group than that in the control group (68 +/- 13% vs 60 +/- 15%, P = 0.054).(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of dobutamine and norepinephrine on oxygen availability in tamponade-induced stagnant hypoxia: a prospective, randomized, controlled study.

OBJECTIVES: To explore the effects of dobutamine and norepinephrine on the global cardiovascular response and on the relationship between oxygen uptake (VO2) and oxygen delivery (DO2) during an acute reduction in blood flow associated with tamponade. DESIGN: Prospective, randomized, controlled acute intervention study. SETTING: University intensive care unit (ICU) laboratory. SUBJECTS: Twenty healthy, anesthetized mongrel dogs, weighing 19 to 28 kg. INTERVENTIONS: Six dogs served as control, seven dogs were given 10 micrograms/kg/min of dobutamine and another seven dogs were given 1 microgram/kg/min of norepinephrine. Data were collected at graded incremental levels of intrapericardial pressure. MEASUREMENTS AND MAIN RESULTS: VO2 was derived from expired gas analysis and DO2 was calculated from the product of thermodilution cardiac index and arterial oxygen content. In each animal, two catheters were inserted into the pericardium to induce tamponade by saline infusion and to measure the intrapericardial pressure. The critical Do2 value, below which VO2 decreased, was found at 9.4 +/- 1.3 mL/kg/min in the control animals. When DO2 decreased to below this critical value, lactic acidosis developed. Dobutamine and norepinephrine, at the dose that was administered, significantly increased cardiac index and DO2. Critical DO2 was slightly higher in the treated than in the control animals (12.1 +/- 1.6 mL/kg/min in dobutamine and 13.2 +/- 0.9 mL/kg/min in norepinephrine, NS). VO2 at critical DO2 was significantly higher in the treated groups than in the control group (7.7 +/- 1.1 mL/kg/min in the dobutamine group and 7.9 +/- 0.9 mL/kg/min in the norepinephrine group vs. 5.4 +/- 0.4 mL/kg/min in control, both p < .01). There was no significant difference in the critical oxygen extraction ratio and the slope of the supply-dependent line between the three groups. In dobutamine-treated animals, cardiac index, DO2, and VO2 were better maintained for any intrapericardial pressure than in the other groups. Critical intrapericardial pressure, at which VO2 started to decrease, was significantly higher in the dobutamine-treated group than in the control group (13.8 +/- 2.3 vs. 9.3 +/- 1.2 mm Hg, p < .05). At critical DO2, the mean blood lactate concentration was also lower in the dobutamine-treated animals than in the other animals (2.1 +/- 0.3 vs. 4.1 +/- 0.7 mmol/L in control and 3.8 +/- 0.4 mmol/L in the norepinephrine group, both p < .05). CONCLUSIONS: During low-flow states associated with tamponade, both dobutamine and norepinephrine at the dose used increased cardiac index, DO2, and VO2, but dobutamine delayed the onset of tissue hypoxia by further increasing blood flow and oxygen availability. In the conditions of the present study, neither agent significantly influenced the oxygen extraction capabilities of the body.

Oxygen extraction is altered by endotoxin during tamponade-induced stagnant hypoxia in the dog.

The present study used a model of cardiac tamponade to investigate the effects of endotoxin on the oxygen extraction capabilities of the body during an acute reduction in blood flow, when blood volume and arterial oxygen content were maintained. In 21 pentobarbital anesthetized, mechanically ventilated dogs, two catheters were introduced into the pericardial space to induce cardiac tamponade, and simultaneously to measure the intrapericardial pressure. Oxygen uptake (VO2) was determined from the expired gases. Oxygen delivery (DO2) was calculated by the product of the thermodilution cardiac index and the arterial oxygen content. Eleven dogs received 2 mg/kg Escherichia coli endotoxin, followed by generous saline infusion (20 ml/kg.hr). Ten dogs served as a control group. In each dog, DO2 was progressively reduced by pericardial saline infusion at a rate of 40 ml/hr for the first hour and 30 ml/hr thereafter. Critical O2 delivery (DO2crit) and critical O2 extraction ratio (O2ERcrit) were determined from a plot of VO2/DO2 for each individual dog. The DO2crit was greater in the endotoxic than in the control group (12.1 +/- 3.1 ml/kg.min vs. 9.6 +/- 1.6 ml/kg.min; P < 0.05). Endotoxin at the dose used did not alter VO2 (or critical VO2). Accordingly, O2ERcrit was significantly lower in the endotoxic than in the control animals (47.2% +/- 5.7% vs. 60.3% +/- 10.6%; P < 0.01). The mixed venous PO2 levels at DO2crit were higher in the endotoxic than in the control group (30.6 +/- 6.1 mm Hg vs. 25.4 +/- 5.2 mm Hg; P < 0.05). Arterial blood lactate concentration was higher in the endotoxic than in the control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)