Impaired Peripheral Perfusion Research Articles

Buerger-Allen exercises' effectiveness for improving lower limb circulation

Impaired peripheral perfusion in the legs is the most common complaint experienced by patients with type 2 Diabetes Mellitus (DM). One nursing intervention in the form of physical exercise that can be administered to DM patients to prevent peripheral perfusion disorders and increase vascularization of the lower extremities is the Buerger-Allen Exercise (BAE). The goal of this study was to analyze the effectiveness of BAE in improving lower extremity circulation. The population consisted of patients with type 2 DM. The research design employed a quasi-experiment with pre-test and post-test, including a control group. A sample of 24 respondents was divided into an intervention group and a control group. The sampling technique used was purposive sampling. Data were obtained through direct Ankle-Brachial Index (ABI) measurement using a Doppler ultrasound and an aneroid sphygmomanometer, temporary blood sugar level measurements using a glucometer, and leg sensitivity measurements using a monofilament tool. Paired T-tests and independent T-tests were used as statistical tests. The results of the Paired T-test for lower limb circulation in the intervention group yielded a p-value of 0.000, indicating a significant difference in the circulation of the lower extremities before and after the intervention. The results of the independent T-test also showed a p-value of 0.000, indicating significance. Thus, BAE can improve lower limb circulation in patients with type 2 DM.

Features of the course of traumatic shock when using respiratory mixtures with a high content of inert gases

This study evaluated the efficiency of using gas mixtures with increased concentrations of inert gases on a hemorrhagic shock model in experimental animals. Massive blood loss is considered a trigger mechanism of severe pathophysiological reactions (impaired peripheral perfusion, acidosis, hemostasis system dysfunction, and multiple organ failure). Inert gases (helium, argon, and xenon) attract attention as potentially useful in various pathological conditions. The study was conducted on 15 same-sex pigs of the same breed, weighing 40–50 kg, randomized into three groups with five each: control group, inhalation of 100% oxygen; “agohhep” group, inhalation of the “Aroxxen” gas mixture: 35% argon, 58% oxygen, 0.2% xenon, and nitrogen as the rest of the volume; and “agohhep-krypto” group, inhalation of the gas mixture “Aroxxen-krypto”: 35% argon, 40% oxygen, 10% krypton, and nitrogen as the rest of the volume. Dynamic monitoring of vital signs and sampling of materials were conducted before blood loss, with blood loss of 20% and 45% of the volume of the circulating blood 60, 120, and 180 min after blood loss. The survival rate of animals and respiratory and circulatory states were evaluated by clinical and laboratory indicators. With blood loss of 45% of the circulating blood volume, no statistically significant differences in mortality were found between the groups. All animals survived for 180 min in the post-hemorrhagic period. In the aggohep-krypto group, average blood pressure values after blood loss and throughout the follow-up period were significantly higher than those in the control and aggohep groups (p 0.05). During shock simulation as a result of blood loss, base deficiency gradually worsened in all groups. However, starting from the second hour of observation, base deficiency began to be compensated in the control and aggohep-krypto groups and the aggohep group, it continued to increase significantly (p 0.01). During the follow-up after blood loss, the level of lactatemia significantly increased in the aggohep group (by 10 times at the end of the follow-up), which is significant different from those in the control and aggohep-krypto groups (p 0.01). Thus, compared with the use of Arroxen gas, the use of Arroxen-krypto gas of the proposed composition in acute massive blood loss makes it possible to achieve a less pronounced attrition of the acid–base balance in experimental animals.

Penerapan Perawatan Kaki Dan Kuku Terhadap Peningkatan Sirkulasi Perifer Pada Penderita Critical Limb Ischemia (CLI)

Background . Critical limb ischemia (CLI) is the most severe stages disease vessels blood chronic , oriented CLI management on effort to anticipate doing amputation by pushing a severe infection happens on wound and healing the wound easier. One wrong possible intervention done to increase peripheral circulation and prevent the occurance of amputation consequence on severe infection is circulation maintenance. Purpose Describe feet application and nail care _ enhancement of peripheral circulation to fill a need safety of patients with Critical Limb Ischemia (CLI) . Method : This is a descriptive study uses a study case approach with a Nursing process approach . Subject of the study was one participant . Results the client felt painful on the feet , it started by feeling numb and cold on her left toes, then purple spots and several days later the spots were changed to be black and widespread to her calf . cold acral, nursing diagnosis enforced impaired peripheral tissue perfusion. Nursing Intervention: feet and nail care, Evaluation: decreased pain scale, increased muscle strength, changed in acral temperature and no changed in capillary refill. Conclusion : Giving circulation maintenance on client Mrs. S with CLI (Critical Limb Ischemia) for 5 days management was effective because on the fifth day client said painful on her left lower extremity decreased so that she could move , and client said she felt comfortable and relax after washing and cleaning her feet using warm water , soap , body lotion and cuting her toenails.
 Keywords : CLI, foot care , peripheral circulation, pain

Abstract #1397695: Use of Continuous Glucose Monitoring to Solve the Mystery of Pseudohypoglycemia

Hypoglycemia (glucose < 55 mg/dL) is uncommon in people without diabetes. Routine monitoring of blood glucose in hospitalized patients usually is performed by fingerstick point of care (POC) glucose testing via glucometer as a measure of capillary whole-blood glucose, correlating with venous plasma glucose. Pseudohypoglycemia is a consideration when POC glucose is low but plasma blood glucose is normal range. It can occur in the setting of impaired peripheral perfusion, such as in patients with Raynaud’s disease, shock, or peripheral vascular disease (PVD). A 63-year-old female was admitted for evaluation of uncontrolled hypertension. Her medical history was significant for previous myocardial infarction, atrial fibrillation, and heart failure with preserved ejection fraction. She had no history of Raynaud's phenomenon, diabetes (HbA1C 5.1%), or known PVD. During hospitalization, she had symptoms of anxiety, diaphoresis, tremors, nausea, forgetfulness, dizziness. POC glucose was 37 mg/dL and the patient was promptly treated with IV dextrose, negating a blood draw for a confirmatory venous plasma glucose. Several similar episodes occurred, even while on dextrose infusion prompting a hypoglycemia laboratory work-up. Off of dextrose, her POC glucose dropped to <50 mg/dL with insulin 97.7 uIU/mL, C-peptide 12.3 ng/mL and proinsulin of 77 pmol/L. However venous glucose was 173 ng/mL and thought to reflect treatment with dextrose prior to the blood draw. A second time, POC glucose was <50 ng/mL with insulin 48.9 uIU/mL and C-peptide 6.0 ng/mL which could support hyperinsulinemia but, again, venous plasma glucose was normal (113 mg/dL). Anti-diabetic medication and insulin antibody screening were negative. A continuous glucose monitoring system (CGMS) was placed on her abdomen to provide alternative peripheral glucose data. The patient manifested glucoses of 32/15/21 mg/dL by glucometer while simultaneous CGMS values were 110/126/156 mg/dL, confirming pseudohypoglycemia. In nondiabetic patients, hypoglycemia fulfilling Whipple’s triad be documented prior to initiating the complex evaluation for causes of hypoglycemia. Our patient is unusual because she did not have usual causes of pseudohypoglycemia such as Raynaud’s disease, diabetes, shock, or PVD. The inaccuracy of POC glucose measurements in patients with impaired microperfusion should be considered when the data are incongruent, as this can cause unnecessary investigations and prolonged length of stay. Should alternative blood glucose monitoring be required in these patients, CGM is a valuable technology.

Perioperative Hemodynamic Monitoring: An Overview of Current Methods.

Perioperative hemodynamic monitoring is an essential part of anesthetic care. In this review, we aim to give an overview of methods currently used in the clinical routine and experimental methods under development. The technical aspects of the mentioned methods are discussed briefly. This review includes methods to monitor blood pressures, for example, arterial pressure, mean systemic filling pressure and central venous pressure, and volumes, for example, global end-diastolic volume (GEDV) and extravascular lung water. In addition, monitoring blood flow (cardiac output) and fluid responsiveness (preload) will be discussed.

Cell-Free Hemoglobin Is Associated With Increased Vascular Resistance and Reduced Peripheral Perfusion in Severe Malaria.

In severe falciparum malaria, unlike sepsis, hypotension on admission is uncommon. We hypothesized that low nitric oxide bioavailability due to the presence of cell-free hemoglobin (CFH) increases vascular tone in severe malaria. Patients with severe malaria (n = 119), uncomplicated malaria (n = 91), or suspected bacterial sepsis (n = 56), as well as healthy participants (n = 50), were recruited. The systemic vascular resistance index (SVRI) was estimated from the echocardiographic cardiac index and the mean arterial pressure. SVRI and hematocrit levels were lower and plasma CFH and asymmetric dimethylarginine levels were higher in patients with malaria, compared with healthy participants. In multivariate linear regression models for mean arterial pressure or SVRI in patients with severe malaria, hematocrit and CFH but not asymmetric dimethylarginine were significant predictors. The SVRI was lower in patients with suspected bacterial sepsis than in those with severe malaria, after adjustment for hematocrit and age. Plasma CFH levels correlated positively with the core-peripheral temperature gradient and plasma lactate levels and inversely with the perfusion index. Impaired peripheral perfusion, as reflected by a low perfusion index or a high core-peripheral temperature gradient, predicted mortality in patients with severe malaria. CFH is associated with mean arterial pressure, SVRI, and peripheral perfusion in patients with severe malaria. This may be mediated through the nitric oxide scavenging potency of CFH, increasing basal vascular tone and impairing tissue perfusion.

Blood lactate increases with the progression of mitral valve disease in dogs

ABSTRACT: In dogs with congestive heart failure, the upregulated sympathetic tone causes vasoconstriction that impairs peripheral blood supply, therefore causing the accumulation of lactate. In this prospective cross-sectional study with a longitudinal component, blood lactate was quantified in 10 healthy and 34 myxomatous mitral valve disease (MMVD) dogs to investigate its potential use as a diagnostic and prognostic biomarker. While there were no differences in lactate concentration between control animals and stages B1 (3.31±0.62mmol/L) and B2 (3.32±0.46mmol/L) dogs, significant differences were found between healthy (2.50±0.69mmol/L) and both C (3.99±0.47mmol/L) and D (6.97±1.23mmol/L) animals. When a cut-off of 3.35mmol/L was used, lactate was able to distinguish dogs with normal and remodeled hearts with a sensitivity of 78.2% and specificity of 63.6%. Also, significant correlations existed between lactate and indicators of cardiac remodeling. Finally, animals with blood lactate &lt;3.5mmol/L carried a better prognosis when compared with dogs in which lactate was &gt;5.0mmol/L. Our results suggest that the progression of MMVD results in accumulation of lactate within the bloodstream, which is likely attributable to the impaired peripheral tissue perfusion. In MMVD dogs, blood lactate may be used as a surrogate for cardiac remodeling, and an increased concentration is associated with a worse prognosis regarding the time to evolve into congestive heart failure.

Reduced arterial vasodilatation in response to hypoxia impairs cerebral and peripheral oxygen delivery in hypertensive men

Hypoxaemia evokes a repertoire of homeostatic adjustments that maintain oxygen supply to organs and tissues including the brain and skeletal muscles. Because hypertensive patients have impaired endothelial-dependent vasodilatation and an increased sympathetic response to arterial oxygen desaturation, we investigated whether hypertension impairs isocapnic hypoxia-induced cerebral and skeletal muscle hyperaemia to an extent that limits oxygen supply. In middle-aged hypertensive men, vertebral and femoral artery blood flow do not increase in response to isocapnic hypoxia, limiting brain and peripheral hyperaemia and oxygen supply. Increased chemoreflex-induced sympathetic activation impairs skeletal muscle perfusion and oxygen supply, whereas an attenuation of local vasodilatory signalling in the posterior cerebrovasculature reduced brain hyperperfusion of hypertensive middle-aged men in response to isocapnic hypoxia. The present study investigated whether hypertension impairs isocapnic hypoxia (IH)-induced cerebral and skeletal muscle hyperaemia to an extent that limits oxygen supply. Oxygen saturation (oxymetry), mean arterial pressure (photoplethysmography) and muscle sympathetic nerve activity (MSNA; microneugraphy), as well as femoral artery (FA), internal carotid artery and vertebral artery (VA) blood flow (BF; Doppler ultrasound), were quantified in nine normotensive (NT) (aged 40±11years, systolic pressure 119±7mmHg and diastolic pressure 73±6mmHg) and nine hypertensive men (HT) (aged 44±12years, systolic pressure 152±11mmHg and diastolic pressure 90±9mmHg) during 5min of normoxia (21% O2 ) and IH (10% O2 ). Total cerebral blood flow (tCBF), brain (CDO2 ) and leg (LDO2 ) oxygen delivery were estimated. IH provoked similar oxygen desaturation without changing mean arterial pressure. Internal carotid artery perfusion increased in both groups during IH. However, VA and FA BF only increased in NT. Thus, IH-induced increase in tCBF was smaller in HT. CDO2 only increased in NT and LDO2 decreased in HT. Furthermore, IH evoked a greater increase in HT MSNA. Changes in MSNA were inversely related to FA BF, LDO2 and end-tidal oxygen tension. In conclusion, hypertension disturbs regional and total cerebrovascular and peripheral responses to IH and consequently limits oxygen supply to the brain and skeletal muscle. Although increased chemoreflex-induced sympathetic activation may explain impaired peripheral perfusion, attenuated vasodilatory signalling in the posterior cerebrovasculature appears to be responsible for the small increase in tCBF when HT were exposed to IH.

Near infrared spectroscopy for measuring changes in bone hemoglobin content after exercise in individuals with spinal cord injury.

Bone blood perfusion has an essential role in maintaining a healthy bone. However, current methods for measuring bone blood perfusion are expensive and highly invasive. This study presents a custom built near-infrared spectroscopy (NIRS) instrument to measure changes in bone blood perfusion. We demonstrated the efficacy of this device by monitoring oxygenated and deoxygenated hemoglobin changes in the human tibia during and after exercise in able-bodied and in individuals with spinal cord injury (SCI), a population with known impaired peripheral blood perfusion. Nine able-bodied individuals and six volunteers with SCI performed a 10 min rowing exercise (functional electrical stimulation rowing for those with SCI). With exercise, during rowing, able-bodied showed an increase in deoxygenated hemoglobin in the tibia. Post rowing, able-bodied showed an increase in total blood content, characterized by an increase in total hemoglobin content due primarily to an increase in deoxygenated hemoglobin. During rowing and post-rowing, those with SCI showed no change in total blood content in the tibia. The current study demonstrates that NIRS can non-invasively detect changes in hemoglobin concentration in the tibia. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:183-191, 2018.

Comparison of oxygen saturation measured by pulse oximetry and arterial blood gas analysis in neonates

Background Arterial blood gas is usually beneficial to discern thenature of gas exchange disturbances, the effectiveness of com-pensation, and is required for adequate management. AlthoughPaO 2 is the standard measurement of blood oxygenation, oxygensaturation measured by pulse oximetry (SapO 2 ) is now a custom-ary noninvasive assessment of blood oxygenation in newborn in-fants.Objective To compare oxygen saturation measured by pulse oxi-metry (SapO 2 ) and arterial blood gas (SaO 2 ), its correlation withother variables, and to predict arterial partial pressure of oxygen(PaO 2 ) based on SapO 2 values.Methods A cross sectional study was conducted on all neonatesadmitted to Pediatric Intensive Care Unit (PICU) during February2001 to May 2002. Neonates were excluded if they had impairedperipheral perfusion and/or congenital heart defects. Paired t-testwas used to compare SapO 2 with SaO 2 . Correlation between twoquantitative data was performed using Pearson’s correlation. Re-gression analysis was used to predict PaO 2 based on SapO 2 val-ues.Results Thirty neonates were included in this study. The differ-ence between SaO 2 and SapO 2 was significant . There were sig-nificant positive correlations between heart rate /pulse rate andTCO 2 , HCO 3 ; respiratory rate and TCO 2 , HCO 3 , base excess (BE);core temperature and HCO 3 , BE; surface temperature and pH,TCO 2, HCO 3, BE; SapO 2 and pH, PaO 2 ; and significant negativecorrelation between SapO 2 and PaCO 2 ; the correlations were weak.The linear regression equation to predict PaO 2 based on SapO 2values was PaO 2 = -79.828 + 1.912 SapO 2 .Conclusion Pulse oximetry could not be used in place of arterialblood gas analysis available for clinical purpose

Using synchrotron radiation angiography with ahighly sensitive detector to identify impaired peripheral perfusion in rat pulmonary emphysema.

Owing to limitations in spatial resolution and sensitivity, it is difficult for conventional angiography to detect minute changes of perfusion in diffuse lung diseases, including pulmonary emphysema (PE). However, a high-gain avalanche rushing amorphous photoconductor (HARP) detector can give high sensitivity to synchrotron radiation (SR) angiography. SR angiography with a HARP detector provides high spatial resolution and sensitivity in addition to time resolution owing to its angiographic nature. The purpose of this study was to investigate whether this SR angiography with a HARP detector could evaluate altered microcirculation in PE. Two groups of rats were used: group PE and group C (control). Transvenous SR angiography with a HARP detector was performed and histopathological findings were compared. Peak density of contrast material in peripheral lung was lower in group PE than group C (p < 0.01). The slope of the linear regression line in scattering diagrams was also lower in group PE than C (p < 0.05). The correlation between the slope and extent of PE in histopathology showed significant negative correlation (p < 0.05, r = 0.61). SR angiography with a HARP detector made it possible to identify impaired microcirculation in PE by means of its high spatial resolution and sensitivity.

C reactive protein: impact on peripheral tissue oxygenation and perfusion in neonates

ObjectiveC reactive protein (CRP) is a sensitive marker of acute inflammation of infectious and non-infectious origin. Aim was to use near-infrared spectroscopy (NIRS) to analyse peripheral oxygenation and perfusion in...

Angiographic findings in patients with postoperative soft tissue defects following total knee arthroplasty

A postoperative defect of the surrounding soft tissue is one main risk factor for implant exposure and infection following total knee arthroplasty (TKR). The main factors that promote infection, tissue ischemia, and hypoxia are strongly associated with arterial insufficiency and the prevalence of impaired peripheral perfusion. We hypothesized that vascular malperfusion is the predisposing reason for soft tissue complications following TKR necessitating plastic reconstructive surgery. A retrospective chart review was made among patients (n = 12) with soft tissue defects due to wound infection following a total knee arthroplasty referred to plastic reconstructive surgery. All patients presented with an exposed implant, and angiographic imaging was performed prior to reconstructive procedures. Eight out of twelve patients (67%) had a pathological vascular status. In three of these patients, interventional procedures were performed to ameliorate perfusion. In ten patients (83%), the defect was covered with a plastic reconstructive regional or free tissue transfer. Four patients received a free latissimus dorsi flap and six patients a pedicled a gastrocnemius muscle flap. In one patient, a secondary wound closure was needed after knee arthrodesis and an amputation was performed in another patient due to a multiresistant staphylococcus aureus infection and massive tissue destruction at the time of admission. We suggest to rule out peripheral occlusive disease among patients undergoing TKR at best prior to orthopedic surgery using pulses and, if in doubt ankle-brachial index and doppler sonography Consequently, if vascular occlusions are then confirmed by angiography, dilatation and stenting or revascularization should be performed, to ameliorate perfusion.

Severe obstructive sleep apnoea exacerbates the microvascular impairment in very mild hypertensives

Different studies have shown that obstructive sleep apnoea syndrome (OSAS), frequently associated with hypertension, represents a harmful and independent risk for cardiovascular diseases. The aim of our study was to ascertain whether the occurrence of OSAS could worsen microcirculatory impairment in very mild hypertensives. One hundred untreated very mild hypertensives underwent polysomnography and subdivided into 32 non-OSAS, 33 mild OSAS and 35 severe OSAS patients on standardized criteria. They underwent routine blood chemistry, ambulatory blood pressure monitoring and anthropometric analysis. Skin capillary density (n mm(-2)) of forearm (FAC) and periungueal (PUC) fields was obtained through videocapillaroscopy. By a venous congestion manoeuvre, PUC was maximized (CVC) and secondary capillary recruitment (GAIN) was calculated. These measurements served as indices of structural and functional capillary rarefaction, respectively. Severe OSAS hypertensives showed reduced FAC (P < 0.001) and PUC (P < 0.001) as compared to those with mild OSAS and non-OSAS, but a greater CVC (P < 0.01) and GAIN (P < 0.001). Multiple regression analysis showed that PUC was inversely related to total sleep time with oxyhaemoglobin saturation at < 90% (TST90) (P < 0.001) and FAC to the apnoea-hypopnoea index (AHI) (P < 0.001) and to the sleep propensity (P < 0.01). CVC was positively associated to AHI (P < 0.001) and GAIN to TST90 (P < 0.05). The findings suggest that OSAS, by means of reduced basal and functional capillarity rarefaction, might pose an additional risk of impaired peripheral perfusion in very mild hypertensives. A microcirculation study therefore should be a part of the clinical approach in patients at high cerebro-cardiovascular risk such as hypertensives and patients with OSAS.

Decreased accuracy of pulse oximetry measurements during low perfusion caused by sepsis: is the perfusion index of any value?

To evaluate the effects of deteriorating perfusion caused by sepsis on the accuracy of pulse oximetry measurements using two more recently available techniques (Nellcor N-395 and Masimo Radical) and to evaluate the perfusion index as a marker of impaired peripheral perfusion to indicate that accuracy of pulse oximetry readings may be affected. Interventional cohort study in a university animal research facility. Thirty-seven adult anesthetized, ventilated rabbits. Pneumonia/sepsis was induced by tracheal instillation of Escherichia coli. Oxygen saturation and perfusion index as a marker of peripheral perfusion were measured by pulse oximetry (SpO2) and recorded continuously for 8 h. Arterial oxygen saturation (SaO2) was measured every 30 min by CO oximetry, and bias (SpO2 - SaO2) was calculated at each time point for each device to assess time-dependent changes in bias. Bias increased significantly across time for both devices tested comparing the first with the second half of the experimental period. Bias measurements during the second half of the experimental time were beyond the +/-3% error limit in 21.4% of cases with Nellcor and in 22.6% with Masimo. A lower perfusion index was associated with increased bias, but sensitivity, specificity, and positive and negative predictive values of this marker for increased bias was very limited. We conclude that accuracy of pulse oximetry measurements was considerably affected with both devices with progressively deteriorating hemodynamics in this animal model of severe sepsis. Perfusion index as a marker for increased risk of bias was not a useful tool.

Angiologische und neurologische Probleme nach Hämodialyse-Shuntanlage am Arm

Vascular access induced complications contribute to the morbidity of patients on regular dialysis treatment. Impaired peripheral perfusion, cardiac stress and nerve lesions are the most common of these complications. In the first part of this paper, angiological problems caused by creating arterio-venous shunts are described. Shunt volumes, blood circulation in the shunt arm and shunt-induced alterations of the circulatory blood volume are discussed as well as the conditions under which these parameters gain pathogenic importance. After describing the different shunt-specific circulatory disturbances in detail, the whole spectrum of preventive interventions are discussed. Based on the author's experience during more than four decades in this field, it is strongly recommended to treat even slight but clinically relevant circulatory disorders caused by arterio-venous shunts. The second part of this paper deals with neurological complications in access surgery for dialysis. The pathogenesis of these complications and the measures necessary to avoid them are discussed. Depending on the skin incision, 5 to 20 % of the patients with fistulas between the radial artery and the cephalic vein at the wrist show lesions of the superficial branch of the radial nerve or of the lateral forearm nerve branches. Fistulas with the ulnar artery at the dorsal aspect of the lower forearm frequently cause irritations of the ulnar nerve's superficial palmar branch. Fistulas with the basilic vein in the upper arm often are associated with lesions of the medial cutaneous nerve of the forearm, especially when the vein is "subcuticularized". Aside from these rather benign lesions, sometimes severe sensomotoric functional losses of the median, radial, and ulnar nerves occur, predominantly after implantation of vascular graft shunts in the upper arm. Similar nerve damage can also be observed in association with severe impairment of the peripheral perfusion caused by this type of shunt. Nerve lesions resulting from severe ischemia are rather rare and most often develop in risk patients with preexisting poor peripheral perfusion.

Elevated plasma amylase levels in advanced chronic heart failure secondary to ischemic or idiopathic dilated cardiomyopathy: correlation with circulating interleukin-6 activity.

It has been reported that proinflammatory cytokine activation is associated with both mesenteric venous congestion and peripheral tissue underperfusion in advanced chronic heart failure. The aim of our study was to investigate if plasma amylase (as an easily approached marker of a low-grade peripheral organ injury caused by elevated systemic venous pressure and reduced cardiac output) is elevated in severe heart failure and if this elevation is correlated with cytokine and neurohormonal activation in the plasma of heart failure patients. Plasma levels of amylase, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), granulocyte-macrophage colony-stimulating factor (GM-CSF), norepinephrine, and renin activity were measured in 43 severe heart failure patients (ischemic, 28; dilated, 15; left ventricular ejection fraction [LVEF] 27 +/- 3%; New York Heart Association [NYHA] classes III-IV), in 37 mild heart failure patients (ischemic, 26; dilated, 11; LVEF, 33 +/- 5%; NYHA classes I-II), and in 20 age-matched and gender-matched healthy controls. NYHA III-IV heart failure patients exhibited significantly higher plasma levels of amylase (342 +/- 19 vs. 174 +/- 13 U/L, p < 0.01), TNF-alpha (6.2 +/- 0.5 vs. 4.2 +/- 0.3 pg/ml, p < 0.01), IL-6 (5.9 +/- 0.3 vs. 4.4 +/- 0.3 pg/ml, p < 0.05), GM-CSF (21.2 +/- 2.7 vs. 4.1 +/- 0.9 pg/ml, p < 0.001), and neurohormones (both p < 0.001) compared with NYHA I-II heart failure patients and healthy controls (amylase, 165 +/- 11 U/L, p < 0.01; TNF-alpha, 2.7 +/- 0.3 pg/ml, p < 0.001; IL-6, 3.2 +/- 0.2 pg/ml, p < 0.01; GM-CSF, 3.1 +/- 0.7 pg/ml, p < 0.001). Only in NYHA III-IV heart failure patients, plasma amylase levels were significantly correlated with plasma IL-6 activity (r = 0.86, p < 0.001), plasma norepinephrine levels (r = 0.82, p < 0.001) and right atrial pressure (r = 0.52, p < 0.05). Additionally, circulating IL-6 was also significantly correlated with plasma norepinephrine (r = 0.86, p < 0.001) and right atrial pressure (r = 0.57, p < 0.01). In conclusion, plasma amylase levels were elevated in severe heart failure patients and correlated well with circulating IL-6 activation, possibly as a result of both mesenteric venous congestion and impaired peripheral tissue perfusion observed in advanced chronic heart failure. However, the lack of association between plasma IL-6 and amylase levels in mild heart failure patients indicates an independent correlation of each variable with the functional status of the disease.

Regional hemodynamic effects of dopamine in the indomethacin-treated preterm infant.

We have previously demonstrated that dopamine induces selective renal vasodilation without affecting cerebral and mesenteric blood flow in < or = 32 weeks' gestation normotensive preterm infants during the first postnatal day. In the present study, we have examined whether pretreatment with indomethacin affects the regional hemodynamic response to dopamine in >1-day-old normotensive preterm infants with similar gestational age. The pulsatility index (PI) was used to assess the dopamine-induced changes in renal, mesenteric, and cerebral blood flow using color Doppler ultrasonography in 20 indomethacin-treated normotensive preterm neonates with patent ductus arteriosus (gestational age: 27.2+/-1.5 weeks; postnatal age: 35.7+/-8.2 hours). Dopamine (5 microg/kg per minute) was started 4.9+/-2.1 hours (range: 2 to 8 hours) after the first dose of indomethacin to combat oliguria and/or impaired peripheral perfusion. Blood flow velocity measurements were obtained immediately before and 10 minutes after the start of dopamine with each subject serving as his/her own control. Dopamine increased heart rate and urine output but did not affect blood pressure at the dose applied. Dopamine decreased the PI in the renal and superior mesenteric artery (2.6+/-1.32 vs. 1.61+/-0.7 and 2.36+/-1.12 vs. 1.76+/-0.64, respectively; p<0.05) whereas the PI in the middle cerebral artery remained unchanged. These results are consistent with a dopamine-induced increase in renal and mesenteric blood flow without an effect on cerebral blood flow. When started at least 2 hours after the first dose of indomethacin, dopamine induces renal and mesenteric vasodilation without affecting cerebral hemodynamics in the >1-day-old indomethacin-treated preterm infant.

Recently published papers: Topical issues in pharmacology

Recently published papers: Topical issues in pharmacology

Revascularization for cardiogenic shock.

Despite the availability of invasive circulatory monitoring, inotropes and thrombolysis, mortality from cardiogenic shock remains in excess of 50%, and continues to account for the deaths of between 7% and 11% of patients admitted with myocardial infarction.1–,3 In the majority of these patients, the problem is one of overwhelming left ventricular damage and, intuitively, revascularization should be the primary therapeutic strategy. However, attempts to prove this have been fraught with difficulty, and the randomized trial paradigm that revolutionized our approach to acute cardiology appears to have faltered. This review examines the features of cardiogenic shock that have hindered attempts to improve its outcome, discusses whether current evidence is sufficient to support a policy of revascularization and explores the potential value of approaches aimed at minimizing reperfusion damage. The development of cardiogenic shock is rarely unexpected, most patients who develop shock do so within 48 hours of admission, with only 10% shocked on arrival.2 As would be expected, shock is associated with larger infarcts, prior infarction, diabetes and infarct extension.4,,5 The diagnosis itself is straightforward, with a systolic blood pressure <90 mmHg for more than 30 min in the absence of hypovolaemia or other potential causes of hypotension. Additional features such as oliguria and impaired peripheral perfusion identify those at particularly high risk of death.6 The widespread availability of bedside echocardiography has rendered the use of invasive haemodynamics, and in particular a requirement for a cardiac index of less than 2.2 l/min/m2, virtually obsolete in the decision‐making process. Echocardiography readily identifies the mechanism of shock and those patients that might benefit from surgery for intra‐ or extra‐myocardial rupture (Figure 1).4,7,,8 Figure 1. Apical four‐chamber echo view with relative incidence of the mechanisms responsible for cardiogenic shock in the SHOCK 8 and MILIS 4 …