atrial-natriuretic-factor and Heart-Arrest

Cardiac arrest (CA) is an extreme stressful situation accompanied by impairment of hypotalamichypophyseal axis resulting from many reasons, specially when cardio-pulmonary resuscitation (CPR) has been delayed or prolonged. The author compares dysfunction of the neurohormonal system, including the release of hypophyseal and adrenal hormones, atrial natriuretic hormone and endothelin in patients in critical illness as well as in those after cardiac arrest. Associated consequences for the maintenance of homeostasis in postresuscitation period have also presented.

Topics: Atrial Natriuretic Factor; Cardiopulmonary Resuscitation; Critical Illness; Heart Arrest; Humans; Hypothalamo-Hypophyseal System; Pituitary-Adrenal System; Time Factors

To evaluate the prognostic potential of serum C-terminal provasopressin (CT-proAVP or Copeptin) and midregional pro-A-type natriuretic peptide (MR-proANP) to predict neurological outcome following resuscitation from cardiac arrest.. In this prospective observational study, we employed novel ultra sensitive immunoassay technology to examine serial serum samples from 134 cardiac arrest patients. Patients were either allocated to mild therapeutic hypothermia using an endovascular device or normothermia. Serial blood samples were obtained from resuscitated cardiac arrest survivors during their first 7 days in an intensive care unit, and serum Copeptin and MR-proANP were measured. Cerebral function assessments were made using cerebral performance categorization (CPC) at discharge from hospital. Copeptin and MR-proANP data were analyzed using dichotomized CPC scores (1-2 versus 3-5).. Sixty-nine patients (51%) had a poor outcome (CPC 3-5) at hospital discharge. MR-proANP and Copeptin peaked on day 1 (i.e. 0-24h) with the medians being 249.3pmol/L and 77.2pmol/L, respectively. In the first 48h maximum levels of MR-proANP and Copeptin showed an AUC in the ROC of 0.743 (95% CI: 0.658-0.828) and 0.677 (95% CI: 0.583-0.771). Binary logistic regression revealed MR-proANP and Copeptin within 48h after ROSC being significantly associated with functional outcome (p<0.05). Copeptin within 48h was also associated with outcome in the hypothermia group (p<0.05).. Systemic levels of MR-proANP and Copeptin peak early in cardiac arrest patients in the 48h post-resuscitation period. MR-proANP and Copeptin were highly predictive for poor outcome in comatose resuscitated patients.

Topics: Adult; Aged; Atrial Natriuretic Factor; Biomarkers; Female; Glycopeptides; Heart Arrest; Humans; Hypothermia, Induced; Male; Middle Aged; Outcome Assessment, Health Care; Predictive Value of Tests; Prognosis; Prospective Studies; Resuscitation

Further characterization of the post-cardiac arrest syndrome (PCAS) is essential to better understand the mechanisms resulting in injury and death. We investigated serial serum concentrations of the stress hormone c-terminal provasopressin (CT-proAVP or copeptin), the cardiac biomarker MR-proANP and a biomarker of oxidation injury, Peroxiredoxin 4 (Prx4) in patients treated with mild hypothermia (MHT) after cardiac arrest, and studied their association to the PCAS and long-term outcome.. Serum samples from cardiac arrest patients were collected serially: at admission, 2, 6, 12, 24, 36, 48 and 72 h after cardiac arrest. CT-proAVP, MR-proANP and Prx4 concentrations were determined and tested for association with two surrogate markers of PCAS (time to return of spontaneous circulation and circulation-SOFA score) and with cerebral performance category (CPC) at 6 months. Good outcome was defined as CPC 1 to 2.. Eighty-four patients were included. CT-proAVP, MR-proANP and Prx4 were early biomarkers with maximum concentrations soon after cardiac arrest and with a significant discriminatory ability between good and poor long-term outcome at most time points. CT-proAVP predicted a poor outcome with the highest accuracy, followed by MR-proANP and Prx4 (area under the receiving operating characteristics curve at 12 h of 0.85, 0.77 and 0.76 respectively). CT-proAVP and MR-proANP showed best correlation to the PCAS.. In 84 resuscitated patients receiving MHT after cardiac arrest, there is a significant difference in concentrations of CT-proAVP, MR-proANP and Prx4 between patients with good and poor outcome. CT-proAVP and MR-proANP have a significant correlation to surrogate markers of the PCAS.

Topics: Aged; Atrial Natriuretic Factor; Biomarkers; Female; Glycopeptides; Heart Arrest; Humans; Hypothermia, Induced; Male; Middle Aged; Peroxiredoxins; Predictive Value of Tests; Prognosis; ROC Curve; Treatment Outcome

Fulminant myocarditis with rapid onset of symptoms and hemodynamic compromise is a rare indication for mechanical support. Because of the potentially reversible nature of this illness, advanced mechanical circulatory support is warranted to achieve recovery or as a bridge to transplantation. Circulatory device options currently available allow for a phased implementation of support modalities in a manner that reduces costs and patient risk. We present a patient with fulminant myocarditis where extracorporeal membrane oxygenation (ECMO) support escalated to short-term Levitronix CentriMag (Levitronix, Waltham, MA) biventricular assist devices (BiVADs). These in turn were exchanged, without major surgery, to long-term paracorporeal VADs (Thoratec, Pleasanton, CA). After rehabilitation and nearly total recovery, the patient was weaned from mechanical circulatory support after 104 cumulative days.

Topics: Adult; Anticoagulants; Atrial Natriuretic Factor; Blood Coagulation; Cardiopulmonary Resuscitation; Echocardiography; Extracorporeal Membrane Oxygenation; Female; Heart Arrest; Heart-Assist Devices; Heparin; Humans; Myocarditis; Natriuretic Peptide, Brain; Shock, Cardiogenic; Stroke Volume; Treatment Outcome

Renal function was measured by clearance technique before and after acute myocardial infarction (MI) induced by left coronary artery ligation in male Sprague-Dawley rats. The animals were anaesthetized with halothane-nitrous oxide, paralysed with pancuronium and artificially ventilated. All parameters were stable throughout the experiment in sham-operated time control animals (n = 8). After MI, rats developed left ventricular dysfunction with increased left ventricular end-diastolic pressure and decreased mean arterial pressure. MI produced antidiuresis and antinatriuresis without changes in glomerular filtration rate (GFR), lithium clearance or renal albumin excretion (n = 8). The antidiuretic and antinatriuretic responses to MI were similar in rats with chronic bilateral renal denervation (n = 5). Three additional rats with chronic bilateral renal denervation had cardiac arrest and were resuscitated with cardiac massage, i.v. lidocaine and intracardiac adrenaline administration. These animals showed a transient increase in urine flow rate, sodium and albumin excretion with maximum 30-60 min after resuscitation, while GFR and lithium clearance were normal. Since cardiac ischaemia and sympathetic stimulation are strong stimuli for the release of atrial natriuretic peptide (ANP), we examined if ANP (0.25, 0.50, and 1.00 microg kg(-1) min(-1), n = 8 per dose) affects urinary albumin excretion. ANP increased dose-dependently the urine/plasma concentration ratio of albumin relative to inulin, which suggests that ANP increases the glomerular permeability for albumin. We conclude that MI causes stimulation of renal tubular sodium and water reabsorption by a mechanism which is independent of intact renal innervation. MI does not produce any change in renal albumin excretion in rats, but transient albuminuria may be observed in rats following cardiac arrest and/or manoeuvres used in cardiac resuscitation. Since ANP produces albuminuria, we speculate that ANP may be an important mediator of albuminuria in states with elevated plasma concentrations of ANP.

Topics: Albuminuria; Animals; Atrial Natriuretic Factor; Blood Pressure; Denervation; Glomerular Filtration Rate; Heart Arrest; Heart Rate; Kidney; Lithium; Male; Myocardial Infarction; Rats; Rats, Sprague-Dawley; Sodium

To determine the relationship of circulating atrial natriuretic peptide concentrations to the pressor response to high-dose epinephrine in patients undergoing cardiopulmonary resuscitation (CPR) for cardiac arrest.. Prospective study.. Fourteen normothermic, adult, prehospital and emergency department patients suffering unexpected cardiac arrest.. Patients received high-dose epinephrine (0.2 mg/kg) i.v. when standard advanced cardiac life support (including multiple 1-mg dosages of epinephrine) failed to result in return of spontaneous circulation.. Cardiac arrest patients were separated into those patients with and without detectable serum atrial natriuretic peptide concentrations, and were termed the "low atrial natriuretic peptide" and "high atrial natriuretic peptide" groups, respectively. Their aortic pressure response to high-dose (0.02 mg/kg) epinephrine was compared. The proportion with positive assays was compared with a group of healthy control subjects. Fourteen patients were studied. Eight patients had low serum atrial natriuretic peptide concentrations and six patients had high circulating atrial natriuretic peptide concentrations. The mean concentration in the high atrial natriuretic peptide group was 151 +/- 82 pg/mL. The proportion with positive assays (six of 14 patients) was greater than in the group in spontaneous circulation (three of 29 patients) (p = .002). The maximal increase in the aortic relaxation-phase pressures after high-dose epinephrine was 9 +/- 7 torr (1.2 +/- 0.9 kPa) in the low atrial natriuretic peptide group and 0 +/- 5 torr (0 +/- 0.7 kPa) in the high atrial natriuretic peptide group (p = .03). The maximal increase in the aortic compression pressures after high-dose epinephrine was 17 +/- 13 torr (2.3 +/- 1.7 kPa) in the low atrial natriuretic peptide group and 2 +/- 10 torr (0.3 +/- 1.3 kPa) in the high atrial natriuretic peptide group (p = .03). Thus, pressor responses after high-dose epinephrine administration were observed in patients in the low atrial natriuretic peptide group, but this response was absent in patients in the high atrial natriuretic peptide group.. Cardiac arrest patients receiving CPR have higher circulating atrial natriuretic peptide concentrations than healthy subjects. High serum atrial natriuretic peptide concentrations may antagonize the vasopressor response to epinephrine. Blocking this effect of atrial natriuretic peptide may improve outcomes in patients suffering cardiac arrest.

Topics: Adult; Aged; Aged, 80 and over; Aorta; Atrial Natriuretic Factor; Blood Pressure; Cardiopulmonary Resuscitation; Epinephrine; Heart Arrest; Humans; Middle Aged; Prospective Studies

Return of spontaneous circulation with CPR is a function of coronary perfusion pressure, which is determined by vasomotor tone and the force of compression. Vasomotor tone is affected by the relative stimulation of arterial vasoconstricting and vasorelaxing receptors by vasoactive substances. We measured the plasma levels of the endogenous vasoactive peptides arginine vasopressin (AVP) angiotensin II (ANG-II) and atrial natriuretic peptide (ANP) during cardiac arrest and resuscitation.. A fibrillatory canine model of canine arrest was used. 'Down time' was greater than 10 min, during which no therapy, including BLS, was given. Standard ACLS was initiated at the end of the down time with manual external chest compression standardized to an esophageal pulse pressure of 50 mmHg. Blood samples were collected through an aortic catheter during spontaneous circulation and 3 min after initiation of ACLS. Peptide levels were measured using standard RIA techniques. Results are reported as the mean +/- S.D. in pg/ml.. AVP levels increased from a baseline of 1.7 +/- 1.0 pg/ml during spontaneous circulation to 29.9 +/- 33.3 during cardiac arrest and CPR (P = 0.01). There was a moderate positive correlation between aortic pressure and circulating AVP levels after the first dose of epinephrine (R = 0.5). There was a trend towards higher AVP levels in animals with return of spontaneous circulation (P = 0.12). ANG-II levels increased from a baseline of 14.7 +/- 12.9 pg/ml during spontaneous circulation to 151 +/- 105 during cardiac arrest and CPR (P < 0.05). ANP levels increased from a baseline of 55 +/- 46 pg/ml during spontaneous circulation to 293 +/- 73 during cardiac arrest and CPR (P < 0.01).. There were significant increases in the levels of these endogenous vasoactive peptides. This reflects the neuroendocrine response to global ischemia and CPR reperfusion. Plasma levels of these peptides may effect the vital organ perfusion pressures, response to exogenous vasopressors, and outcome of resuscitative efforts. Future therapies may be directed at enhancing or blocking the effect of these peptides so as to optimize perfusion pressure which is one of the principle determinants of outcome during CPR.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Atrial Natriuretic Factor; Cardiopulmonary Resuscitation; Dogs; Heart Arrest; Hemodynamics; Neurosecretory Systems; Time Factors

Topics: Adult; Arrhythmia, Sinus; Atrial Natriuretic Factor; Bradycardia; Female; Heart Arrest; Humans