pituitrin and Shock--Cardiogenic

Shock occurs when failure of the cardiovascular system compromises tissue perfusion. When fluid administration fails to restore adequate arterial pressure and organ perfusion in patients with shock, therapy with vasoactive agents should be initiated. The key to selecting among vasoactive agents is to make the choice in the context of the goals of therapy. The ultimate goals of hemodynamic therapy in shock are to restore effective tissue perfusion and to normalize cellular metabolism. The clinician needs to consider ways of achieving those goals and the mechanisms of action of potential therapies. Armed with this knowledge, it becomes easier to match the mechanism of action of a particular agent to the goals of therapy. When this is done, differences among various agents are seen primarily as differences in mechanisms of action, and discussions about which agent is "best" are transformed into consideration of which agent is best suited to implement the therapeutic strategy that has been selected in a given clinical context. Despite the complex pathophysiology of shock, use of vasoactive agents for hemodynamic support of patients with shock can be guided by an underlying approach in which clinicians define specific goals and end points, titrate therapies to those end points, and evaluate the results of their interventions on an ongoing basis.

Topics: Cardiotonic Agents; Critical Care; Dopamine; Female; Hemodynamics; Humans; Intensive Care Units; Male; Norepinephrine; Prognosis; Randomized Controlled Trials as Topic; Risk Assessment; Shock; Shock, Cardiogenic; Shock, Hemorrhagic; Survival Analysis; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Arginine vasopressin (AVP or antidiuretic hormone) is one of the key hormones in the human body responsible for a variety of cardiovascular and renal functions. It has so far escaped introduction into the routine clinical laboratory due to technical difficulties and preanalytical errors. Copeptin, the C-terminal part of the AVP precursor peptide, was found to be a stable and sensitive surrogate marker for AVP release. Copeptin behaves in a similar manner to mature AVP in the circulation, with respect to osmotic stimuli and hypotension. During the past years, copeptin measurement has been shown to be of interest in a variety of clinical indications, including cardiovascular diseases such as heart failure, myocardial infarction, and stroke. This review summarizes the recent progress on the diagnostic use of copeptin in cardiovascular and renal diseases and discusses the potential use of copeptin measurement in the context of therapeutic interventions with vasopressin receptor antagonists.

Topics: Arginine Vasopressin; Biomarkers; Blood Volume; Cardiovascular Diseases; Cardiovascular System; Glycopeptides; Heart Failure; Humans; Kidney; Kidney Diseases; Myocardial Infarction; Prognosis; ROC Curve; Shock, Cardiogenic; Stroke; Vasopressins

Cardiogenic shock after acute myocardial infarction continues to exhibit a high mortality rate. The prognosis can be improved with acute revascularization. Use of the intra-aortic balloon pump is also an established treatment concept. Administration of catecholamines should be limited as far as possible; monitoring hemodynamic parameters based on cardiac power output or cardiac power index can be very helpful. New treatment approaches such as the calcium sensitizer levosimendan, NO synthase inhibition, complement inhibition, or vasopressin therapy have not yet yielded convincing results. Future therapies will likely address the anti-inflammatory aspect of cardiogenic shock.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Cardiotonic Agents; Catecholamines; Complement C5; Complement Inactivating Agents; Humans; Hydrazones; Intra-Aortic Balloon Pumping; Myocardial Infarction; Myocardial Revascularization; Nitric Oxide Synthase; Pyridazines; Randomized Controlled Trials as Topic; Shock, Cardiogenic; Simendan; Survival Rate; Vasopressins

Cardiovascular failure in critically ill patients carries a high mortality. Identification and treatment of the underlying etiology simultaneously with prompt therapy are indicated to avoid the consequences of prolonged shock. Physicians should assess patients using all available clinical, radiologic, and laboratory data to avoid the pitfalls associated with use of single measures of regional or global perfusion. Continued evidence of inadequate perfusion despite fluid resuscitation warrants consideration of placement of a pulmonary artery catheter or pharmacologic support of the cardiovascular system. Finally, the dynamic nature of physiology in critically ill patients requires constant patient reassessment and flexibility in treatment to tailor therapy individually as the pathologic state evolves.

Topics: Algorithms; Blood Vessels; Catheterization, Swan-Ganz; Glucocorticoids; Heart; Heart Conduction System; Heart Diseases; Heart Failure; Humans; Myocardial Infarction; Oxygen Consumption; Shock, Cardiogenic; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Topics: Anaphylaxis; Child; Crystalloid Solutions; Fluid Therapy; Hemodynamics; Humans; Isotonic Solutions; Shock; Shock, Cardiogenic; Shock, Septic; Vasopressins

Topics: Animals; Blood Pressure; Humans; Shock, Cardiogenic; Shock, Septic; Vasodilation; Vasopressins

Cardiogenic shock (CS) is the most serious complication of acute myocardial infarction (AMI) with high mortality, and the conventional nursing mode can not meet the clinical needs. Studies have shown that integrated care model has advantages for critical and chronic diseases. However, there is no clinical study to evaluate the clinical efficacy of this nursing model on cardiogenic shock induced by acute myocardial infarction (CS-AMI).. This is a prospective randomized controlled trial to study the clinical efficacy of integrated care combined with vasopressin in the treatment of CS-AMI. Participants will be randomized in a 1:1 ratio to receive integrated care combined with vasopressin in the treatment group and conventional care combined with vasopressin in the control group. The patients will be followed up for 3 months after systematic treatment. Observation indicators include: length of hospital stay, quality of life score, blood pressure level, and nursing satisfaction score. Finally, SPASS 20.0 software will be used for statistical analysis of the data.. This study will evaluate the clinical efficacy of integrated nursing combined with vasopressin in the treatment of CS-AMI. The results of this study will provide a reference for selecting appropriate nursing programs for CS-AMI patients.. OSF Registration number: DOI 10.17605/OSF.IO/K8CN4.

Topics: Delivery of Health Care, Integrated; Humans; Myocardial Infarction; Prospective Studies; Quality of Life; Randomized Controlled Trials as Topic; Shock, Cardiogenic; Treatment Outcome; Vasopressins

Acute heart failure (AHF) due to acute myocardial infarction (AMI) is likely to involve cardiogenic shock (CS), with neuro-hormonal activation. A relationship between AHF, CS and vasopressin response is suspected. This study aimed to investigate the implication of vasopressin on hemodynamic parameters and tissue perfusion at the early phase of CS complicating AMI. Experiments were performed on male Wistar rats submitted or not to left coronary artery ligation (AMI and Sham). Six groups were studied Sham and AMI treated or not with either a vasopressin antagonist SR-49059 (Sham-SR, AMI-SR) or agonist terlipressin (Sham-TLP, AMI-TLP). Animals were sacrificed one day after surgery (D

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Heart Failure; Male; Myocardial Infarction; Rats; Rats, Wistar; Shock, Cardiogenic; Stroke Volume; Vasopressins; Ventricular Function, Left

Topics: Cohort Studies; Humans; Retrospective Studies; Shock, Cardiogenic; Vasopressins

Vasopressors are a commonly used treatment in beta-blocker poisoning despite evidence they may be ineffective or harmful. The primary objective of the present study is to use previously collected data from two prior studies (high-dose insulin (HDI) versus vasopressin + epinephrine and a placebo-controlled HDI study) to compare survival between vasopressin + epinephrine and placebo. Secondary outcomes included a comparison with HDI as well as comparisons with hemodynamic parameters, including mean arterial pressure (MAP), cardiac output (CO), heart rate (HR), and systemic vascular resistance (SVR).. Cardiogenic shock was induced in healthy pigs with a bolus of 0.5 mg/kg of intravenous propranolol followed by an infusion of 0.25 mg/kg/minute until the point of toxicity, defined as (0.75 × initial HR × initial MAP), at which point the infusion was reduced to 0.125 mg/kg/minute for 240 (vasopressin + epinephrine or HDI) or 360 minutes (placebo) or until death.. Survival was significantly lower in pigs receiving vasopressin + epinephrine (0%, 0/5) than in pigs receiving placebo (50%, 2/4) (p < 0.01). Survival was significantly higher with HDI compared with both groups (100%, 5/5) (p < 0.01). All vasopressin + epinephrine pigs died within 100 minutes after reaching toxicity. Over the course of the resuscitation, we observed a statistically significant steady decrease in CO and HR in the vasopressin + epinephrine group compared with placebo (p < 0.01). In contrast, we observed a statistically significant change in MAP and SVR that followed a parabolic arc, with MAP and SVR rising significantly initially in the vasopressin + epinephrine group then rapidly falling until death (p < 0.01).. Mortality was higher with vasopressors compared with placebo in this porcine model of propranolol poisoning. Further studies are warranted to define the optimal timing and role of vasopressors in beta-blocker poisoning.

Topics: Adrenergic beta-Antagonists; Animals; Cardiotoxicity; Disease Models, Animal; Drug Administration Schedule; Epinephrine; Hemodynamics; Propranolol; Risk Assessment; Shock, Cardiogenic; Sus scrofa; Time Factors; Vasoconstrictor Agents; Vasopressins

Cardiovascular dysfunction in asphyxiated neonates contributes significantly to their morbidity and mortality. We have recently shown that a low-dose vasopressin infusion (0.005 - 0.01 units/kg per hour) may improve myocardial oxygen transport balance in a swine model of neonatal hypoxia-reoxygenation. We aimed to compare the systemic and regional hemodynamic effects of low-dose vasopressin to dobutamine, a synthetic beta-adrenoreceptor agonist. Piglets (1 - 5 days old, 1.6 - 2.2 kg) were anesthetized and instrumented to continuously monitor systemic hemodynamic parameters, including cardiac output and mesenteric flow indices. After 2 h of hypoxia (10% - 15% O2), piglets had normoxic reoxygenation for 4 h. In a blinded randomized fashion, piglets received infusion of either vasopressin (0.01 units/kg per hour started at 30 min of reoxygenation) or dobutamine (20 μg/kg per minute started at 2 h of reoxygenation) (n = 8 per group). Hypoxia-reoxygenation controls (placebo, n = 8) and sham-operated (n = 5) piglets were also studied. Tissue lactate, glutathione, glutathione disulfide, and lipid hydroperoxides levels and histology of the left ventricle and the small bowel were analyzed. Plasma was also analyzed for troponin-I and intestinal fatty acid-binding protein levels. Piglets subjected to hypoxia-reoxygenation had cardiogenic shock and metabolic acidosis, which improved on reoxygenation. During recovery, cardiac output and mesenteric flows gradually deteriorated and were increased similarly in vasopressin- and dobutamine-treated piglets (P < 0.05 vs. controls). Plasma troponin-I and left ventricular lactate levels were lower in the vasopressin and dobutamine groups (P < 0.05 vs. controls), with no difference in the histological analysis among groups. The intestinal GSSG/GSH ratio and lipid hydroperoxides level were lower in the vasopressin and dobutamine groups (P < 0.05 vs. controls). This study is the first to demonstrate that a low-dose vasopressin infusion used in the setting of neonatal swine model of hypoxia-reoxygenation is associated with an improvement in cardiac output and mesenteric perfusion.

Topics: Animals; Animals, Newborn; Asphyxia Neonatorum; Cardiac Output; Dobutamine; Glutathione; Heart Ventricles; Hypoxia; Lactic Acid; Lipid Peroxides; Mesenteric Artery, Superior; Oxygen; Reperfusion Injury; Shock, Cardiogenic; Swine; Troponin I; Vasopressins

Topics: Anti-Inflammatory Agents; Cardiopulmonary Resuscitation; Controlled Clinical Trials as Topic; Drug Therapy, Combination; Epinephrine; Greece; Heart Arrest; Hospital Mortality; Hospitalization; Humans; Hydrocortisone; Methylprednisolone; Neurologic Examination; Shock, Cardiogenic; Survival Rate; Vasoconstrictor Agents; Vasopressins

We assessed the hemodynamic effects of guideline therapy in experimental cardiogenic shock and compared this treatment with a combination containing an alternative vasopressor (arginine vasopressin, AVP). Our hypothesis was that combined dobutamine-norepinephrine still is the superior inopressor therapy assessed by ventriculoarterial matching in both systole and diastole. Cardiogenic shock (CS) was induced by coronary microembolization in 16 pigs. Dobutamine (Dobu, 2ug/kg/min) alone and combined with either norepinephrine (NE, 100 ng/kg/min) or the pure vasopressor AVP (0.001 u/kg/min) were infused. In CS, Dobu increased cardiac output (CO) and central venous oxygen saturation (SVO₂) from 74 ± 3 mL/kg and 37 ± 2% to 103 ± 8 mL/kg and 49 ± 3%. Adding NE resulted in a further improvement of CO (125 ± 9 mL/kg) and SVO₂ (59 ± 4%) because of an increased heart rate and contractility with minimal change in systemic vascular resistance. Also, energy transfer from the ventricle to the arterial system was restored partly by Dobu and was normalized by supplementing NE. In contrast, supplemental AVP further worsened the shock state by decreasing CO (70 ± 6 mL/kg) and SVO₂ (45 ± 5%) compared with Dobu alone. Combined Dobu-NE has an efficient hemodynamic profile in CS. A pure afterload increasing substance used in acute ischemic CS aggravates the shock state by causing a ventriculoarterial mismatch despite its use in combination with an inotropic compound.

Topics: Animals; Cardiotonic Agents; Disease Models, Animal; Dobutamine; Drug Therapy, Combination; Heart Failure; Hemodynamics; Male; Norepinephrine; Orchiectomy; Shock, Cardiogenic; Swine; Vasodilator Agents; Vasopressins; Ventricular Function, Left

To evaluate vasopressin as a rescue therapy in catecholamine-refractory septic and cardiogenic shock in very-low-birthweight (VLBW) infants.. Prospective assessment of vasopressin therapy in three VLBW infants with catecholamine-refractory septic shock (24 + 6 wk, 600 g) and cardiogenic shock (26 + 1 wk, 890 g; 26 + 1 wk, 880 g) at a university hospital.. Adequate systemic arterial blood pressure could only be restored after vasopressin administration as a continuous infusion over a 36-h period in the preterm suffering from septic shock; in the two neonates with cardiogenic shock, only a transient stabilization in mean arterial pressure was observed, which did not impact on the poor prognosis.. Although vasopressin appears to be a suitable rescue therapy in catecholamine-resistant septic shock in VLBW infants, further evaluation in controlled clinical trials is warranted.

Topics: Diseases in Twins; Humans; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Infant, Very Low Birth Weight; Norepinephrine; Shock, Cardiogenic; Shock, Septic; Treatment Failure; Vasoconstrictor Agents; Vasopressins

In a retrospective study of 36 patients who developed cardiogenic shock after myocardial infarction, intravenous vasopressin therapy increased mean arterial pressure from 56 to 73 mm Hg at 1 hour (p < 0.001) and maintained it for 24 hours without changing pulmonary capillary wedge pressure, cardiac index, urine output, or other inotropic requirements. After norepinephrine administration, mean pulmonary capillary wedge pressure increased at 1 hour from 21 to 24 mm Hg (p = 0.04); however, this increase was not sustained at 12 and 24 hours. Norepinephrine was associated with a significant increase in cardiac power index at 24 hours, whereas there was only a trend for an increase in cardiac power with vasopressin therapy. In a cohort of patients who developed refractory cardiogenic shock after myocardial infarction, vasopressin was associated with increased mean arterial pressure and no adverse effect on other hemodynamic parameters.

Topics: Aged; Blood Pressure; Cardiac Output; Female; Follow-Up Studies; Humans; Male; Myocardial Infarction; Norepinephrine; Pulmonary Wedge Pressure; Retrospective Studies; Shock, Cardiogenic; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Topics: Adenosine Triphosphate; Blood Pressure; Brain Ischemia; Calcium Channels; Hemostatics; Humans; Hypotension; Muscle, Smooth, Vascular; Shock; Shock, Cardiogenic; Shock, Septic; Vasoconstrictor Agents; Vasodilation; Vasopressins

To assess the sublingual microcirculation in a patient during vasopressin administration for a distributive shock after cardiopulmonary bypass.. Case-report in the Department of Intensive Care of a university hospital.. A 53 year-old man developed severe distributive shock after cardiac transplant, requiring massive doses of vasopressor agents.. Vasopressin administered twice at a dose of 0.02 U/min increased mean blood pressure and allowed partial weaning of other vasopressor drugs. Microcirculatory alterations were assessed by orthogonal polarization spectral technique: 50% and 60% of capillaries were perfused at baseline, and these proportions did not worsen when vasopressin was administered.. Despite its strong vasopressor effects vasopressin infusion did not worsen microcirculatory alterations in this patient with distributive shock following cardiac surgery.

Topics: Blood Pressure; Cardiomyopathies; Cardiopulmonary Bypass; Central Venous Pressure; Fluorescence Polarization; Heart Rate; Heart Transplantation; Hemodynamics; Humans; Infusions, Intravenous; Male; Microcirculation; Middle Aged; Mouth Floor; Oxygen Consumption; Pulmonary Wedge Pressure; Shock, Cardiogenic; Spectrometry, Fluorescence; Vasoconstrictor Agents; Vasopressins

The hypotension of septic shock is due to systemic vasodilation. On the basis of a clinical observation, we investigated the possibility that a deficiency in vasopressin contributes to the vasodilation of septic shock.. In 19 patients with vasodilatory septic shock (systolic arterial pressure [SAP] of 92 +/- 2 mm Hg [mean +/- SE], cardiac output [CO] of 6.8 +/- 0.7 L/min) who were receiving catecholamines, plasma vasopressin averaged 3.1 +/- 1.0 pg/mL. In 12 patients with cardiogenic shock (SAP, 99 +/- 7 mm Hg; CO, 3.5 +/- 0.9 L/min) who were also receiving catecholamines, it averaged 22.7 +/- 2.2 pg/mL (P < .001). A constant infusion of exogenous vasopressin to 2 patients with septic shock resulted in the expected plasma concentration, indicating that catabolism of vasopressin is not increased in this condition. Although vasopressin is a weak pressor in normal subjects, its administration at 0.04 U/min to 10 patients with septic shock who were receiving catecholamines increased arterial pressure (systolic/diastolic) from 92/52 to 146/66 mm Hg (P < .001/P < .05) due to peripheral vasoconstriction (systemic vascular resistance increased from 644 to 1187 dyne.s/cm5; P < .001). Furthermore, in 6 patients with septic shock who were receiving vasopressin as the sole pressor, vasopressin withdrawal resulted in hypotension (SAP, 83 +/- 3 mm Hg), and vasopressin administration at 0.01 U/min, which resulted in a plasma concentration (approximately 30 pg/mL) expected for the level of hypotension, increased SAP from 83 to 115 mm Hg (P < .01).. Vasopressin plasma levels are inappropriately low in vasodilatory shock, most likely because of impaired baroreflex-mediated secretion. The deficiency in vasopressin contributes to the hypotension of vasodilatory septic shock.

Topics: Adult; Blood Pressure; Cardiac Output; Dopamine; Epinephrine; Heart Rate; Hemodynamics; Humans; Norepinephrine; Shock, Cardiogenic; Shock, Septic; Sodium; Vascular Resistance; Vasodilation; Vasopressins

Plasma atrial natriuretic factor, aldosterone, renin activity, and antidiuretic hormone were studied in low output heart failure syndromes: cardiogenic shock in ten patients with acute myocardial infarction of the anterior wall (first group), hypovolemic shock after melena from peptic ulcer in ten subjects (second group), and hypotension with bradycardia syndrome in ten patients with acute myocardial infarction of the inferior wall (third group). Circulating atrial natriuretic factor in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) was significantly higher than in healthy volunteers matched for sex and age (8.4 +/- 0.3 pg/ml). In these patients there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the second and third groups were within normal range. Plasma aldosterone was high in all groups, plasma renin activity was elevated in the first and third groups, and high antidiuretic hormone was observed in the first and second groups. These findings indicate that in low output heart failure syndromes only hemodynamic changes affecting the atria stimulate atrial natriuretic factor release. No correlations were found between plasma atrial natriuretic factor and other hormones. In particular, high atrial natriuretic factor levels in the patients with cardiogenic shock did not inhibit release of aldosterone, renin, or antidiuretic hormone. It may be surmised that in these patients the hemodynamic effects override the inhibitory effects of atrial natriuretic factor.

Topics: Adult; Aldosterone; Atrial Natriuretic Factor; Blood Volume; Bradycardia; Cardiac Output, Low; Female; Heart Failure; Humans; Male; Melena; Middle Aged; Myocardial Contraction; Myocardial Infarction; Peptic Ulcer Hemorrhage; Renin; Shock, Cardiogenic; Vascular Resistance; Vasopressins; Venous Pressure

The aim of this paper was to study plasma atrial natriuretic factor, renin activity, aldosterone and antidiuretic hormone in low-output heart failure syndromes such as cardiogenic shock, hypovolemic shock and hypotension with bradycardia syndrome. A total of 30 patients were investigated: 10 with cardiogenic shock due to acute myocardial infarction of the anterior wall (systolic and diastolic blood pressure 56.0 +/- 3.7/40.5 +/- 2.0 mmHg; heart rate 119.7 +/- 1.2 beats/min; central venous pressure 16.2 +/- 0.6 cmH2O) (I group), 10 with hypovolemic shock induced by melena in peptic ulcer (systolic and diastolic blood pressure 74.5 +/- 1.5/57.5 +/- 1.7 mmHg; heart rate 111.0 +/- 1.4; central venous pressure 6.3 +/- 0.5 cmH2O) (II group), 10 with hypotension with bradycardia syndrome which occurred in patients during acute myocardial infarction of the inferior wall (systolic and diastolic blood pressure 71.9 +/- 2.0/58.0 +/- 2.6 mmHg; heart rate 52.0 +/- 2.2 beats/min; central venous pressure 4.6 +/- 0.4 cmH2O) (III group). Plasma atrial natriuretic factor values were measured using radioimmunoassay after chromatographic pre-extraction; plasma renin activity, aldosterone and antidiuretic hormone values were calculated using radioimmunoassay. Circulating atrial natriuretic factor was significantly (p less than 0.01) higher in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) than in healthy volunteers (8.4 +/- 0.3 pg/ml). In the former there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the IInd and IIIrd groups of patients were in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Bradycardia; Cardiac Output, Low; Female; Hemodynamics; Humans; Hypotension; Male; Middle Aged; Myocardial Infarction; Renin; Shock; Shock, Cardiogenic; Vasopressins

The pituitaries and adrenals of 30 patients died from extensive fresh myocardial infarction and of 25 patients died from other diseases were studied. In myocardial infarction the mean weight of the above glands was significantly higher than in other diseases. In most cases an increase in number of pituitary ACTH-cells was observed with the immunoperoxidase method. In non-cardiogenic shock (another 9 cases) gland weight was also increased but without a significant increase in the number of ACTH-cells. Hyperactivity of the anterior pituitary-adrenal system is due to a number of known factors. It may be assumed that patients who have infarction are either exposed to an extraordinary amount of stress stimuli or are more susceptible to stress than normal subjects. The findings may indicate the morphological basis of this situation. Of the shock phenomena, incomplete necrosis and haemorrhage of the adrenal cortex are frequent. In the pituitary neural lobe the neurosecretory material, which proved to be vasopressin with the PAP-method, was found to be increased more frequently in myocardial infarction than after other diseases.

Topics: Adrenal Cortex; Adrenocorticotropic Hormone; Adult; Aged; Aged, 80 and over; Female; Humans; Immunoenzyme Techniques; Male; Middle Aged; Myocardial Infarction; Organ Size; Pituitary Gland, Anterior; Shock; Shock, Cardiogenic; Vasopressins

Topics: Adolescent; Adult; Aged; Animals; Blood Circulation; Blood Pressure; Child; Female; Humans; Male; Microcirculation; Middle Aged; Ornithine; Rats; Shock; Shock, Cardiogenic; Shock, Hemorrhagic; Vasopressins

Topics: Adrenal Cortex Hormones; Blood Circulation; Cardiac Output; Humans; Microcirculation; Shock; Shock, Cardiogenic; Time Factors; Vasopressins

Topics: Adrenal Cortex Hormones; Blood Circulation; Cardiac Output; Humans; Microcirculation; Shock; Shock, Cardiogenic; Time Factors; Vasopressins

Topics: Angina Pectoris; Coronary Disease; Digoxin; Electrocardiography; Hydrochlorothiazide; Hypercholesterolemia; Hypertension; Metaraminol; Nitroglycerin; Shock; Shock, Cardiogenic; Vasopressins; Warfarin