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Having outlined the principal physiological and pathological aspects of the atrial natriuretic factor (ANF) on the basis of data found in the literature, the authors report the results of their research on variations of ANF plasma level during hyperkinetic atrial arrhythmia, acute myocardial infarction with and without complications as well as hypotensive and renal effects of synthetic ANF in congestive heart failure. Regardless of the cause of hyperkinetic atrial arrhythmia, high ANF levels were normalized or significantly reduced after the return to sinus rhythm whereas with the sole reduction of ventricular rate ANF remained raised. In uncomplicated myocardial infarction ANF level was raised to an extent inversely proportional to the ejection fraction. In cardiogenic shock, ANF values were high and correlated to the high central venous pressure and heart rate. On the contrary, in the hypotensive bradycardia syndrome ANF values were normal even when the syndrome had occurred in the acute stage of infarction. In congestive heart failure, ANF administration had contradictory effects in that diuresis was induced by lower doses, and hypotension by higher ones.

We examined the cardiovascular and metabolic response to RBC transfusion in patients with circulatory shock after volume resuscitation. Data were analyzed from 36 transfusions in 32 patients who were undergoing continuous hemodynamic monitoring. Transfusions were administered for moderate to severe anemia, mean Hgb 8.3 g/dl. The diagnosis were sepsis (19/36), cardiogenic shock (14/36), connective tissue disease (2/36), and severe hypocalcemia (1/36). Benefit from transfusion was defined as an improvement in tissue oxygen utilization (increased oxygen consumption [VO2] or decreased lactate), a decrease in myocardial VO2 (MAP x HR), or a decrease in myocardial work (left ventricular work index). Mean transfusion volume was 577 ml over 4.5 h. Hgb and oxygen delivery (DO2) increased by 27% and 28%, respectively, while pulmonary artery wedge pressure and cardiac index were unchanged. No significant change was noted in VO2, or lactate, after augmentation of red cell mass. An increase occurred in myocardial work indices and MAP x HR. No changes were identified when subgroups were analyzed based on diagnosis, pretransfusion Hgb, lactate, or VO2 levels. We conclude that selective increase in DO2 by augmentation of RBC mass and oxygen-carrying capacity did not improve the shock state in these volume-resuscitated patients, regardless of the etiology of the shock.

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.

STUDY OBJECTIVE - The aim of the study was to measure plasma neuropeptide Y, which is related to sympathetic nerve stimulation, in patients admitted to a coronary care unit and to relate the findings to clinical information. DESIGN - Plasma neuropeptide Y was measured on admission and the results were related to the cause of admission and to clinical information collected prospectively and retrospectively. SUBJECTS - Plasma subjects were obtained from 377 consecutive daytime admissions to the coronary care unit at Södersjukhuset. Results of only the first sample in each patient are included in this study, so 45 cases observed more than once (readmitted patients) were omitted. Six samples were abandoned because of technical failures. The study therefore comprises 326 patients. Clinical diagnoses were defined as acute myocardial infarction, arrhythmia, angina pectoris, and miscellaneous (all other diagnoses). Heart failure was defined according to a modified Killip scheme. MEASUREMENTS and RESULTS - Neuropeptide Y like immunoreactivity was measured by radio-immunoassay. Plasma concentrations above normal (greater than 30 pmol.litre-1) were found in association with: increased age, female sex, diuretic treatment, tachycardia, arterial hypotension, increased respiratory rate, and mortality in the unit. There was a strong relationship between high neuropeptide Y concentrations and: moderate left heart failure (63%), pulmonary oedema (90%), and cardiogenic shock (100%). Of patients without heart failure only 25% had raised neuropeptide Y. In multivariate analysis, the severity of heart failure (Killip class), heart rate and respiratory rate were the only variables that were significantly and independently related to plasma neuropeptide Y. CONCLUSIONS - The presence and degree of circulatory disturbance, in particular tachycardia and left heart failure, were strongly related to increased plasma concentrations of neuropeptide Y in coronary care patients.

After ingestion of an unknown amount of formalin with suicidal intent, a 55-year-old female and a 34-year-old male were admitted to the hospital with extensive gastrointestinal corrosive damage, circulatory shock, metabolic acidosis, respiratory insufficiency and impairment of renal function, which rapidly progressed to acute renal failure. Metabolic acidosis was in part due to high plasma levels of formic acid, the main metabolite of formaldehyde, and hyperlactatemia. Both patients underwent hemodialysis and hemofiltration treatment. In the male patient, a gastrectomy had to be performed. The further clinical course in the patients was characterized by sepsis and protracted pulmonary complications. Both patients died after developing adult respiratory distress syndrome and global cardiac insufficiency. In vitro experiments on formaldehyde reactivity to proteins yielded evidence for almost complete but reversible binding to plasma and blood. Formaldehyde probably exerts systemic toxicity in the form of its labile Schiff's base with proteins, but not as free formaldehyde.

The cardiac resuscitation records of 458 patients who received advanced cardiac life support at Detroit General Hospital during the last two years were reviewed to identify patients who had pulseless idioventricular rhythm (PIVR) recognized and treated with dexamethasone. Twenty-five cases were identified. The initial successful resuscitation rate of 52% in these patients contrasts sharply with other published data indicating 100% failure with the use of conventional chronotropic drugs. The most common etiology of cardiac arrest in our patients who display PIVR during resuscitation is hypoperfusion shock. Dexamethasone may counteract the lethal arrhythmia by causing the release of aditional adenosine triphosphate into the cytoplasm from the mitochondria.

Eighteen patients in whom shock developed after acute myocardial infarction are described. There was electrocardiographic evidence of acute inferior infarction in 11, of inferolateral infarction in three, and of anteroseptal infarction in four. In all cases the right atrial pressure was the same as or exceeded the end expiratory pulmonary artery wedge pressure. Plasma volume expansion of 100-2500 ml was needed to produce an optimum pulmonary artery wedge pressure. Eleven patients needed additional inotropic support with dopamine. Despite the absence of a critical increase in pulmonary artery wedge pressure, potential or actual hypoxia was almost always present. Six patients needed endotracheal intubation and mechanical ventilation because they had severe hypoxia that was unresponsive to supplemental inspired oxygen. Life threatening arrhythmias were also common (ventricular fibrillation in seven patients and complete heart block in four). Five patients died. All surviving patients are well and only one requires treatment for heart failure.

Serum catecholamine and glucocorticoid levels, kinin activity and major lipids were measured in 144 patients with acute myocardial infarction aggravated by cardiogenic shock. Sympatho-adrenal and kinin activity, and glucocorticoid levels were increased considerably, whereas transcortine reserve binding capacity and serum lipid content were decreased. These parameters underwent the greatest change in patients with the true cardiogenic shock as the condition deteriorated. The demonstrated neuro-humoral changes may be of diagnostic and predictive value.

The hepatic hemodynamic response to cardiogenic shock was investigated in a porcine model produced by pericardial tamponade to better understand the pathophysiology of postshock hepatic insufficiency. Reductions of cardiac output to 50 percent of baseline levels produced marked hepatic ischemia by causing disproportionate reductions in blood flow through the celiac and hepatic arteries and portal vein. These were due to selective vasoconstriction of the splanchnic resistance vessels that was mimicked without tamponade by the infusion of angiotensin II, ablated by angiotensin-converting enzyme blockade, unaffected by alpha-adrenergic ablation, and correlated closely with levels of plasma renin activity. The ischemic liver injury of cardiogenic shock appears to be largely due to an exquisite responsiveness of the splanchnic vascular smooth muscle to endogenously released angiotensin II.

The high density lipoprotein (HDL) cholesterol concentrations of frozen specimen obtained in 1972-73 are reported from 93 men aged 40-49 years who later developed coronary heart disease (CHD), and for 186 controls. Mean HDL cholesterol of CHD-patients was 7.9% lower than that of controls matched for smoking habits and serum concentrations of triglycerides and total cholesterol (p 0.05 for 82 men who had myocardial infarction, n.s. difference for 11 with sudden coronary death), and 10.2% lower (p 0.05) than that of controls who were not matched for the parameters mentioned. The present prospective study confirms that HDL cholesterol is inversely associated with the risk of developing CHD in middle-aged men.

This vignette discusses the use of blood gas determination in the diagnosis and management of cardiogenic shock complicating an acute MI. Both arterial and venous samplings are used to assess cardiac output. Results of therapy can be followed by noting directional changes in cardiac output, i.e., changes in A-VDO2.

The data obtained by the author testifies to the fact that in various clinical forms of myocardial infarction, there are definite correlations between biologically active substances, reflecting the reactivity of the cholinergic and adrenergic systems. In non-complicated myocardial infarction the predominance of catecholamines is noted, as a rule. In complicated course of the disease with a favourable outcome, the absolute content of the biologically active substances is at maximum and the predominance of catecholamines remains; in some cases, however, the predominance of acetylcholine is observed. In myocardial infarction with a fatal outcome, there is practically no stable predominance of this or that substance with a distinct tendency to the growth of the acetylcholine content and an inadequate change in the content of catecholamines.

Plasma fibronectin concentrations were determined in 16 patients with sepsis and shock. In all patients a definite decrease was observed during the course of the disease which did not correlate with coagulative function. Fibronectin in plasma rose to normal levels with improvement in the clinical picture. It is possible that plasma fibronectin indicates the functioning of the reticuloendothelial system.

The inotropic and electrophysiological effects of plasma obtained from patients and experimental dogs during cardiogenic shock following acute myocardial infarction were studied. Changes in the isometric contraction and the intracellular action potential were determined in isolated papillary muscles of rabbits. Control plasma collected from normal subjects produced no significant changes in the contraction or the electrical parameters. Plasma from shock patients decreased peak force by 42% and the maximum rate of force development by 38% in comparison to control values; the time to peak of contraction, the relaxation time and the action potential parameters were not significantly altered. Corresponding results were obtained with plasma from dogs before and during experimental cardiogenic shock. Biochemical determinations failed to identify a single specific "myocardial depressant factor" in the plasma of patients and dogs with cardiogenic shock. The results suggest that (1) various humoral factors released during cardiogenic shock may depress the contractile function of cardiac muscle and (2) that the observed negative intropic effect is not due to electrical changes in the cell membrane.

In patients with shock the metabolic activity of the red blood cells was studied following separation according to cell-age by density layer centrifugation using Stractan II-Urografin solutions. Metabolic acidosis in patients with cardiogenic shock (n = 8) and with postoperative shock (n = 7) induced a pronounced fall in 2,3-diphosphoglycerate (2,3-DPG) levels and in adenosine triphosphate (ATP), in contrast to a raised lactate-pyruvate ratio. 2,3-DPG values were higher than normal in patients with hypoglycemic shock (n = 12), whereas further measured substrate levels were markedly decreased. The levels of these compounds of the red blood cells revealed a significant difference in the hemolysates derived from cells separated according to cell-age. The shock syndrome was also observed in patients suffering from severe congestive heart failure (n = 10) who received dopamine (300 mug/min) for its known action in improving hemodynamics and renal function. Following drug administration for 150 min a clinical improvement was associated with a change of extent and pattern of the red blood cell metabolic disorder.

The activity of glutamino-oxaloacetic transaminase was studied in 85 and that of creatinophosphokinase, total lactate-dehydrogenase and its isoenzymes in 58 patients with macrofocal myocardial infarction complicated by a shock. The maximal transaminase activity in patients with myocardial infarction attended by a shock was on the average greater than in similar patients without any shock. In patients with myocardial infarction attended by a shock who presented, at the same time, congestive manifestations in the systemic ciruclation demonstrated a higher transaminase activity and its normalization at a later date than this was in the case of patients with a shock, but without congestion in the systemic circulation. In patients suffering from myocardial infarction with a shock the activity of creatinophosphokinase and total lactate-dehydrogenase averaged higher than in those without shock. In the blood serum of such patients the proportions of the lactate-dehydrogenase isoenzymes were found to undergo substantial changes, which consisted in an increased activity of the LDH1 and LDH5 fractions. The main factor responsible for a considerable rise in the activity of the blood serum transaminase, creatinophosphokinase, total lactate-dehydrogenase and the LDH1 fraction occurring in patients with myocardial infarction attended by a shock is the great extent of the necrotic focus in the myocardium.

Endothelin (ET) is a recently discovered, endothelium-derived peptide that may be the most potent vasoconstrictor yet identified. Although there is much interest in the possible systemic actions of circulating ET in vivo, there is no data on ET levels under physiological conditions, or in cardiovascular disease. We used a radioimmunoassay that was sufficiently sensitive to detect ET immunoreactivity (irET) in the SepPak-extracted plasma from 14 healthy volunteers in a range from 0.03 to 0.69 pg/ml (mean 0.26 +/- 0.236 pg/ml). ET levels were not significantly different from normal in 5 patients with stable congestive heart failure (0.46 +/- 0.36 pg/ml). However, irET was increased markedly in 6 patients in cardiogenic shock (3.65 +/- 1.14 pg/ml), and (less so) in 6 patients on chronic dialysis (1.05 +/- 0.41) and in 4 with pulmonary hypertension (1.52 +/- 0.45) (p less than 0.001). The present results suggest that circulating irET concentration is responsive to altered cardiovascular conditions, and therefore support a potential role for ET as a vasoactive hormone.

Thirteen patients in severe cardiogenic shock, persisting despite the use of adrenergic agents, were treated with enoximone, a recently available phosphodiesterase inhibitor. Cardiogenic shock was characterized by low cardiac output (less than 2.5 liter.min-1.m-2), elevated pulmonary artery balloon-occluded pressure (greater than or equal to 15 mm Hg), decreased urine output (less than 20 ml.hour-1) and increased blood lactate (greater than or equal to 2.0 mEq.liter-1). Ten patients were mechanically ventilated. A short-term intravenous infusion of 0.5 mg.kg-1 in 20 minutes of enoximone resulted in significant increases in cardiac index (from 1.8 +/- 0.3 to 2.9 +/- 0.3 liter.min-1.m-2, p less than 0.001) and stroke index (from 17.8 +/- 3.3 to 21.9 +/- 5.1 ml.m-2, p less than 0.001) and significant decrease in pulmonary artery balloon-occluded pressure (from 21.7 +/- 5.8 to 19.8 +/- 6.0 mm Hg, p less than 0.01) without a consistent change in mean arterial pressure (from 79 +/- 8 to 76 +/- 9 mm Hg, difference not significant). Enoximone administration decreased arterial oxygen tension (from 108 +/- 42 to 94 +/- 36 mm Hg, p less than 0.01) and increased venous admixture (from 12.8 +/- 6.5 to 16.0 +/- 8.0%, p less than 0.01). In 8 patients, a second infusion of 0.5 mg.kg-1 immediately thereafter amplified these changes. All patients but one survived the episode of cardiogenic shock and 5 patients left the hospital alive. These results indicate that the addition of enoximone to adrenergic agents in the treatment of cardiogenic shock can markedly increase cardiac output and stroke volume without substantial effects on arterial pressure.

The aim of this study was to determine the oxigen affinity actually present in vivo in blood from patients with acute myocardial infarction. Patients with uncomplicated acute myocardial infarction had normal value of P50 in vivo (partial pressure of oxygen at which 50 percent of the hemoglobin is saturated with oxygen at fixed levels of pHand PC02 present in vivo). Also the values of P50 in vivo of blood from patients with low cardiac output with mild or severe heart failured did not differ from the normal mean. This was the consequence of an increase of 2, 3-diphosphoglycerate levels (which reduces the oxygen affinity of hemoglobin) and of the immediate effect of alkalosis (Bohr effect). By contrast, the values of P50 in vivo were significantly increased in patients with cardiogenic shock. This could be ascribed to the state of acute acidiosis present in these patients. In these conditions the changes in the values of P50 in vivo play an important role in the oxygen delivery to the tissues. However, high values of P50 do not enhance oxygen delivery when a severe arterial hypoxemia (P02 smaller than 40-45 mm Hg) is also present.

To determine whether the extensive myocardial injury associated with cardiogenic shock in some patients results from a progressive rather than a discrete massive insult, a study was made of 15 selected patients who had cardiogenic shock within 48 hours of admission, 5 patients with hypovolemic shock without myocardial infarction and 11 patients with myocardial infarction without shock. Peak plasma MB creatine kinase (CK) activity was significantly higher in the seven patients with cardiogenic shock associated with initial infarction (213 international units [IU]/liter) than in patients with shock and previous infarction (98 IU/liter) and in patients with uncomplicated myocardial infarction (125 IU/liter). A prolonged time to peak MB CK activity (averaging 26 hours) and a plateau of elevated MB CK activity were seen in patients with shock associated with initial infarction. Because shock itself did not slow the rate of apparent MB CK disappearance, results obtained suggest that cardiogenic shock associated with initial infarction in selected patients results from progressive myocardial damage underlying continuing release of MB CK into the circulation. The findings are compatible with the concept that, in these patients, cardiogenic shock reflects a vicious cycle of spreading myocardial injury, progressive compromise of cardiac function, exacerbation of ischemia and perpetuation of myocardial damage.

Hemorrhagic shock caused by gastrointestinal bleeding in seven pigs and by external bleeding in another six pigs and cardiogenic shock induced by intravenous infusion of the tricyclic antidepressant drug nortriptyline in yet another eight pigs caused a significant increase in serum cationic trypsin-like immunoreactivity together with formation of complexes between cationic trypsin, on the one hand, and alpha-2-macroglobulin and alpha-1-antitrypsin, on the other hand, compatible with what happens in acute pancreatitis.

The authors examined the concentrations of zinc, HGH, insulin and glucose in blood serum of 40 patients with acute myocardial infarction. Zinc and HGH concentrations in blood serum correlated well with changes in the clinical state in these patients. The more severe the condition of the patient, the greater zinc concentration fall and HGH concentration rise in blood serum were noted. All the changes were statistically significant (P less than 0.001) in cases of severe clinical course and most distinct in cardiogenic shock. On the other hand, in MI of mild course, zinc concentration fall in blood serum was not accompanied by HGH rise. A positive correlation between the concentrations of zinc and HGH found in normal subjects became negative in patients with acute MI of severe course. The changes of zinc and HGH concentrations seem to be due to the non-specific effect of acute myocardial stress, particularly enhanced in MI with severe course and cardiogenic shock, Observation of the intensity of changes may have prognostic significance due to the fact that they were most distinctive in MI of most severe course.

Thirty-six patients with acute myocardial infarction aggravated by acute left ventricular failure (pulmonary edema, cardiogenic shock) were studied for their blood rheologic properties. The impairments of the blood rheologic properties were classified as Stage I and II syndromes of high and low blood viscosity and were characterized by a phasic nature of their course. The rheologic disorders associated with pulmonary edema and reversed cardiogenic shock were decompensated (Stage II syndrome of high blood viscosity--Stage I syndrome of low blood viscosity), but reversible following intensive rheologic therapy. Irreversible cardiogenic shock was characterized by Stage II syndrome of low blood viscosity which was intractable. In acute myocardial infarction without concomitant acute left ventricular failure, rheologic disorders were characterized by Stage I syndrome of high blood viscosity, i. e. they were compensated and did not require intensive rheologic therapy. The management of rheologic impairments attending acute left ventricular failure should be combined, the intensity of therapeutic measures, the nature of combinations and the dosage of drugs being dependent on the degree and phase of rheologic disturbances.

The use of continuous arterial PO2 monitoring with the aid of intra-arterial electrodes is discussed with reference to 50 patients in an intensive care unit specializing in internal medicine. Monitoring time ranged from 2 h to 15 days. There were no serious complications which could, with certainty, be attributed to the intravascular measurement of PO2. The advantages of this method lie particularly in the early detection of hypoxemias, in the uninterrupted monitoring of artificial respiration and in the immediate indication of favorable and unfavorable response to therapy. Finally, a list is given of possible indications in which this method can be used in intensive medicine.

In 29 cardiosurgical patients in cardiogenic shock after extracorporal circulation complicated by acute pulmonary failure, it was impossible to restore normal postoperative arterial oxygen tension, in-spite of optimal pharmacotherapy and ideal conditions with a conventional volume-controlled respirator. These patients were subject to continuous arteriovenous haemofiltration; in all of them the start of haemofiltration immediately led to a significant reduction of respiratory oxygen supply with an increase in arterial oxygen tension. Pulmonary shunt volume decreased. At the same time there was an increase in arteriovenous oxygen difference, arterial oxygen content and oxygen transport capacity. Pulmonary artery pressure as well as pulmonary vascular resistance decreased noticeably, whereas there was an increase in total peripheral vascular resistance. Starting haemofiltration with decreasing left ventricular filling pressure, accompanied by a rise in blood pressure and an increase in total peripheral resistance, led to an improvement of the haemodynamic situation as well as pulmonary oxygen diffusion, thereby ensuring oxygen perfusion of peripheral tissue. The results suggest a causal relation between the improvement of the clinical condition of the patient and the elimination of cardiopulmonary toxic agents like myocardial depressant factor (MDF) and shock mediators due to arteriovenous haemofiltration.

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)