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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 66-year-old patient with chronic obstructive pulmonary disease (COPD) complicated by arterial hypoxemia and repeated episodes of respiratory and right ventricular failure, a satisfactory level of oxygenation could not be maintained despite controlled oxygen therapy. To enable oxygen to be administered without depression ventilation, artificial respiration by means of phrenic nerve stimulation (diaphragm pacing) has been employed. Evidence of clinical improvement since pacing was begun 32 months ago include fewer episodes of respiratory failure and better control of congestive heart failure despite a gradual worsening of pulmonary function.
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PMID:Diaphragm pacing. Application to a patient with chronic obstructive pulmonary disease. 30 48

Calcium chloride is frequently administered to patients immediately after separation from cardiopulmonary bypass to improve the contractile state of the myocardium. Animal studies suggest that calcium chloride may produce increases in pulmonary vascular resistance, which can precipitate right ventricular failure. In an attempt to determine the effect of calcium chloride administration after cardiopulmonary bypass on right ventricular function, this study was designed to evaluate patients with normal and elevated pulmonary vascular resistance. Fifty patients scheduled for elective cardiac surgery were prospectively studied for changes in ionized calcium levels before and after bypass. The impact of calcium administration on right ventricular function was assessed by a pulmonary artery catheter modified for the measurement of right ventricular ejection fraction. In all patients the level of ionized calcium decreased during bypass from a mean of 4.91 to 4.29 mg.dl-1. However, the infusion of calcium chloride (10 mg.kg-1) after bypass resulted in increasing the ionized calcium levels to prebypass levels. Administration of calcium chloride after bypass to patients with normal right ventricular function resulted in a transient increase in both cardiac output and right ventricular ejection fraction without any change in pulmonary vascular resistance. Eight patients with both elevated pulmonary vascular resistance and depressed right ventricular function were evaluated to determine the effect of calcium chloride after bypass on pulmonary vascular resistance and right ventricular ejection fraction. Administration of calcium chloride (10 mg.dl-1) to these patients did not result in any significant increase in pulmonary vascular resistance or depression of right ventricular performance. More important, in these patients, right ventricular ejection fraction and cardiac output were significantly increased after calcium chloride administration. In summary, the results of this study fail to demonstrate any increase in pulmonary vascular resistance or deterioration of right ventricular function with the administration of calcium chloride (10 mg.kg-1) after bypass in patients with elevated pulmonary vascular resistance.
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PMID:The effect of calcium on pulmonary vascular resistance and right ventricular function. 149 94

Sudden release of platelet-activating factor (PAF) into the circulation can cause hypotension, tachycardia, and circulatory collapse. To further examine this response, we performed detailed studies of cardiovascular function after PAF administration to young domestic pigs and newborn piglets. Our results indicate that circulatory dysfunction after PAF reflects severe constriction of pulmonary resistance vessels and consequent acute right ventricular failure. Although PAF-induced coronary artery constriction and contractile depression may be complicating problems, left ventricular underperfusion and dysfunction after PAF are mainly the result of systemic arterial hypotension and diminished left ventricular filling. The adverse hemodynamic effects of PAF are accompanied by substantial release of thromboxane A2 (TxA2). These effects are mimicked by the TxA2 agonist U-46619 and partially blocked by specific and nonspecific inhibitors of TxA2 synthesis (OKY-046 and indomethacin). Even more potent blockade of PAF action is exerted by the TxA2 receptor blocker, SQ 29,548. Taken together, these findings indicate that severe pulmonary vascular constriction and hemodynamic collapse soon after intravenous PAF are at least partially mediated by PAF-induced TxA2 release. Tachyphylaxis to PAF influence has been observed in studies of leukocyte and platelet function. We hypothesized that tachyphylaxis to PAF might also occur in our studies of constrictor responses in pulmonary vessels. Recently, we have examined the capacity of PAF to produce sustained pulmonary vasoconstriction in open-chested, anesthetized newborn piglets. Infusions sufficient to produce 100% increase in mean pulmonary artery pressure after 3 min showed no loss of efficacy when sustained for 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular effects of platelet-activating factor. 181 12

Holter recordings of subjects apparently free from cardiovascular disease have demonstrated a moderate sinusal and nodal depression during sleep. This depression does not seem to be sufficient to create overt cardiovascular disorders in apparently healthy subjects, but it may aggravate or even reveal an underlying disorder of rhythm or conduction in elderly people or in patients taking drugs that potentiate its effects. In sleep apnea syndrome prolonged episodes of apnea may produce a paroxysmal, then permanent increase in pulmonary arterial pressure, which may lead to right heart failure. These episodes also increase the pre- and after-load and decrease myocardial contractility, thus facilitating the occurrence of left ventricular failure, potentiated by systemic arterial hypertension, overweight or even coronary disease, all conditions that are often present in these subjects. Arterial hypertension is so frequent in sleep apnea syndrome that some authors advocate a systematic search for the syndrome by Holter recordings before the hypertension is pronounced "essential". All studies confirm the existence of rhythm and conduction disorders directly related to apneic episodes. These disorders decrease or regress after a well-conducted treatment of the sleep apnea syndrome. They are mainly of the "hypokinetic" type, created by depression of sinus activity and conduction pathways. Their frequency, their severity and, in particular, the risk of sudden death they carry seem to have been overestimated, especially since no evidence has ever been produced of a potentially lethal rhythm disorder occurring during sleep apnea. Nevertheless, there is no certainty that these patients are not at risk of sudden death related to their sleep apnea syndrome.
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PMID:[Cardiovascular disorders during sleep]. 214 78

A 14-year-old girl was admitted with chief complaints of edema and chest pain. She had hepatomegaly, but did not have heart murmur and accentuation of the pulmonary component of the second heart sound. The electrocardiogram showed right axis deviation, negative T wave in V3,4 and ST depression in III, aVF. But right ventricular hypertrophy was not dominant. Chest radiography showed a cardiothoracic ratio of 54% and a slight prominence of proximal pulmonary arteries. The edema was soon diminished only by the diuretics, but it appeared again without the diuretics. At the cardiac catheterization 3 months after the onset of symptoms, the pulmonary arterial pressure was 150/85 mmHg and the pulmonary resistance was 3,232 dyn/sec/cm5. The right atrial pressure was 9.5 mmHg and oxygen saturation at the pulmonary artery was 31.0%. Prostaglandin E1 reduced the pulmonary artery pressure only a little, but raised the systemic pressure. The patient was treated with several vasodilators, but her condition deteriorated rapidly and she developed severe right ventricular failure. She died only 8 months after the onset of symptoms and 5 months after the catheterization. At autopsy, histological examination demonstrated intimal fibrotic thickening of the small-sized pulmonary arteries and organizing thrombus. But there was not plexiform lesion. Heart failure was easily improved when she was first admitted. But after 3 months the cardiac catheterization revealed that her condition was already severe. Several vasodilators was not effective to such a rapidly progressive primary pulmonary hypertension.
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PMID:[A case of rapidly progressive pulmonary pulmonary hypertension in a 14-year-old girl]. 259 31

The hemodynamic manifestations of right ventricular dysfunction after ischemic injury depend not only on the severity of injury but also on the degree of coexistent left ventricular dysfunction. A better understanding of right ventricular failure and of optimal therapies has been hindered in part by lack of suitable experimental models of selective and differential ventricular injury. Therefore, we developed a technique of differential ventricular myocardial protection during a period of global cardiac ischemia and examined the effect of such an injury on intrinsic right and left ventricular myocardial function, metabolism, and regional blood flow. Twenty-six dogs were subjected to 30 minutes of ischemia while being supported by cardiopulmonary bypass. During ischemia, right and left ventricular myocardial temperatures were independently varied by selective ventricular endomyocardial thermal regulation. Nine dogs underwent right and left ventricular normothermic ischemia, eight underwent right and left ventricular hypothermic ischemia, and nine underwent right ventricular normothermic and left ventricular hypothermic ischemia. In both ventricles, normothermic ischemia resulted in greater depression of ventricular ability to generate stroke work as a function of end-diastolic dimension (p less than 0.05), greater depletion of myocardial adenine nucleotide content (p less than 0.05), and greater subendocardial reperfusion hyperemia (p less than 0.05). Myocardial temperature of the contralateral ventricle during ischemia had no effect (p = not significant) on intrinsic ventricular functional, metabolic, or regional blood flow response to injury. For a given degree of right ventricular injury assessed by these parameters, the degree of left ventricular injury could be independently varied by as much as 50%. This is a particularly suitable model for the investigation of acute right ventricular failure.
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PMID:Differential ventricular ischemic injury: an experimental model of right ventricular failure with a variable degree of left ventricular dysfunction. 317 5

Postoperative low cardiac output is the most common cause of death in patients undergoing elective repair of tetralogy of Fallot. The incidence is much higher than in elective adult bypass operations for coronary artery disease. To explain this difference, we investigated 16 children having elective repair of tetralogy (mean age 6.3 years). Myocardial biopsy specimens obtained during bypass before arrest, at the end of cold arrest by blood cardioplegia, and after 30 minutes of reperfusion were studied for adenosine triphosphate and lactate levels. Myocardium was submitted for microscopic study shortly after the onset of ischemia. The operation was successful in reducing right ventricular-pulmonary artery gradients from 82 +/- 28 to 9 +/- 1 mm Hg, yet seven patients required significant inotropic support (dopamine, greater than 5 micrograms/kg/min) for more than 24 hours and 12 patients needed prolonged use of digoxin and diuretics for right ventricular failure. Tissue levels of adenosine triphosphate and lactate in the tetralogy groups were compared with those in 20 adults with coronary artery disease having similar myocardial protection techniques. Adenosine triphosphate levels in the tetralogy group decreased during cross-clamping (41 +/- 8 minutes) from 24 +/- 3 to 16 +/- 2 mmol/kg dry weight (mean +/- 1 standard error), with a marked further drop after reperfusion to 9 +/- 2 mmol/kg (p less than 0.01). Adenosine triphosphate levels in the group with coronary disease also decreased from 20 +/- 1 to 16 +/- 1 mmol/kg after a longer cross-clamp time (70 +/- 17 minutes) but remained at 15 +/- 2 mmol/kg after reperfusion. Tissue lactate levels in the tetralogy group rose markedly during ischemia and remained elevated after reperfusion. In contrast, lactate levels in the group with coronary disease rose moderately during ischemia and returned to normal early on reperfusion. Microscopic study revealed focal myocyte necrosis in tetralogy of Fallot. Our findings, which demonstrate inadequate myocardial protection of patients with tetralogy during repair, with depression of adenosine triphosphate and increased lactate during ischemia and reperfusion, suggest a defect in oxidative metabolism. The drop in adenosine triphosphate after reperfusion in the patients with tetralogy implicates reperfusion injury as a mechanism of myocardial damage.
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PMID:Inadequate myocardial protection with cold cardioplegic arrest during repair of tetralogy of Fallot. 325 36

The ventilation-perfusion match under therapy with captopril was registered in 14 patients with secondary pulmonary hypertension and right heart failure caused by chronic obstructive lung disease. In none of the cases, changes of cranialisation of the perfusion or increasing ventilation-perfusion mismatch was found, but a significant fall in O2 was seen in all patients. This O2-depression is due to decreasing stroke volume of the right to left shunt.
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PMID:[Decrease in arterial PO2 with captopril administration in secondary pulmonary hypertension and right heart failure]. 331 70

Right ventricular (RV) function in terms of hemodynamics and RV wall motion was studied in 14 mongrel dogs during left heart bypass (LHB) using a centrifugal blood pump. The wall motion was analyzed by two-dimensional echocardiography (2D-echo). Incremental changes in LHB flow ratios of 0% (controls), 25%, 50%, 75% and a maximum 85-100% were accompanied by decrements of segmental shortening of the interventricular septum (IVS) by 54 +/- 12%, 43 +/- 5%, 42 +/- 2%, 35 +/- 0% and 0%, respectively. In addition to akinesis of the IVS during maximum flow, a specific part of the RV free wall adjacent to the IVS also had marked depression of contractions and overall RV contraction was nearly dependent on the RV free wall opposite to the IVS. Maximum LHB flow induced complete depression of the left ventricular cavity, a marked increase in RV volume, and depression of the RV ejection fraction on 2D-echo. Excessive or prolonged LHB reduces the RV wall motion capability and may lead to right heart failure. Our results suggest that an LHB ratio of about 75% is optimum to maintain normal cardiac function, particularly that of the right heart.
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PMID:Two-dimensional echocardiographic evaluation of right ventricular function during left heart bypass. 384 2

In anesthesized pigs, hemodynamic measurements and gated bloodpool scintigraphy were performed during and after infusion of live Escherichia coli (2 X 10(8)/kg). Ejection fractions (EF) as well as the relation between end-diastolic volumes (EDV) and stroke work (SW) were used to evaluate changes in left (LV) and right ventricular (RV) function. Porcine E. coli sepsis proved to be characterized by pulmonary vascular hypertension (PVH) and systemic arterial hypotension, accompanied by a reflex increase in heart rate. Systemic flow remained essentially unchanged. E. coli infusion resulted in pronounced and opposite changes in LV and RV preload. RVEDV increased initially and then returned to the value observed before E. coli infusion. LVEDV showed a continuous decrease during the observation of 3 hours. Alterations in LVSW and RVSW appeared to parallel the changes in LVEDV and RVEDV. No significant changes in LVEF and RVEF were found. It is concluded that porcine E. coli sepsis might be a suitable model for human sepsis complicated by PVH. In this animal model no clear signs of myocardial depression or evidence of right heart failure were observed.
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PMID:Left and right ventricular function in porcine Escherichia coli sepsis. 388 76


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