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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In acute and chronic left heart failure peripheral resistance is elevated due to increased sympathetic tone. This should compensate the decrease in stroke volume. In the diseased left ventricle however the augmentation of afterload leads to further reduction of stroke volume and to increase of heart size and myocardial oxygen consumption. This vitious cycle may be interrupted by vasodilators. Drugs like nitroglycerin, mainly acting on the venous system, reduce preload and thereby relieve symptoms of pulmonary congestion (backward failure). Phentholamin on the other hand primarily reduces afterload by an action on the resistance vessels and thereby increases cardiac output (forward failure). Nitroprusside has effects on both, the capacity and resistance vessels. So nigroglycerin is the remedy of choice in acute pulmonary edema. Nitroprusside in leftf heart failure in acute myocardial infarction and Phentolamin in acute left ventricular failure due to critical rise in blood pressure. For long term treatment of chronic left heart failure (coronary heart disease, cardiomyopathy, rheumatic heart disease) hydralazin or prazosin may be used as well as long acting nitrates.
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PMID:[Progress in the therapy of acute and chronic cardiac insufficiency by means of systemic vasodilators. Studies with prazosin and nitroglycerin]. 12 80

Artificial ventilation with positive end-expiratory pressure (PEEP) reduces venous return by raising intrathoracic pressure. To determine whether PEEP decreases cardiac output further by depressing myocardial function, we constructed Starling curves, using rapid dextran infusion in 7 anesthetized dogs ventilated with zero (ZEEP) and 20 cm PEEP. The changes in stroke volume and in left ventricular stroke work (LVSW) when PEEP was added or removed were significantly greater than could be attributed to the corresponding change in transmural left ventricular end-diastolic pressure (LVEDPTM) on these Starling curves. To the extent that PEEP did not alter left ventricular diastolic volume-pressure characteristics, these data indicated PEEP depressed ventricular function. Identical changes with PEEP in cardiac output (-30%), esophageal pressure (+10 cmH2O), and left ventricular function were observed after pulmonary edema was induced with oleic acid. These results confirm and extend recent suggestions that high levels of PEEP depress left ventricular function in dogs, accounting for about half of the reduction in cardiac output before and during acute pulmonary edema.
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PMID:Effect of positive end-expiratory pressure on ventricular function in dogs. 37 68

Nifedipine induces vascular smooth muscle relaxation through a calcium antagonistic action. The possibility of clinical use of the drug as a ventricular unloading agent has been explored in this study. In patients with hypertensive (seven cases), primary (seven cases) or rheumatic (aortic insufficiency five cases, mitral regurgitation five cases) cardiac disease, nifedipine, administered in a single sublingual dose (10 mg), relieved acute pulmonary edema. Circulatory variations from control were the following: decrease of systemic and pulmonary arterial pressures, and of vascular resistances, of pulmonary wedge pressure, of left ventricular diastolic and systolic dimensions (echocardiography); increase of cardiac and stroke index, of left ventricular mean rate of circumferential fiber shortening, of left and right mean pre-ejection delta P/delta t and mean rate of ejection; improvement of forward output in primary and rheumatic disease. Nifedipine benefits acute congestive heart failure by sustained fall of both preload and afterload and, possibly, by an enhanced contractility. It seems to have an appropriate indication in cases in which left ventricular afterload reduction is desirable.
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PMID:Clinical use of a calcium antagonistic agent (nifedipine) in acute pulmonary edema. 44 58

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

Stroke volume was determined from the pulmonary artery pressure record by application of the pulse contour method. Pulmonary artery pressure records were obtained in 17 patients using a high fidelity catheter-tip pressure transducer and simultaneous measurements of cardiac output were obtained from indicator dilution curves. The formula used was SV = KP sa (i plus T s/Td) where Psa is the planimetered area beneath the systolic portion of the pulmonary artery pressure curve. Ts and Td are the durations of systole and diastole, and K is a constant. Stroke volume was altered by isometric handgrip exercise and/or pharmacological agents in 15 patients. Serial measurementswere made in 2 patients in acute pulmonary oedema after myocardial infarction. Comparison of a wide range of values of stroke volume by the pulse contour method with those obtained from dye dilution curves showed a good correlation (r plus 0.97, P smaller than 0.001) regression line y = 1.01 times - 0.47. Measurement of stroke volume from the pulmonary artery pressure contour is a technique of potential value in serial haemodynamic monitoring.
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PMID:Measurement of stroke volume from pulmonary artery pressure record in man. 80 78

If the failing left ventricle could be given an effective push, other approaches to the treatment of heart failure would not be needed. We have inotropes only for short-term parenteral use. We have no safe inotrope for chronic oral use. The effect of digitalis is only feeble and the phosphodiesterase inhibitors seem to increase mortality from sudden death. Diuretics are dramatic for acute pulmonary oedema and the mainstay for chronic fluid retention but do not improve the pump and by reducing blood volume stimulate the renin angiotensin system to vasoconstriction, further fluid retention and hypokalaemia. Nitrates drop pre-load without reducing blood volume but tolerance is a problem and stroke volume does not increase. Reduction of afterload helps the failing ventricle to empty, the pull and output increases. The angiotensin converting enzyme inhibitors (ACEI) are now the cornerstone of heart failure treatment, reducing mortality in severe heart failure (CONSENSUS) and superior to standard vasodilator therapy (V-HeFT-2) at improving the survival of patients with mild to moderate heart failure. ACEI can reduce the incidence of ventricular ectopy and probably do this through improving left ventricular function, from decreasing sympathetic tone, reducing myocardial oxygen demand or increasing serum potassium but ACEI did not diminish the incidence of sudden death in the SOLVD trial despite reducing mortality. Disappointingly little improvement in exercise tolerance and persistence of chronic fatigue in heart failure concentrated attention on the periphery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The push, the pull and the periphery. 144 45

To assess the influence of mental stress on ventricular pump function in coronary patients, 88 postinfarction patients (mean age, 53 +/- 10 years) performed mental arithmetic during Swan-Ganz catheterization monitoring a mean of 44 +/- 16 days after myocardial infarction. The test lasted 3 minutes in 66 patients and 10 minutes in 22 patients. Two patients suffered acute pulmonary edema a few minutes after mental arithmetic, but no others complained of symptoms. Mean heart rate increased from 76 +/- 14 to 92 +/- 17 beats/min, mean systolic blood pressure increased from 138 +/- 22 to 160 +/- 27 mm Hg, mean diastolic blood pressure increased from 89 +/- 10 to 101 +/- 15 mm Hg, mean pulmonary wedge pressure increased from 13 +/- 6 to 19 +/- 8 mm Hg (p less than 0.001), and mean stroke volume decreased from 72 +/- 18 to 65 +/- 18 ml (p less than 0.001) during mental arithmetic. The changes in central hemodynamics during mental arithmetic were not predictable from noninvasive parameters. In the 22 patients who performed 10-minute mental arithmetic, the changes persisted throughout mental exercise. Eighty-one patients underwent supine bicycle ergometry after mental arithmetic: Absolute mental arithmetic-pulmonary wedge pressure values correlated with those during exercise at the first stage (25 W) (r = 0.63, p less than 0.001) and at maximal load (77 +/- 29 W) (r = 0.49, p less than 0.001), and pulmonary wedge pressure change between stress values and baseline during mental arithmetic did not correlate with those during the first stage of exercise (r = 0.09, p = NS) or during maximal load (r = 0.11, p = NS). Twenty-nine patients repeated the study 1 year after myocardial infarction, and the same hemodynamic changes were observed during mental arithmetic. In conclusion, it appears that mental stress can cause deteriorations of central hemodynamics that can be independent of changes in heart rate and blood pressure and are not predictable from exercise-induced changes; stress-induced cardiovascular activation can last for at least 10 minutes and is stable over long time periods.
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PMID:Influence of mental stress on ventricular pump function in postinfarction patients. An invasive hemodynamic investigation. 200 23

There has been increasing interest in the use of calcium antagonists as arterial vasodilator agents in the management of patients with congestive heart failure. Because congestive heart failure is mostly secondary to coronary artery disease, calcium antagonist drugs seem particularly appealing because of their anti-ischemic properties. The potent vasodilating action of calcium antagonists decreases impedance and improves ejection phase indexes of left ventricle function. However, these drugs interfere with calcium availability for myocardial contraction, and concern has been expressed about their potential depressant effect on myocardial performance. The net hemodynamic effect depends on the relative vascular versus myocardial potency of each calcium antagonist and on the indirect effects of reflex sympathetic activation. Balance between these factors is still influenced by the intrinsic status of left ventricle of the patient. Generally, the negative inotropic direct effect of the calcium antagonists is counteracted by the beneficial influence of the decrease of systemic vascular resistance. Because of its relatively more pronounced negative inotropic action, verapamil is not advisable in patients with left ventricular failure. Limited experience with diltiazem show no significant negative inotropic action. Nifedipine has been studied in its acute and long term effects. The use of sublingual nifedipine is established in the emergency management of acute pulmonary edema, specially in patients with arterial hypertension, or when acute ventricular dysfunction is associated with mitral or aortic insufficiency. Patients with chronic congestive heart failure have shown after nifedipine an increase in stroke volume and cardiac index at rest and during exercise, as well as decreases of pulmonary capillary wedge pressure during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of calcium antagonists in the pharmacologic treatment of heart insufficiency]. 269 18

Rotating tourniquets are traditionally part of the treatment of acute pulmonary edema. However, their effectiveness has been questioned. A radioisotope technique was therefore used to evaluate directly the increments in the blood volume of the leg after venous occlusion using a pressure of 60 mmHg in 26 patients with left ventricular (LV) dysfunction following myocardial infarction. The increment in mean radionuclide count at serial 15-second intervals (reflecting the blood volume in the leg distal to the occlusion) increased significantly from the pre-occlusion value by 46 +/- 26% (p less than 0.0005). Thus satisfactory trapping of blood is achieved even in LV failure. However, mean ejection fraction decreased slightly but significantly from 0.23 +/- 0.10 to 0.21 +/- 0.10 (p less than 0.05), a decrease observed in 18 of the 26 patients. LV end-diastolic and end-systolic volume equivalents tended to decrease slightly, but not in all patients. Mean stroke volume and cardiac output equivalents were reduced by 14% (p less than 0.0005), while calculated peripheral resistance increased significantly. The present study fails to support the hypothesis that preload reduction by tourniquets improves LV function.
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PMID:[Effect of tourniquet occlusion on peripheral blood pooling and ventricular function]. 270 60

Opiates and loop diuretics are the mainstay of treatment of acute pulmonary oedema, but it is now recognized that immediate response to intravenous loop diuretics is acute vasoconstriction with impaired cardiac performance. It therefore seemed appropriate to compare the effects of intravenous isosorbide 5-mononitrate and frusemide on systemic and coronary haemodynamics in a group of patients with chronic cardiac failure at cardiac catheterization. Intra-arterial blood pressure was recorded from the ascending aorta, pulmonary capillary wedge pressure and cardiac output were measured using a Swan-Ganz thermodilution catheter. Coronary venous blood flow was measured using a thermodilution technique and A-V oxygen difference across the myocardium was obtained from simultaneous blood sampling in the aorta and coronary sinus. Absolute myocardial nutrient blood flow was measured using a 133Xe clearance technique. Frusemide in a dosage of 0.5 mg/kg given intravenously provoked acute vasoconstriction with falls in cardiac output and stroke volume. Pulmonary capillary wedge pressure was unchanged in the first 60 min after administration of frusemide. Isosorbide 5-mononitrate in a dosage of 15 mg intravenously, significantly reduced the pulmonary capillary wedge pressure within 5 min, and with the subsequent fall in systolic arterial blood pressure, cardiac output was maintained. These results suggest that intravenous isosorbide 5-mononitrate could well be of value in the immediate management of the patient with acute pulmonary oedema.
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PMID:A comparison of intravenous elantan and frusemide in patients with chronic cardiac failure. 360 6


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