Hemodynamics

Elestolol sulfate is a nonselective, ultrashort acting P-adrenoceptor blocker. It has no ISA and produces weak inhibition of the fast sodium channel. The dmg is under clinical investigation for supraventricular tachyarrhythmias, unstable angina, and acute MI. In humans, flestolol has hemodynamics and electrophysiologic effects similar to those of other P-adrenoceptor blockers. The pharmacokinetics of flestolol are similar to those of esmolol. It is 50 times more potent than esmolol and the elimination half-life is 7.2 min. Recovery from P-adrenoceptor blockade is 30—45 min after stopping iv infusions. The dmg is hydrolyzed by tissue esterases and no active metabohtes of flestolol have been identified (41). 

In normal human subjects, ANP infusion for one hour causes increased absolute and fractional sodium excretion, urine flow, GFR, and water clearance (53—55). As shown in many in vitro and in vivo animal studies, ANP achieves this by direct effect on the sodium reabsorption in the inner medullary collecting duct, ie, by reducing vasopressin-dependent free-water and sodium reabsorption leading to diuresis and by indirect effect through increased hemodynamic force upon the kidney. ANP inhibits the release of renin and aldosterone resulting in the decreased plasma renin activity and aldosterone concentration (56,57). 

Ascites. Patients with cirrhosis, especially fiver cirrhosis, very often develop ascites, ie, accumulation of fluid in the peritoneal cavity. This is the final event resulting from the hemodynamic disturbances in the systemic and splanchnic circulations that lead to sodium and water retention. When therapy with a low sodium diet fails, the dmg of choice for the treatment of ascites is furosemide, a high ceiling (loop) diuretic, or spironolactone, an aldosterone receptor antagonist/potassium-sparing diuretic. 

Few areas of organic medicinal chemistry in recent memory have had so many closely spaced pulses of intense research activity as the prostaglandins. Following closely on the heels of the discovery of the classical monocyclic prostaglandins (prostaglandin El, F2, A2, etc.), with their powerful associated activities, for example, oxytocic, blood pressure regulating, and inflammatory, was the discovery of the bicyclic analogues (the thromboxanes, prostacyclin) with their profound effects on hemodynamics and platelet function. More recently, the non-... 

Circulation Leakage of fluid from the vasculature into the surrounding tissue causes edema, drop in blood pressure and finally hemodynamic shock. 

Newly developed class III drugs comprise dofetilide, a specific Ik, blocker, and ibutilide, which blocks IKl and activates the slow iNa- Both drugs lack hemodynamic side effects. These drugs are scheduled for the treatment of atrial fibrillation and atrial flutter. As with class HI drugs, they can induce torsade de pointes arrhythmia. 

Vasopressin (antidiuretic hormone [ADH]) secretion increases in response to decreased blood volume and/or reductions in effective blood volume via a decrease in inhibitory tone from both low-pressure and high-pressure baroreceptors to the hypothalamus. The neuronal pathways that mediate hemodynamic regulation of... 

All three classes also inhibit depolarization-induced contraction of venous smooth muscle in vitro. However, venous relaxation does not substantially contribute to the hemodynamic actions of Ca2+ channel blockers. 

Inhaled NO has been used for treatment of persistent pulmonary hypertension of newborn infants, critical respiratory failure of preterm infants, and acute hypertension of adult cardiac surgery patients. PDE-5 inhibitors such as sildenafil are also effective for treatment of pulmonary hypertension. The combination of PDE-5 and NO inhalation yields additive beneficial effects on pulmonary hemodynamics. On the other hand, measurement of exhaled NO is a noninvasive and reproducible test that is a surrogate measure of airway inflammation in patients with bronchial asthma. 

The adrenergic drugs are useful in improving hemodynamic status by improving myocardial contractility and increasing heart rate, which results in increased cardiac output. Peripheral resistance is increased by vasoconstriction. In cardiogenic shock or advanced shock associated with low cardiac output, die adrener-... 

Monitoring the patient in shock requires vigilance on the part of the nurse The patient s heart rate, blood pressure, and ECG are monitored continuously. The urinary output is measured often (usually hourly), and an accurate intake and output is taken. Monitoring of central venous pressure via a central venous catheter will provide an estimation of the patient s fluid status. Sometimes additional hemodynamic monitoring is necessary with a pulmonary artery catheter. The use of a pulmonary artery catheter allows the nurse to monitor a number of parameters, such as cardiac output and peripheral vascular resistance The nurse adjusts therapy according to the primary health care provider s instructions. 

Cardiac hypertrophy appears to be mediated by HS proteins (Izumo et al., 1988). Cardiac myocytes exposed to a hemodynamic stress have been found to increase their levels of heat shock proteins (Delcayre et al., 1988). Although experiments involving interference with HS protein synthesis were not done in these studies. 

Delcayre, C., Samuel, J.L., Marotte, F., Best, B.M., Mercadier, J.J., Rappaport, L. (1988). Synthesis of stress proteins in rat cardiac myocytes 2-4 days after imposition of hemodynamic overload. J. Clin. Invest. 82,460-468. 

Smedegard G. Revenas B. Arfors KE Anaphylaxis in the monkey hemodynamics and blood flow distribution. Acta Physiol Scand 1979 106 191. 

We examined the effects of selective activation of histamine Hj receptors on coronary hemodynamics in two groups patients with atypical chest pain and normal coronary arteries, and patients with vasospastic angina [48]. Selective Hj receptor stimulation was achieved by infusing histamine intravenously (0.5 pg/kg/min) for 5 min after pretreatment with cimetidine to antagonize the H2 receptors. Heart rate was kept constant (100 beats/min) by coronary sinus pacing. 

In a third study the time course of the effects of intravenous and intracoronary injections of cysteinyl leukotrienes on metabolic parameters and systemic and coronary hemodynamics was examined in patients with normal coronary arteries [32]. LTD4 (3 nmol, injected into the left coronary artery) induced an early (20 s), transient fall in mean arterial pressure paralleled by rises in heart rate and plasma levels of epinephrine and norepinephrine, all of which had returned to baseline by 10 min. CVR rose at 10 and 15 min and myocardial oxygen extraction at 15 min. Thus, small doses of cysteinyl leukotrienes may induce both an early, transient fall in mean arterial pressure, with secondary sympathoadrenergic activation, and a later increase in small coronary arteriolar resistance. 

Interestingly, these studies provided the important information that the hemodynamic effects of mediators depend on both the underlying cardiovascular conditions and the pharmacologic treatment (e.g. H2 blockade). 

Hanashiro PK, Weil MH Anaphylactic shock in man. Report of two cases with detailed hemodynamic and metabolic studies. Arch Intern Med 1967 119 129. 

Vigorito C, Giordano A. De Caprio L, Vitale DE, Maurea N, Silvestri P, Tuccillo B, Ferrara N, Marone G, Rengo F Effects of histamine on coronary hemodynamics in man role of H, and H2 receptors. J Am Coll Cardiol 1987 10 1207. 

Anaphylactic patients with impending shock, for example, those with incontinence, sudden loss of hearing or vision, dizziness, or collapse, and those with profound or persistent hypotension, require slow intravenous infusion of a dilute epinephrine solution [0.1 mg in 1 ml (1 10,000)]. Continuous hemodynamic monitoring and dose titration by trained and experienced healthcare professionals are essential. Maximum infusion rates of 5-15 ig/min are recommended in adults [2,18,22]. 

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