Right atrial

Central venous (right atrial) Less than 5 mm Hg... 

Notes CO cardiac output VR venous return HR heart rate SV stroke volume EDV end-diastolic volume ESV end-systolic volume O blood flow AP pressure gradient R resistance r vessel radius P systolic pressure Piiastoik- diastolic pressure MAP mean arterial pressure TPR total peripheral resistance, P venous pressure Era- right atrial pressure Rv venous resistance. 

The pressure gradient, or the inflow pressure minus the outflow pressure, is determined by the pressure at the beginning of the venous system (Pv) and right atrial pressure (Prblood flow the slightly stiffer large veins offer a small degree of resistance (Rv). 

Placement of a CVP line provides a useful (although indirect and insensitive) estimate of the relationship between increased right atrial pressure and CO. 

The central venous pressure is the hydrostatic pressure generated by the blood in the great veins. It can be used as a surrogate of right atrial pressure (mmHg). 

Bunaftine (21) is a naphthalenecarboxamide derivative, that has been developed as an antiarrhythmic agent. The compound exhibits both Class I and Class III electrophysiological effects. Fenici and co-workers studied bunaftine in patients with paroxysmal atrial tachyarrhythmia and recorded right atrial monophasic action potentials [72]. A mean increase of 18% in atrial repolarization time and an increase in monophasic APD during pac-... 

In the rat, we observed a decrease of the spontaneous frequency of right atrial preparations and biphasic inotropic effects in left atrial preparations. Negative effects were not antagonized by atropine. The positive inotropic effect was modified very little by prior reserpinization or prior exposure to propranolol and phentolamine but was sensitive to Mn ions. On the other hand. 

Cardiac lesions Autopsies did not reveal right atrial or other hemorrhage pathology of the kind seen in animals. 

Since Kantrovitz et al. described the concept of counterpulsation in 1968 [3], the lABP has been the mainstay for temporarily augmenting the cardiac output and improving hemodynamics in acutely decompensated refractory HF [4, 5]. lABP use has been shown to reduce heart rate, left ventricular end-diastolic pressure, mean left atrial pressure, afterload, and myocardial oxygen consumption by at least 20-30%. The lABP also modestly increases coronary perfusion pressure and decreases the right atrial pressure, pulmonary artery pressure, and pulmonary vascular resistance [6]. 

The IV administration of propafenone is accompanied by an increase in right atrial, pulmonary arterial, and pulmonary artery wedge pressures in addition to an increase in vascular resistance and a decrease in the cardiac index. A significant decrease in ejection fraction may be observed in patients with preexisting left ventricular dysfunction. In the absence of cardiac abnormalities, propafenone has no significant effects on cardiac function. 

B. Intravenous furosemide causes a significant decrease in pulmonary capillary wedge pressure and right atrial pressure, concomitantly decreasing stroke volume and increasing vascular resistance. This effect in many cases occurs before diuresis begins. 

Carvedilol significantly reduces systemic blood pressure, pulmonary artery pressure, right atrial pressure, systemic vascular resistance, and heart rate, while stroke volume index is increased. 

In 142 patients with symptomatic heart failure (New York Heart Association classes III and IV) randomized to double-blind, placebo-controlled short-term treatment with a single intravenous dose of conivaptan 10, 20, or 40 mg, conivaptan significantly reduced pulmonary capillary wedge pressure and right atrial pressure and increased urine output (1). 

Hemodynamic effects During treatment with ACE inhibitors, systemic vascular resistance is decreased along with the pulmonary capillary wedge pressure and right atrial pressure (4). End-diastolic and end-systolic dimensions are reduced. Long-term ACE inhibition decreases echocardiographic left ventricle (LV) dimensions and increases the shortening fraction (5). 

Before insertion the device needs to be evacuated from air by expanding and refolding the wire mesh in saline. Once accomplished, the device is loaded into the delivery catheter and percutaneously introduced. Self-expansion of the left and right atrial discs is achieved by pushing the delivery cable and retrieving the catheter stepwise. After checking for proper device position and configuration, the device is released. 

The AV node is a subendocardial right atrial construct that is located within a fibrous stroma in the triangle of Koch. It is connected to both sympathetic and parasympathetic nerves. The bimdle of His arises from the distal section of the AV node and goes to the summit of the... 

Hodkinson, J., Couper-Smith, J., Kew, M.C. Inferior vena cava and right atrial thrombosis complicating an amebic hepatic abscess. Amer. J. Gastroenterol. 1988 83 786 - 788... 

Feingold, MX., Litwak, R.L., Geller, S.S., Baron, M.M. Budd-Chiari-syndrome caused by a right atrial tumor. Arch. luteru. Med. 1971 127 292 - 295... 

In pulmonary hypertension, both verapamil and nifedipine increase mean right atrial pressure in association with hypotension, chest pain, dyspnea, and hypoxemia the severe hemodynamic upset resulted in cardiac arrest in two patients after verapamil and death in another after nifedipine (54). A patient with pulmonary hypertension also developed pulmonary edema whilst taking nifedipine (55) and another seems to have developed this as an allergic reaction (56). 

Phosphate infusion Calcified right atrial thrombus (30)... 

Spencer K, Weinert L, Pentz WH. Calcified right atrial mass in a woman receiving long-term intravenous... 

Milrinone is a phosphodiesterase type III/IV inhibitor that has vasodilatory properties and increases the force of contraction and velocity of relaxation of cardiac muscle. Milrinone has not been evaluated fully in the equine clinical setting. It produces a dose-dependent increase in heart rate, cardiac output, arterial blood pressure and ejection fraction and a reduction in right atrial, pulmonary artery pressures and systemic vascular resistance in normal anesthetized horses (Muir 1995). These changes persisted for 30 min after the termination of a constant i.v. infusion of milrinone. 

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