Atrial pressure

ACS Symposium Series American Chemical Society Washington, DC, 1980. 

Increased intracellular Ca2+ activity also activates secretory cells (25). Inhibition studies Indicate that the Inotropic effect of monensln Is mediated In part by the release of catecholamines from the adrenals and/or the heart Itself (22). Ifonensln also discharges catecholamines from disaggregated bovine chromaffin cells In culture (26.27), and Induces the release of acetylcholine at the neuromuscular jxmctlon (28). Thus, the secretion stimulatory activity of monensln also supports the concept that Increased Intracellular Na activity produces a rise in intracellular Ca2+ activity sufficient to stimulate Ca2+-activable cells. 

Two hypotheses for the conversion of a primary Increase in Intracellular Na activity to a subsequent increase in intracellu- 

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The atrial natriuretic peptide (ANP) belongs to a family of hormones that have structural similarity and some biological actions in common, such as natriuresis and haemoconcentration. It is synthesized and secreted by the cardiac atrium in response to increased atrial pressure. ANP is believed to act physiologically in an opposing manner to AVP... 

Atrial natriuretic peptide A type of peptide, 28 amino acids in length, secreted by the atria of the heart when atrial pressure and stretch are increased. 

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). 

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]. 

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. 

Adenosine affects vascular smooth muscle tone in the pulmonary circulation. In the feline pulmonary vascular bed, under conditions of controlled pulmonary blood flow and constant left atrial pressure, adenosine was shown to produce dose-dependent, tone-dependent responses (Neely and Matot 1996 Cheng et al. 1996). At low baseline pulmonary vascular tone adenosine induces vasoconstriction via A3AR and the release of prostanoids, whereas at elevated pulmonary vascular tone it produces vasodilatation by acting on A2AR, without nitric oxide release or the activation of guanylate cyclase or KATp channels (Neely and Matot 1996 Cheng et al. 1996). 

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). 

I. The rate of conversion with digoxin is no better than placebo. Digoxin may restore sinus rhythm when AF is due to heart failure (73,74). In this setting, reversion is the result of improved hemodynamics and a reduction in left atrial pressure. 

More specific treatment to combat cardiotoxic effects is usually necessary in only a minority of instances in the series reported above (40), five patients (14%) had marked hypotension. Initial low left ventricular filling pressures were corrected within 3 hours by infusion of isotonic saline. Systemic hypotension persisted and was corrected by infusion of sympathomimetic amines. Routine insertion of a pulmonary artery catheter, with continuous monitoring of blood gases, pulmonary arterial pressure, left atrial wedge pressure, and cardiac output have been recommended (40). Volume expansion is suggested for low left atrial pressure,... 

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). 

Injection into the left ventricle or the proximal aorta is likely to produce more marked effects. Cardiac rate, stroke volume, and cardiac output increase. There is a rise in right and left atrial pressures and left ventricular end-diastolic pressure. The pulmonary arterial pressure is also increased. The blood volume expands and peripheral blood flow increases and then decreases as systemic resistance falls. The hematocrit falls and venous pressure gradually rises. As the systemic arterial pressure falls, the heart rate increases. These responses are largely due to the injection of strongly hypertonic solutions, which promote a rapid expansion of the plasma volume water shifts from the extravascular fluid spaces to the blood and moves out of the erythrocytes, which shrink and become crenated. Blood viscosity rises, but plasma viscosity does not increase significantly. The erythrocytes give up potassium to the plasma and this might contribute to the observed reduction in peripheral vascular resistance. 

A 16-year-old boy who took long-term verapamil after a Mustard operation for transposition of the great arteries developed severe congestive heart failure, which did not respond to diuretics. Systemic vascular resistance was increased by 75% and pulmonary vascular resistance by 150% the cardiac index was reduced from 3.0 to 1.8 1/minute/m. Ejection fraction and atrial pressure were unchanged and neurohormonal causes were excluded. The heart failure resolved after withdrawal of verapamil. 

The jugular venous pressure (J VP) is used as a measure of right atrial pressure. The JVP is measured in centimeters from the sternal angle and is best visualized with the patient s head rotated to the left. The JVP is described for its quality and character, effects of respiration, and patient position-induced changes. When reporting a JVP, both the measure and the patient position must be reported. The JVP can be reported as actual centimeters above the manubrium, or... 

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