Blood volume, effective arterial

Aldosterone acts on the distal tubule of the nephron to increase sodium reabsorption. The mechanism of action involves an increase in the number of sodium-permeable channels on the luminal surface of the distal tubule and an increase in the activity of the Na+-K+ ATPase pump on the basilar surface of the tubule. Sodium diffuses down its concentration gradient out of the lumen and into the tubular cells. The pump then actively removes the sodium from cells of the distal tubule and into the extracellular fluid so that it may diffuse into the surrounding capillaries and return to the circulation. Due to its osmotic effects, the retention of sodium is accompanied by the retention of water. In other words, wherever sodium goes, water follows. As a result, aldosterone is very important in regulation of blood volume and blood pressure. The retention of sodium and water expands the blood volume and, consequently, increases mean arterial pressure. 

Low-pressure receptors. The low-pressure receptors are located in the walls of the atria and the pulmonary arteries. Similar to baroreceptors, low-pressure receptors are also stretch receptors however, stimulation of these receptors is caused by changes in blood volume in these low-pressure areas. An overall increase in blood volume results in an increase in venous return an increase in the blood volume in the atria and the pulmonary arteries and stimulation of the low-pressure receptors. These receptors then elicit reflexes by way of the vasomotor center that parallel those of baroreceptors. Because an increase in blood volume will initially increase MAP, sympathetic discharge decreases and parasympathetic discharge increases so that MAP decreases toward its normal value. The simultaneous activity of baroreceptors and low-pressure receptors makes the total reflex system more effective in the control of MAP. 

T Renin — T angiotensin II —> T aldosterone -4 T Na+ reabsorption Net effects 4 urine output T blood volume T mean arterial pressure... 

Net effects 4 urine output 4 blood volume 4 mean arterial pressure... 

Spontaneous bacterial peritonitis (SBP) is a serious complication of cirrhotic ascites, arising most frequently in those with advanced liver disease. Its development leads to a further reduction in the effective arterial blood volume, and it has a mortality rate equivalent to that of a variceal bleed [202], Since hepatic blood flow and func-... 

FIGURE 78-1. Diagnostic algorithm for the evaluation of hyponatremia. (CHF, congestive heart failure EABV, effective arterial blood volume SIADH, syndrome of inappropriate antidiuretic hormone UNa, urine sodium concentration Uosm, urine osmolality.)... 

Despite their successful use for at least 20 years, the mechanisms by which they lower the blood pressure remain uncertain. Theories to explain the antihypertensive effectiveness of the diuretic agents have included a) alteration of sodium and water content on arterial smooth muscle, b) the induction of a decreased vascular response to catecholamines, c) a decrease in blood volume and total extracellular fluid volume, and d) a direct vasodilator action independent from the diuretic effect(12). 

Angiotensin 11 can raise blood pressure in different ways, including (1) vasoconstriction in both the arterial and venous limbs of the circulation (2) stimulation of aldosterone secretion, leading to increased renal reabsorption of NaCl and water, hence an increased blood volume (3) a central increase in sympathotonus and, peripherally, enhancement of the release and effects of norepinephrine. 

Sodium retention and hypo albumin aemi a are constant features. The former appears consequent on disturbed blood volume distribution, withslanch-nic dilatation and reduced effective central arterial blood volume leads to sodium retention. Hypoalbu-minaemia associated with reduced hepatic albumin synthesis, and raised portal pressure associated with obstruction to flow, as well as active sodium retention all predispose to ascites. Hypoalbuminaemia is associated with reduced hepatic synthesis. 

A common reason for diuretic use is for reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases that reduce blood delivery to the kidney. This reduction is sensed as insufficient effective arterial blood volume and leads to salt and water retention and edema formation. Judicious use of diuretics can mobilize this interstitial edema without significant reductions in plasma volume. However, excessive diuretic therapy may lead to further compromise of the effective arterial blood volume with reduction in perfusion of vital organs. Therefore, the use of diuretics to mobilize edema requires careful monitoring of the patient s hemodynamic status and an understanding of the pathophysiology of the underlying illness. 

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,... 

Ultimately, decompensation of the water and electrolyte balance is the result of (1.) splanchnic and peripheral arterial vasodilation, (2.) subsequent marked reduction in the effective arterial blood volume, (3.) increase in renin, aldosterone, vasopressin and noradrenaline, 4.) renal vasoconstriction with retention of sodium and water, and (5.) inadequate compensation of the plasma volume as a result of progressive hypalbuminaemia. 

Paracentesis should be combined with an i.v. solution of albumin (our own experience has shown that an i.v. solution of 20 — 40 ml plasma expander directly before i.v. albumin administration increases the oncotic pressure, so that albumin remains efficacious for a longer time in the blood circulation). Apparently, 3 mg terlipressin is as effective as i.v. albumin in preventing a decrease in effective arterial blood volume, (s. p. 309)... 

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. 

Patients at greatest risk are those dependent on angiotensin 11 to maintain Wood pressure and renal efferent arteriolar constriction. These include patients with hemodynamicaUy significant renal artery stenosis, particularly bilateral stenosis, and those with decreased effective arterial renal blood flow, particularly those with congestive heart failure, volume depletion from excess diuresis or gastrointestinal fluid loss, hepatic cirrhosis with ascites, and the nephrotic syndrome." ... 

Nonosmotic release of ADH occurs when the effective arterial blood volume (EABV) decreases by approximately 5% to 10%. The EABV is the vascular component of the ECF that is responsible for organ perfusion. A change in the EABV promotes an afferent response from baroreceptors in the chest and neck and activation of the renin-angiotensin system, leading to synthesis of angiotensin 11. Angiotensin 11 then stimulates both nonosmotic release of ADH and thirst. The volume stimulus overrides osmotic inhibition of ADH release, and conservation of water fosters restoration of blood pressure and EABV at the expense of hypo-osmolality. 

Due to its lack of effect on venous compliance, the drug has little or no effect on circulating blood volume. It does, however, have a potent effect on arterial smooth muscle. Thus, it increases systolic blood pressure to a greater degree than diastolic blood pressure. 

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