Blood volume hypotension

The principal mechanism of the hypotensive effect of diuretics (qv) is salt and fluid depletion, leading to reduction in blood volume (200,240). Acute effects lead to a decrease in cardiac output and an increase in total peripheral resistance. However, during chronic adrninistration, cardiac output and blood volume return toward normal and total peripheral resistance decreases to below pretreatment values. As a result, the blood pressure falls. The usual reduction in blood volume is about 5%. A certain degree of sustained blood volume contraction has to occur before the blood pressure decreases. The usual decrease in blood pressure achieved using a diuretic is about 20/10 mm Hg (2.7/1.3 kPa) (systoHc/diastoHc pressures. 

The principal function of the circulatory system is to supply oxygen and vital metabolic substrates to cells throughout the body, as well as removal of metabolic waste products. Circulatory shock is a life-threatening condition whereby this principal function is compromised. When circulatory shock is caused by a severe loss of blood volume or body water it is called hypovolemic shock, the focus of this chapter. Regardless of etiology, the most distinctive manifestations of hypovolemic shock are arterial hypotension and metabolic acidosis. Metabolic acidosis is a consequence of an accumulation of lactic acid resulting from tissue hypoxia and anaerobic... 

Reabsorption of water is a fundamental function of the kidney because loss of fluid volume and reduction in blood pressure (hypotension) would have devastating consequences on all other tissues, possibly leading to severe metabolic disruption or even death. Blood pressure is monitored by the kidney and regulated by secretion of a proteolytic enzyme called renin, which initiates a cascade involving angiotensin and aldosterone to restore blood volume. 

Counter-regulation in acute hypotension due to vasodilators (B). Increased sympathetic drive raises heart rate (reflex tachycardia) and cardiac output and thus helps to elevate blood pressure. Patients experience palpitations. Activation of the renin-angioten-sin-aidosterone (RAA) system serves to increase blood volume, hence cardiac output. Fluid retention leads to an increase in body weight and, possibly, edemas. These counter-regulatory processes are susceptible to pharmacological inhibition ( 3-blockers, ACE inhibitors, ATI-antagonists, diuretics). 

Massive use of diuretics entails a hazard of adverse effects (A) (1) the decrease in blood volume can lead to hypotension and collapse (2) blood viscosity rises due to the increase in eryth-ro- and thrombocyte concentration, bringing an increased risk of intravascular coagulation or thrombosis. 

Secondary hypotension is a sign of an underlying disease that should be treated first. If stroke volume is too low, as in heart failure, a cardiac glycoside can be given to increase myocardial contractility and stroke volume. When stroke volume is decreased due to insufficient blood volume, plasma substitutes will be helpful in treating blood loss, whereas aldosterone deficiency requires administration of a mineralocor-ticoid (e.g., fludrocortisone). The latter is the drug of choice for orthostatic hypotension due to autonomic failure. A parasympatholytic (or electrical pacemaker) can restore cardiac rate in bradycardia. 

Hypotensive effect Narcotic analgesics may cause severe hypotension in individuals whose ability to maintain blood pressure has been compromised by a depleted blood volume, or coadministration of drugs such as phenothiazines or general anesthetics. Renal toxicity Avinza doses over 1,600 mg/day contain a quantity of fumaric acid that has not been demonstrated to be safe, which may result in serious renal toxicity. 

Frequent serum electrolyte analysis is essential during therapy with the high-ceiling diuretics. Overdose may result in a rapid reduction of blood volume, dizziness, headache, orthostatic hypotension, hyponatremia, and hypokalemia. Nausea, vomiting, diarrhea, and loss of appetite are especially common with ethacrynic acid. 

A hypotensive patient suspected of having internal bleeding is given a dose lower than the usual amount of an intravenous anesthetic. An acceptable level of anesthesia occurs. How is it possible to achieve anesthesia in this patient with a dose of anesthetic that may be inadequate in a normoten-sive patient with adequate blood volume ... 

Abnormalities of fluid and electolyte imbalance are the most common forms of clinical toxicity, overdose may result in rapid reduction of blood volume, dizziness, orthostatic hypotension, headache, hypokalemia. 

Patients with decreased intravascular blood volume should have hypotension, but many nephrotic patients (apart from nephrotics with minimal change disease) are hypertensive (K28). Adults with nephrotic syndrome were repeatedly demonstrated to have normal or increased (not decreased) plasma volume (G4). 

Contrast-induced nephropathy (CIN) is the most serious complication associated with the use of CM and can negatively affect long-term patient morbidity and mortality (4-10). CIN is usually defined as an acute decline in renal function characterized by an absolute rise of 0.5mg/dl (44jumol/l) in serum creatinine (SCr) or a 25% increase from baseline, occurring after the systemic administration of CM in the absence of other risk factors such as atheroembolic disease, hypotension and lew blood volume, surgery, or nephrotoxins (1,2,6,7,10-13). 

The decrease in blood volume can lead to hypotension and collapse. 

In severe anaphylaxis, hypotension is due to vasodilation and loss of circulating volume through leaky capillaries. Colloid is more effective at restoring blood volume than crystalloid and 1-21 of plasma substitute should be infused rapidly. Oxygen and artificial ventilation may be necessary. Advice on the management of anaphylactic shock may be altered from time to time check the UK Resuscitation Council website (www.resus.org.uk) for current information. 

Morphine and disease. When intense peripheral vasoconstriction accompanies, e.g. trauma, morphine administered s.c. or i.m. may appear to be ineffective because it fails quickly to enter the systemic circulation repeating the dose before the first has been absorbed may lead to poisoning when the vasoconstriction passes off. In such circumstances morphine should be given slowly i.v. (2.5 mg every 2-3 min). If the blood volume is low, morphine may cause serious hypotension. 

Since blood pressure can be considered a product of volume and vasoconstriction, the logical initial treatment of orthostatic hypotension is to expand blood volume using a sodium-retaining adrenocortical steroid (fludrocortisone ) or desmopressin (p. 716) — plus elastic support stocking to reduce venous pooling of blood when erect. 

Smaller vessels may be obstructed with cholesterol emboli, vascular lesions, or platelet plugs, all of which will present as isolated decreased perfusion of the glomeruli. The serum creatinine frequently is increased since the lesions are usually diffuse. However, the urinalysis most commonly will be normal since the kidney itself is not ischemic and the glomeruli are not involved. The urinary indices suggest prerenal azotemia (i.e., a low urine sodium concentration and a low fractional excretion of sodium) in the absence of systemic hypotension or a decrease in effective blood volume. The urine volume may or may not be diminished. However, the onset of oliguria sec-... 

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