Renal perfusion

Phenylephrine 10-1000 pg/minute Seconds Bradycardia, coronary vasoconstriction, decreased renal perfusion, metabolic acidosis Alpha-1, increased cardiac output (CO), decreased systemic vascular resistance (SVR)... 

Epinephrine 1-12 pg/minute Seconds Increased myocardial demand, flushing, arrhythmia, decreased renal perfusion Alpha-1, beta-1, beta-2, increased CO, variable SVR... 

Since the discovery of renin over 100 years ago, the RAAS has been extensively studied as a prime target or site of action for many effective antihypertensives.15 Renin is produced and stored in the juxtaglomerular cells of the kidney, and its release is stimulated by impaired renal perfusion, salt depletion, and pr adrenergic stimulation. The release of renin is the rate-limiting... 

Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the central nervous system (CNS) is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. This results from several factors, including loss of appetite, malabsorption due to gastrointestinal edema, elevated metabolic rate, and elevated levels of proinflammatory cytokines. 

Calculated fractional excreted sodium (FeNa) less than 1% in patients with compromised baseline renal function, and less than 0.2% in patients with normal baseline renal function indicates dehydration and reduced renal perfusion. 

As previously discussed, increased portal pressure triggers the release of nitric oxide to directly vasodilate the splanchnic arterial bed and decrease portal pressure. Unfortunately, nitric oxide also dilates the systemic arterial system, causing a decrease in blood pressure and a decrease in renal perfusion by lowering the effective intravascular volume. The kidney reacts by activating the renin-angiotensin-aldosterone system, which increases plasma renin activity, aldosterone production, and sodium retention. This increase in intravascular volume furthers the imbalance of intravascular oncotic pressure, allowing even more fluid to escape to the extravascular spaces. 

The zona glomerulosa is responsible for the production of the mineralocorticoids aldosterone, deoxycorticosterone, and 18-hydroxy-deoxycorticosterone. Aldosterone promotes renal sodium retention and excretion of potassium. Its synthesis and release are regulated by renin in response to decreased vascular volume and renal perfusion. Adrenal aldosterone production is regulated by the renin-angiotensin-aldosterone system. 

Dopamine is a a- and P-adrenergic agent with dopaminergic activity Low doses of dopamine (1 to 5 mcg/kg per minute) maintain renal perfusion, higher doses (greater than 5 mcg/kg per minute) exhibit a- and P-adrenergic activity and are frequently utilized to support blood pressure and to improve cardiac function. Low doses of dopamine should not be used for renal protection as part of the treatment of severe sepsis.24,27-28... 

Normal saline or dopamine at renal perfusion dose of 2 mcg/kg per minute for oliguria monitor for electrolyte abnormalities and replace as indicated. 

Renal function can be grossly assessed by hourly measurements of urine output, but estimation of creatinine clearance based on isolated serum creatinine values in critically ill patients may yield erroneous results. Decreased renal perfusion and aldosterone release result in sodium retention and, thus, low urinary sodium (<30 mEq/L). 

Risk factors for ARF include advanced age, acute infection, preexisting chronic respiratory or cardiovascular disease, dehydration, and chronic kidney disease (CKD). Decreased renal perfusion secondary to abdominal or coronary bypass surgery, acute blood loss in trauma, and uric acid nephropathy also increase risk. 

Nephrotoxin administration (e.g., radiocontrast dye) should be avoided whenever possible. When patients require contrast dye and are at risk of contrast dye-induced nephropathy, renal perfusion should be maximized through strategies such as assuring adequate hydration with normal saline or sodium bicarbonate solutions and administration of oral acetylcysteine 600 mg every 12 hours for four doses. Strict glycemic control with insulin in diabetics has also reduced the development of ARF. 

The kidney s ability to adjust to abrupt changes in sodium intake is diminished in patients with ESRD. Sodium restriction beyond a no-added-salt diet is not recommended unless hypertension or edema is present. A negative sodium balance can decrease renal perfusion and cause a further decline in GFR. 

The enumeration of these effects of prostaglandins makes it understandable that the inhibition of the cycloxigenases will result in antiinflammatory, analgesic and antipyretic effects. Another important function of PGE2 is the vasodilatation it can induce in the renal circulation. Locally produced PGE2 increases the renal perfusion. 

Hepato-renal syndrome rapid progressive (type I) with rising serum creatinine levels, or non-progressive and less severe (type II) impairment of renal function, often consequent on bacterial peritonitis, with persistent ascites responds to vasoconstrictor treatment, typically with terlipressin through constriction of splanchnic vessels and improved renal perfusion. Withdrawal of treatment does not seem to lead inevitably to recurrence. Haemodialysis may also stabilise patients. 

In most forms of shock, intense vasoconstriction, mediated by reflex sympathetic nervous system activation, is present. Indeed, efforts aimed at reducing rather than increasing peripheral resistance may be more fruitful to improve cerebral, coronary, and renal perfusion. A decision to use vasoconstrictors or vasodilators is best made on the basis of information about the underlying cause, which may require invasive monitoring. 

Liver disease is often associated with edema and ascites in conjunction with elevated portal hydrostatic pressures and reduced plasma oncotic pressures. Mechanisms for retention of Na+ by the kidney in this setting include diminished renal perfusion (from systemic vascular alterations), diminished plasma volume (due to ascites formation), and diminished oncotic pressure (hypoalbuminemia). In addition, there may be primary Na+ retention due to elevated plasma aldosterone levels. 

Other current applications of Ir-191m angiography include diagnosis of congenital circulatory defects (i.e., tetrology of Fallot) and vena caval obstruction. Potential applications that remain to be explored include measurement of ventricular volume, renal perfusion, cerebral blood flow, and evaluation of blood flow to tumors and organs by selective arterial infusion. 

Dopamine (Intropin) [Vasopressor/Adrenergic] Uses Shortterm use in cardiac decompensation secondary to X contractility when no hypovolemia is present T organ perfusion (at low dose) Action Renal dose 2-5 mcg/kg/min Inotropic dose 5-10 mcg/kg/min Pressor dose >10 mcg/kg/min Dose Adults Peds. 5-20 mcg/kg/min by cont inf, start at 5 and T by 5 mcg/kg/min to 20 mcg/kg/min max to effect (mix 400 mg in 250 mL D5W to make 1600 mcg/mL) (see Table 1-3) Caution [C, ] Contra Pheochromocytoma (adrenal gland tumor), VF, sulfite sensitivity Disp Inj 40, 80, 160 mg/mL, premixed 0.8, 1.6, 3.2 mg/mL SE Tach, vasoconstriction, X BP, HA, N/V, dyspnea Notes >10 mcg/kg/min 1 renal perfusion Interactions T Effects W/ a-blockers, diuretics, ergot alkaloids, MAOIs, BBs, anesthetics, phenytoin 1 effects W/ guanetliidine EMS Correct hypovolemia before use use microdrip set or inf pump check soln- discolored... 

Renal damage is the most significant toxic reaction. Renal impairment occurs in nearly all patients treated with clinically significant doses of amphotericin. The degree of azotemia is variable and often stabilizes during therapy, but can be serious enough to necessitate dialysis. A reversible component is associated with decreased renal perfusion and represents a form of prerenal renal failure. An irreversible component results from renal tubular injury and subsequent dysfunction. 

Of the prophylactic agents, hydration is unanimously endorsed, Its theorized mechanism of action is the enhancement of renal perfusion and, conversely, the minimization of ischemia. While it has become the standard of care based on a multitude of early trials (85,86), no large, prospective studies have been conducted. The optimal method of hydration has yet to be decided, with one study showing benefit of normal saline (0.9% NS) over half NS (0.45%) (87), and another study suggesting that 154 mEq/L of sodium bicarbonate is superior to NS alone, Of note, the total volume in the latter study was less than that was used in other trials, making it difficult to compare (88). Thus, currently, NS should be used unless the patient is highly intolerant to volume administration, In such a case, 154 mEq/L of sodium bicarbonate can be administered over a shorter time period,... 

Correct answer = D. It is important to increase the cardiac output to improve oxygen delivery and thus minimize anaerobic metabolism and improve CNS and renal perfusion. Since this patient apparently does not have a heart condition, such as congestive heart failure, she could benefit from fluid therapy. An inotropic agent, such as dopamine, would lead to an increased cardiac output and dilation of the renal vasculature. [Note At high doses, however, it may constrict the renal beds due to interaction on a receptors.] Antibiotic administration is also important but will not improve the patient s hemodynamics. 

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