Septic shock dopamine

More potent than dopamine and may be more effective in managing hypotension in septic shock... 

Norepinephrine is a potent a-adrenergic agent with less pronounced P-adrenergic activity. Doses of 0.01 to 3 mcg/kg per minute can reliably increase blood pressure with small changes in heart rate or cardiac index. Norepinephrine is a more potent agent than dopamine in refractory septic shock.24,27-28... 

Vasopressin causes vasoconstrictive effects that, unlike adrenergic receptor agonists, are preserved during hypoxia and severe acidosis. It also causes vasodilation in the pulmonary, coronary, and selected renal vascular beds that may reduce pulmonary artery pressure and preserve cardiac and renal function. However, based on available evidence, vasopressin is not recommended as a replacement for norepinephrine or dopamine in patients with septic shock but may be considered in patients who are refractory to catecholamine vasopressors despite adequate fluid resuscitation. If used, the dose should not exceed 0.01 to 0.04 units/min. 

A medication order for a nine-month-old child weighing 8 kg includes dopamine in a dose of 5 mcg/kg/min. The drug available is dopamine 400 mg/5 mL. The physician ordered 70 mg of dopamine in 200 mL of D5W to be administered at 6.75 mL per hour to this child who is in septic shock. Check for the accuracy of the dilution order. 

Dopamine is used in the treatment of shock owing to inadequate cardiac output (cardiogenic shock), which may be due to myocardial infarction or congestive heart failure. It is also used in the treatment of septic shock, since renal circulation is frequently compromised in this condition. An advantage of using dopamine in the treatment of shock is that its inotropic action increases cardiac output while dilating renal blood vessels and thereby increasing renal blood flow. 

Prompt intensive treatment with corticosteroids may be lifesaving when an excessive inflammatory reaction has resulted in septic shock. A massive infusion of corticosteroids can restore cardiac output and reverse hypotension by sensitizing the response of adrenoceptors in the heart and blood vessels to the stimulating action of catecholamines. This protective role of steroids may be due to a direct effect on vascular smooth muscle. The combination of glucocorticoids and dopamine therapy preserves renal blood flow during shock. 

Dobutamine is widely used to increase myocardial contractility, cardiac output, and stroke volume in the peri-operative period. It is less likely to increase heart rate than dopamine. There is evidence that dobutamine can increase both myocardial contractility and coronary blood flow. This makes it particularly suitable for use in patients with acute myocardial infarction. Dobutamine is also suitable for treating septic shock associated with increased filling pressures and impaired ventricular function. Owing to the competing a and 3 activity there is usually little change in mean arterial pressure. 

Oj effects noradrenaline (with slight P effect on heart) is selectively released physiologically where it is wanted as therapeutic agents for hypotensive states (excepting septic shock) dopamine and dobutamine are preferred (for their cardiac inotropic effect). Also having predominantly effects are imidazolines (xylometazoline, oxymeta-... 

Hannemann, L. Reinhart, K. The effects of low-dose dopamine on splanchnic blood flow and oxygen uptake in patients with septic shock. Intensive Care Med. 1997, 23, 11. 

Arger et al 1999) however, the coadministration of dopamine opposes this effect and increases renal blood flow (Schaer et al 1985). Coadministration of norepinephrine (noradrenaline) and dobuta-mine to foals with septic shock increased urine production and blood pressure (Corley et al 2000). Norepinephrine (noradrenaline) should be reserved for horses with sepsis and used in conjunction with inotropes and monitoring of urine output. The recommended i.v. dose rates are shown in Table 12.3. 

Dopamine often is recommended as the initial catecholamine in sepsis because it increases blood pressure by increasing myocardial contractility and vasoconstriction. Dopamine has been described to have dose-related receptor activity at DAj-, DA2-, fi -, and i-receptors. Unfortunately, this dose-response relationship has not been confirmed in critically ill patients. In patients with septic shock, there is a great overlap of hemodynamic effects even at doses as low as 3 mcg/kg per minute. Tachydysrhythmias are common owing to the release of endogenous norepinephrine by dopamine entering the sympathetic nerve terminal. Dopamine may increase the PAOP through pulmonary vasoconstriction. This drug also may depress ventilation and worsen hypoxemia in patients dependent on the hypoxic ventilatory drive. 

Dopamine is frequently the initial vasopressor used in septic shock. Doses of 5 to 10 mcg/kg per minute are initiated to improve MAP. Most studies in patients with septic shock have shown that at these doses dopamine increases Cl by improving contractility and heart rate, resulting primarily from its effects. It increases arterial pressure and SVR as a result of both the increased cardiac output and, at higher doses (>10 mcg/kg per minute), as a result of the i effects. 

The clinical utility of dopamine as a vasopressor in the setting of septic shock is limited because large doses frequently are necessary to maintain cardiac output and blood pressure. At doses exceeding 20 mcg/kg per minute, there is limited further improvement in cardiac performance and regional hemodynamics. Its clinical use frequently is hampered by tachycardia and tachydysrhythmias, which may lead to myocardial ischemia. Although tachydysrhythmias theoretically should not be expected to occur until 5 to 10 mcg/kg per minute of dopamine, these fii effects are observed with doses as low as 3 mcg/kg per minute. They seem to be more prevalent in patients... 

Although splanchnic blood flow and DO2 may increase with dopamine, there is no preferential increase in the splanchnic perfusion as a fraction of cardiac output and systemic increases in D02. One study found an inverse relationship between fractional splanchnic flow at baseline and the change in fractional splanchnic blood flow such that dopamine was effective in increasing the fractional splanchnic blood flow in those in whom it was normal but worsened it in those with high baseline values, such as occurs with redistribution of regional blood flow in septic shock. Clinically, it is difficult to distinguish prospectively either subset of patients. 

Furthermore, tolerance to the vasodilatory effects of dopamine after 24 to 48 hours is evident in nonohguric patients with sepsis syndrome and has been reported in others. The lack of response to dopamine in septic shock patients on vasopressors and the tolerance that develops in responders to low-dose dopamine may be explained in part by time- and disease-dependent desensitization of the dopamine receptors this may not occur in those with sepsis syndrome or normal volunteers. Furthermore, differences in the extent of preexisting vasodilation and the pathophysiology of renal dysfunction in oliguric and septic shock patients also may contribute to the inconsistent responses seen to the administration of low doses of dopamine. 

There are three clinical trials using phenylephrine in septic shock evaluating 38 patients. Phenylephrine (0.5 to 9 mcg/kg per minute), when used alone or in combination with dobutamine or low doses of dopamine, improves blood pressure and myocardial performance in fluid-resuscitated septic patients. Incremental doses of phenylephrine over 3 hours result in linear dose-related increases in MAP, SVR, heart rate, and stroke index when administered as a single agent in stable, nonhypotensive but hyperdynamic, volume-resuscitated... 

De Backer D, Creteur J, Silva E, Vincent JL. Effects of dopamine, norepinephrine, and epinephrine on the splanchnic circulation in septic shock Which is best Crit Care Med 2003 31 1659-1667. 

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