Mean arterial blood pressure

Mean arterial blood pressure A calculated measure of arterial blood pressure mean arterial blood pressure = (2 x diastolic blood pressure + systolic blood pressure)/3. 

Systemic vascular resistance The portion of resistance to blood flow leaving the heart that is determined by vascular tone (constriction or relaxation). Systemic vascular resistance = mean arterial blood pressure/cardiac output. 

Other factors regulating ADH secretion include blood volume and blood pressure. A decrease in blood volume of 10% or more causes an increase in ADH secretion sufficient to cause vasoconstriction as well as antidiuresis. A decrease in mean arterial blood pressure of 5% or more also causes an increase in ADH secretion. The resulting water conservation and vasoconstriction help increase... 

Cardiac index and blood pressure must be sufficient to ensure adequate organ perfusion, as assessed by alert mental status, creatinine clearance sufficient to prevent metabolic azotemic complications, hepatic function adequate to maintain synthetic and excretory functions, a stable heart rate and rhythm, absence of ongoing myocardial ischemia or infarction, skeletal muscle and skin blood flow sufficient to prevent ischemic injury, and normal arterial pH (7.34 to 7.47) with a normal serum lactate concentration. These goals are most often achieved with a cardiac index greater than 2.2 L/min/m2, a mean arterial blood pressure greater than 60 mm Hg, and PAOP of 25 mm Hg or greater. 

An effect on blood pressure was shown in the study by Clark and Litchfield (1969) in which subcutaneous injections of PGDN to anesthetized rats at 5, 10, 20, 40, 80, or 160 mg/kg resulted in a dose-related fall in mean arterial blood pressure (measured in the cannulized femoral artery) within 30 min with recovery over the next 12 h. The maximum drop in blood pressure correlated with the maximum concentration of PGDN in the blood. However, a drop in blood pressure did not occur in human volunteers who inhaled 0.5 ppm PGDN for 7.3 h. Rather, a mean elevation of diastolic blood pressure of 12 mm Hg was associated with severe and throbbing headaches (Stewart et al. 1974). A drop in blood pressure and decreasing stroke volume can result in brain ischemia, causing the dizziness and weakness reported by one subject after exposure at 0.5 ppm for 6 h in the Stewart et al. (1974) study as well as in occupationally exposed workers (Horvath et al. 1981). 

In another study, decreases in heart rate and mean arterial blood pressure occurred in dogs following a single exposure to 0.5 mL/kg kerosene by aspiration, although these values returned to the control values within 60 minutes (Goodwin et al. 1988). The actual dose entering the lungs by aspiration cannot be determined. This study is limited, however, because only one dose was tested. 

Any sudden alteration in the mean arterial blood pressure tends to produce compensatory reflex changes in heart rate, contractility, and vascular tone, which will oppose the initial pressure change and restore the homeostatic balance. The primary sensory mechanisms that detect changes in the mean arterial blood pressure are stretch receptors (baroreceptors) in the carotid sinus and aortic arch. 

The injection of a vasoconstrictor, which causes an increase in mean arterial blood pressure, results in activation of the baroreceptors and increased neural input to the cardiovascular centers in the medulla oblongata. The reflex compensation for the drug-induced hypertension includes an increase in parasympathetic nerve activity and a decrease in sympathetic nerve activity. This combined alteration in neural firing reduces cardiac rate and force and the tone of vascular smooth muscle. As a consequence of the altered neural control of both the heart and the blood vessels, the rise in blood pressure induced by the drug is opposed and blunted. 

Injection of a drug that causes a fall in the mean arterial blood pressure triggers diametrically opposite reflex changes. There is decreased impulse traffic from the cardiac inhibitory center, stimulation of the cardiac accelerator center, and augmented vasomotor center activity. These changes in cardiac and vasomotor center activity accelerate the heart and increase sympathetic transmission to the vasculature thus, the drug-induced fall in blood pressure is opposed and blunted. 

An increase in sympathetic tone constricts blood vessels in most vascular beds and therefore causes a net increase in total peripheral resistance. Increased sympathetic tone increases neural release of norepinephrine and its interaction both with 3-adrenoceptors on cardiac cells and with a-adrenoceptors on vascular smooth muscle cells. As a consequence, the systolic and diastolic blood pressures are elevated. It follows that the mean arterial blood pressure must also be increased. 

Dofetilide does not significantly alter the mean arterial blood pressure, cardiac output, cardiac index, stroke volume index, or systemic vascular resistance. There is a slight increase in the delta pressure/delta time (dP/dt) of ventricular myocytes. 

Anesthesia induction with propofol causes a significant reduction in blood pressure that is proportional to the severity of cardiovascular disease or the volume status of the patient, or both. However, even in healthy patients a significant reduction in systolic and mean arterial blood pressure occurs. The reduction in pressure appears to be associated with vasodilation and myocardial depression. Although propofol decreases systemic vascular resistance, reflex tachycardia is not observed. This is in contrast to the actions of thiopental. The heart rate stabilization produced by propofol relative to other agents is likely the result of either resetting or inhibiting the baroreflex, thus reducing the tachy-cardic response to hypotension. 

Hypotensive activity. Tincture of the gland, administered intravenously to rabbits, was active " """. Water extract of the dried gum resin, administered intravenously to dogs at variable doses, was active " """. Gum extract, administered to anaesthetized rats at doses of 0.3-2.2 mg/100 g body weight, significantly reduced the mean arterial blood pressure " """. 

Chapter 12 contains additional discussion of vasodilators. All the vasodilators that are useful in hypertension relax smooth muscle of arterioles, thereby decreasing systemic vascular resistance. Sodium nitroprusside and the nitrates also relax veins. Decreased arterial resistance and decreased mean arterial blood pressure elicit compensatory responses, mediated by baroreceptors and the sympathetic nervous system (Figure 11-4), as well as renin, angiotensin, and aldosterone. Because sympathetic reflexes are intact, vasodilator therapy does not cause orthostatic hypotension or sexual dysfunction. 

Diazoxide is an effective and relatively long-acting parenterally administered arteriolar dilator that is occasionally used to treat hypertensive emergencies. Injection of diazoxide results in a rapid fall in systemic vascular resistance and mean arterial blood pressure associated with substantial tachycardia and increase in cardiac output. Studies of its mechanism suggest that it prevents vascular smooth muscle contraction by opening potassium channels and stabilizing the membrane potential at the resting level. 

For example, because an adequate dose of hydralazine causes a significant decrease in peripheral vascular resistance, there will initially be a drop in mean arterial blood pressure, evoking a strong response in the form of compensatory tachycardia and salt and water retention (Figure 11-5). The result is an increase in cardiac output that is capable of almost completely reversing the effect of hydralazine. The addition of a B-blocker prevents the tachycardia addition of a diuretic (eg, hydrochlorothiazide) prevents the salt and water retention. In effect, all three drugs increase the sensitivity of the cardiovascular system to each other s actions. 

MAP, mean arterial blood pressure i.v., intravenous administration... 

Discrepancies between results from the preliminary studies and the larger, multicenter trials remain to be elucidated. Significant intercenter variance in patient management (fluids, mean arterial blood pressure, ICP, and CPP) and treatment may have adversely affected the results of one of these trials (The National Acute Brain Injury Study Hypothermia) (61). Despite the overall negative findings, however, it is quite possible that certain subgroups of patients may benefit from treatment with mild hypothermia. 

A significant reduction of the ICP was seen, which was similar to the results of Marion and Shiozaki, who used hypothermic therapy in traumatic brain injuries (37,38). With an unaffected mean arterial blood pressure (MABP) and increased cerebral perfusion pressure (CPP), hypothermic therapy appeared to benefit stroke patients, as uncontrolled intracranial hypertension is the main cause of death in the first week after stroke. However, rewarming the patients consistently led to a secondary rise of ICP, which required additional ICP therapy with mannitol. In some cases it even exaggerated the initial ICP levels (Fig. 3). 

Cardiopulmonary parameters and rectal body temperature are determined while the rabbit is in the sling and also at 15 min intervals following induction of anesthesia with the rabbit in lateral recumbency. Heart rate, mean arterial blood pressure, respiratory rate and respiratory pattern are calculated from tracings from the physiological recorder. Arterial blood pH, partial pressure of oxygen (PaQz), and partial pressure of... 

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