Arterial pressure

Midazolam and diazepam decrease arterial pressure without a change ia heart rate. Like thiopeatoae, midazolam is a respiratory depressant. Advantages of midazolam are its amnestic effect, coupled with less postoperative depression (102). A reversal agent for the benzodiazepiaes has also become available. Flumazenil [78755-81-4] C25H24FN2O2, (5) displaces the beazodiazepiaes from their receptor but has Httie demoastrable activity of its owa (103,104). 

Moreover, digitahs has indirect effects on the circulation, which in normal hearts results in a small increase in arterial pressure, peripheral resistance, and cardiac output (114). The effects of digitahs on the circulation of an individual experiencing congestive heart failure are much more dramatic, however. The increased cardiac output, for example, increases renal blood flow which can reheve in part the edema of CHF associated with salt and water retention (114). 

Diuretics have become the cornerstone of all treatment regimens of CHF (III—II3). They can reheve symptoms of pulmonary and peripheral edema. In mild CHF, the thia2ide-type diuretics are adequate unless the GFR falls below 30 ml,/min, as compared to 120 ml,/min in normal subjects. Diuretics improve left ventricular function in CHF due in part to decrease of preload. Indapamide has been shown to cause reduction of pulmonary arterial pressure and pulmonary wedge pressure. 

Mean arterial pressure and cardiac output, an expression of the amount of blood that the heart pumps each minute, are the key Indicators of the normal functioning of the cardiovascular system. Mean arterial pressure is strictly controlled, but by changing the cardiac output, a person can adapt, e.g., to increased oxygen requirement due to increased workload. Blood flow in vital organs may vary for many reasons, but is usually due to decreased cardiac output. However, there can be very dramatic changes in blood pressure, e.g., blood pressure plummets during an anaphylactic allergic reaction. Also cytotoxic chemicals, such as heavy metals, may decrease the blood pressure. 

According to Ra rmond-Hamet, evodiamine and rutaecarpine on injection induce increased arterial pressure. 

Primary pulmonary hypertension is a disease of unclear etiology that is characterized by abnormally high mean pulmonary arterial pressures, in the absence of a demonstrable cause. A wide variety of pulmonary and cardiac diseases can lead to secondary pulmonary hypertension. 

Vasodilators are a group of dtugs, which relax the smooth muscle cells of the blood vessels and lead to an increased local tissue blood flow, a reduced arterial pressure and a reduced central venous pressure. Vasodilators reduce the cardiac pre-load as well as after-load and thereby reduce cardiac work. They are used in a variety of conditions including hypertension, cardiac failure and treatment/prevention of angina pectoris. Major groups are Ca2+-channel blockers (e.g. dihydropyridines), NO-donators (e.g. organic nitrates), K+-channel openers (minoxidil), phosphodiesterase inhibitors (e.g. sildenafil), Rho-kinase inhibitors (e.g. Y27632) or substances with unknown mechanism of action (e.g. hydralazine). Inhibitors of the... 

In a third study the time course of the effects of intravenous and intracoronary injections of cysteinyl leukotrienes on metabolic parameters and systemic and coronary hemodynamics was examined in patients with normal coronary arteries [32]. LTD4 (3 nmol, injected into the left coronary artery) induced an early (20 s), transient fall in mean arterial pressure paralleled by rises in heart rate and plasma levels of epinephrine and norepinephrine, all of which had returned to baseline by 10 min. CVR rose at 10 and 15 min and myocardial oxygen extraction at 15 min. Thus, small doses of cysteinyl leukotrienes may induce both an early, transient fall in mean arterial pressure, with secondary sympathoadrenergic activation, and a later increase in small coronary arteriolar resistance. 

Cysteinyl leukotrienes can induce an early, transient fall in arterial pressure associated with sympathoadrenergic activation, plus a late rise in small coronary arteriolar resistance [32]. Using specific antagonists of CysFTi and CysFT2 [63] it will be possible to assess the each receptor s contribution to the cardiovascular effects of these vasoactive mediators. 

If PCWP between 15 and 18 mmHg and symptomatic o If adequate mean arterial pressure (MAP)... 

Reduce mean arterial pressure (MAP) by 20-25% or to a diastolic blood pressure of 110 mmHg in hypertensive emergencies... 

Aim for a 10-15% reduction in mean arterial pressure (MAP) ° Nitroprusside—0.25-0.5 mcg/kg/min continuous IV infusion increase in increments of 0.25-0.5 mcg/kg/min until desired hemodynamic effect. Usual doses up to 2-3 mcg/kg/min. High-alert medication—read package insert before use... 

Systolic blood pressure (SBP) <90 mmHg or a mean arterial pressure (MAP) <60 mmHg for >1 h or hypotension requiring vasopressor pharmacotherapy... 

FIGURE 10-4. Treatment algorithm for the management of moderate to severe hypovolemia. BP, blood pressure CVP, central venous pressure ECG, electrocardiogram MAP, mean arterial pressure PA, pulmonary artery PAOP, pulmonary artery occlusion pressure PRBCs, packed red blood cells SBP, systolic blood pressure. 

Arterial blood gases for evaluating partial arterial pressure of carbon dioxide (Pco2) should be considered for patients in severe distress, suspected hypoventilation, or when PEF or FEYT, is less than or equal to 30% after initial treatment. 

FIGURE 11-3. Emergency department and hospital-based management of asthma exacerbation. FEV-, forced expiratory volume in 1 second Pco2, partial arterial pressure of carbon dioxide PEF, peak expiratory flow 02, oxygen. (From Kelly HW, Sorkness CA. Asthma. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 517, with permission.)... 

Pco2 partial arterial pressure of carbon dioxide... 

Increased intrahepatic resistance to portal flow increases pressure on the entire splanchnic bed an enlarged spleen (splenomegaly) is a common finding in cirrhotic patient and can result in thrombocytopenia due to splenic sequestration of the platelets. Portal hypertension mediates systemic and splanchnic arterial vasodilation through production of nitric oxide and other vasodilators in an attempt to counteract the increased pressure gradient. Nitric oxide causes a fall in systemic arterial pressure unfortunately, this activates both the renin-angiotensin-aldosterone and sympathetic nervous systems and... 

Vasodilation and decreased arterial pressure are also detected centrally. The sympathetic nervous system is activated to increase blood pressure, which in turn increases portal pressure. Unchecked, these combined effects enable the cycle of portal pressure and ascites to continue, setting up a self-perpetuating loop of ascites formation. 

Systemic blood pressure correlates with glomerular pressure and elevations in both systemic blood pressure and glomerular pressure contribute to glomerular damage. The rate of GFR decline is related to elevated systolic blood pressure and mean arterial pressure. The decline in GFR is estimated to be 14 mL/minute per year with a systolic blood pressure of 180 mm Hg. Conversely, the decline in GFR decreases to 2 mL/minute per year with a systolic blood pressure of 135 mm Hg.11... 

---