Systemic arterial pressures

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... 

Nitroprusside is effective in the short-term management of severe HF in a variety of settings (e.g., acute MI, valvular regurgitation, after coronary bypass surgery, decompensated HF). Generally, it will not worsen, and may improve, the balance between myocardial oxygen demand and supply. However, an excessive decrease in systemic arterial pressure can decrease coronary perfusion and worsen ischemia. 

Figure 1. Principal Nervous and Humoral Pathways Involved in Maintenance of Systemic Arterial Pressure...

Figure 2. Possible Contributions to Maintenance of Systemic Arterial Pressure during Neurogenic Hypertension and Its Subsequent "Cure by Sympathectomy or Adrenergic Blockade A. Normal...

Cerebral blood flow depends on cerebral perfusion pressure and cerebrovascular resistance. The perfusion pressure is the difference between systemic arterial pressure at the base of the brain when in the recumbent position and the venous pressure at exit from the subarachnoid space, the latter being approximated by the intracranial pressure. Cerebral perfusion pressure divided by cerebral blood flow gives the cerebrovascular resistance. In normal humans, cerebral blood flow remains almost constant when the mean systemic blood pressure is between approximately 50 and 170mmHg, which, under normal circumstances when the intracranial venous pressure is negligible, is the same as the cerebral perfusion pressure. This homeostatic mechanism to maintain a constant cerebral blood flow in the face of changes in cerebral perfusion pressure is known as autoregulation (Reed and Devous 1985 Powers 1993). Autoregulation is less effective in the elderly, and so postural hypotension is more likely to be symptomatic (Wollner et al. 1979 Parry et al. 2006). 

Overall systemic arterial pressure is also maintained until a late stage. These responses follow neuroendocrine activation when the heart begins to fail. 

Rapid peripheral intravenous injection of concentrated ionic contrast media produces a brief rise in systemic arterial pressure followed by a prolonged fall the diastolic pressure decreases more than the systolic pressure and the heart slows the pulse contour changes, and the venous pressure rises the arterial hypotension is more marked if injection is rapid. The electrocardiogram can show flattening, splitting, or T-wave inversion tachycardia is probably compensatory, as are the concomitant increases in venous pressure and pulmonary arterial pressure. Hypotension associated with a vasovagal reaction probably explained four deaths from acute coronary insufficiency (two each with iodoalphionic acid and iopa-noic acid) in patients with ischemic heart disease. 

Injection into the left ventricle or the proximal aorta is likely to produce more marked effects. Cardiac rate, stroke volume, and cardiac output increase. There is a rise in right and left atrial pressures and left ventricular end-diastolic pressure. The pulmonary arterial pressure is also increased. The blood volume expands and peripheral blood flow increases and then decreases as systemic resistance falls. The hematocrit falls and venous pressure gradually rises. As the systemic arterial pressure falls, the heart rate increases. These responses are largely due to the injection of strongly hypertonic solutions, which promote a rapid expansion of the plasma volume water shifts from the extravascular fluid spaces to the blood and moves out of the erythrocytes, which shrink and become crenated. Blood viscosity rises, but plasma viscosity does not increase significantly. The erythrocytes give up potassium to the plasma and this might contribute to the observed reduction in peripheral vascular resistance. 

Calcium channel blockers inhibit L-type calcium channels in cardiac and smooth muscle. As a result, inhibition of calcium influx into cells occurs, causing a decrease in myocardial contractility and rate, resulting in reduced oxygen demand. Cardiac rate is slowed by the ability of calcium channel blockers to block electrical conduction through the atrioventricular (AV) node. In addition, calcium channel blockers can reduce systemic arterial pressure by relaxing arterial smooth muscle and decreasing systemic vascular resistance. 

Cannabinoids are able to cause different effects at the level of various systems and/or organs the most important effects occur on the central nervous system and on the cardiovascular system. In fact, they are able to affect mood, memory, motor coordination and cognition, and they increase heart rate and variate the systemic arterial pressure. Furthermore, it is well known the capability of cannabinoids to reduce intraocular pressure and to affect the respiratory and endocrine systems (L. E. Hollister, Health Aspects of Cannabis, Pharmacological Reviews, 38,1-20,1986). More recently, it was found that they suppress the cellular and humoral immune response and have antiinflammatory properties (A. W. Wirth et al.. Antiinflammatory Properties of Cannabichromene, Life Science, 26,1991-1995,1980). 

An important advance in NO inhalation therapy would be to develop an ambulatory treatment regime that allows the patient to leave the hospital and resume normal activities without being bmdened by cumbersome gas handling equipment. With this in mind, Hampl et al. tested the ability of periodically administered DETA/NO (Figure 2) to relieve pulmonary hypertension in rats whose lungs had been injured by monocrotaline exposure (20). They found that once-a-day inhalation of aerosolized DETA/NO lowered these animals PAP to normal levels with no observed effect on overall blood pressure (i.e., mean systemic arterial pressure, or MAP) or other signs of toxicity. 

The result of the combination of myogenic mechanisms and tubuloglomerular feedback is that the net filtration pressure or Pccap is kept reasonably constant over a very wide range of systemic arterial pressures. It should be noted that renal blood flow and GFR change across this range of systemic pressures but to a significantly smaller extent than would be predicted if these autoregulatory mechanisms were not in place. 

Pulmonary hypertension is characterized by a chronically elevated pulmonary artery pressure. As described in previous sections of this chapter, under normal conditions, the pulmonary artery pressure has a systolic value of 18 to 25 mm Hg, a diastolic value of 6 to 10 mm Hg, and a mean value ranging from 12 to 16 mm Hg. Pulmonary hypertension exists when the pulmonary artery systolic and mean pressures exceed 30 and 20 mm Hg, respectively. In the disease state, the pressure in the pulmonary artery may fluctuate widely and is often so high that it equals the blood pressure in the systemic arterial bed. As would be expected, pulmonary vascular resistance is also extremely high in patients with pulmonary hypertension. In addition, patients with this disease exhibit an enlarged right ventricle and an enlargement of the main pulmonary artery and its branches. Systemic hemodynamic parameters, however, such as cardiac output, cardiac index, systemic artery pressure, and pulmonary artery wedge pressure are usually not elevated. 

Direct vascular smooth-muscle relaxants evaluated in primary pulmonary hypertension include hydralazine, isosorbide dinitrate, and diazoxide. In general, the hemodynamic effects of these drugs include modest reduction in mean pulmonary artery pressure, which parallels a significant reduction in systemic arterial pressure, decreased pulmonary vascular resistance, and increased cardiac output. 

The calcium channel blocking drugs may prove to be very useful in the treatment of patients following acute stroke. In particular, nimodipine has been found to have selective actions on cerebral vascular smooth muscle without affecting systemic arterial pressure [16]. After intravenous administration, nimodipine increases hemispheric cerebral blood flow in patients with acute ischaemic stroke [235]. A placebo-controlled double-blind trial has shown that nimodipine significantly decreases the occurrence of severe neurologic deficits from spasm alone in patients who have had subarachnoid haemorrhage [236],... 

Nesiritide is a human B-type natriuretic peptide, which binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells, leading to dose-dependent reductions in pulmonary capillary wedge pressure and systemic arterial pressure in patients with heart failure. It is indicated in the treatment of patients with acutely decompensated CHF who have dyspnea at rest or with minimal activity. 

In postoperative patients, a parenteral dose of 2-3 mg butorphanol produces analgesia and respiratory depression approximately equal to that produced by 10 mg morphine or 80-100 mg meperidine the onset, peak, and duration of action are similar to those that follow the administration of morphine. The plasma t of butorphanol is -3 hours, like pentazocine, analgesic doses of butorphanol produce an increase in pulmonary arterial pressure and in the work of the heart systemic arterial pressure is slightly decreased. 

ACE inhibitors are more potent arterial than venous dilators. In response to ACE inhibition, mean arterial pressure (MAP) may decrease or be unchanged the change in MAP will be determined by the stroke volume response to afterload reduction. Heart rate typically is unchanged, even when there is a decrease in systemic arterial pressure, a response that hkely refiects a decrease in sympathetic tone in response to ACE inhibition. The decrease in left ventricular afterload results in increased stroke volume and cardiac output. Venodilation results in decreases in right and left heart filling pressures and end-diastolic volumes. 

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