Systemic arterial pressures hypotension

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). 

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. 

FIGURE 8 Bedside monitor recording of pulmonary artery pressure (PAP) and systemic artery pressure (SAP) in a 1-day-old postoperative patient after repair of obstructed total anomalous pulmonary venous connection. Stable PAP and SAP are achieved with 15-ppm nitric oxide (NO). When the NO was transiently discontinued, there was a prompt increase in PAP and profound systemic hypotension. With reinstitution of NO, recovery occurred. Subsequently, the child was easily weaned from NO. 

In 9 healthy subjects, oral indometacin 50 mg every 6 hours for 4 doses abolished the hypotensive response to intravenous hydralazine 150 mierograms/kg, and the subjects only responded when given another dose of hydralazine 30 minutes later. A study in 7 patients with pulmonary hypertension given indometacin 50 mg and hydralazine 350 mierograms/kg, both intravenously, either alone, or concurrently, also found that the effects of hydralazine (reduction in systemic arterial pressure, heart rate, cardiac index) were reduced by indometacin. In contrast, another study in 9 healthy subjects found that oral indometacin 25 mg four times daily for 2.5 days did not affect the hypotensive response to a single 200-mierogram/kg intravenous dose of hydralazine. 

Syncope Because of the risk of syncope, monitor vital signs while initiating iloprost. In patients with low systemic blood pressure, take care to avoid further hypotension. Do not initiate iloprost in patients with systolic blood pressure less than 85 mm Hg. Be alert to the presence of concomitant conditions or drugs that might increase the risk of syncope. Syncope can also occur in association with pulmonary arterial hypertension, particularly in association with physical exertion. 

A unique property of bretylium as an antiarrhythmic agent is its positive inotropic action. This effect, related to its actions on the sympathetic nervous system, includes an initial release of neuronal stores of norepinephrine followed shortly by a prolonged period of inhibition of direct or reflex-associated neuronal norepinephrine release. The onset of bretylium-induced hypotension is delayed 1 to 2 hours because the initial catecholamine release maintains arterial pressure before this time. 

The vasodilators decrease total peripheral resistance and thus correct the hemodynamic abnormality that is responsible for the elevated blood pressure in primary hypertension. In addition, because they act directly on vascular smooth muscle, the vasodilators are effective in lowering blood pressure, regardless of the etiology of the hypertension. Unlike many other antihypertensive agents, the vasodilators do not inhibit the activity of the sympathetic nervous system therefore, orthostatic hypotension and impotence are not problems. Additionally, most vasodilators relax arterial smooth muscle to a greater extent than venous smooth muscle, thereby further minimizing postural hypotension. 

More specific treatment to combat cardiotoxic effects is usually necessary in only a minority of instances in the series reported above (40), five patients (14%) had marked hypotension. Initial low left ventricular filling pressures were corrected within 3 hours by infusion of isotonic saline. Systemic hypotension persisted and was corrected by infusion of sympathomimetic amines. Routine insertion of a pulmonary artery catheter, with continuous monitoring of blood gases, pulmonary arterial pressure, left atrial wedge pressure, and cardiac output have been recommended (40). Volume expansion is suggested for low left atrial pressure,... 

Rapid i.v. administration of tetracyclines can result in hypotension and collapse. This has been attributed to intravascular chelation of calcium and/or a decrease in blood pressure owing to the drug vehicle. The i.v. administration of doxycycline to horses causes tachycardia, systemic arterial hypertension, collapse and death. This reaction may be caused by the highly lipid-soluble doxycycline chelating intracellular calcium, resulting in cardiac neuromuscular blockade. 

Although a1B-knockout mice showed significantly reduced blood pressure, they displayed reduced, instead of increased, systemic arterial blood pressure compared to WT (39) and a normal contractile response of mesenteric segments to a,-agonists (39). The mechanism of the hypotension is likely the autonomic failure that characterizes the a1B-transgenic mice, indicating that a1B-ARs are not significant players in vasoconstriction. 

Renal hypoperfusion without systemic hypotension most commonly results from bilateral renal artery occlusion, or unilateral occlusion in a patient with a single functioning kidney. In these conditions, the sodium-retentive hormones are activated by the decline in renal parenchymal perfusion. However, systemic arterial blood pressure is usually elevated, leading to an inhibition of antidiuretic hormone release. Consequently, the urinary indices will reflect enhanced sodium reabsorption (i.e., a low fractional excretion of sodium), but the urinary solutes may not be maximally concentrated. 

The ijn vivo effects of leukotrienes on blood pressure and heart rate are quite cenplex. Generally, there is a biphasic response consisting of an initial transient increase in systemic blood pressure followed by a sustained systemic hypotension after a bolus of 1-10 pg/kg of LTC. or LTD.. 8 8 Intravenous LTC. decreases cardiac output and rate tdiile increasing total peripheral resistance.Pretreatment with indcmethacin potentiates the initial increase in blood pressure and attenuates the sustained hypotension and changes in cardiac function due to ETC.. Low doses of LTD. injected into the left circumflex corona artery of sheep result in coronary vasoconstriction and irpaired ventricular function. ... 

There are three potential drawbacks in the use of vasodilators First, vasodilators can lead to a baroreceptor-mediated reflex stimulation of the heart (increased heart rate and inotropy) from systemic vasodilation and arterial pressure reduction. Second, they can impair the normal baroreceptor-mediated reflex vasoconstriction when a person stands up, which can lead to orthostatic hypotension and syncope on standing. Third, they can lead to renal retention of sodium... 

Complications which were common in the early days of haemoperfusion, seldom happen in the modem extracorporeal treatment. Most fiequently patients undergoing HP develop mild fever, hypotension, bleeding and perturbation of the blood clotting system. Sometimes hypotension could be significant with arterial pressure dropping by 35-40%. Patients with severe poisonings followed by liver iailure are particularly prone to hypotension. This reaction to... 

The cardiovascular action of SM to lower systemic blood pressure in the rats has been demonstrated. Langendorff cardiac preparation in guinea pig and four types of vasculature in dog, including coronary, renal, femorid, and mesenteric arteries are performed. SM induces dose-related hypotension without changing heart rate. Atropine, propranolol, and chlorpheniramine plus cimetidine antagonize the hypotensive effect. In the isolated whole-heart preparation, SM injection increases coronary blood flow and causes a positive inotropic action. SM relaxes all arteries at low concentration and contracts all, but the coronary artery, at high concentration (7P). 

Guanethidine reduces blood pressure by its ability to diminish vascular tone both the arterial and venous sides of the circulatory system are involved. The resulting venous pooling contributes to orthostatic hypotension, a prominent feature of guanethidine treatment. The reduction in blood pressure is more prominent when the patient is standing than recumbent. 

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. 

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. 

Most types of smooth muscle are dependent on transmembrane calcium influx for normal resting tone and contractile responses. These cells are relaxed by the calcium channel blockers (Figure 12-3). Vascular smooth muscle appears to be the most sensitive, but similar relaxation can be shown for bronchiolar, gastrointestinal, and uterine smooth muscle. In the vascular system, arterioles appear to be more sensitive than veins orthostatic hypotension is not a common adverse effect. Blood pressure is reduced with all calcium channel blockers. Women may be more sensitive than men to the hypotensive action of diltiazem. The reduction in peripheral vascular resistance is one mechanism by which these agents may benefit the patient with angina of effort. Reduction of coronary artery tone has been demonstrated in patients with variant angina. 

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