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Hypertension and the Kidney

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Hypertension and the Kidney 8.16 Hypertension and the Kidney 2 MAP, mm Hg Heart rate, beats/min Cardiac index, L/min/m AHHF 200 200 120 5.0 NF 150 B B 90 mm Hg 100 NP 100 60 2.5 NP 50 Mean arterial 30 pressure, AHHF NF 0 0 0 0 P<0.005 P<0.005 NS NS NS Stroke work index, g m/m2 LVEDP, mm Hg LVEDV, mL/m2 40 B 150 60 200 L/min 9 30 NP 45 mm Hg 6 NP 20 75 30 100 B B NP 3 10 LVEDP, B NP 15 Cardiac output,Cardiac 0 0 0 0 0 P<0.005 NS P<0.005 P<0.025 NS P<0.005 NS Hemodynamic parameters at baseline (B) and during nitroprusside (NP) infusion A Baseline hemodynamics in acute hypertensive heart failure (AHHF) vs no failure (NF) B in both groups had electrocardiographic evidence of LV hypertrophy 60 AHHF: baseline caused by long-standing hypertension. AHHF: with nitroprusside A, Baseline hemodynamic measurements before treatment No failure: baseline 50 No failure: with nitroprusside revealed that the following measurements were the same in both groups: mean arterial pressure (MAP), heart rate, cardiac index, systemic vascular resistance, and stroke work index. Likewise, the 40 LV end-diastolic volume (LVEDV) was similar in both groups. In fact, the only hemodynamic difference between the groups was a mm Hg significant elevation of LV filling pressure (LVFP) (pulmonary capil- 30 lary wedge pressure) in the group with pulmonary edema. In acute LVFP, hypertensive heart failure the finding of elevated LV end-diastolic 20 pressures (LVEDPs), despite normal ejection fraction and cardiac index, implies the presence of isolated diastolic dysfunction. The increased LV end-diastolic pressure (LVEDP), despite similar 10 LVEDV, can only be explained by a decrease in LV compliance in patients with acute hypertensive heart failure. B, The importance 0 of an acute decrease in LV compliance in the pathogenesis of acute 40 80 120 160 200 240 hypertensive heart failure (AHHF) was confirmed in these patients LVEDV, mL/m2 by the hemodynamic response to vasodilator therapy. Sodium C Left ventricular compliance at baseline and with nitroprusside nitroprusside infusion resulted in prompt resolution of pulmonary edema in the group having AHHF, with the LVEDP decreasing from a mean of 43 to 18 mm Hg. C, The decrease in filling pres- FIGURE 8-23 sure during nitroprusside therapy in patients with AHHF was not Pathogenesis of acute hypertensive heart failure. Both malignant caused by venodilation with decreased venous return because the hypertension and severe benign hypertension can be complicated by LVEDV actually increased during nitroprusside infusion. Thus, the acute pulmonary edema caused by isolated diastolic dysfunction. In response to sodium nitroprusside therapy was mediated through a acute hypertensive heart failure the compromise of left ventricular (LV) decrease in systemic vascular resistance that led to an immediate diastolic function occurs as a result of a decrease in LV compliance improvement in LV compliance and reduction in wedge pressure caused by an increased workload imposed on the heart by the marked despite an increase in LVEDV. These findings suggest that the prox- elevation in systemic vascular resistance. Illustrated are the hemody- imate cause of AHHF is an elevation of the systemic vascular resis- namic derangements in acute hypertensive heart failure in a study that tance that precipitates acute diastolic dysfunction (decreased LV compared five patients with severe essential hypertension complicated compliance) with elevated pulmonary capillary wedge pressure, by acute pulmonary edema with a control group of five patients with resulting in pulmonary edema. NS— not significant. (Adapted from equally severe hypertension but no pulmonary edema [28]. Patients Cohn and coworkers [28]; with permission.) Hypertensive Crises 8.17 FIGURE 8-24 Treatment of acute hypertensive heart failure. The left ventricular 60 (LV) end-diastolic pressure-volume relationships (compliance curves) in acute hypertensive heart failure (AHHF) before and after 50 treatment with sodium nitroprusside are represented schematically. In AHHF, the pressure-volume curve is shifted up and to the left, 40 reflecting an acute decrease in LV compliance caused by severe Nitroprusside systemic hypertension. In this setting, a higher than normal LV , mm Hg 30 end-diastolic pressure (LVEDP) is required to achieve any given level of LV end-diastolic volume (LVEDV). Normal LV systolic pressure function (ejection fraction and cardiac output) is maintained but 20 at the expense of a very high wedge pressure that results in acute AHHF Left end-diastolic ventricular pulmonary edema. Treatment with sodium nitroprusside causes Normal 10 a reduction in the elevated systemic vascular resistance, with a concomitant decrease in impedance to LV ejection. As a result, LV 0 compliance improves. Pulmonary edema resolves owing to a reduc- 40 80 120 160 200 240 tion in LVEDP, despite the fact that LVEDV actually increases dur- Left ventricular end-diastolic volume, mL/m2 ing treatment. Sodium nitroprusside is the preferred drug for treat- ment of AHHF. There is no absolute blood pressure goal. The infu- sion should be titrated until signs and symptoms of pulmonary edema resolve or the blood pressure decreases to hypotensive lev- els. Rarely is it necessary to lower the blood pressure to this extent, however, because reduction to levels still within the hypertensive range is usually associated with dramatic clinical improvement. Although hemodynamic monitoring is not always required, it is essential in patients in whom concomitant myocardial ischemia or compromised cardiac output is suspected. After the hypertensive crisis has been controlled and pulmonary edema has resolved, oral antihypertensive therapy can be substituted as the patient is weaned from the nitroprusside infusion. As in the treatment of hypertensive patients with chronic congestive heart failure symp- toms owing to isolated diastolic dysfunction, agents such as ␤- blockers, angiotension-converting enzyme inhibitors, or calcium channel blockers may represent logical first-line therapy. These agents directly improve diastolic function in addition to reducing systemic blood pressure. In patients with malignant hypertension or resistant hypertension, however, adequate control of blood pres- sure may require therapy with more than one drug. Potent direct- acting vasodilators such as hydralazine or minoxidil may be used in conjunction with a ␤-blocker to control reflex tachycardia and a diuretic to prevent reflex salt and water retention. 8.18 Hypertension and the Kidney FIGURE 8-25 Aortic dissection Aortic dissection. Classification of aortic dissection is based on the presence or absence of involvement of the ascending aorta [29]. Transverse aortic arch Descending The dissection is defined as proximal if there is involvement of the aorta ascending aorta. The primary intimal tear in proximal dissection may arise in the ascending aorta, transverse aortic arch, or descending Ascending aorta. In distal dissections, the process is confined to the descending aorta aorta without involvement of the ascending aorta, and the primary intimal tear occurs most commonly just distal to the origin of the left subclavian artery. Proximal dissections account for approximately 57% and distal dissections 43% of all acute aortic dissections. Acute aortic dissection is a hypertensive crisis requiring immediate antihypertensive treatment aimed at halting the progression of the dissecting hematoma. The three most frequent complications of aortic dissection are acute aortic insufficiency, occlusion of major arterial branches, and rupture of the aorta with fatal hemorrhage (location of rupture-hemorrhage: ascending aorta–hemopericardium Proximal Distal with tamponade, aortic arch–mediastinum, descending thoracic (Type A) (Type B) aorta–left pleural space, abdominal aorta– retroperitoneum). Patients with acute dissection should be stabilized with intensive antihypertensive therapy to prevent life-threatening complications before diagnostic evaluation with angiography. The initial therapeutic goal is the elimination of pain that correlates with halting of the dissection, and reduction of the systolic pressure to the 100 to 120 mm Hg range or to the lowest level of blood pressure compatible with the maintenance of adequate renal, cardiac, and cerebral perfusion [30]. Even in the absence of systemic hypertension the blood pressure should be reduced. Antihypertensive therapy should be designed not only to lower the blood pressure but also to decrease the steepness of the pulse wave. The most commonly used treatment regimens consist of initial treatment with intravenous ␤-blockers such as propranolol, metoprolol, or esmolol followed by treatment with sodium nitroprusside. After control of the blood pressure, angiography or transesophageal echocardiography, or both, should be performed. The need for surgical intervention is determined based on involvement of the ascending aorta. In proximal dissections, sur- gical therapy is clearly superior to medical therapy alone (70% vs 26% survival, respectively). In contrast, in patients with distal dissection, intensive drug therapy alone leads to an 80% survival rate compared with only 50% in patients treated surgically. The explanation for the advantage of surgical therapy in proximal dissection is probably that the risks of complications such as cerebral ischemia, acute aortic insufficiency, and cardiac tamponade are higher and managed more effectively with surgery. Because these complications do not occur in distal dissection, in the absence of occlusion of a major arterial branch or development of a saccular aneurysm during long-term follow-up, medical therapy is preferred. Patients with distal dissection tend to be elderly with more advanced aortic atherosclerosis and therefore are at higher risk of complications from operative intervention. (Adapted from Wheat [29]; with permission.) .
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