- Email: [email protected]
Postcardiac surgical hypertension
REVIEW
ARTICLE
Theodore Stanley, MD, Editor
Postcardiac
Surgical
Hypertension
Richard J. Gray, MD
H
YPERTENSION occurs in 30% to 60% of patients after cardiac surgery.‘-’ It can develop several hours after surgery, but is usually present within one to two hours, and is often established by the time the patient returns to the intensive care unit (ICU). Various definitions have been used for postoperative hypertension, including an absolute level of mean arterial pressure (MAP) >lOS mmHg,4 or a 20 mmHg increase in MAP.’ Since systolic pressures tend to predominate and can result in potentially damaging excessive aortic shear forces, it has also been defined as a systolic blood pressure >140 mmHg.6 Although hypertension is common after all types of cardiac operations, its appearance and severity tend to favor cardiac valve surgery, especially relief of aortic stenosis.’ The hazards of postoperative hypertension, especially if severe, can include cerebral vascular accidents, suture line disruption, and dissection of the aorta due to associated aortic pathology. A more subtle risk is that of greater aortic impedance that places heavy metabolic demands on the myocardium which is just recovering from an ischemic insult.8*9 Hypertension is also one of many possible causes for the common “nonspecific” ST and T wave electrocardiographic changes seen after cardiac surgery. An additional risk is hypertension-mediated intimal damage to saphenous vein graft endothelium, which may contribute to future graft closure and premature atherosclerosis.” From the Department of Thoracic & Cardiovascular Surgery, CedarsSinai Medical Center, Los Angeles. Address reprint requests to Richard Gray, MD, Cedars-Sinai Medical Center, 8700 Beverly Blvd. Rm 6215, LAMAngeles, CA 90048. o I988 by Grune & Stratton, Inc. 0888~6296/88/0205-001S$03.00/0
67%
PREDISPOSING FACTORS
Mechanisms that have been implicated in postoperative hypertension include elevated levels of plasma epinephrine and norepinephrine (NE),11-‘3 renin and angiotensin,14 vasopressin,” excessive sympathetic nervous system activity,3 and certain reflexes originating in the heart or great vessels.16*”Although the events of anesthesia, cardiopulmonary bypass (CPB), surgical stimulation, and hypothermia have all been associated with increases in catecholamine levels, ‘*J~J*J~there still is a question as to the causative role of catecholamine excess, since plasma catecholamine levels are elevated in most patients irrespective of the presence or absence of hypertension.*’ In a broad survey of catecholamine responses to cardiac surgery, epinephrine levels are most profoundly elevated,‘***’but NE elevations may also persist for several days (Fig l).*’ It should be remembered that epinephrine is the consequence of adrenomedullary secretion, whereas NE is the neurotransmitter released from sympathetic nerve endings; thus, plasma values of NE provide an index of sympathetic nervous system activity. Infusions of NE result in intense hypertension due to a-adrenergic constriction. Indeed, postoperative hypertension has been linked to a markedly positive peripheral NE gradient. ** In the study of Gray et aP of 20 cardiac surgical patients, only the NE level was consistently elevated (two- to sevenfold in all patients), whereas epinephrine and renin levels were either normal or modestly elevated (Table 1). This implication of sympathetic nervous system stimulation is consistent with the observation that hypertension is often lessened following extubation and adequate sedation. Clinically, a preoperative history of hypertension3 and preoperative use of propranololm
Journalof CardiothofacicAnesthesia, Vol2, No 5 (October),
1988: pp
678-682
POSTOPERATIVE HYPERTENSION
679
--Norepinephrme -Epmephrme
E 24OOr
2 1600 aI ; 1200 .$ 800. $
400-P 1
1
I
Preop
Fig 1.
Day
1
1
Day2
I
I
Day3
The serum norapinephrina and apinaphrina levels associated with cardiac surgary. Reprinted with parmis-
sion?’
have been linked to acute postoperative hypertension. Preoperative left ventricular ejection fraction is usually lower in patients remaining normotensive than in those who become hypertensive, implying that adequate left ventricular function is an important ingredient in hypertension.’ As with its more common counterpart, essential hypertension, the basic mechanisms remain unknown; however, certain physiologic features are common. Current data support the importance of sympathetic nervous system stimulation and elevated NE levels with varying cardiovascular responses based on preoperative hypertension, P-blocker usage, adequacy of cardiac function, and type of anesthesia, possibly working through alterations in adrenergic receptor number and function.
safely administered by nursing personnel, and be free of short-term side effects. Since it possesses most of these features, nitroprusside has been used extensively for treatment.2455 It allows for titration of MAP to the desired level, with significant reductions in SVR and cardiac filling pressures.’ Cardiac output usually increases but may not if cardiac filling pressures are lowered excessively.4 Usually a modest reflex tachycardia occurs with prolonged usage, especially at high doses (>4 hg/kg/min). Starting at a dosage of 0.5 pg/kg/min, an average effective dose is 1 to 2 pg/kg/min. Toxicity can develop with nitroprusside, consisting of tachyphylaxis, metabolic acidosis, or elevations of sodium thiocyanate and cyanide levels. A potentially serious drawback, especially in older patients and individuals with limited
CLINICAL FEATURES AND TREATMENT
In addition to the hypertension, hemodynamic measurements often reveal a normal, slightly elevated, or slightly reduced cardiac output and moderate-to-significant elevations of systemic vascular resistance (SVR). Guidelines for successful drug therapy in this condition require an agent that must address the prevailing hemodynamic characteristics, be rapid in onset as well as offset to allow titration, be easily and
Table 1. Postoparstiva Catacholamina Levels Narepinephrine WLI
Epinephrine (W/L)
Renin WmLlh)
Mean
664
94
2.9
SD
242
51
5.3
Range
266-l
,452
21-195
O-23.2
NOmld (mean + SD) Normal + 2 SD
146 f 45
42 i 35
0.5 f 0.3
236
112
1.1
RICHARD J. GRAY
680
ho2
PVO,
(mm Hg)
(mm Hg)
(ml Anin)
48-
1
AaDO,
MVO,
t
Q,/Qt
(mm Hg)
360
26
T 24 22
320
-
36-
20
32 -
18
28 -
16 I T
Pulmonary and tissue gas exchange variables measured at an inspired oxygen concentration of 100% during the Fig 2. control period and during the last ten minutes of each intervention in a subgroup of eight patients. NP. nitroprusside: TNG, nitroglycerin: PaO*, arterial oxygen tension; PvG,. mixed venous oxygen tension; MvG,, tissue oxygen use; AaDO*, alveolar-arterial oxygen gradient: GslQt. intrapulmonary shunting. (0) Control; Ef1)NP: ( 1 TNG, (a) P < 0.06 vs control: ( + 1 P < 0.01 NP v TNG: f + + 1P < 0.001 NP v TNG. Reprinted with permission.’
pulmonary function, is the occurrence of a marked decrease in PaO,, suggesting the presence of a ventilation-perfusion mismatch. The mechanism by which nitroprusside worsens intrapulmonary shunting appears to be inhibition of hypoxic vasoconstriction in the pulmonary bed, resulting in increased perfusion of poorly ventilated regions.26-28Figure 2 illustrates variables of pulmonary gas exchange comparing nitroprusside with a nitroglycerin infusion.’ Despite a reduction in global myocardial oxygen requirements, marked reductions in coronary blood flow due to excessive lowering of diastolic blood pressure can lead to myocardial ischemia with use of nitroprusside.4 Coronary steal can also result in myocardial ischemia with nitroprusside administration. The mechanism is not fully understood, but factors important to the process include the presence of significant obstructive coronary disease in a vessel adjacent to a branch without significant obstruction. Maximal dilation of downstream resistance vessels without effect upon the upstream conductance vascular segment results in the large vessel obstruction becoming the critical factor regulating local blood flow. This worsens the maldistri-
bution of coronary blood flow away from the obstructed zone. 29Maldistribution of blood flow and the potential for myocardial ischemia are worsened by any significant reduction in coronary perfusion pressure resulting from vasodilator administration.29 This is especially true of an agent that particularly lowers diastolic blood pressure. Nitroprusside, with its potent direct small vessel vasodilating action, is capable of such effects, as is dipyridamole.29 Neither drug has significant effects on the larger conductance vessels, nor do the drugs appear to have significant ability to dilate the atherosclerotic segment. This lack of conductance effect is in contrast to that of nitroglycerin, which has been demonstrated to alter vascular tone throughout29*30and also appears capable of dilating certain diseased segments.30 For these reasons, intravenous (IV) nitroglycerin has been suggested for postoperative hypertension. In one study, it was able to achieve blood pressure control equivalent to that of nitroprusside in 14 of 17 patients and did not result in worsening of intrapulmonary shunting.5 Patients with chronic congestive heart failure and elevated filling pressures tolerated nitroglycerin particularly well. The average’infusion
POSTOPERATIVE HYPERTENSION
681
rate of nitroglycerin for successful control of blood pressure is 1 to 2 rg/kg/min. Postoperative hypertension is often seen in the setting of overall hyperdynamic cardiovascular function with sinus tachycardia, elevated cardiac output, and modestly elevated systemic vascular resistance. /3-adreneric blocker therapy seems particularly useful in this type of patient, especially in view of the elevation of catecholamines that often occurs and the frequent history of preoperative B-blocker use. Intermittent dosing with IV propranolol, 1 to 5 mg, every six hours, has been successful; however, propranolol has not traditionally been used as a continuous infusion. The IV ultra-short-acting b-blocker, esmolol, given as a continuous infusion, appears to provide effective control of hypertension in most patients, with minimum reduction of cardiac function. The principal advantages to this approach are the lack of any deleterious effects on intrapulmonary shunting, titratable onset and offset of action, and freedom from excessive lowering of diastolic blood pressure.” Table 2 summarizes these effects with data from a study that compared nitroprusside to esmolol in patients with postoperative hypertension after coronary artery surgery.23 Labetalol, an agent with both a- and fiblocking effects, available both orally and IV, has also been used successfully in early postoperative hypertension. Incremental bolus doses of 10 to 40 mg are associated with reductions in blood pressure and heart rate (HR),3’ and appear to be as successful at controlling postoperative hypertension as hydralazine, but without the tendency for the increased HR that occurs with hydralazine.32 Continuous IV infusion has also been used with similar success at a dosage of 2 mg/min. A decrease in HR with labetalol in this clinical situation is less certain than blood pressure reduction, but a significant decline in both HR and cardiac index with no reduction in systemic resistance have also been reported, suggesting that @-blockade may predominate over a-blocking effects, especially when labetalol is used in IV form.33 Calcium channel blocking drugs have been
Table 2.
Treatment
of Poatoperative
Esmolol v Nitropruaaide:
PaMllaSr Heart rate
Summary
Hypertension: of Differences
Esmdol (%I
NitroprUtide (%)
a-14
t
?? -20 ?? -8 ?? -23
t
-31.
t
+7
+7*
8lood pressure Systolic Diastolic Cardiac index Stroke volume Left ventricular SWI
-18.
-7.5
-0.3
?? -30
-199
PaO,
-0.1
t
0, saturation
-0.1
t
-39. -54
Abbreviation: SWI, stroke work index. +P < 0.05 Baseline Y dug. tP < 0.05 esmolol Y nitropruaside.
increasingly used for control of chronic outpatient hypertension, and as IV formulations become widely available they are likely to be used for control of acute hypertension as well. One such agent, nicardipine, has little or no discernible negative inotropic or chronotropic effects, and when given as either an IV bolus or infusion, it has rapid enough onset and offset of action to allow titration of blood pressure.34 It has been found to be capable of controlling hypertension while increasing cardiac output and HR. Several hours’ therapy with an IV agent may be sufficient if hypertensive tendencies decrease with rewarming and relief of pain and anxiety. Other patients, particularly those with hypertension preoperatively, will require longer therapy. Successful weaning from IV to oral control has been achieved with hydralazine, 10 to 50 mg, every six hours; aldomet, 250 to 500 mg, every six hours; or clonidine, 0.1 to 0.2 mg, every six to eight hours. More recently, however, nifedipine, 10 to 20 mg, every six hours, orally or sublingually, has been used successfully and is well tolerated. In general, it is wise to resume preoperative antihypertensive regimens that may have been well tolerated; however, daily adjustments in dosage may be necessary. Regimens that include chronic thiazide diuretics should be reevaluated in view of possible rapid postoperative changes in electrolytes and intravascular volume, as well as long-term adverse effects on serum lipids.
REFERENCES 1. Estafanous FG, Tarazi RC, Viljoen JF, et al: Systemic hypertension following myocardial revascularization. Am Heart J 85:732-738, 1972
2. Hoar PF, Hickey RF, Ullyot DJ: Systemic hypertension following myocardial revascularization. J Thorac Cardiovasc Surg 71:859-864, 1976
662
3. Roberts AJ, Niarchos AP, Subramanian VA, et al: Systemic hypertension associated with coronary artery bypass surgery. Predisposing factors, hemodynamic characteristics, humoral profile, and treatment. J Thorac Cardiovast Surg 74:846-859,1977 4. Fremes SE, Weisel RD, Baird RJ, et al: Effects of postoperative hypertension and its treatment. J Thorac Cardiovasc Surg 8647-57, 1983 5. Flaherty JT, Magee PA, Gardner TL, et al: Comparison of intravenous nitroglycerin and sodium nitroprusside for treatment of acute hypertension developing after coronary artery bypass surgery. Circulation 65:1072-1077,1982 6. Gray RJ, Batenman TB, Czer LSC, et al: Use of esmolol in hypertension after cardiac surgery. Am J Cardiol 56:49F-56F, 1985 7. Cooper TJ, Clutten-Brock TH, Jones SN, et al: Factors relating to the development of hypertension after cardiopulmonary bypass. Br Heart J 5491-95.1985 8. Kaplan JA, Jones EL: Vasodilator therapy during coronary surgery: Comparison of nitroglycerin and nitroprusside. J Thorac Cardiovasc Surg 77:301-309, 1979 9. Hilton JD, Weisel RD, Barid RJ, et al: The hemodynamic and metabolic response to pacing after aortocoronary bypass. Circulation 64:1148-1153,198 1 10. Brody WR, Kosek JC, Angel1 WW: Changes in vein grafts following aortocoronary bypass induced by pressure and ischemia. J Thorac Cardiovasc Surg 64847-854, 1972 11. Wallach R, Karp RB, Reves JG, et al: Pathogenesis of paroxysmal hypertension developing during and after coronary bypass surgery: A study of hemodynamic and humoral factors. Am J Cardiol46:559-565, 1980 12. Reves JG, Karp RB, Buttner EE, et al: Neural and adrenomedullary catecholamine release in response to cardiopulmonary bypass in man. Circulation 66:49-55, 1982 13. Hoar PF, Stone JG, Faltas AN, et al: Hemodynamic and adrenergic responses to anesthesia and operation for myocardial revascularization. J Thorac Cardiovasc Surg S&242-248, 1980 14. Taylor KM, Morton IJ, Brown JJ: Hypertension and the renin-angiotensin system following open heart surgery. J Thorac Cardiovasc Surg 74840-845, 1977 15. Hawkins SS, Aveling W, Treasure T, et al: Hypertension, vasopressin and renin in coronary artery surgery. Br J Anesth 55:1161,1983 16. Fouad FM, Estafanous FG, Bravo EL, et al: Possible role of cardioaortic reflexes in post-coronary bypass hypertension. Am J Cardiol44:866-872, 1979 17. James TN, Hageman GR, Uthaler F: Anatomic and physiologic considerations of a cardiogenic hypertensive chemoreflex. Am J Cardiol44:850-859, 1979 18. Lillehei RC, Lillehei CW, Grismer JT, et al: Plasma catecholamines in open heart surgery: Prevention of their pernicious effects by pretreatment with dibenzyline. Surg Forum 14:269-271,1963 19. Chee-Ken T, Glisson SN, El-Etr A, et al: Levels
RICHARD J. GRAY
of circulating norepinephrine and epinephhne before, during, and after cardiopulmonary bypass in man. J Thorac Cardiovast Surg 71:928-931, 1976 20. Whelto PK, Flaherty JT, MacAllister NP, et al: Hypertension following coronary artery bypass surgery. Role of preoperative propranolol therapy. Hypertension 2:291298,1983 21. Engleman RM, Haag B, Lemeshaw S, et al: Mechanism of plasma catecholamine increases during coronary artery bypass and valve procedures. J Thorac Cardiovast Surg 86:608-615,1983 22. Young YD, Jones M, Hanowell ST, et al: Changes in peripheral vascular and cardiac sympathetic activity before and after coronary artery bypass surgery: Interrelationships with hemodynamic alterations. Am Heart J 102:972-979,198l 23. Gray RJ, Bateman TB, Czer LX, et al: Comparison of esmolol and nitroprusside for acute post-cardiac surgical hypertension. Am J Cardiol59:887-892, 1987 24. Estafanous FG, Tarazi RC: Systemic arterial hypertension associated with cardiac surgery. Am J Cardiol 46:685-694, 1980 25. Gall WE, Clarke WR, Dota DB: Vasomotor dynamics associated with cardiac operations. I. Venous tone and the effects of vasodilators. J Thorac Cardiovasc Surg 83:724-731, 1982 26. Colley PS, Cheney FW: Sodium nitroprusside increases Qs/Qt in dogs with regional atelectasis. Anesthesiology 47:338-341, 1977 27. Hill AB, Chir B, Sykes MK, et al: A hypoxic pulmonary vasoconstrictor response in dogs during and after infusion of sodium nitroprusside. Anesthesiology 50:484-488, 1979 28. Benumof JL: Hypoxic pulmonary vasoconstriction and infusion of sodium nitroprusside. Anesthesiology 50~481-483, 1979 29. Becker L: Conditions for vasodilator-induced coronary steal in experimental myocardial ischemia. Circulation 57:1103-1110, 1978 30. Brown BG, Bolson E, Peterson RB, et al: The mechanisms of nitroglycerin action: Stenosis vasodilatation as a major component of the drug response. Circulation 64:1089-1097,198l 31. Morel DR, Forster A, Suter PM: IV labetalol in the treatment of hypertension following coronary artery surgery. Br J Anaesth 54:1191-l 196, 1982 32. Gabrielson G, Lingham R, Dimich I, et al: Comparative study of labetalol and hydralazine in the treatment of postoperative hypertension. Anesth Analg 66S63, 1987 33. Meretoja OA, Allonen H, Arola M, et al: Combined alpha- and beta-blockade with labetalol in post-open heart surgery hypertension. Reversal of hemodynamic deterioration with glucagon. Chest 78:810-815, 1980 34. Lambert CR, Hill JA, Nichols WW, et al: Coronary and systemic hemodynamic effects of nicardipine. Am J Cardiol55:652-657, 1985
ARTICLE
Theodore Stanley, MD, Editor
Postcardiac
Surgical
Hypertension
Richard J. Gray, MD
H
YPERTENSION occurs in 30% to 60% of patients after cardiac surgery.‘-’ It can develop several hours after surgery, but is usually present within one to two hours, and is often established by the time the patient returns to the intensive care unit (ICU). Various definitions have been used for postoperative hypertension, including an absolute level of mean arterial pressure (MAP) >lOS mmHg,4 or a 20 mmHg increase in MAP.’ Since systolic pressures tend to predominate and can result in potentially damaging excessive aortic shear forces, it has also been defined as a systolic blood pressure >140 mmHg.6 Although hypertension is common after all types of cardiac operations, its appearance and severity tend to favor cardiac valve surgery, especially relief of aortic stenosis.’ The hazards of postoperative hypertension, especially if severe, can include cerebral vascular accidents, suture line disruption, and dissection of the aorta due to associated aortic pathology. A more subtle risk is that of greater aortic impedance that places heavy metabolic demands on the myocardium which is just recovering from an ischemic insult.8*9 Hypertension is also one of many possible causes for the common “nonspecific” ST and T wave electrocardiographic changes seen after cardiac surgery. An additional risk is hypertension-mediated intimal damage to saphenous vein graft endothelium, which may contribute to future graft closure and premature atherosclerosis.” From the Department of Thoracic & Cardiovascular Surgery, CedarsSinai Medical Center, Los Angeles. Address reprint requests to Richard Gray, MD, Cedars-Sinai Medical Center, 8700 Beverly Blvd. Rm 6215, LAMAngeles, CA 90048. o I988 by Grune & Stratton, Inc. 0888~6296/88/0205-001S$03.00/0
67%
PREDISPOSING FACTORS
Mechanisms that have been implicated in postoperative hypertension include elevated levels of plasma epinephrine and norepinephrine (NE),11-‘3 renin and angiotensin,14 vasopressin,” excessive sympathetic nervous system activity,3 and certain reflexes originating in the heart or great vessels.16*”Although the events of anesthesia, cardiopulmonary bypass (CPB), surgical stimulation, and hypothermia have all been associated with increases in catecholamine levels, ‘*J~J*J~there still is a question as to the causative role of catecholamine excess, since plasma catecholamine levels are elevated in most patients irrespective of the presence or absence of hypertension.*’ In a broad survey of catecholamine responses to cardiac surgery, epinephrine levels are most profoundly elevated,‘***’but NE elevations may also persist for several days (Fig l).*’ It should be remembered that epinephrine is the consequence of adrenomedullary secretion, whereas NE is the neurotransmitter released from sympathetic nerve endings; thus, plasma values of NE provide an index of sympathetic nervous system activity. Infusions of NE result in intense hypertension due to a-adrenergic constriction. Indeed, postoperative hypertension has been linked to a markedly positive peripheral NE gradient. ** In the study of Gray et aP of 20 cardiac surgical patients, only the NE level was consistently elevated (two- to sevenfold in all patients), whereas epinephrine and renin levels were either normal or modestly elevated (Table 1). This implication of sympathetic nervous system stimulation is consistent with the observation that hypertension is often lessened following extubation and adequate sedation. Clinically, a preoperative history of hypertension3 and preoperative use of propranololm
Journalof CardiothofacicAnesthesia, Vol2, No 5 (October),
1988: pp
678-682
POSTOPERATIVE HYPERTENSION
679
--Norepinephrme -Epmephrme
E 24OOr
2 1600 aI ; 1200 .$ 800. $
400-P 1
1
I
Preop
Fig 1.
Day
1
1
Day2
I
I
Day3
The serum norapinephrina and apinaphrina levels associated with cardiac surgary. Reprinted with parmis-
sion?’
have been linked to acute postoperative hypertension. Preoperative left ventricular ejection fraction is usually lower in patients remaining normotensive than in those who become hypertensive, implying that adequate left ventricular function is an important ingredient in hypertension.’ As with its more common counterpart, essential hypertension, the basic mechanisms remain unknown; however, certain physiologic features are common. Current data support the importance of sympathetic nervous system stimulation and elevated NE levels with varying cardiovascular responses based on preoperative hypertension, P-blocker usage, adequacy of cardiac function, and type of anesthesia, possibly working through alterations in adrenergic receptor number and function.
safely administered by nursing personnel, and be free of short-term side effects. Since it possesses most of these features, nitroprusside has been used extensively for treatment.2455 It allows for titration of MAP to the desired level, with significant reductions in SVR and cardiac filling pressures.’ Cardiac output usually increases but may not if cardiac filling pressures are lowered excessively.4 Usually a modest reflex tachycardia occurs with prolonged usage, especially at high doses (>4 hg/kg/min). Starting at a dosage of 0.5 pg/kg/min, an average effective dose is 1 to 2 pg/kg/min. Toxicity can develop with nitroprusside, consisting of tachyphylaxis, metabolic acidosis, or elevations of sodium thiocyanate and cyanide levels. A potentially serious drawback, especially in older patients and individuals with limited
CLINICAL FEATURES AND TREATMENT
In addition to the hypertension, hemodynamic measurements often reveal a normal, slightly elevated, or slightly reduced cardiac output and moderate-to-significant elevations of systemic vascular resistance (SVR). Guidelines for successful drug therapy in this condition require an agent that must address the prevailing hemodynamic characteristics, be rapid in onset as well as offset to allow titration, be easily and
Table 1. Postoparstiva Catacholamina Levels Narepinephrine WLI
Epinephrine (W/L)
Renin WmLlh)
Mean
664
94
2.9
SD
242
51
5.3
Range
266-l
,452
21-195
O-23.2
NOmld (mean + SD) Normal + 2 SD
146 f 45
42 i 35
0.5 f 0.3
236
112
1.1
RICHARD J. GRAY
680
ho2
PVO,
(mm Hg)
(mm Hg)
(ml Anin)
48-
1
AaDO,
MVO,
t
Q,/Qt
(mm Hg)
360
26
T 24 22
320
-
36-
20
32 -
18
28 -
16 I T
Pulmonary and tissue gas exchange variables measured at an inspired oxygen concentration of 100% during the Fig 2. control period and during the last ten minutes of each intervention in a subgroup of eight patients. NP. nitroprusside: TNG, nitroglycerin: PaO*, arterial oxygen tension; PvG,. mixed venous oxygen tension; MvG,, tissue oxygen use; AaDO*, alveolar-arterial oxygen gradient: GslQt. intrapulmonary shunting. (0) Control; Ef1)NP: ( 1 TNG, (a) P < 0.06 vs control: ( + 1 P < 0.01 NP v TNG: f + + 1P < 0.001 NP v TNG. Reprinted with permission.’
pulmonary function, is the occurrence of a marked decrease in PaO,, suggesting the presence of a ventilation-perfusion mismatch. The mechanism by which nitroprusside worsens intrapulmonary shunting appears to be inhibition of hypoxic vasoconstriction in the pulmonary bed, resulting in increased perfusion of poorly ventilated regions.26-28Figure 2 illustrates variables of pulmonary gas exchange comparing nitroprusside with a nitroglycerin infusion.’ Despite a reduction in global myocardial oxygen requirements, marked reductions in coronary blood flow due to excessive lowering of diastolic blood pressure can lead to myocardial ischemia with use of nitroprusside.4 Coronary steal can also result in myocardial ischemia with nitroprusside administration. The mechanism is not fully understood, but factors important to the process include the presence of significant obstructive coronary disease in a vessel adjacent to a branch without significant obstruction. Maximal dilation of downstream resistance vessels without effect upon the upstream conductance vascular segment results in the large vessel obstruction becoming the critical factor regulating local blood flow. This worsens the maldistri-
bution of coronary blood flow away from the obstructed zone. 29Maldistribution of blood flow and the potential for myocardial ischemia are worsened by any significant reduction in coronary perfusion pressure resulting from vasodilator administration.29 This is especially true of an agent that particularly lowers diastolic blood pressure. Nitroprusside, with its potent direct small vessel vasodilating action, is capable of such effects, as is dipyridamole.29 Neither drug has significant effects on the larger conductance vessels, nor do the drugs appear to have significant ability to dilate the atherosclerotic segment. This lack of conductance effect is in contrast to that of nitroglycerin, which has been demonstrated to alter vascular tone throughout29*30and also appears capable of dilating certain diseased segments.30 For these reasons, intravenous (IV) nitroglycerin has been suggested for postoperative hypertension. In one study, it was able to achieve blood pressure control equivalent to that of nitroprusside in 14 of 17 patients and did not result in worsening of intrapulmonary shunting.5 Patients with chronic congestive heart failure and elevated filling pressures tolerated nitroglycerin particularly well. The average’infusion
POSTOPERATIVE HYPERTENSION
681
rate of nitroglycerin for successful control of blood pressure is 1 to 2 rg/kg/min. Postoperative hypertension is often seen in the setting of overall hyperdynamic cardiovascular function with sinus tachycardia, elevated cardiac output, and modestly elevated systemic vascular resistance. /3-adreneric blocker therapy seems particularly useful in this type of patient, especially in view of the elevation of catecholamines that often occurs and the frequent history of preoperative B-blocker use. Intermittent dosing with IV propranolol, 1 to 5 mg, every six hours, has been successful; however, propranolol has not traditionally been used as a continuous infusion. The IV ultra-short-acting b-blocker, esmolol, given as a continuous infusion, appears to provide effective control of hypertension in most patients, with minimum reduction of cardiac function. The principal advantages to this approach are the lack of any deleterious effects on intrapulmonary shunting, titratable onset and offset of action, and freedom from excessive lowering of diastolic blood pressure.” Table 2 summarizes these effects with data from a study that compared nitroprusside to esmolol in patients with postoperative hypertension after coronary artery surgery.23 Labetalol, an agent with both a- and fiblocking effects, available both orally and IV, has also been used successfully in early postoperative hypertension. Incremental bolus doses of 10 to 40 mg are associated with reductions in blood pressure and heart rate (HR),3’ and appear to be as successful at controlling postoperative hypertension as hydralazine, but without the tendency for the increased HR that occurs with hydralazine.32 Continuous IV infusion has also been used with similar success at a dosage of 2 mg/min. A decrease in HR with labetalol in this clinical situation is less certain than blood pressure reduction, but a significant decline in both HR and cardiac index with no reduction in systemic resistance have also been reported, suggesting that @-blockade may predominate over a-blocking effects, especially when labetalol is used in IV form.33 Calcium channel blocking drugs have been
Table 2.
Treatment
of Poatoperative
Esmolol v Nitropruaaide:
PaMllaSr Heart rate
Summary
Hypertension: of Differences
Esmdol (%I
NitroprUtide (%)
a-14
t
?? -20 ?? -8 ?? -23
t
-31.
t
+7
+7*
8lood pressure Systolic Diastolic Cardiac index Stroke volume Left ventricular SWI
-18.
-7.5
-0.3
?? -30
-199
PaO,
-0.1
t
0, saturation
-0.1
t
-39. -54
Abbreviation: SWI, stroke work index. +P < 0.05 Baseline Y dug. tP < 0.05 esmolol Y nitropruaside.
increasingly used for control of chronic outpatient hypertension, and as IV formulations become widely available they are likely to be used for control of acute hypertension as well. One such agent, nicardipine, has little or no discernible negative inotropic or chronotropic effects, and when given as either an IV bolus or infusion, it has rapid enough onset and offset of action to allow titration of blood pressure.34 It has been found to be capable of controlling hypertension while increasing cardiac output and HR. Several hours’ therapy with an IV agent may be sufficient if hypertensive tendencies decrease with rewarming and relief of pain and anxiety. Other patients, particularly those with hypertension preoperatively, will require longer therapy. Successful weaning from IV to oral control has been achieved with hydralazine, 10 to 50 mg, every six hours; aldomet, 250 to 500 mg, every six hours; or clonidine, 0.1 to 0.2 mg, every six to eight hours. More recently, however, nifedipine, 10 to 20 mg, every six hours, orally or sublingually, has been used successfully and is well tolerated. In general, it is wise to resume preoperative antihypertensive regimens that may have been well tolerated; however, daily adjustments in dosage may be necessary. Regimens that include chronic thiazide diuretics should be reevaluated in view of possible rapid postoperative changes in electrolytes and intravascular volume, as well as long-term adverse effects on serum lipids.
REFERENCES 1. Estafanous FG, Tarazi RC, Viljoen JF, et al: Systemic hypertension following myocardial revascularization. Am Heart J 85:732-738, 1972
2. Hoar PF, Hickey RF, Ullyot DJ: Systemic hypertension following myocardial revascularization. J Thorac Cardiovasc Surg 71:859-864, 1976
662
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