The goal mean arterial pressure (MAP) is typically set as greater than 65 mm Hg. A higher goal may be needed with chronic hypertensives in whom the autoregulatory curve of the brain and kidney have shifted to accommodate long-standing elevated systemic pressures. In addition, patients with known vascular stenoses of the carotid or renal arteries, as well as those with unrepaired coronary artery disease may require a higher perfusion pressure to overcome these potentially flow-limiting lesions. A lower MAP may be required for a time in patients with a friable aorta to decrease the risk of bleeding.
MAP is defined as MAP = CO × SVR, where SVR denotes systemic vascular resistance. As CO itself is defined as HR times stroke volume (SV), the equation may be further defined as: MAP = HR × SV × SVR. Thus, hypotension may be conceptualized as being affected by 1 of these 3 major variables.
HR may be a factor in hypotension. The process of cooling and arresting of the myocardium during cardiac surgery renders the muscle less compliant and induces diastolic dysfunction.12 This resultant increase in the “stiffness” of the ventricles can limit the stroke volume and render the CO more dependent on HR. Thus, a HR that is too slow, even if not strictly bradycardic, may limit CO and decrease MAP. The responsivity of the blood pressure to pacing with epicardial wires to a HR of 90 to 100 beats/minute may be tested. If both atrial and ventricular wires are present, pacing can be accomplished with maintenance of atrial kick. However, if only ventricular wires are available, the hemodynamic benefit of increasing HR with ventricular pacing may be diminished by loss of contribution to stroke volume from loss of atrial kick. In fact, an increased pressor requirement may be observed in patients who lose atrioventricular (AV) synchrony and the atrial contribution to SV due to the development of an arrhythmia such as atrial fibrillation.
SV is affected by preload, contractility, and afterload. Hypotension, especially in the patient with a labile blood pressure, may be due to decreased preload and low SV from hypovolemia. Low preload may be due to an obvious process such as chest tube drainage or to a more occult occurrence such as retroperitoneal bleeding in the patient who has undergone femoral arterial cannulation. The volume responsiveness of the patient can be tested empirically by 250 to 500 cc fluid boluses with subsequent assessment of the effect upon blood pressure. Both normal saline and lactated ringers may be used for resuscitation although 5% albumin is frequently utilized with the intention of administering an agent with a greater intravascular half-life. Transfusion with packed red blood cells may be indicated in the setting of significant anemia, especially with a concurrent vasopressor requirement. The data on hydroxyethyl starch (HES) agents discourage its use in the cardiac surgical ICU. One study randomized 45 patients to receive either 15 mL/kg HES solution or 4% albumin after admission to the cardiac ICU and found that the HES group demonstrated thromboelastometry tracings indicative of impaired fibrin formation and clot strength.13 Although the 2 groups demonstrated similar chest tube outputs, a subsequent meta-analysis of 18 trials comparing HES solutions with albumin for fluid management in CPB surgery found that HES solutions increased blood loss, reoperation for bleeding, and the rate of blood transfusion.14 Given these results, it seems prudent to avoid the use of HES solutions for resuscitation in the postcardiac surgery patient. Hypotension from decreased preload and low SV may be secondary to mechanical obstructive process rather than hypovolemia. Conditions such as tamponade and tension pneumothorax prevent adequate venous return, depress SV and CO, and can result in hypotension and shock with rising pressor requirement and lactate and oliguria. Tamponade is further discussed under section “Bleeding.”
Hypotension may also be secondary to low SV from decreased contractility. A temporary decrease in myocardial function is to be expected in the postcardiac surgery patient.4,5,6 One study examining 24 patients undergoing elective coronary artery bypass surgery with serial hemodynamic measurements and radionuclide evaluation of ventricular function found that 96% experienced left- and right-sided myocardial depression postprocedure. The left-sided EF dropped from 58% preoperative to 37% with the nadir occurring 4.4 hours after coronary bypass. Recovery back to 55% occurred approximately 7.1 hours after coronary bypass.6 An earlier study of 22 patients undergoing coronary artery bypass surgery found that those with an EF of more than 55% recovered ventricular function within 4 hours of bypass but that those with an EF more than 45% demonstrated a more profound decrease in function and a delayed recovery to baseline even after 24 hours.5 Thus, the immediate postoperative cardiac patient may demonstrate a temporary inotropic or vasopressor requirement until myocardial contractility has fully recovered. However, a high index of suspicion for differentiating between this known and expected decrease in function and concurrent detrimental processes should be maintained. Other independent causes of decreased myocardial contractility include new onset myocardial infarction from unrepaired disease or from CABG thrombosis or vasospasm. Diagnosis of a new ischemic insult may be accomplished with an electrocardiogram or with echocardiography demonstrating a new wall motion abnormality. In addition to hemodynamic instability, the onset of new arrhythmias such as ventricular tachycardia (VT) may be a manifestation of myocardial supply-demand mismatch. Troponins are of limited utility in detecting ischemia as they are typically elevated postcardiac surgery; however, some advocate trending the values. Management may include the administration of nitroglycerin to vasodilate the coronary arteries and to increase coronary perfusion pressure by decreasing preload and hence left ventricular end-diastolic pressure, cardiac catheterization to remove thrombus, or reexploration in the operating room to visually inspect the grafts.
Systemic Vascular Resistance
Hypotension may also be caused by insufficient systemic vascular resistance. Some patients arrive to the ICU hypothermic despite adequate rewarming on CPB due to a phenomenon called afterdrop—a redistribution hypothermia secondary to a cool periphery. These patients require active rewarming, which results in vasodilation of the peripheral vasculature and can uncover or worsen a vasopressor requirement. CPB causes a systemic inflammatory response that can lead to decreased SVR and a form of postbypass hypotension known as vasodilatory shock,15,16 generally described as a MAP less than 70 mm Hg in the setting of an adequate CI of more than 2.5 L/min/m2. Increased levels of vasodilators such as nitric oxide and bradykinin have been implicated in the pathogenesis of this phenomenon. The increase in bradykinin may be related to lack of deactivation by angiotensin converting enzyme (ACE) due to decreased blood flow to the lungs during CPB.17,18 Vasodilatory shock may also be caused by a relative vasopressin deficiency.19,20 One prospective study of 145 patients measured vasopressin levels 5 minutes after weaning from CPB. Those with vasodilatory shock demonstrated lower levels of vasopressin than those with postbypass hypotension due to decreased CI, and infusion with exogenous vasopressin improved MAP.19 This study found the incidence of vasodilatory shock to be 8%, although the incidence was higher (27%) in those with an EF of less than 35%; in addition, preoperative ACE-inhibitors, commonly part of a heart failure regimen, were found to be a risk factor for the development of vasodilatory shock. A retrospective study of 2823 patients found a 20% rate of vasoplegia; clinical risk factors included observation of a clinically significant decline in MAP at the onset of CPB, length of bypass, and preoperative use of β blockers and ACE-inhibitors among others.21
Another way to conceptualize the hemodynamic changes of the postoperative period, especially in patients with valvular lesions, is to consider whether the myocardium is pressure-overloaded or volume-overloaded. Lesions such as aortic stenosis give rise to pressure-overloaded ventricles. In this situation, chronic obstruction to left ventricular ejection results in concentric hypertrophy as a compensatory response to increased wall stress. The increase in ventricular wall thickness results in a ventricle with decreased diastolic compliance or greater “stiffness.” As a result, the resultant limitation in SV can result in a decrease in CO with lower HRs. Conversely, excessively high HRs may limit diastolic filling time, SV, and may also compromise CO. The stiffness of the ventricle impedes filling and makes the myocardium more dependent on atrial kick for stroke volume. Hence, the development of a nonsinus rhythm such as atrial fibrillation may result in a decrease in SV that decreases CO and MAP. The pressure-overloaded ventricle is more prone to ischemia than the normal ventricle. The increase in muscle mass increases the basal metabolic rate of the entire ventricle. In addition, the increase in stiffness of the pressure-overloaded myocardium results in an increase in the left ventricular end-diastolic pressure (LVEDP). This results in a decrease in the gradient for coronary perfusion pressure (CPP = aortic diastolic pressure [AoDP] – LVEDP/coronary vascular resistance) rendering the myocardium more vulnerable ischemia with decreases in blood pressure. Tachycardia is particularly detrimental not only because it limits SV by decreasing diastolic filling time but also because it reduces the duration of diastolic coronary perfusion and increases myocardial oxygen demand. The hemodynamic considerations in the pressure-overloaded ventricle are summarized in Table 54–3.
Table 54–3Hemodynamic goals in the pressure-overloaded ventricle. ||Download (.pdf) Table 54–3Hemodynamic goals in the pressure-overloaded ventricle.
|Rhythm || |
|Heart rate || |
Avoid bradycardia to avoid decreased CO (CO = HR × SV)
Avoid tachycardia to avoid ischemia (increased myocardial oxygen demand, decreased duration of diastolic coronary perfusion)
|Blood pressure || |
Although hypotension is to be carefully avoided in the pressure-overloaded myocardium, patients with preserved LV function often present to the ICU hypertensive, as the left ventricle has not yet had time to adapt to the removal of the stenotic aortic lesion. In this case, institution of a vasodilator such as nicardipine can control blood pressure in the acute setting. The patient with decompensated aortic stenosis may have decreased contractility and may have presented with decompensated heart failure.
Lesions such as aortic and mitral regurgitation result in volume-overloaded ventricles. Chronic volume overload results in eccentric hypertrophy where overall muscle mass is increased but chamber enlargement is greater than the increase in ventricular wall thickness. This gradual increase in LV size and compliance usually causes little change in the LVEDP. Chronic volume overload may result in a dilated cardiomyopathy with decreased LV systolic function and may require the use of inotropes to separate from bypass and their continued use in the ICU until myocardial stunning resolves. Decreased CO after correction of mitral regurgitation may also be secondary to decreased volume loading of the left ventricle from the resolution of regurgitation. Reports of the ejection prior to and after resolution of mitral regurgitation may be somewhat misleading. For example, a preoperative EF of 55% with a postoperative EF of 30% may not reflect any actual change in the contractility. The estimated EF prior to surgery reflects a SV that includes both forward flow and retrograde flow into the left atrium, and the effective EF taking only forward flow into account may have been 30% from the start. Because left ventricular afterload increases acutely after correction of mitral regurgitation, the left ventricle may benefit from pharmacologic afterload reduction. Chronic volume overload differs greatly from the volume overload resulting from acute aortic or mitral insufficiency where LVEDP increases dramatically and can result in sudden pulmonary edema and decreased CO prior to surgical correction.
Mitral regurgitation and stenosis may result in left atrial hypertension and dilation that can predispose to atrial fibrillation. In addition, pulmonary hypertension secondary to chronic venous congestion may be present with concomitant right ventricular dysfunction due to long-standing increases in RV afterload.
The hemodynamic problem of low CO (CO = HR × SV) may be broken down by examining the HR as well as the factors affecting SV (preload, afterload, and contractility). In the situation where low CO is accompanied by bradycardia, the CO may be augmented by increasing the HR. This can be accomplished either by electrical pacing with an external epicardial wire, reprogramming the rate of an internal pacemaker, or increasing the HR chemically with an agent with chronotropic properties. If a low CO is accompanied by a low afterload state and hypotension, the blood pressure should first be supported with vasopressors until more definitive therapies can be instituted. If the patient is volume-responsive, the SV and CO may be augmented with additional preload. If the patient does not demonstrate improvement with volume, then the depressed CO may be secondary to decreased contractility. Epinephrine, an inoconstrictor, provides inotropic support along with vasoconstriction that should increase MAP. The inodilators dobutamine and milrinone may also be used but because they vasodilate the peripheral vasculature, vasopressor initiation or increase may be necessary to counteract a further drop in blood pressure. SV and CO may also be limited due to excessive afterload. The patient with high MAP and depressed CO may benefit from afterload reduction with a systemic vasodilator.
A high CO in the presence of a low HR does not need any intervention. If accompanied by low MAP, the low SVR state may be counteracted with vasoconstrictors such as norepinephrine and vasopressin. A high CO state with high MAP should be treated, as a high MAP may increase the risk of bleeding and will increase the oxygen demand of the myocardium; a decrease in blood pressure should, however, always be made in the context of baseline blood pressure and with an evaluation of the risk of hypoperfusion to pressure-dependent organs. The various possible therapies for disordered blood pressure and CO are detailed in Table 54–4.22
Table 54–4Therapies for abnormal blood pressure and cardiac output. ||Download (.pdf) Table 54–4Therapies for abnormal blood pressure and cardiac output.
The details of various vasopressors and inotropes are included in Tables 54–5 and 54–6.23 The vasopressors are utilized for their ability to increase MAP by increasing SVR (MAP = CO × SVR). Norepinephrine, an α1 agonist that provides β1 inotropy is typically chosen in favor of phenylephrine, a pure α1 agonist that only increases afterload and does not provide inotropic assistance. Vasopressin may be useful in the vasoplegic patient with low SVR postbypass as a supplement to norepinephrine. In addition, as it has minimal pulmonary vasoconstrictive effects at low doses (< 4 U/h), vasopressin may be useful in patients with significant pulmonary hypertension or right ventricular dysfunction. Dopamine at low doses produces renal and splanchnic vasodilation, an effect that has not been shown to impact outcomes. Dopamine is the precursor to norepinephrine; at higher doses, the effect of dopamine becomes more similar to that of norepinephrine with the addition of inotropic and then vasoconstrictive properties. Epinephrine, dobutamine, and milrinone provide inotropy with varying effects upon the blood pressure. Epinephrine, due to greater α1 constriction than β2 vasodilation, has the overall effect of increasing blood pressure. Dobutamine and milrinone, both inodilators, increase inotropy but at the cost of increased vasodilation and the potential need for initiation or escalation of vasopressors. Compared with dobutamine, milrinone produces a greater decrease in SVR. Dobutamine and milrinone both increase levels of cyclic adenosine monophosphate (cAMP) (and subsequently calcium and contractility) in the cardiac myocyte but by different mechanisms: through the β1 receptor, dobutamine activates the Gs/adenylate cyclase pathway while milrinone inhibits phosphodiesterase III, an enzyme that degrades cAMP. These 2 agents, hence, are synergistic and lower levels of each medication may be coadministered with fewer side effects. Although all β1 agonists demonstrate some degree of chronotropy, isoproterenol demonstrates a particularly strong ability to increase HR and is colloquially known as the chemical pacemaker.
Table 54–5Vasopressors, inotropes, and afterload reducers (mechanisms and receptors). ||Download (.pdf) Table 54–5Vasopressors, inotropes, and afterload reducers (mechanisms and receptors).
| ||Classification ||Receptors ||Dose |
|DA-1 ||α1 ||β1 ||β2 ||Other |
|Phenylephrine ||Vasopressor ||0 ||++ ||0 ||0 || ||1-200 μg/min |
|Vasopressin ||Vasopressor ||0 ||0 ||0 ||0 ||V1 (also V2) || |
0.02-0.04 U/min up to 0.1
(1.4-2.4 U/h up to 6)
|Norepinephrine ||Inoconstrictor ||0 ||+++ ||++ ||0 || ||1-20 μg/min |
|Dopamine ||Inoconstrictor || |
|± || || |
|Epinephrine ||Inoconstrictor ||0 ||+++ ||+++ ||++ || ||1-20 μg/min |
|Dobutamine ||Inodilator ||0 ||0 ||+++ ||+++ || ||2-20 μg/kg/min |
|Milrinone ||Inodilator ||0 ||0 ||0 ||0 ||PDE3 inhibitor ||0.125-0.5 μg/kg/min |
|Isoproterenol ||Inodilator ||0 ||0 ||+++ ||+++ || ||1-5 μg/min |
Table 54–6Vasopressors, inotropes, and afterload reducers (effects). ||Download (.pdf) Table 54–6Vasopressors, inotropes, and afterload reducers (effects).
| ||Classification ||Vasoconstriction ||Vasodilation ||Contractility ||HR ||Other |
|Phenylephrine ||Vasopressor ||3+ ||0 ||0 ||0 ||Reflex bradycardia |
|Vasopressin ||Vasopressor ||4+ ||0 ||0 ||0 ||Lacks pulmonary vasoconstrictor activity at doses < 4 U/h |
|Norepinephrine ||Inoconstrictor ||4+ ||0 ||2+ ||1+ || |
|Inoconstrictor || |
|Epinephrine ||Inoconstrictor ||4+ ||3+ ||4+ ||4+ ||May induce transient hyperlactatemia |
|Dobutamine ||Inodilator ||0 ||2+ ||4+ ||2+ ||Pulmonary vasodilator |
|Milrinone ||Inodilator ||0 ||3+ ||3-4+ ||0 ||Pulmonary vasodilator; half-life hours, accumulates in renal failure |
|Isoproterenol ||Inodilator ||0 ||4+ ||4+ ||4+ || |
In addition to chronotropy and inotropy, the different β1 agonists also demonstrate varying degrees of bathmotropy (arrhythmogenicity) and dromotropy (increased conduction through the AV pathway). High doses of norepinephrine, dopamine, epinephrine, and dobutamine may induce tachycardia or arrhythmias such as atrial fibrillation with rapid ventricular response. Milrinone also has a proarrhythmogenic tendency but is less than that of dobutamine.
The half-lives of these inotropes and vasopressors, with the exception of vasopressin and milrinone, are on the order of minutes, thus enhancing their titratability. Vasopressin has a half-life of approximately 10 to 20 minutes. Milrinone's terminal elimination half-life is approximately 2 hours, which renders it less titratable than other more rapid-offset inotropes such as dobutamine. It accumulates with prolonged infusions as well as in patients with renal insufficiency.
Epinephrine has been associated with the development of hyperglycemia and a type B lactic acidosis, that is, lactate generation in the absence of clinical evidence of tissue hypoperfusion (in contrast to type A which is associated with poor oxygen delivery). One study randomized 36 patients to receive norepinephrine or epinephrine for hypotension after CPB. They found that 6 of 19 patients who received epinephrine developed increased lactate levels peaking between 6 and 10 hours after CPB (lactate to ~3.8 mmol/L, pH 7.34) while 0 of 17 patients who received norepinephrine demonstrated the same phenomenon. The lactate normalized by 22 to 30 hours after bypass. There was no difference in the oxygen-delivery index calculated between the 2 groups. The authors postulated that because epinephrine inhibits the pyruvate dehydrogenase complex, the increased levels of pyruvate get shunted to generate more lactate in order to preserve the normal balance of lactate:pyruvate needed to maintain the oxidized form of nicotinamide adenine dinucleotide (NAD).24 Another study conducted in a medical ICU studying patients with dopamine-resistant cardiogenic shock randomized patients to receive norepinephrine-dobutamine or epinephrine. This study found that patients in the epinephrine group demonstrated an increase in lactate that peaked at 4.9 mmol/L at 6 hours with a pH of 7.26; this finding was notably absent in the dobutamine-norepinephrine group.25 Thus, lactic acidosis in the context of epinephrine therapy may not necessarily indicate hypoperfusion as it may reflect generation of endogenous lactate by another unrelated mechanism, especially if oxygen delivery is calculated to be adequate; however, use of epinephrine may obscure the utility of lactate as a marker of hypoperfusion.
The use of a vasodilator may be necessary with excessive hypertension that cannot be resolved with the usual doses of sedative and analgesics (Table 54–7). Nicardipine is a dihydropyridine calcium channel blocker whose main effect is vasodilation of the systemic, coronary, and cerebral circulations with essentially no AV nodal blocking activity or negative inotropy. Both nitroglycerin and nitroprusside release nitric oxide, a potent vasodilator that activates guanylyl cyclase, increase cyclic guanosine monophosphate (cGMP), and results in decreased intracellular calcium and vascular smooth muscle relaxation. Nitroglycerin predominantly causes venodilation, which decreases preload and the volume work of the heart. It is particularly useful when myocardial ischemia is suspected as CPP (AoDP – LVEDP/coronary vascular resistance) is improved by 2 mechanisms: by decreasing preload which decreases LVEDP and by decreasing coronary vascular resistance by promoting coronary vasodilation. Nitroprusside causes both venodilation and arterial dilation. High doses may result in cyanide toxicity.
Table 54–7Vasodilators. ||Download (.pdf) Table 54–7Vasodilators.
| ||Classification ||Mechanism ||Dose ||Considerations |
|Nicardipine ||Arterial dilator ||Calcium channel blocker ||5-15 mg/h || |
|Nitroglycerin ||Venodilator ||Nitric oxide ||5-400 μg/min || |
|Nitroprusside ||Balance arterial and venodilator ||Nitric oxide ||0.25-4 μg/kg/min (max 10 μg/kg/min) ||Cyanide toxicity, especially with doses > 8 μg/kg/min |
These 3 vasodilators provide rapid onset of action within minutes. Nicardipine has an elimination half-life of approximately 45 minutes while the elimination half life of both nitroglycerin and nitroprusside is approximately 5 minutes. Vasodilators may result in a reflex tachycardia. Tachyphylaxis can be seen, as well as rebound hypertension on sudden discontinuation of the drip. All vasodilators can reverse hypoxic vasoconstriction and worsen hypoxia by increasing shunt in atelectatic areas of the lung. In addition, those with intracranial hypertension may experience an increase in intracranial pressure due to an increase in cerebral blood flow secondary to cerebral vasodilation.