Fig. 9.1
Kaplan-Meier estimates of the rates of death at 3 years from cardiovascular (CV) causes, re-infarction, congestive heart failure (CHF), stroke, resuscitation after cardiac arrest, and the composite end point, according to the estimated glomerular filtration rate (GFR) at baseline. Modified from the original version [2, 3]
Chronic and acute heart failure patients frequently have renal dysfunction caused by a complex disease process that is broadly referred to as cardiorenal syndrome (Fig. 9.2). Renal and systemic ischemia and congestive nephropathy and hepatopathy from high central venous pressure (CVP ) and low cardiac output cause neurohumoral stimulation with upregulation of the renin-angiotensin-aldosterone system and increased catecholamines, antidiuretic hormone, and inflammatory cytokines (Figs. 9.3, 9.4, and 9.5) [5–8]. Renal function may also be negatively affected by the use of diuretics, angiotensin II receptor blockers or angiotensin II-converting enzyme inhibitors, and intravenous contrast agents [6]. Over time, this leads to a decline in renal function with renal fibrosis [6]. ESHD frequently occurs in older patients and therefore in the presence of low renal reserve (nephronopenia) and chronic metabolic acidosis, both of which may cause renal fibrosis [9].
Fig. 9.2
Congestive heart failure (CHF) and cardiorenal syndrome
Fig. 9.3
Effect of increasing central venous pressure (CVP) on glomerular filtration rate (GFR) in rats with constant blood pressure. The curvilinear model had the following individual polynomial components for the relationship between CVP and estimated GFR (eGFR): first order, Y = −25.8·(CVP + 1)/10 (Wald 28.2, p < 0.0001), and second order, Y = 35.7·([CVP + 1]/10)0.5 (Wald 17.4, p < 0.0001). Modified from the original version [4]
Fig. 9.4
CVP and renal blood flow on GFR. Modified from Damman K et al., Eur J Heart Fail 2007; 9:872–878
Fig. 9.5
Pathophysiology of the relationship between venous congestion and reduced glomerular filtration rate (GFR). ANP atrial natriuretic peptide, SNS sympathetic nervous system, RAAS renin-angiotensin-aldosterone system. Numbers in circles represent the targets for specific therapies as follows: (1) ultrafiltration, diuretics, sodium, and water restriction and arginine vasopressin receptor antagonists. (2) Ultrafiltration, diuretics, and sodium and water restriction. (3) Angiotensin II-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers. (4) Statin therapy. (5) Beta-blocker therapy. (6) Angiotensin II receptor blockers. (7) Neutral endopeptidase inhibitors. (8) Urodilatin. Modified from the original version [5]
Preoperative abnormal renal function (i.e., GFR <60 mL/min/1.73 m2) is associated with an increased incidence of acute kidney injury/acute tubular necrosis (AKI/ATN) and a reduced rate of survival 1 year after left ventricular assist device (LVAD ) placement [10]. Other studies have confirmed that adverse outcomes are associated with preoperative renal dysfunction [10, 11]. An INTERMACS (Interagency Registry for Mechanically Assisted Circulatory Support) risk score of 1 vs. 2 or 3 predicts poor renal outcomes [12]. Studies have shown that postoperative AKI/ATN is associated with the following preoperative characteristics: angiotensin II-converting enzyme inhibitor or angiotensin II receptor blocker use, renal size <10 cm, older age, small left ventricle, and diastolic dysfunction with high CVP (both likely signs of right heart failure and known association of diastolic dysfunction with chronic kidney disease) (Table 9.1) [13–15]. However, in a review of 100 consecutive continuous-flow LVAD (CF-LVAD ) implantations, Borgi and colleagues [14] did not find a statistically significant association between postoperative AKI/ATN and preoperative diabetes mellitus, hypertension, or renal dysfunction (7). The difference in these study findings may be attributed to the later era of the Borgi study, which has been proposed to be a period when patients received implants earlier in their disease process at a higher INTERMACS score . Operative and perioperative risk factors for AKI/ATN have been studied, and longer cardiopulmonary bypass (CPB) time (122 ± 55 vs. 78 ± 17 min), higher intraoperative blood loss and replacement (>1 L), and need for reoperation all increase the risk of postoperative AKI/ATN (Table 9.2) [13, 16–19]. Postoperative AKI/ATN is associated with a high risk of mortality, but death is most likely to occur within the first year after AKI/ATN, as the survival rate after the first year is not affected by the occurrence of postoperative AKI/ATN [15].
Table 9.1
Preoperative factors associated with postoperative acute kidney injury
1. Glomerular filtration rate <60 mL/min |
2. INTERMACS score of 1 vs. 2 or 3 |
3. Preoperative use of angiotensin II-converting enzyme inhibitors or angiotensin II receptor blockers |
4. Renal size <10 cm |
5. Diastolic dysfunction and high central venous pressure, likely reflective of right heart dysfunction |
Table 9.2
Perioperative factors associated with postoperative acute kidney injury
1. Cardiopulmonary bypass time >90 min |
2. Blood loss >500–1000 mL |
3. Right heart dysfunction |
4. Need for return to the operating room |
Studies have shown that CF-LVAD placement can often lead to postoperative liver and renal recovery, especially for (but not limited to) patients with mild preoperative renal dysfunction (e.g., creatinine levels between 1.4 and 1.9 mg/dL) [10, 11, 20–30]. Despite an early recovery in GFR (measured by serum creatinine) in patients after CF-LVAD implantation, a late (i.e., greater than 1 year post implantation) decline in GFR (measured by an increase in serum creatinine) has been observed. The reason for this decline is unclear [10, 23, 31–35]. Possible causes include low muscle mass at the time of implantation with a subsequent increase in muscle mass, continued (albeit less intense) neurohumoral and inflammatory cytokine stimulation, and hypertensive damage from the “new physiology” of chronic high diastolic perfusion. Animal and human studies have shown an abnormal inflammatory response in the arterial wall after exposure to a CF-LVAD [36–43]. Notably, at higher pump speeds, low-grade continuous hemolysis occurs, which has been proposed as a cause of chronic hemoglobinuria, reduced availability of nitric oxide, and oxidative stress with peritubular inflammation [16, 18]. In an ovine model, micro-emboli have been seen in the renal microvasculature [17].
Most contemporary pumps are continuous-flow assist devices. Therefore, this chapter will focus on the care of patients with renal dysfunction after placement of a CF-LVAD . Currently, ESRD is an exclusion criterion for destination therapy (DT) LVAD placement, so patients with ESRD have been approved for LVAD placement only if they have been approved for dual-organ transplant or bridge to transplant (BTT). The number of patients in whom ESRD develops after LVAD implantation for DT has grown. We will discuss the successful care of these post-LVAD patients with ESRD by a specialized dialysis clinic and management team.
Other renal-related syndromes in LVAD patients are worthy of attention in this new and relatively unstudied physiology, which is characterized by minimal pulsatile flow with high diastolic and low systolic pressure and low-grade, continuous hemolysis. Postoperative mediastinal and pericardial tamponade is a cause of sudden oliguria. Partial-flow constriction from a clot, pannus over the inflow, or “kinking” of the inflow cannula or the aortic graft that causes acute or subacute massive hemoglobinuria in the presence of reduced cardiac output can cause AKI [43]. Renal or splenic infarcts may develop in patients, accompanied by acute pain syndrome. Hyponatremia often continues after LVAD implantation, and, although not yet studied, correction may lead to improved functional status.
The First 48 h
Performing LVAD surgery generally requires the patient to undergo CPB. As in all cardiovascular surgeries, limiting CPB time to <90 min can help prevent postoperative AKI [13]. Perioperative bleeding is a confounding complication with a progressive increase in the risk of AKI with >500–1000 mL of blood loss and replacement [13]. Right heart dysfunction after LVAD placement is a common risk factor for postoperative AKI because of the reduced cardiac output and high venous pressure [6, 7, 14]. Pulmonary hypertension frequently develops in patients with chronic heart failure; in fact, an LVAD is usually placed as DT or as a “bridge to candidacy” in patients with increased pulmonary vascular resistance (>4 WU) to allow pulmonary pressure to normalize so that transplantation can be considered. Right ventricular failure causes high right-sided pressure and increased CVP . Right heart failure may be affected by the LVAD itself, as discussed in Chap. 18. The septum may be displaced to the left, adversely affecting right ventricular function. This is dependent on the LVAD pump speed and its effect on the anatomy of the left ventricle. Ideally, to help protect the septum, the pump is adjusted so that the aortic valve opens with each beat and the left ventricle remains mildly dilated. High venous return with increased pump flow may further overload the right ventricle and cause dilation and strain, especially if there is not a concomitant reduction in the pulmonary pressure and cardiac output. The end result may be right ventricular failure and increased central and renal venous pressure. This outcome may be further complicated by tricuspid regurgitation, which is common in chronic heart failure, especially in patients with high preoperative pulmonary artery (PA) pressure . Congestive hepatopathy and nephropathy are also common and may worsen renal function and cause a poor diuretic response (Figs. 9.3, 9.4, and 9.5) [5–8, 14].
Low systemic blood pressure in postoperative LVAD patients compounds right heart failure and high central and renal venous pressures. Causes of low systemic blood pressure include sedation, pain medications, and frequent use of vasodilatory inotropes and pulmonary vasodilators. A continuous-flow pump cannot pump against high pressure, so it is important to keep the systemic pressure high enough to provide adequate renal perfusion, taking the adverse effects of high venous pressure into account. Care should be taken, however, not to increase the systemic pressure high enough to reduce output from the continuous-flow pump [44].
The nephrologist should confer closely with the intensivist, cardiologist, and LVAD surgeon. The best plan for accomplishing this is to perform daily team rounds.
In the immediate postoperative period, we minimize the use of casual fluid (i.e., fluid given as a carrier for drips, medications, and electrolytes) and administer therapeutic fluid according to a weight-based protocol by using a balanced electrolyte solution with some bicarbonate equivalent rather than normal saline. Postoperative volume-related weight gain has been associated with poor outcomes [45], and fluid-restricted protocols in the postoperative period have been associated with either worse [46] or improved [47] outcomes. González-Fajardo and colleagues [48] have shown improved outcomes in patients undergoing abdominal vascular surgery with the use of a fluid-restricted protocol [45]. In addition, at CHI/St. Luke’s Texas Heart Institute, we are initiating a trial of a fluid-sparing regimen in CF-LVAD patients . The goal PA pressure is <45 mmHg, and the goal CVP is initially <12 mmHg and is reduced to <10 mmHg once the patient is hemodynamically stable. Milrinone is often required to support right ventricular function and to lower PA pressure. In patients with a low GFR , which affects milrinone clearance, drug accumulation may cause low systemic and renal perfusion pressure. For patients with a low GFR (<30–40 mL/min/1.73 m2) or low urine output (<0.5 mL/kg/h), we prefer to reduce the milrinone dose to <0.25 μg/kg/min, but we confer regularly with the cardiology team (Table 9.3) (Figs. 9.6 and 9.7) [50].
Table 9.3
Fluid therapy choice in the AKI ICU
Alternatives | |
|---|---|
Drug | Hazard/disadvantages |
0.9% saline | Acidosis, ?AKI |
Lactated Ringer’s | Hypotonic, Ca++ |
Plasmalyte | Gluconate, acetate |
Albumin | Cost, ?AKI |
HES | AKI, bleeding, pruritus |
Gelatin | Anaphylaxis |
Fig. 9.6
Favor-balanced fluid not NS. Modified from Shaw, et al. Ann Surg. 2012 Mar 30
Although diuretics generally are not recommended early because of the risk of venous dilatation, low blood pressure, and reduced LV filling, loop diuretics may be necessary to prevent severe volume overload, especially in patients with right heart dysfunction [51]. Judicious fluid management, however, should be the mainstay of fluid therapy.
In patients with fluid overload , pulmonary congestion, and high right-sided filling pressures, we initiate loop diuretics while minimizing fluid intake. The latter requires coordination with the pharmacy and members of the intensive care unit (ICU) team. A low dose of a loop diuretic (20–40 mg of furosemide or 0.5–1 mg of bumetanide) is given, while the patient’s response and blood pressure are monitored. The dose can then be titrated either with higher intermittent doses or with a continuous drip (5–20 mg/h of furosemide or 0.25–1 mg/h of bumetanide). For patients who do not respond, we confer with the team to ensure that no other cause for low renal perfusion pressure can be identified (e.g., excessive sedation, pain medication, vasodilators such as milrinone, or tamponade). A lack of response, again, may indicate a poor right heart function or a need to increase the LV output, and the cardiologist may need to make pump speed adjustments. These adjustments may be made under echocardiographic or PA catheter guidance. The next step that we have found helpful is the addition of a distal tubule blocker (usually chlorothiazide, 250–500 mg administered intravenously). Loop diuretics and distal tubular blockers cause alkalosis and hypokalemia. We use potassium chloride, carbonic anhydrase inhibitors, or amiloride in this situation. Amiloride has a shorter half-life and a more immediate onset than mineralocorticoid inhibitors and will ameliorate alkalosis and hypokalemia as well.
From a renal perspective, ideal postoperative values include a CVP of <10 mmHg, PA pressure of <45 mmHg with the LVAD adjusted so that the valve is opening, and a mean systemic pressure of 70–80 mmHg, as well as an even fluid balance (Table 9.4).
Table 9.4
Ideal hemodynamics for renal function
1. Central venous pressure <10 mmHg |
2. Pulmonary pressure <45 mmHg |
3. “Mean arterial pressure” 70–80 mmHg |
4. Adequate cardiac output to ensure stable and normal end-organ function; patient should be awake, alert, and neurologically stable (confer with cardiology) |
A sudden reduction in urine output should trigger suspicion of bleeding , especially bleeding into the mediastinum with functional tamponade or into the pleural space with a sudden reduction in cardiac output or mean pressure. Tamponade will usually be associated with increased central pressures, but this is occasionally subtle and may cause low urine output, even in the setting of a minimal change in PA pressure and CVP. Right heart dysfunction is always a consideration; thus, we further emphasize the importance of conferring with the LVAD team (Table 9.5). Often, an adjustment of inotropic drugs or pump speed is successful. However, the patient may require reoperation for bleeding and pericardial decompression or placement of a right ventricular support device, but we have a standard action plan (Table 9.6).
Acute Oliguria Post Continuous-Flow LVAD
- 1.
Lower urinary tract obstruction
- 2.
Severe RH dysfunction with decrease in cardiac output
- 3.
Tamponade/due to mediastinal bleeding
- 4.
Bleeding/look for hemothorax
- 5.
Pump malfunction/inflow or outflow obstruction—rare in post-op period
- 6.
Sepsis or drug-induced hypotension—consider milrinone
Table 9.5
Acute oliguria after continuous-flow LVAD implantation
1. Lower urinary tract obstruction |
2. Severe right heart dysfunction with decreased cardiac output |
3. Tamponade due to mediastinal bleeding |
4. Bleeding (look for hemothorax) |
5. Pump malfunction, inflow or outflow obstruction (rare in the postoperative period) |
6. Sepsis- or drug-induced hypotension (consider milrinone) |
Table 9.6
Acute oliguria after continuous-flow LVAD implantation : action plan
1. Ensure that the bladder is decompressed |
2. Look for a sudden decrease in hemoglobin levels |
3. Confer with the ICU team to adjust pump or drips |
4. Perform chest radiography: computed tomography or echocardiography |
5. Check urine indices, if appropriate 6. Look for nephrotoxic drugs |
If the above-described measures do not improve the patient’s condition, intervention with renal replacement is necessary. For patients who remain on the ventilator and need fluid removal, we prefer to use continuous renal replacement therapy (CRRT) , which allows more continuous ultrafiltration (UF) adjustment with excellent clearance. At our institution, we often keep the patient on CRRT in the operating room to control fluid volume and electrolytes. Our ICU nurse, who is familiar with the patient, manages CRRT in the operating room. Adjustments are made by the anesthesia team, but the nephrologist is always available.
We have found that the blood flow rate does not affect blood pressure or hemodynamic stability, so we recommend adjusting this rate as close to 300 mL/min as possible to prevent system thrombosis. The clearance, which is controlled by the dialysate flow and the dialysate content, is based on the concentrations of blood urea nitrogen, creatinine, and potassium, as well as the acid-base status, just as in the standard ICU patient. However, we prefer a dialysate and UF fluid flow of at least 35 mL/kg/h (Fig. 9.8).
Fig. 9.8
Dose of CVVH in AKI. Modified from [52]
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