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Cardiorenal Syndrome Type 1

David L. Brown

OUTLINE

Deﬁnition and Classiﬁcation, 216 Prevalence, 216 Prognosis, 216 Risk Factors, 218 Diagnosis, 218

Pathophysiology, 218 Prevention, 220 Management, 221 Summary, 222

Various organ systems within the body are intimately connected to each other and communicate via organ crosstalk, the complex biologic communication and feedback between organ systems mediated by soluble and cellular messengers. In the normal state, this crosstalk helps to maintain homeostasis and optimal function of the body and all its component systems. However, during disease, this crosstalk can transfer signals from the diseased organ that initiate and perpetuate dysfunction in other organs.

1,2

DEFINITION AND CLASSIFICATION

Combined disorders of the heart and kidney are referred to as cardiorenal syndromes (CRSs) and have been deﬁned as “a complex pathophysiological disorder of the heart and the kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ.”3 The CRSs are classiﬁed into four subtypes based on the primary organ that is dysfunctional, either “cardiorenal” syndromes (types 1 or 2) or “renocardiac” syndromes (types 3 or 4) and whether the organ dysfunction is acute (types 1 and 3) or chronic (types 2 and 4). A ﬁfth subtype is characterized by simultaneous cardiac and renal dysfunction in the setting of a systemic illness. The ﬁve subtypes are summarized in Table 22.1. of the organ dysfunction and which problem predominates can also be used to distinguish types 1 or 2 (cardiac ﬁrst) from types 3 or 4 (renal ﬁrst).4 Furthermore, the classiﬁcation is not static, as patients may transition between different CRS subtypes both in and out of the hospital.5 For example, a patient with chronic congestive heart failure (CHF) and chronic kidney disease (CKD) who is considered to have CRS type 2 may develop acute decompensated heart failure (ADHF) requiring hospitalization complicated by acute kidney injury (AKI); the patient would then be diagnosed with CRS type 1. Successful treatment of the ADHF with resolution of the AKI will return the patient to CRS type 2. Likewise, the same patient could progress to end-stage renal disease and develop acute pulmonary edema requiring

The temporal sequence

emergent dialysis, in which case the diagnosis would be CRS type 3. In the cardiac intensive care unit (CICU) environment, the most commonly encountered CRS is type 1, which will be the focus of this chapter.

CRS type 1 is characterized by an acute deterioration in cardiac function that then leads to a reduction in glomerular ﬁltration rate (GFR) and AKI (Fig. 22.1). The most common precipitants of acute cardiac dysfunction in the CICU that result in AKI are cardiogenic shock, ADHF, acute myocardial infarction (MI), acute mitral or aortic regurgitation, pericardial tamponade, constrictive pericarditis, or prolonged arrhythmias with associated hypotension or cardiogenic shock. For any given patient, there are four patterns of CRS type 1: (1) de novo cardiac injury leading to de novo kidney injury; (2) de novo cardiac injury leading to acute-on-chronic kidney injury; (3) acute on chronic cardiac decompensation leading to de novo kidney injury; and (4) acute-on-chronic cardiac decompensation leading to acuteon-chronic kidney injury.

PREVALENCE

CRS type 1 has been described in 27% to 45% of hospitalized patients with ADHF coronary syndromes (ACS). who present with ADHF, approximately 60% will develop AKI.4 AKI can be present on admission or can develop after admission. Approximately 20% to 30% of heart failure patients develop an increase in serum creatinine of more than 0.3 mg/dL lowing admission. The rise in serum creatinine usually occurs in the ﬁrst 3 to 5 days of hospitalization for ADHF.

6–12

and in 9% to 54% of patients with acute

13–19

Of patients with preexisting CKD

9,20–23

fol-

PROGNOSIS

The development of CRS type 1 is associated with worse clinical outcomes, more rehospitalizations, and greater health care expenditures.

11,12,15,25

The mortality risk associated with CRS type

216

CHAPTER 22 Cardiorenal Syndrome Type 1 216.e1

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Keywords

Cardiorenal syndrome acute decompensated heart failure heart failure acute kidney injury chronic heart failure chronic kidney disease hemodialysis continuous renal replacement treatment

CHAPTER 22 Cardiorenal Syndrome Type 1 217

ular-

Increased

Reduced renal

Uremic milieu

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TABLE 22.1 Classiﬁcation of the Cardiorenal Syndromes

Class Type Description Examples

1 Acute cardiorenal syndrome Acute worsening of cardiac function resulting in

AKI

2 Chronic cardiorenal syndrome Chronic abnormalities of cardiac function leading

to CKD

3 Acute renocardiac syndrome Abrupt worsening of renal function leading to

acute cardiac dysfunction

4 Chronic renocardiac syndrome CKD leading to chronic cardiac dysfunction Left ventricular hypertrophy in CKD 5 Secondary cardiorenal syndrome Systemic disorders causing cardiac and renal

dysfunction

ADHF, acute decompensated heart failure; AKI, acute kidney injury; CHF, congestive heart failure; CIN, contrast-induced nephropathy; CKD, chronic kidney disease. Modiﬁed from Cruz DN. Cardiorenal syndrome in critical care: the acute cardiorenal and renocardiac syndromes. Adv Chronic Kidney Dis. 2013; 20:56–66.

ADHF Cardiac surgery Acute coronary syndromes CIN Hypertension CHF Acute pulmonary edema in AKI Arrhythmia due to acidosis or electrolyte abnormalities

or volume overload

CIN leading to CHF

Sepsis Systemic lupus erythematosus Diabetes

Relative

decrease in

cardiac output

ADHF

Increased preload

Arterial

underfilling

Sympathetic nervous system

Endothelial relaxin factor

RAAS

Arginine vasopressin

Endothelin

Ineffective

natriuretic peptides

Kinin-kallikrein system

Prostaglandins

autoregulation

Vasoconstriction

Decreased

perfusion

pressure

Functional (pre-renal)

AKI

Parenchymal

damage

susceptibility

Glomer interstitial damage

Sclerosis Fibrosis

Fig. 22.1 Pathogenesis of CRS type 1. Acute decompensated heart failure (ADHF) via arterial

underﬁlling and venous congestion sets off a series of changes in neurohormonal and hemodynamic factors that culminate in acute kidney injury (AKI). CKD, Chronic kidney disease; CRS, cardiorenal syndrome; RAAS, renin-angiotensin-aldosterone system. (Modiﬁed from Ronco C, Cicoira M, McCullough PA. Cardiorenal syndrome type 1. Pathophysiological crosstalk leading to combined heart and kidney dysfunction in the setting of acute decompensated heart failure. J Am Coll Cardiol. 2012;60:1031–1042.)

Venous

congestion

Increased venous

pressure

Related episodes of AKI

CKD

218 PART IV Noncoronary Diseases: Diagnosis and Management

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1 is most pronounced early25 but an increased risk of death has been observed 10 years after the index hospitalization for acute MI patients who develop AKI.18 Furthermore, a biologic gradient has been observed between the severity of CRS type 1 and mortality risk.

17,25

In ADHF, any reduction in GFR is generally associated with a worse prognosis, whether it is present at baseline or develops during treatment. A systematic review of 16 studies including more than 80,000 patients with heart failure20 categorized renal function as normal (estimated GFR [eGFR] 90 mL/min or higher), mildly impaired (eGFR 53 to 89 mL/min), or moderately to severely impaired (eGFR <53 mL/min). The mortality rate at a follow-up of 1 year or more was 24% in those with a normal eGFR compared with 38% and 51% in patients with mild and moderate to severe reductions in eGFR, respectively (adjusted hazard ratios, 1.6 and 2.3, respectively). It is estimated that mortality increases by approximately 15% for every 10 mL/min reduction in eGFR. However, the relationship between change in GFR and prognosis is complex. Patients with improving renal function may also experience worse outcomes. Fluctuating renal function may reﬂect a sicker cohort of patients with signiﬁcantly worse survival than those with stable renal function. An analysis of 401 patients enrolled in the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial found that patients with an improvement or a decline in estimated GFR during treatment of ADHF had similar outcomes.26 Compared to patients with a stable GFR, those with either an improvement or a decline in GFR were signiﬁcantly more likely to have a reduced cardiac index and to require intravenous inotrope and vasodilator therapy. These patients also experienced a signiﬁcantly higher rate of all-cause mortality.

Additionally, the mechanism of worsening renal function in heart failure impacts its prognostic signiﬁcance. An analysis of 6337 subjects enrolled in the Studies of Left Ventricular Dysfunction (SOLVD) trial showed that early worsening of renal function was associated with increased mortality in the overall population.27 However, in the enalapril group, early worsening of renal function was not associated with increased mortality, while in the placebo group, the association with mortality was signiﬁcant. A signiﬁcant survival beneﬁt from enalapril therapy was observed in patients who continued enalapril despite early worsening renal function. These ﬁndings suggest that worsening renal function is not always a marker of adverse clinical outcome. On the contrary, in the case of angiotensin-converting enzyme (ACE) inhibitor administration, it is a manifestation of the agent’s pharmacologic properties, which exert a favorable effect on long-term outcome.

RISK FACTORS

Several predisposing risk factors for CRS type 1 have been identiﬁed. Nonmodiﬁable risk factors include a history of diabetes, prior admissions for ADHF or MI, and more severe cardiac dysfunction at the time of presentation (pulmonary edema, tachyarrhythmias, worse Killip class or lower ejection fraction). kidney function on admission has consistently been associated with higher risk for CRS type 1. Modiﬁable risk factors include

10,13,14,28

Impaired

high doses of diuretics (e.g., daily furosemide dose >100 mg/day or in-hospital use of thiazides) and/or vasodilator therapy as well as higher contrast volumes (e.g., contrast media volume-to-creatinine clearance ratio [V/CrCl] >3.7) during cardiac catheterization and intervention.

6,7,10,12,24,29,30

DIAGNOSIS

Among patients with heart failure who have an elevated serum creatinine and/or a reduced estimated GFR, it is important to distinguish between underlying kidney disease and impaired kidney function due to CRS type 1.31 This distinction may be difﬁcult since many patients have both. Findings suggestive of underlying kidney disease include signiﬁcant proteinuria (usually >1000 mg/day), an active urine sediment with hematuria with or without pyuria or cellular casts, and/or small kidneys on radiologic evaluation. However, a normal urinalysis, which is typically present in CRS without underlying kidney disease, can also be seen in variety of renal diseases, including nephrosclerosis and obstructive nephropathy.31 Ultimately, the diagnosis of CRS type 1 is made retrospectively after treatment to improve cardiac performance results in improvement in renal function.

PATHOPHYSIOLOGY

ADHF may reduce GFR by several mechanisms, including neurohumoral adaptations, reduced renal perfusion, increased renal venous pressure, and right ventricular (RV) dysfunction (see Fig. 22.1). In addition, exposure to nephrotoxins may precipitate CRS type 1. The pathophysiology of CRS type 1 may vary at different time points during a single hospitalization. For example, early in a CICU admission, AKI may be related to a low cardiac output state and/or marked increase in central venous pressure (CVP). However, later in the hospital course, exposure to nephrotoxins—such as contrast media or medications that impair renal perfusion, including nonsteroidal antiinﬂammatory drugs (NSAIDs) or ACE inhibitors—may contribute to the development of CRS type 1. Iatrogenic causes of CRS type 1 are presented in Fig. 22.2.

Impaired LV function leads to several hemodynamic derangements, including reduced stroke volume and cardiac output, arterial underﬁlling, elevated atrial pressures, and venous conges-

These hemodynamic derangements trigger a variety of

tion. compensatory neurohormonal adaptations, including activation of the sympathetic nervous system and the renin-angiotensinaldosterone system and increases in the release of vasopressin and endothelin-1, which promote salt and water retention as well as systemic vasoconstriction. These pathways lead to the disproportionate reabsorption of urea compared with that of creatinine.

37–39

In the setting of ADHF, blood urea nitrogen therefore represents a surrogate marker of neurohormonal activation.

40,41

These adaptations overwhelm the vasodilatory and natriuretic effects of natriuretic peptides, nitric oxide, prostaglandins, and bradykinin.

11,34,42

In the short term, neurohumoral adaptations contribute to preservation of perfusion to vital organs (the brain and heart) by maintenance of systemic pressure via arterial vasoconstriction

32–35

CHAPTER 22 Cardiorenal Syndrome Type 1 219

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Heart

ailure

Drug accumulation

↓ contractility

Tumor lysis,

urate-mediated

dysfunction

↑ Afterload

arrhythmias

imbalance

1/V2

Accumulation

Imaging

↓ Afterload

↑ Contractility

Metformin

Chemotherapy

Antibiotics

NSAIDs

Contrast

media

ACEi - ARB

Aldosterone receptor blockers

AVP receptor blockers

Urate precipitation interstitial damage

Toxic damage

Transient ischemia

Oxidative stress

↓ Filtration fraction

↓ Tubuloglomerular

feedback

↓ Na reabsorption

Lactic acidosis

interstitial damage

Acute

kidne

injury

Hyperkalemia

Polyuria

Overhydration

dehydration

Diuretics

↑ Diuresis

Hypovolemia

Fig. 22.2 Iatrogenic causes of CRS type 1. Multiple sources of iatrogenic injury, some of which

may be unavoidable, can result in either cardiac, renal, or cardiorenal impairment and kidney damage in patients with acutely decompensated heart failure (ADHF). ACEi, Angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; AVP, arginine vasopressin; NSAIDs, nonsteroidal antiinﬂammatory drugs. (Modiﬁed from Ronco C, Cicoira M, McCullough PA. Cardiorenal syndrome type 1. Pathophysiological crosstalk leading to combined heart and kidney dysfunction in the setting of acute decompensated heart failure. J Am Coll Cardiol. 2012;60:1031–1042.)

in other circulations, including the renal circulation, and by increasing myocardial contractility and heart rate. However, over the long term, systemic vasoconstriction increases cardiac afterload and reduces cardiac output, which can further reduce renal perfusion. The maladaptive nature of these adaptations is evidenced by the slowing of disease progression and reduction in mortality with the administration of ACE inhibitors and β-blockers in patients with heart failure and reduced ejection fraction.

In the absence of shock, impaired renal perfusion is an uncommon cause of CRS type 1 in ADHF. Hypotension is an uncommon ﬁnding in patients hospitalized for ADHF. In the Acute Decompensated Heart Failure National Registry (ADHERE) of over 100,000 patients, 50% had a systolic blood pressure of 140 mm Hg or higher, while less than 2% had a systolic blood pressure below 90 mm Hg.22 ADHF patients with reduced ejection fraction have little or no reduction in cardiac output with loop

diuretic therapy because they are on the ﬂat part of the FrankStarling curve, where changes in left ventricular end-diastolic pressure (LVEDP) have little or no effect on cardiac performance. Furthermore, the ESCAPE trial of 433 patients with ADHF6 found no correlation between the cardiac index and either the baseline GFR or worsening kidney function. Increasing the cardiac index did not improve renal function after discharge. In contrast, patients with ADHF and preserved systolic function are on a steep Starling curve such that, for every unit reduction in LVEDP induced by diuresis, there is a signiﬁcant fall in stroke volume. These patients are more sensitive to diuresis; excessive diuresis can reduce preload and cardiac output, leading to hypotension, a reduction in renal perfusion, and CRS type 1 (Fig. 22.3).

Increased intraabdominal or central venous pressure, which

increases renal venous pressure, reduces GFR.

32,43

Raising the intraabdominal venous pressure to about 20 mm Hg reduces renal plasma ﬂow and GFR of 24% and 28%, respectively, in

220 PART IV Noncoronary Diseases: Diagnosis and Management

Risk of cardiorenal syndrome

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Dehydration Fluid balance Overhydration

Diuretics

ultrafiltration

Hypotension Tachycardia Shock Organ hypoperfusion Oliguria

Normal heart

Volume depletion

arterial underfilling

Low Blood pressure High

Fig. 22.3 Volume and blood pressure management window. Patients at risk for cardiorenal

syndrome type 1 have a narrow window for management of both blood pressure and volume; extremes in either parameter can be associated with worsened renal function. (Modiﬁed from Ronco C, Cicoira M, McCullough PA. Cardiorenal syndrome type 1. Pathophysiological crosstalk leading to combined heart and kidney dysfunction in the setting of acute decompensated heart failure. J Am Coll Cardiol. 2012;60:1031–1042.)

Diseased heart

Management

window

Optimal status

At-risk

kidneys

Normal kidneys

Liberal intake

positive balance

Hypertension

Peripheral edema

Impaired oxygenation

Organ congestion

Acute

decompensation

normal adults.44 Studies in heart failure patients demonstrate an inverse relationship between venous pressure and GFR when the central venous pressure was measured directly jugular venous pressure was diagnosed on physical examination.

RV dilation and dysfunction may adversely affect kidney function through at least two mechanisms31: (1) the associated elevation in CVP elevation can lower the GFR; and (2) RV dilation impairs LV ﬁlling and, therefore, forward output, via ventricular interdependence (the reverse Bernheim phenomenon).49 Increased pressure within a distended RV increases LV extramural pressure, reducing LV transmural pressure for any given intracavitary LV pressure and inducing leftward interventricular septal bowing, thereby diminishing LV preload and distensibility and reducing stroke volume and forward ﬂow. a role in ventricular interdependence but is not critical to the interaction.52 Thus, a reduction in RV ﬁlling pressure during treatment of ADHF may lead to an increase in GFR, both by reducing renal venous pressure and by diminishing the impairment of LV ﬁlling.

Some drugs commonly prescribed for the treatment of ADHF can also contribute to development of AKI by disturbing systemic and renal hemodynamics (see Fig. 22.2). Diuretics are recommended in ADHF to reduce dyspnea and edema, but their overuse may result in excessive intravascular volume depletion and further compromise kidney perfusion (see Fig. 22.3). resistance may also complicate the clinical picture of CRS type 1 by acutely or chronically increasing sodium retention.56 ACE inhibitors, angiotensin receptor blockers (ARBs), and aldosterone receptor antagonists are guideline-directed therapies for heart

45–47

or elevated

50,51

An intact pericardium plays

54,55

Diuretic

failure57 because these drugs have been shown to signiﬁcantly improve survival of these patients.

58–64

However, they affect renal

hemodynamics, and their use must be carefully monitored to

avoid the development of AKI in decompensated patients.

Another important iatrogenic nephrotoxin in ADHF and ACS is iodinated contrast media commonly used for vascular imaging procedures (see Fig. 22.2). These agents induce intense and prolonged vasoconstriction at the corticomedullary junction of the kidney and directly impair the autoregulatory capacity of the kidney through a reduction in nitric oxide synthesis. effects, coupled with direct tubular toxicity of iodinated radiocontrast, can lead to overt acute tubular necrosis and AKI.

PREVENTION

CRS type 1 is a result of the interaction between complex pathogenic factors; once it becomes clinically apparent, it is difﬁcult to abort and is often irreversible. Most important, CRS type 1 is associated with adverse outcomes, even if the AKI resolves. practice with an aim to identify and avoid precipitating factors as well as to use measures to maintain optimal functioning of the heart and kidneys. This may involve multimodality and multidisciplinary preventive strategies, working via diverse therapeutic targets. Although evidence-based guidelines currently exist for management of ADHF, are no clear recommendations for the management of CRS type

1.73 The multitude of pathophysiologic interactions and their complexity render the management of CRS challenging.

11,15

Thus, prevention of CRS is paramount in clinical

67,68

ACS,

69–71

and AKI,72 there

65,66

These

CHAPTER 22 Cardiorenal Syndrome Type 1 221

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BOX 22.1 Renoprotective Strategies in the

Cardiac Intensive Care Unit

• Regular monitoring of ﬂuid intake/output, urine output, renal function, blood

pressure

•

Accurate and frequent monitoring of volume status

• Hold ACE inhibitors/ARBs in patients with worsening renal function

• Optimize volume status

• Adjust diuretic doses based on volume status

• Pharmacovigilance (drug monitoring, avoid nephrotoxins, attention to drug

interactions)

•

Initial use of vasodilators (nitrates, hydralazine) in ADHF if blood pressure

is adequate

•

Avoid unnecessary use of iodinated contrast agents

• Optimize volume status before use of iodinated contrast agents

• Minimize volume of iodinated contrast agents

ACE, Angiotensin-converting enzyme; ADHF, acute decompensated heart failure; ARBs, angiotensin receptor blockers. Modiﬁed from Cruz DN. Cardiorenal syndrome in critical care: the acute cardiorenal and renocardiac syndromes. Adv Chronic Kidney Dis. 2013;20:56–66.

Improving the natural history of heart failure and avoiding acute decompensation are the cornerstones of prevention of CRS type 1.74 Strategies for prevention in these patients should follow those recommended by the American College of Cardiology/ American Heart Association (ACC/AHA) for stage A and stage B heart failure.75 These include coronary artery disease risk factor modiﬁcation and avoidance of medications that may precipitate salt and water retention, including NSAIDs and thiazolidinediones. More important, use of renin-angiotensin-aldosterone system antagonists and β-blockers should be optimized. In patients with CKD, efforts must be made to cautiously introduce these cardioprotective agents with close monitoring of kidney function.

Another mainstay of prevention is to recognize patients at risk for CRS. Patients who develop CRS type 1 are generally older, have a history of previous hospitalizations for heart failure or MI, and often have baseline kidney dysfunction and hypertension. Risk prediction scores for AKI have been published for ADHF24 for contrast-induced AKI after percutaneous coronary intervention,76 after cardiac surgery,77 and in hospitalized patients.78 Such scoring systems can be used to recognize preemptively the patients at a high intrinsic risk of developing AKI. Renoprotective measures can then be selectively instituted in high-risk patients to reduce the risk of acute CRS79 (Box 22.1).

MANAGEMENT

No medical therapies directly increase the GFR (manifested clinically by a decline in serum creatinine) in patients with heart failure. On the other hand, improving cardiac function can result in increases in GFR, indicating that CRS type 1 has substantial reversible components.

AKI induced by primary cardiac dysfunction implies inadequate renal perfusion until proven otherwise.81 Inadequate perfusion may be a consequence of a low cardiac output state, increased CVP leading to renal congestion, or both. Elevated CVP leading to renal venous hypertension is a product of right

heart function, blood volume, and venous capacitance—all of which are heavily inﬂuenced by neurohormonal systems.4 A careful history and physical examination can usually differentiate a volume-depleted patient from one who is severely volume overloaded. Diuretics, typically beginning with a loop diuretic, are ﬁrst-line therapy for managing volume overload in patients with ADHF as manifested by peripheral and/or pulmonary edema. In patients with heart failure, an elevated BUN/creatinine ratio should not deter diuretic therapy if clinical evidence of congestion is present.80 That aggressive diuresis improves outcomes is suggested in two studies, ESCAPE82 and Efﬁcacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST),83 in which hemoconcentration, an indicator of aggressive diuresis, was found to be associated with worsening of renal function in the hospital but an improvement in survival after discharge. These ﬁndings provide support for the recommendation included in the 2013 ACC/AHA heart failure guidelines that the goal of diuretic therapy is to eliminate clinical evidence of ﬂuid retention, such as an elevated jugular venous pressure and peripheral edema.84 The rapidity of diuresis can be slowed if the patient develops hypotension or worsening renal function. However, the goal of diuretic therapy is to eliminate ﬂuid retention even if this leads to asymptomatic mild to moderate reductions in blood pressure or renal function.

The optimal diuretic regimen has not been determined in randomized controlled trials. Continuous intravenous infusion of diuretics has traditionally been considered more effective than bolus in severe ADHF.

85,86

However, in the recent Diuretic Optimization Strategies Evaluation (DOSE) randomized trial, there were no signiﬁcant differences in patients’ symptoms or in the change in kidney function when diuretic therapy was administered by bolus as compared with continuous infusion or at a high dose (2.5 times the previous outpatient oral dose) as compared with a low dose (equivalent to the previous oral dose).87 The high-dose strategy was associated with greater diuresis and more favorable outcomes in some secondary measures but also with transient worsening of kidney function (23% vs. 14% in low dose, P = .04). It is frequently overlooked that the median hourly dose of furosemide by continuous infusion in the DOSE trial was only 5 mg in the low-dose arm and 10.7 mg in the high-dose arm. These doses are signiﬁcantly below the 20- to 40 mg/h doses frequently required in CRS type 1 patients. In addition, ADHF patients with serum creatinine greater than 3 mg/dL were excluded from the DOSE trial. Those patients are more likely to need higher doses of furosemide and are more susceptible to develop CRS type 1 during hospitalization for ADHF.

Intravenous administration of inotropic drugs—such as dobutamine, dopamine, and milrinone—has a role in the treatment of patients who develop cardiogenic shock. However, both routine use of short-term intravenous therapy in patients with ADHF and prolonged therapy with oral inotropic drugs other than digoxin has been associated with an increase in mortality. As a result, the main role of inotropic drugs other than digoxin is in the management of cardiogenic shock. The role of inotropes in patients with CRS is uncertain and the routine use of inotropes is not recommended given their lack of proven efﬁcacy and their association with adverse events when used in patients other than

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those with cardiogenic shock or ADHF who are deteriorating toward cardiogenic shock.

Ultraﬁltration is an alternative to loop diuretics for the management of ﬂuid overload in patients with ADHF and worsening kidney function. The Ultraﬁltration versus Intravenous Diuretics for Patients Hospitalized for Acute Decompensated Congestive Heart Failure (UNLOAD) trial randomized 200 ADHF patients to ultraﬁltration or intravenous diuretics and found that ultraﬁltration safely produced greater weight loss and ﬂuid removal than intravenous diuretics and reduced readmissions for heart failure.88 However, in the Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trial,89 the use of a stepped pharmacologic-therapy algorithm was superior to a strategy of ultraﬁltration for the preservation of renal function at 96 hours, with a similar amount of weight loss with the two approaches. Ultraﬁltration was associated with a higher rate of adverse events. Thus, although ultraﬁltration may be helpful for ﬂuid removal in ADHF in patients unresponsive to diuretic therapy, the available evidence does not establish ultraﬁltration as ﬁrst-line therapy for ADHF or as an effective therapy for CRS type 1. The 2009 ACC/AHA guidelines state that ultraﬁltration is reasonable for patients with refractory congestion not responding to medical therapy.

Intravenous vasodilators used in the treatment of ADHF include nitroglycerin, nitroprusside, and nesiritide. In the ADHERE database of almost 100,000 patients, worsening of renal function was signiﬁcantly more common when intravenous diuretics were given with nitroglycerin or nesiritide compared with intravenous diuretics alone (relative risk, 1.20 and 1.44, respectively).90 However, a causal effect could not be distinguished from patients requiring combination therapy because they had worse heart failure.

There are no randomized trials of nitroglycerin or nitroprusside. Randomized trials have yielded conﬂicting results on the effect of nesiritide therapy on renal function in the treatment of ADHF. The largest trial, the Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure (ASCEND-HF), nesiritide was not associated with a worsening of renal function but was associated with increased rates of hypotension.91 Similarly, the Renal Optimization Strategies Evaluation (ROSE) trial found that low-dose nesiritide did not enhance decongestion or alter renal function when added to diuretic therapy.92 Overall, nesiritide has not been found to be of beneﬁt in ADHF and it is not currently recommended for the prevention of AKI.

SUMMARY

In summary, CRS type 1 is a complex and multidimensional entity that is commonly encountered in the CICU and has a signiﬁcant effect on morbidity and mortality. Preventive strategies in general for all patients at risk for CRS type 1 will help decrease the incidence of AKI. The management of CRS type 1 is

The full reference list for this chapter is available at

ExpertConsult.com.

challenging because of the many complex pathophysiologic interactions between the heart and kidney. Although evidencebased guidelines currently exist for management of ADHF, ACS, and AKI, at present there are no clear recommendations for the management of CRS type 1.

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