CRITICAL CARE IN THE ICU
From the annual Survey of Current Issues in Surgical Anesthesia, sponsored by the Cleveland Clinic Foundation,
November 14-17, 2004
Michael S. O’Connor, DO, MPH, Staff Anesthesiologist, Department of Cardiothoracic Anesthesia, and Co-
Director, Fellowship Program, Cleveland Clinic, Cleveland
| ACUTE RENAL FAILURE (ARF)
|
 | Incidence: 5% to 7% of all hospitalized patients; increases to 15% in intensive care unit (ICU); depends on clinical
context (≈50% in patients with septic shock)
|
| Definition: increase in serum creatinine >0.5 mg/dL if baseline <2.5 mg/dL; often associated with decreased urine
output
|
| Etiology: renal hypoperfusion most common cause of acute tubular necrosis (ATN) in ICU; perioperative renal failure
also common due to insufficient cardiac output, hypovolemia, vasodilatation, and nephrotoxic insults; paradigms
include hemodynamic-nephrotoxic model (views renal failure as continuum of hemodynamic compromise,
either from ischemia or from toxic insults evolving into prerenal insufficiency, ATN, and bilateral cortical necrosis)
|
| Risk factors: include advanced age, preexisting renal insufficiency (related to congestive heart failure [CHF], diabetes,
hypertension, or liver failure; mild insults may cause ARF), sepsis, shock, multiple organ dysfunction, exposure
to endogenous toxins (eg, bilirubin) or exogenous toxins (eg, cyclosporin, radiocontrast dyes), and high-
risk procedures (eg, vascular procedure, bypass, urologic procedure, trauma, biliary tract procedure, and transplantation
[with exposure to nephrotoxic agents])
|
| Cardiac surgery: ARF uncommon with normal renal function and normal left ventricular (LV) function
|
| Patterns of postoperative ARF: pattern A—aortal clamping results in abrupt decrement in renal function; over 4
to 8 days, renal function improves and patient returns to baseline; as creatinine clearance increases, serum creatinine
also increases (serum creatinine unreliable marker of renal function); pattern B—surgery with impaired
cardiac function; over 20 days, cardiac function improves, but recovery incomplete; pattern C—
surgery followed by abrupt decline in creatinine clearance; improvement begins but recovery incomplete;
septic shock, hypovolemia, or other insult then develops (prerenal insufficiency) and leads to renal failure; renal
recovery does not occur (50% to 60% mortality)
|
| Detection of renal dysfunction: oliguria (<15 mL/hr; not reliable index of renal function); urinary sodium; creatinine
clearance
|
| Strategies for renal protection: important to treat hypovolemia; fluid challenge patient; if oliguria persists, optimize
hemodynamics by placing central venous pressure (CVP) line or pulmonary artery catheter, then give diuretics;
if oliguria persists, implement diuretic-resistance protocol (eg, furosemide infusion, metolazone)
|
| Management principles: include monitoring, fluid resuscitation, and optimizing hemodynamics; supportive measures
important (good ICU care provides prophylaxis against stress ulcers and deep venous thrombosis [DVT]); patient
requires early nutritional support; speaker suggests nephrology consultation may be necessary
|
| Loop diuretics: decrease O2 consumption; maximize proximal tubular urine flow; induce renocortical vasodilatation;
studies show no benefit for renal function or outcome; better prognosis in nonoliguric renal failure; patients
who convert from oliguric to nonoliguric renal failure with furosemide and who do not require renal
replacement therapy also have better prognosis; effective in acute management of hypovolemia and high potassium;
risk for hypovolemia, particularly with diabetes, chronic renal insufficiency, or radiocontrast ARF
|
| Low-dose dopamine: increases renal blood flow; ameliorates vasoconstrictive effects of other agents; increases
urine output; no proven efficacy in preventing or improving renal outcome; increased plasma renin activity
counteracts effect of dopamine; diuresis may be harmful in oliguric critically ill patient (may lead to gut necrosis);
blunts ventilatory drive
|
| Fenoldopam: selective dopamine agonist; approved by Food and Drug Administration (FDA) for hypertensive
emergencies; increasing doses decrease blood pressure (BP) but maintain renal perfusion; also effective in
contrast nephropathy
|
| Other agents: include nesiritide (B-type natriuretic peptide [BNP]) and anaritide (atrial natriuretic peptide; outcome
studies show no benefit)
|
| Vasopressor therapy: arginine vasopressin (AVP) used in profound shock; restores normal circulating AVP; give infusion
of 1 to 6 U per hour; evidence-based interventions for sepsis that may prevent renal failure include vasopressin,
hydrocortisone, normal glycemia, drotrecogin (activated protein C), and early goal-directed resuscitation
|
| Renal replacement therapy (RRT): concerns include volume overload, leading to hypoxemia, hyperkalemia,
metabolic acidemia, and uremic complications; techniques include intermittent hemodialysis (requires technician
at bedside) and continuous RRT (speaker uses continuous venovenous hemodialysis [CVVHD]; preferred
in unstable patient; less risk for hypotension; preferred method in patient with elevated intracranial
pressure or hypophosphatemia; no mortality or survival benefit in prospective studies)
|
| Prognosis: 45% to 70% mortality in ICU patients (20% mortality rate overall); no improvement in outcome, despite
advances in RRT; increased severity of illness in ICU patients (greater proportion of patients have ARF
with sepsis and multiple organ dysfunction); ARF specific and independent predictor of poor outcome
|
| MANAGEMENT OF ACUTE POSTOPERATIVE HEART FAILURE (HF)
|
| Epidemiology: HF afflicts 5 million Americans; ≈500,000 new cases diagnosed yearly (but only 2200 heart transplants
yearly); prevalence increases with advancing age; $25 billion spent on acute HF patients annually; major
public health problem (no national screening efforts); preventable (with good BP control); risk factor identification
from American College of Cardiology (ACC) and American Heart Association (AHA)
|
| New York Heart Association (NYHA) classification for severity of HF: Class I—asymptomatic; Class IV—symptomatic
at rest with shortness of breath or pulmonary congestion
|
| Stages of HF: A—high-risk with no symptoms (hypertension, diabetes, coronary artery disease [CAD], previous
exposure to cardiotoxic drugs, and family history of cardiomyopathy); B—structural heart disease with no
symptoms (LV hypertrophy, previous myocardial infarction [MI], LV systolic dysfunction, and valvular heart
disease); C—structural disease with previous or current symptoms (NYHA Class I, II, III, IV); D—refractory
symptoms requiring special interventions
|
| Syndrome of HF: traditional view of inadequate ventricular performance leading to HF; new view of structural,
functional, and biologic changes leading to progressive HF; multiple models used to understand HF
|
| Pathophysiology: hemodynamic model—increased preload; improved stroke volume; patient eventually becomes
symptomatic; further increases in preload lead to acute decompensated HF; vasodilators and inotropes important);
neurohumoral model—norepinephrine, angiotensin, aldosterone, and endothelin important; improve cardiac
output, but at some point, become deleterious; counter-regulatory hormones, eg, natriuretic peptides and
bradykinin, oppose action of renin, aldosterone, and angiotensin; other factors include genetic background, environmental
factors (eg, alcohol, tobacco), and coexisting conditions (eg, diabetes mellitus, hypertension, renal
disease, CAD, and anemia)
|
| Mechanisms that result in development of HF: multiple etiologies; final common pathway involves myocardial
dysfunction, reduced perfusion, sympathetic system activation, renin-angiotensin-aldosterone system (RAAS)
activation
|
| Remodeling: involves mechanical, neurohumoral, and genetic factors; alters ventricular shape, size, and function;
may be due to MI, cardiomyopathy, hypertension, and valvular heart disease; characteristics include hypertrophy,
loss of myocytes, and increased interstitial fibrosis; reverse remodeling involves use of
angiotensin-converting enzyme (ACE) inhibitors, β-adrenergic antagonists, and cardiac resynchronization
therapy
|
| Therapeutic interventions: step-wise approach using ACC/ AHA guidelines; stage A—risk-factor reduction, particularly
treatment of hypertension, diabetes, and dyslipidemia using ACE inhibitors; stage B—ACE inhibitor or
angiotensin receptor blocker; β-blockers in selected patients; stage C—ACE inhibitors and β-blockers in all
patients; dietary sodium restriction; cardiac resynchronization therapy; revascularization and mitral valve surgery;
aldosterone antagonists; nesiritide; stage D—inotropes; LV-assist devices; transplantation; hospice care
|
| Strategies for management of acute perioperative HF
|
| Goals: improve hemodynamic parameters; relieve symptoms; improve survival
|
| Drug classifications: diuretics; inotropic agents; vasodilators (eg, nesiritide)
|
| Diuretics: cornerstone of treatment of chronic HF; adverse effects include hypomagnesemia, hypokalemia,
and activation of RAAS
|
| Inotropic agents: improve LV contractility and cardiac index; common drugs include epinephrine and milrinone
(speaker rarely uses dobutamine); adverse effects include increased myocardial O2 consumption, demand,
and arrhythmogenicity, acceleration of disease progression, and increased mortality
|
| Vasodilators: indicated for fluid overload and elevated filling pressures; common drugs include nitroglycerin
(primarily venous vasodilator) and sodium nitroprusside (arterial vasodilator); have no effect on RAAS; adverse
effects include tolerance and increased heart rate (HR); need to be continually titrated
|
| Nesiritide: recombinant form identical to endogenous BNP; opposes action of RAAS; opposes sympathetic
nervous system; decreases preload and afterload (leading to increased contractility); causes natural diuresis
and natriuresis; no effect on HR; study of intravenous nesiritide vs nitroglycerin for treatment of decompensated
HF showed more dramatic reduction in filling pressures with nesiritide, but no qualitative difference
in symptoms; also no significant difference in adverse effects (eg, hypotension); nesiritide did show lower
trend toward readmission; candidates for therapy include patients with acute decompensated HF, symptoms
of congestion, “reasonable” systolic BP, and difficult-to-diurese patients; also used in cases of elevated creatinine
and impaired LV contractility; should not be used in patients presenting with shock
|
| Nonpharmacologic therapy: cardiac resynchronization therapy (involves 3-lead system; shown to reverse remodeling,
decrease heart size, and improve ejection fraction); revascularization; Dor procedure (endoventricular
patch to reduce size of ventricle over areas of aneurysmal dilatation); mitral valve repair; transplantation
(epidemiologically insignificant in treatment of HF); ventricular-assist devices—initially conceived as bridge
to transplantation; currently destination therapy; reverse neurohumoral effects; improve hemodynamic effects;
reverse effects on cardiac myocytes; improve effects on cardiac structure and function [prevent remodeling])
|
| Conclusion: HF major public health problem; clinical syndrome (final common pathway for multiple diseases);
new research and clinical trials have changed scope of therapies; acute therapy includes diuretics, inotropes, vasodilators,
and ventricular-assist devices; nesiritide represents new treatment for specific subgroup of patients
with acute HF
|
Educational Objectives
| The goal of this activity is to educate the listener about acute renal failure and management of acute postoperative heart failure.
After hearing and assimilating this program, the participant will be better able to:
|
| 1. Describe the epidemiology of acute renal failure (ARF) in the intensive care unit (ICU).
|
| 2. Summarize the management principles of ARF in the ICU.
|
| 3. Review the pathophysiology of heart failure (HF).
|
| 4. Define the mechanisms that result in the development of HF.
|
| 5. Describe the therapeutic interventions available for HF.
|
Discussed on This Program
Acetylcysteine (N -acetylcysteine) [Mucomyst, others]
Anaritide acetate [Auriculin]
Aprotinin [Trasylol]
Bupivacaine HCl (several trade names)
Dobutamine [Dobutrex]
Dopamine HCl [Intropin, Dopamine HCl in 5% Dextrose]
Drotrecogin alfa (activated protein C) [Xigris]
Epinephrine (several trade names)
Fenoldopam mesylate [Corlopam]
Fentanyl [Sublimaze]
Furosemide [Lasix]
Hetastarch (hydroxyethyl starch; HES) [Hespan, Hextend, Voluven]
Hydrocortisone (cortisol) [many trade names]
Metolazone [Mykrox, Zaroxolyn]
Milrinone lactate [Primacor]
Nesiritide [Natrecor]
Nitroglycerin (several trade names)
Nitroprusside sodium [Nitropress, Sodium Nitroprusside]
Norepinephrine bitartrate (levarterenol) [Levophed]
Vasopressin (8-arginine-vasopressin) [Pitressin]
Suggested Reading
Bellomo R et al: Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial. Australian
and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet 356:2139, 2000; Burger AJ et
al: Prospective Randomized Evaluation of Cardiac Ectopy with Dobutamine or Natrecor Therapy. Effect of nesiritide (B-
type natriuretic peptide) and dobutamine on ventricular arrhythmias in the treatment of patients with acutely decompensated
congestive heart failure: the PRECEDENT study. Am Heart J 144:1102, 2002; Chertow GM et al: Independent association
between acute renal failure and mortality following cardiac surgery. Am J Med 104:343, 1998; Cuffe MS et al:
Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA
287:1541, 2002; Debaveye YA et al: Is there still a place for dopamine in the modern intensive care unit? Anesth Analg
98:461, 2004; Entwistle JW 3rd et al: Postoperative nesiritide use following high-risk mitral valve replacement. Heart
Surg Forum 7:E189, 2004; Higgins TL et al: Stratification of morbidity and mortality outcome by preoperative risk factors
in coronary artery bypass patients. A clinical severity score. JAMA 267:2344, 1992 (Erratum in: JAMA 268:1860,
1992); Holmes CL et al: Bad medicine: low-dose dopamine in the ICU. Chest 123:1266, 2003; Ip-Yam PC et al: Renal
function and proteinuria after cardiopulmonary bypass: the effects of temperature and mannitol. Anesth Analg 78:842,
1994; Jessup M et al: Heart failure. N Engl J Med 348:2007, 2003; Kitzman DW et al: Pathophysiological characterization
of isolated diastolic heart failure in comparison to systolic heart failure. JAMA 288:2144, 2002; Mehta RL et al:
Nephrology consultation in acute renal failure: does timing matter? Am J Med 113:456, 2002; Metnitz PG et al: Effect of
acute renal failure requiring renal replacement therapy on outcome in critically ill patients. Crit Care Med 30:2051, 2002;
Nohria A et al: Medical management of advanced heart failure. JAMA 287:628, 2002; Paganini EP et al: Severity scores
and outcomes with acute renal failure in the ICU setting. Contrib Nephrol 132:181, 2001; Publication Committee for the
VMAC Investigators (Vasodilatation in the Management of Acute CHF): Intravenous nesiritide vs nitroglycerin for treatment
of decompensated congestive heart failure: a randomized controlled trial. JAMA 287:1531, 2002 (Erratum in: JAMA
288:577, 2002); Rahman TM et al: Management of acute renal failure on the intensive care unit. Clin Med 2:108, 2002;
Ramsay JG: Cardiac management in the ICU. Chest 115:138S, 1999; Roger VL et al: Trends in heart failure incidence
and survival in a community-based population. JAMA 292:344, 2004; Singri N et al: Acute renal failure. JAMA 289:747,
2003; Southworth MR: Treatment options for acute decompensated heart failure. Am J Health Syst Pharm 60 Suppl 4:S7,
2003.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty
reported nothing to disclose.
Dr. O’Connor spoke in Naples, Florida at Survey of Current Issues in Surgical Anesthesia, held November 14-17, 2004,
and sponsored by The Cleveland Clinic Foundation. The Audio-Digest Foundation thanks Dr. O’Connor and The Cleveland
Clinic Foundation for their cooperation in the production of this program.
|
