HF - CTI

Insuficiencia Cardíaca en UCI
Arturo Briva
Definición
HF is a complex clinical syndrome that results from any structural or functional
impairment of ventricular filling or ejection of blood.
The cardinal manifestations of HF are dyspnea and fatigue, which may limit
exercise tolerance, and fluid retention, which may lead to pulmonary and/or
splanchnic congestion and/or peripheral edema
Journal of the American College of Cardiology
! 2013 by the American College of Cardiology Foundation and the American Heart Association, Inc.
Published by Elsevier Inc.
Vol. 62, No. 16, 2013
ISSN 0735-1097/$36.00
http://dx.doi.org/10.1016/j.jacc.2013.05.020
PRACTICE GUIDELINE
2013 ACCF/AHA Guideline for the Management
of Heart Failure: Executive Summary
A Report of the American College of Cardiology Foundation/
American Heart Association Task Force on Practice Guidelines
Developed in Collaboration With the American College of Chest Physicians, Heart Rhythm Society,
and International Society for Heart and Lung Transplantation
Determinantes del Gasto Cardiaco
www.voer.edu.vn
Yano et al. JCI 2005.
Acoplamiento excitacion-contracción.
Relación fuerza/estiramiento.
Consumo de O2 miocárdico.
Desempeño Ventricular
http://ccnmtl.columbia.edu/projects/heart/exercises/MechPropHeart/lecture.html
Aumentan RVS y PAM.
Cae VS
Aumento primario de
contractilidad
Aumento de FC
Aumenta contractilidad
con aumento de VDF
Activación neuro-humoral: adaptación y cronicidad
Giordano et al. JCI 2005.
IC crónica: repercusión sistémica tisular
Giordano et al. JCI 2005.
Journal of the American College of Cardiology
! 2013 by the American College of Cardiology Foundation and the American Heart Association, Inc.
Published by Elsevier Inc.
Vol. 62, No. 16, 2013
ISSN 0735-1097/$36.00
http://dx.doi.org/10.1016/j.jacc.2013.05.020
PRACTICE GUIDELINE
2013 ACCF/AHA Guideline for the Management
of Heart Failure: Executive Summary
A Report of the American College of Cardiology Foundation/
American Heart Association Task Force on Practice Guidelines
Developed in Collaboration With the American College of Chest Physicians, Heart Rhythm Society,
and International Society for Heart and Lung Transplantation
Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation
WRITING COMMITTEE MEMBERS
Clyde W. Yancy, MD, MSc, FACC, FAHA, Chairyz;
Mariell Jessup, MD, FACC, FAHA, Vice Chair*y; Biykem Bozkurt, MD, PhD, FACC, FAHAy;
Javed Butler, MBBS, FACC, FAHA*y; Donald E. Casey, Jr, MD, MPH, MBA, FACP, FAHAx;
1502
Yancy et al.
2013 ACCF/AHA Heart Failure Guidelines: Executive Summary
JACC Vol. 62, No. 16, 2013
October 15, 2013:1495–539
Table 3. Definitions of HFrEF and HFpEF
Classification
EF (%)
Description
I. Heart failure with reduced ejection fraction (HFrEF)
!40
Also referred to as systolic HF. Randomized controlled trials have mainly enrolled
patients with HFrEF, and it is only in these patients that efficacious therapies
have been demonstrated to date.
II. Heart failure with preserved ejection fraction (HFpEF)
"50
Also referred to as diastolic HF. Several different criteria have been used to
further define HFpEF. The diagnosis of HFpEF is challenging because it is
largely one of excluding other potential noncardiac causes of symptoms
suggestive of HF. To date, efficacious therapies have not been identified.
a. HFpEF, borderline
41 to 49
These patients fall into a borderline or intermediate group. Their characteristics,
treatment patterns, and outcomes appear similar to those of patients with
HFpEF.
b. HFpEF, improved
>40
It has been recognized that a subset of patients with HFpEF previously had HFrEF.
These patients with improvement or recovery in EF may be clinically distinct
from those with persistently preserved or reduced EF. Further research is
needed to better characterize these patients.
EF indicates ejection fraction; HF, heart failure; HFpEF, heart failure with preserved ejection fraction; and HFrEF, heart failure with reduced ejection fraction.
prevalence continues to rise (40). In the Medicare-eligible
population, HF prevalence increased from 90 to 121 per
1000 beneficiaries from 1994 to 2003 (41). HFrEF and
HFpEF each make up about half of the overall HF burden
(43). One in 5 Americans will be >65 years of age by 2050
(44). Because HF prevalence is highest in this group, the
number of Americans with HF is expected to significantly
5. Initial and Serial Evaluation of the
HF Patient: Recommendations
5.1. Clinical Evaluation
See Table 5 for multivariable clinical risk scores.
men, (46) with blacks having a greater 5-year mortality rate
than whites (47). HF in non-Hispanic black males and
females has a prevalence of 4.5% and 3.8%, respectively,
versus 2.7% and 1.8% in non-Hispanic white males and
females, respectively (40).
(Level of Evidence: C)
2. In patients with idiopathic dilated cardiomyopathy, a 3generational family history should be obtained to aid in
establishing the diagnosis of familial dilated cardiomyopathy. (Level of Evidence: C)
Table 4. Comparison of ACCF/AHA Stages of HF and NYHA Functional Classifications
ACCF/AHA Stages of HF (37)
NYHA Functional Classification (38)
A
At high risk for HF but without structural heart
disease or symptoms of HF
B
Structural heart disease but without signs or
symptoms of HF
I
No limitation of physical activity. Ordinary physical activity
does not cause symptoms of HF.
C
Structural heart disease with prior or current
symptoms of HF
I
No limitation of physical activity. Ordinary physical activity
does not cause symptoms of HF.
II
Slight limitation of physical activity. Comfortable at rest,
but ordinary physical activity results in symptoms of HF.
III
Marked limitation of physical activity. Comfortable at rest,
but less than ordinary activity causes symptoms of HF.
IV
Unable to carry on any physical activity without symptoms of HF,
or symptoms of HF at rest.
IV
Unable to carry on any physical activity without symptoms of HF,
or symptoms of HF at rest.
D
Refractory HF requiring specialized interventions
None
ACCF indicates American College of Cardiology Foundation; AHA, American Heart Association; HF, heart failure; and NYHA, New York Heart Association.
1504
Yancy et al.
2013 ACCF/AHA Heart Failure Guidelines: Executive Summary
JACC Vol. 62, No. 16, 2013
October 15, 2013:1495–539
Table 6. Recommendations for Biomarkers in HF
Biomarker, Application
Setting
COR
LOE
References
Ambulatory, Acute
I
A
64–70,92–98
Prognosis of HF
Ambulatory, Acute
I
A
69,71–76,96,99–106
Achieve GDMT
Ambulatory
IIa
B
77–84
Acute
IIb
C
107,108
Acute, Ambulatory
I
A
85–88,96,101,104–115
Ambulatory
IIb
B
89–91
Acute
IIb
A
96,101,104,106–108,110,112–115
Natriuretic peptides
Diagnosis or exclusion of HF
Guidance for acutely decompensated
HF therapy
Biomarkers of myocardial injury
Additive risk stratification
Biomarkers of myocardial fibrosis
Additive risk stratification
COR indicates Class of Recommendation; GDMT, guideline-directed medical therapy; HF, heart failure; and LOE, Level of Evidence.
2. Measurement of BNP or NT-proBNP and/or cardiac troponin
is useful for establishing prognosis or disease severity
in acutely decompensated HF (96,99–106). (Level of
Evidence: A)
CLASS IIb
1. The usefulness of BNP- or NT-proBNPLguided therapy
for acutely decompensated HF is not well established
and to detect alternative cardiac, pulmonary, and other
diseases that may cause or contribute to the patient’s
symptoms. (Level of Evidence: C)
2. A 2-dimensional echocardiogram with Doppler should be
performed during initial evaluation of patients presenting
with HF to assess ventricular function, size, wall thickness,
wall motion, and valve function. (Level of Evidence: C)
days) and early telephone follow-up (within 3 days) of hospital
discharge
Yancy
et al. are reasonable (345,346). (Level of Evidence: B)
(Level of Evidence: B)
JACC
Vol
ancy1516
et al.
JACC Vol. 62,
2013
3. Surgical aortic valve replacement is reasonable
for No. 16,
2. Use
of clinical
risk-prediction
tools Summary
and/orExecutive
biomarkersSummary patients with critical aortic stenosis and a predicted
ACCF/AHA
Heart
Failure
Guidelines:
October 1
013 ACCF/AHA2013
Heart
Failure
Guidelines:
Executive
Octobersurgical
15, 2013:1495–539
to identify patients at higher risk for postdischarge clinical
mortality of no greater than 10% (353). (Level of Evidence: B)
events are reasonable (62). (Level of Evidence: B)
4. Transcatheter aortic valve replacement after careful candidate consideration is reasonable for patients with critical
aortic stenosis who are deemed inoperable (354). (Level of
Evidence: B)
8. Important Comorbidities in HF
CLASS IIb
1. CABG may be considered with the intent of improving
survival in patients with ischemic heart disease with
severe LV systolic dysfunction (EF <35%) and operable
coronary anatomy whether or not viable myocardium is
present (352,355,356). (Level of Evidence: B)
Although there are additional and important comorbidities that
occur in patients with HF as referenced in Table 24, it remains
uncertain how best to generate specific recommendations,
given the status of current evidence.
Table 24. Ten Most Common Co-Occurring Chronic Conditions Among Medicare Beneficiaries With Heart Failure (N[4,947,918), 2011
Beneficiaries Age !65 y (N¼4,376,150)*
Beneficiaries Age <65 y (N¼5,71,768)y
N
%
N
%
Hypertension
3,685,373
84.2
Hypertension
461,235
80.7
Ischemic heart disease
3,145,718
71.9
Ischemic heart disease
365,889
64.0
Hyperlipidemia
2,623,601
60.0
Diabetes
338,687
59.2
Anemia
2,200,674
50.3
Hyperlipidemia
325,498
56.9
Diabetes
2,027,875
46.3
Anemia
284,102
49.7
Arthritis
1,901,447
43.5
Chronic kidney disease
257,015
45.0
Chronic kidney disease
1,851,812
42.3
Depression
207,082
36.2
COPD
1,311,118
30.0
Arthritis
201,964
35.3
Atrial fibrillation
1,247,748
28.5
COPD
191,016
33.4
Alzheimer’s disease/dementia
1,207,704
27.6
Asthma
888,16
15.5
*Mean No. of conditions is 6.1; median is 6.
yMean No. of conditions is 5.5; median is 5.
COPD indicates chronic obstructive pulmonary disease.
Data source: Centers for Medicare and Medicaid Services administrative claims data, January 2011#December 2011, from the Chronic Condition Warehouse (CCW),
ccwdata.org (347).
SPECIAL CONTRIBUTION
Early Management of Patients With Acute
Heart Failure: State of the Art and Future
Directions—A Consensus Document from the
SAEM/HFSA Acute Heart Failure Working
Group
Sean P. Collins, MD, MSc, Alan B. Storrow, MD, Phillip D. Levy, MD, MPH, Nancy Albert, PhD,
Javed Butler, MD, Justin A. Ezekowitz, MD, G. Michael Felker, MD, Gregory J. Fermann, MD,
Gregg C. Fonarow, MD, Michael M. Givertz, MD, Brian Hiestand, MD, MPH, Judd E. Hollander, MD,
David E. Lanfear, MD, Peter S. Pang, MD, MSc, W. Frank Peacock, MD, Douglas B. Sawyer, MD, PhD,
John R. Teerlink, MD, and Daniel J. Lenihan, MD
Abstract
Heart failure (HF) afflicts nearly 6 million Americans, resulting in 1 million emergency department (ED)
visits and over 1 million annual hospital discharges. The majority of inpatient admissions originate in the
ED; thus, it is crucial that emergency physicians and other providers involved in early management
understand the latest developments in diagnostic testing, therapeutics, and alternatives to hospitalization.
This article discusses contemporary ED management as well as the necessary next steps for ED-based
acute HF research.
ACADEMIC EMERGENCY MEDICINE 2015;22:94–112 © 2015 by the Society for Academic Emergency
Medicine
101
ACADEMIC EMERGENCY MEDICINE • January 2015, Vol. 22, No. 1 • www.aemj.org
H
eart failure (HF) afflicts nearly 6 million Americans, resulting in 1 million emergency department (ED) visits and over 1 million annual
hospital discharges.1,2 An aging population and
improved survival from cardiovascular diseases is
expected to further increase HF prevalence.3 By 2030 an
estimated 25% increase in HF prevalence will result in
an additional 3 million affected individuals.1,4 Of the
$39.2 billion spent on HF care in the US in 2010, inpatient admissions accounted for the single largest pro-
Table 5
Associated Clinical Characteristics and Treatment Approaches Based on ED Presentation Phenotype
From the Department of Emergency Medicine, Vanderbilt University, Nashville Veterans Affairs Medical Center (SPC, ABS, DBS),
Nashville, TN; the Department of Emergency Medicine, Wayne State University (PDL), Detroit, MI; the Department of Emergency
Medicine, University of Cincinnati (GJF), Cincinnati, OH; the Department of Emergency Medicine, Harvard Medical School
(MMG), Boston, MA; the Department of Emergency Medicine, Wake Forest University (BH), Winston-Salem, NC; the Department
of Emergency Medicine, Thomas Jefferson University (JEH), Philadelphia, PA; the Department of Emergency Medicine, Northwestern University (PSP), Chicago, IL; the Department of Emergency Medicine, Baylor University (WFP), Houston, TX; the Division of Cardiology, Cleveland Clinic (NA), Cleveland, OH; the Division of Cardiology, Emory University (JB), Atlanta, GA; the
Division of Cardiology, University of Alberta (JAE), Edmonton, Alberta, Canada; the Division of Cardiology, Duke University
(GMF), Durham, NC; the Division of Cardiology, Ronald Reagan-UCLA Medical Center, (GCF) Los Angeles, CA; the Division of
Cardiology, Wayne State University (DEL), Detroit, MI; the Division of Cardiology, San Francisco Veterans Affairs Medical Center,
University of California at San Francisco (JRT), San Francisco, CA; and the Division of Cardiology, Vanderbilt University, Nashville Veterans Affairs Medical Center (DJL), Nashville, TN.
Received August 23, 2014; accepted August 24, 2014.
The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
The authors have no relevant financial information to disclose.
Editor’s note: This paper is a planned copublication of J Card Fail 2014 Jul 17 [epub]. doi: 10.1016/j.cardfail.2014.07.003.
Supervising Editor: David C. Cone, MD.
Address for correspondence and reprints: Sean P. Collins, MD, MSc; e-mail: [email protected].
ED Presentation Phenotype
94
94
Clinical Characteristics
Treatment
Low BP (SBP < 100 mm Hg)
Known/suspected low LVEF
Diuretics (+++)
Inotropes/Pressors (++)
Mechanical support (+)
Normal BP (SBP 100–140 mm Hg)
Subacute systems
Preserved or reduced LVF
Dietary/medication indiscretion
Diuretics (++)
IV vasodilators (+)
Topical nitrates (++)
History of HTN
Abrupt system onset
Flash pulmonary edema
Multiple non-CV comorbidities
Topical/SL nitrates (++)
Diuretics (+)
IV vasodilators (+++)
NIV
ISSN 1069-6563
94
PII ISSN 1069-6563583
© 2015 by the Society for Academic Emergency Medicine
doi: 10.1111/acem.12538
High BP (SBP > 140 mm Hg)
+ = Relative intensity of use; BP = blood pressure; CAD = coronary artery disease; CRI = chronic renal insufficiency; CV = cardiovascular; HTN = hypertension; IV = intravenous; LVEF = left ventricle ejection fraction; NIV = NIV = noninvasive ventilation;
SBP = systolic blood pressure; SL = sublingual.
DISPOSITION DECISION MAKING: CAN A SUBSET
OF ED PATIENTS BE SENT HOME?
The ED is increasingly being relied on to evaluate more
AHF clinical profiles safe for either ED discharge, or
discharge after a brief period of treatment and observation, would be of even greater utility. Unfortunately, risk
prediction instruments in AHF have been largely unsuc-
Table 3
Synopsis of Recommended AHF Therapies Based on ESC, HFSA and ACCF/AHA, and CCS Guidelines
Recommendation
Diuretic use
AHF patients with
fluid overload
should receive
diuretics
Dosing
Inadequate diuresis
Ultrafiltration
ESC
HFSA
ACCF/AHA
I/B
B
I/B
SR/MQ
IV, to symptom
improvement,
consider high-dose
regimen, NSR.
IV, titrate to symptom
relief, minimize AE
(C)
Initial IV dose
should equal or
exceed oral daily
dose, then adjust
based on
response (I/B)
Consider doubling
loop diuretic (NSR)
Consider adding
thiazide
Consider dopamine
@ 2.5 lg/kg/min
(NSR)
Consider in refractory
cases (NSR)
Increase dose (C)
Continuous infusion
(C)
Add thiazide (C)
Add thiazide (IIa/B)
Increase loop dose
(IIa/B)
Consider renal
dose dopamine
(IIb/B)
We recommend a loop diuretic, such
as furosemide, for most patients
with HF and congestive symptoms.
When acute congestion is cleared,
the lowest dose should be used that
is compatible with stable signs and
symptoms (SR/LQ).
Increases in loop diuretics, cautious
addition of a second diuretic (a
thiazide or low-dose metolazone)
(WR/MQ).
Refractory cases (C)
In lieu of diuretics—
selected patients (C)
In refractory cases
of overload (IIb/
B)
Pulmonary
congestion (IIb/
C)
In pulmonary
congestion and SBP
>110 mm Hg (IIa/B)
caution in aortic/
mitral stenosis
NSR
+ diuretic and no
hypotension (B)
+ diuretic therapy
(IIb/A)
+ diuretic therapy
(IIb/A)
Severe volume
overload and Na
< 135 (IIb/B)
Vasodilators, other
pharmacologic
therapy
Nitrates
Nesiritide
CCS
Patients with persistent congestion
despite diuretic therapy, with or
without impaired renal function,
may, under experienced
supervision, receive continuous
venovenous ultrafiltration. (Practical
tip)
Titrated to SBP > 100 mm Hg, for
relief of dyspnea in
hemodynamically stable patients
(SBP > 100 mm Hg)
SR/MQ
Vasopressin
antagonist
NSR
After first-line therapy
(C)
NSR
Opiates +/–
antiemetic
Fluid restriction
IIa/C
NSR
NSR
NSR
<2 L/days if Na <
130 mEq/L; stricter if
<125 mEq/L (C)
NSR
I/A
If no contraindication
(B)
1.5–2 L/day
especially in Na <
135 and
congestion (IIa/C)
UFH, LMWH (I/B)
If SaO2 < 90% (I/C)
If hypoxia (C)
NSR
For RR > 20, caution
in SBP < 85 mm Hg
(IIa/B)
SBP < 85 mm Hg or
hypoperfusion (IIa/C)
In severe dyspnea (A)
NSR
If hypoxia, titrated to an SaO2 > 90%
(SR/MQ)
We recommend CPAP or BiPAP not
be used routinely (SR/MQ)
In selected
hypotensive patient
(C)
In short-term
support of
selected patients
(IIb/B)
Thromboembolism
prophylaxis
Respiratory support
Oxygen
NIV
Inotropic support
WR/HQ
Symptomatic or severe
hyponatremia (<130 mmol/L) and
persistent congestion despite
standard therapy, to correct
hyponatremia and the related
symptoms (WR/MQ)
NSR
NSR
We recommend hemodynamically
stable patients do not routinely
receive inotropes like dobutamine,
dopamine, or milrinone (SR/HQ).
ACCF/AHA = American College of Cardiology Foundation/American Heart Association; AHF = acute heart failure; BiPAP = bilevel
positive airway pressure; CCS = Canadian Cardiovascular Society; CPAP = continuous positive airway pressure; ESC = European
Society of Cardiology; HFSA = Heart Failure Society of America; NIV = noninvasive ventilation; NSR = no specific recommendation; SR/HQ = strong recommendation, high-quality evidence; SR/LQ = strong recommendation, low-quality evidence;
SR/MQ = strong recommendation, moderate-quality evidence; WR/HQ = weak recommendation, high-quality evidence;
WR/MQ = weak recommendation, moderate-quality evidence.
104
Collins et al. • EARLY MANAGEMENT OF PATIENTS WITH ACUTE HEART FAILURE
Figure 1. A conceptual model of acute heart failure risk stratification in the ED based on known predictors of risk for mortality or
serious adverse events, presence of absence of comorbidities, and self-care issues. Such an algorithm may augment clinical judgment in disposition decisions. ICU = intensive care unit.
However, patients with a mildly elevated troponin are at
increased risk for “failing” observation care and requir97
consideration, but it can take time for certain perturbations to manifest, and intervention before adequate
18. Figure
ESC Definition
of Advanced
HF algorithm. CRT indicates cardiac resynchronization therapy; CRT-D, cardiac resynchronization
2. Indications
for CRT therapy
therapy-defibrillator; GDMT, guideline-directed medical therapy; HF, heart failure; ICD, implantable cardioverter-defibrillator; LBBB, left
bundle-branch
block;
LVEF,and/or
left ventricular
fraction; MI, myocardial infarction; and NYHA, New York Heart Association.
ere symptoms
of HF with
dyspnea
fatigue at ejection
rest or with
mal exertion (NYHA class III or IV)
Table
ESC (pulmonary
Definition and/or
of Advanced
odes of
fluid 18.
retention
systemicHFcongestion, peripheral
ma) and/or reduced cardiac output at rest (peripheral hypoperfusion)
1. Severe symptoms of HF with dyspnea and/or fatigue at rest or with
ctive evidence
severe(NYHA
cardiac
dysfunction
minimal of
exertion
class
III or IV) shown by at least 1 of the
wing:2. Episodes of fluid retention (pulmonary and/or systemic congestion, peripheral
VEF <30%
edema) and/or reduced cardiac output at rest (peripheral hypoperfusion)
seudonormal or restrictive mitral inflow pattern
3. Objective evidence of severe cardiac dysfunction shown by at least 1 of the
ean PCWP
>16 mm Hg and/or RAP >12 mm Hg by PA catheterization
following:
gh BNP a.or LVEF
NT-proBNP
<30% plasma levels in the absence of noncardiac causes
b. Pseudonormal
or restrictive
inflow
ere impairment
of functional
capacitymitral
shown
by pattern
1 of the following:
c. exercise
Mean PCWP >16 mm Hg and/or RAP >12 mm Hg by PA catheterization
ability to
High distance
BNP or NT-proBNP
-Minuted.walk
!300 mplasma levels in the absence of noncardiac causes
_4.2Severe
impairment
of functional capacity shown by 1 of the following:
<12 to
14 mL/kg/min
eak Vo
a. Inability to exercise
ory of "1 HF hospitalization in past 6 mo
b. 6-Minute walk distance !300 m
_ 2 <12 features
ence of c.allPeak
the previous
despite “attempts to optimize” therapy,
to 14 mL/kg/min
Vo
uding 5.diuretics
and
unless these
are poorly
History of
"1GDMT,
HF hospitalization
in past
6 mo tolerated or
raindicated, and CRT when indicated
6. Presence of all the previous features despite “attempts to optimize” therapy,
including
diuretics
and GDMT,
unless
these
are poorly
tolerated or
indicates
B-type
natriuretic
peptide;
CRT,
cardiac
resynchronization
and CRT
indicatedGDMT, guideline-directed
; ESC, contraindicated,
European Society
of when
Cardiology;
l therapy;
heart B-type
failure;natriuretic
LVEF, left
ventricular
ejectionresynchronization
fraction;
BNP HF,
indicates
peptide;
CRT, cardiac
BNP, therapy;
N-terminal
NYHA,
New guideline-directed
York Heart
ESC,pro-B-type
European natriuretic
Society of peptide;
Cardiology;
GDMT,
therapy;artery;
HF, heart
failure;
LVEF, left
ventricular
fraction;
ation;medical
PA, pulmonary
PCWP,
pulmonary
capillary
wedgeejection
pressure;
NT-proBNP,
N-terminal pro-B-type natriuretic peptide; NYHA, New York Heart
P, right
atrial pressure.
Association;
PA,al.pulmonary
ted from
Metra et
(33). artery; PCWP, pulmonary capillary wedge pressure;
and RAP, right atrial pressure.
Adapted from Metra et al. (33).
Table 19. Clinical Events and Findings Useful for Identifying
Patients With Advanced HF
Repeated ("2) hospitalizations or ED visits for HF in the past year
Table 19. Clinical Events and Findings Useful for Identifying
Progressive
in renal
Patientsdeterioration
With Advanced
HFfunction (e.g., rise in BUN and creatinine)
Weight loss without other cause (e.g., cardiac cachexia)
Repeated ("2) hospitalizations or ED visits for HF in the past year
Intolerance to ACE inhibitors due to hypotension and/or worsening renal
Progressive deterioration in renal function (e.g., rise in BUN and creatinine)
function
Weight loss without other cause (e.g., cardiac cachexia)
Intolerance to beta blockers due to worsening HF or hypotension
Intolerance to ACE inhibitors due to hypotension and/or worsening renal
Frequent
systolic blood pressure <90 mm Hg
function
Persistent
dyspnea
with
dressing
requiring
rest
Intolerance
to beta
blockers
dueortobathing
worsening
HF or hypotension
Inability
to walk
1 block
the level
ground
Frequent
systolic
bloodonpressure
<90
mm Hgdue to dyspnea or fatigue
Recent
need todyspnea
escalate
volume rest
status, often reaching
Persistent
withdiuretics
dressingtoormaintain
bathing requiring
daily
furosemide
doselevel
overground
160 mg/d
useoroffatigue
supplemental
Inability
to walk equivalent
1 block on the
due toand/or
dyspnea
metolazone
therapy
Recent need to escalate diuretics to maintain volume status, often reaching
Progressive
decline in equivalent
serum sodium,
usually
to <133
daily furosemide
dose over
160 mg/d
and/ormEq/L
use of supplemental
metolazone therapy
Frequent
ICD shocks
Progressive decline in serum sodium, usually to <133 mEq/L
ACE indicates angiotensin-converting enzyme; BUN, blood urea nitrogen; ED,
Frequent ICD shocks
emergency department; HF, heart failure; and ICD, implantable cardioverterACE indicates angiotensin-converting enzyme; BUN, blood urea nitrogen; ED,
defibrillator.
emergency
HF,(274).
heart failure; and ICD, implantable cardioverterAdapted
fromdepartment;
Russell et al.
defibrillator.
Adapted from Russell et al. (274).
Factores frecuentes de descompensacion
No adherencia a tto (fármacos, sodio sobrecarga hídrica)
Isquemia miocárdica
HTA
FA y otras taquiarritmias
Efecto secundario inotrópico negativo (Amiodarona, diltiazem, beta bloqueantes)
TEP
Fármacos que aumentan retención hidrosalina (corticoides, AINE).
Ingesta de alcohol u otros tóxicos.
Endocrinopatia (diabetes, hiper/hipotiroidismo)
Infección
Enfermedad CV asociada (Endocarditis, patología aortica)
Estrategia
1.- Predominio de la insuficiencia:
izquierda (más frecuente) o derecha
2.- Función afectada
sistolica (contractilidad, FEVI, dilatación VI)
diastólica (relajación, asociado al llenado ventricular y contractilidad)
Mecanismos de disfuncion sistolica
1.- perdida de masa ventricular
-
- patología coronaria
- trastornos infecciosos/inflamatorios
- traumático
- cardiomiopatia adquirida (post parto, por ej).
-
2.- miocardiopatía primaria
-
-
- infiltración
- depósitos glicogeno alterados
- distrofia muscular
- patología metabólica
- neoplasia
- genética
-
3.- trastorno mecánico
-
- valvular
- congénito.
-
-
-
Manejo farmacológico.
Falla sistolica de VI
1.- HTA
2.- Normotension
3.- Hipotensión
Falla sistolica + HTA
( PCP alta + GC bajo + HTA)
1.- Vasodilatadores
2.- Diuréticos (Hipervolemia asociada)
Falla sistolica + Normotension
(isquemia miocárdica, miocarditis, ICC crónica)
1.- Dobutamina/Milrinona
2.- Diuréticos (Hipervolemia asociada)
Falla sistolica + Hipotensión.
1.- Dobutamina/Dopamina/Nadr/Adr
2.- Aporte volumen i.v. (Hipovolemia asociada)
3.- Soporte mecánico.
Mecanismos de disfuncion diastólica
1.- relajación anormal
- isquemia
- HV post HTA
-
2.- aumento rigidez
-
- infiltración
-
3.- transmisión extrínseca
-
- HTP
- patología pericardica
- PEEP/ARM
-
Falla diastólica.
Incidencia en forma pura: desconocida
Tto: Inotrópicos con acción irregular, aporte de volumen
limitado (igual que diuréticos).
Verapamil y beta bloqueantes pueden estar indicados
RV failure in the setting of chronic heart and lung disease.
Management of RV failure is directed at optimizing right-sided
filling pressures and reducing afterload. Due to a lower level of
vascular tone, vasoactive medications have less salient effects
on reducing vascular resistance in the pulmonary than in the
systemic circulation. Successful management requires reversal of
FOCUSED REVIEW
patients with acute RV failure who fail to respond to
management while the underlying cause of their RV f
addressed.
Keywords: right-sided heart failure; pulmonary hype
critical care
Management of Acute Right Ventricular Failure in the Intensive
(Received in original form December 13, 2013; accepted in final form April 21, 2014 )
Care
Unit
Supported by National Institutes of General Medical Sciences grant P20 GM103652 and American Heart Association grant 11FTF7400032.
Correspondence
and requests
for reprints
should be addressed to James R. Klinger, M.D., Division of Pulmonary and Critical Care Medicine,
Corey
E. Ventetuolo
and James
R. Klinger
Hospital, 593 Eddy Street, Providence, RI 02903. E-mail: [email protected]
Division of Pulmonary, Sleep and Critical Care Medicine, Rhode Island Hospital, Alpert Medical School of Brown University, Providence,
Ann Am
Thorac Soc Vol 11, No 5, pp 811–822, Jun 2014
Rhode
Island
Copyright © 2014 by the American Thoracic Society
DOI: 10.1513/AnnalsATS.201312-446FR
Internet address: www.atsjournals.org
Abstract
any conditions that heighten pulmonary vascular tone and the
use of selective pulmonary vasodilators at doses that do not
Right ventricular (RV) failure occurs when the RV fails to maintain induce systemic hypotension or worsening of oxygenation.
enough blood flow through the pulmonary circulation to achieve
Systemic systolic arterial pressure should be kept close to RV
adequate left ventricular filling. This can occur suddenly in
systolic pressure to maintain RV perfusion. When these efforts
a previously healthy heart due to massive pulmonary embolism or
fail, the judicious use of inotropic agents may help improve
right-sided
myocardial infarction,
RVcare
contractility
to maintain
cardiac exercise
output. is associated with
Several developments
have led tobuta many
greatercases encountered
during
in the intensive
unit withenough
emphasis
on
infocus
the intensive
unit involve
Extracorporeal
support and
is increasingly
being
to support
on right care
ventricular
(RV)worsening
function of
in compensated
increase
inused
blood
pressure. The d
fluid management,
afterload life
reduction,
RV failure in the setting of chronic heart and lung disease.
with acute RV failure who fail to respond to medical
critically ill patients. These include the rapid
augmentation patients
of contractility
using vasoactive between the two circulations is b
Management of RV failure is directed at optimizing right-sided
management while the underlying cause of their RV failure is
growth
in our and
understanding
of pulmonary
medications,
an introduction to the rapidly the ability of the lung to recruit
filling
pressures
reducing afterload.
Due to a lower
level of and
addressed.
vasculartone,
biology
and themedications
subsequenthave less salient
expanding
vascular
vasoactive
effects field of extracorporeal life support. collapsed or unused vessels as car
development
of several
new classes
of
the relatively low d
on
reducing vascular
resistance
in the pulmonary
than in the
Keywords: right-sided heart failure; increases
pulmonaryand
hypertension;
systemic
circulation.
Successful
management
pulmonary
vasodilator
medications.
The requires reversal of critical care
vascular motor tone in the proxi
widespread treatment of patients with
pulmonary vascular bed. In the
The Normal Pulmonary
pulmonary arterial hypertension has also
circulation, a large drop between
Circulation and RV
enhanced our clinical expertise in managing
venous pressure is created by m
(Received in original form December 13, 2013; accepted in final form April 21, 2014 )
acute RV failure toward the end of their
The pulmonary circulation is a low-pressure arterioles that act as resistors an
Supported by National Institutes of General Medical Sciences grant P20 GM103652 and American Heart Association grant 11FTF7400032.
disease. Finally, technical advances in
to redistribute blood flow to diffe
circuit both at rest and during exercise.
Correspondence and requests for reprints should be addressed to James R. Klinger, M.D., Division of Pulmonary and Critical Care Medicine, Rhode Island
extracorporeal
support
haveRIprovided
us [email protected]
Despite a rise in cardiac output during heavy as needed. In contrast, the differen
Hospital,
593 Eddy life
Street,
Providence,
02903. E-mail:
d,
ns
the outflow region expands the proximal
pulmonary artery, priming it to receive the
Because they share a common septum,
abnormalities in the function of one
ng the
erably
ntricle
walled
of its
more
At end
mm in
in
maller
he RV
nd
tening
oduces
much
RV to
he LV
rences
forces
Figure 2. Differences between right ventricular (RV) and left ventricular (LV) response to increasing
afterload (left panel) and increasing preload (right panel). RV stroke volume falls sharply as mean
! is increased from 20 to 30 mm Hg in the pulmonary artery, but LV stroke volume
vascular pressure (P)
stays fairly constant as mean aortic pressure is increased from 100 to 140 mm Hg. In contrast, LV
stroke work increases rapidly as left atrial pressure is raised from 10 to 20 cm H2O, while the
increase in RV stroke work in response to the same elevation or right atrial pressure is much more
modest. Reproduced by permission from Reference 113.
AnnalsATS Volume 11 Number 5 | June 2014
RV and LV end-diastolic pressure is
maintained. Similarly, increased RV
preload increases RV output, thereby
raising LV end-diastolic pressure and
maintaining the right-to-left end-diastolic
pressure difference. As pulmonary vascular
resistance increases, however, the RV
becomes incapable of maintaining LV
filling pressure. RV end-diastolic pressure
begins to riseFOCUSED
as LV end-diastolic
pressure
REVIEW
Figure 5. Pulmonary vascular resistance in intra- and extra-alveolar vessels relative to lung volume.
Interstitial pressure becomes more negative during lung expansion in the spontaneously breathing
patient, favoring enlargement of most pulmonary vessels and a fall in their resistance to blood flow.
Intra-avleolar vessels, however, become compressed by expansion of surrounding alveoli during lung
inflation, leading to increased vascular resistance in these vessels. Total pulmonary vascular resistance
is lowest at functional residual capacity, where vascular resistance in both intra- and extra-alveolar
vessels is intermediate. TLC = total lung capacity. Reproduced by permission from Reference 114.
(56–59). These agents inhibit the
metabolism of cGMP, the second
messenger that mediates the vasodilatory
effects of nitric oxide and the natriuretic
peptides. In animal studies, PDE5
inhibitors increase contractility in
hypertrophied RV, but not in normal RV
(60). Thus, these agents may improve
Detection and Monitoring of
RV Function in Critically
Ill Patients
Assessment of RV function in the critically
ill patient begins with physical exam and
consideration of the patient’s presentation
and medical history. Evidence of elevated
right-sided filling pressures, as suggested
RV function in patients with chronic
pulmonary hypertension who develop acute
RV failure. PDE5 inhibitors must be
used cautiously in patients who are
hemodynamically unstable (61, 62),
because they have systemic vasodilator
effects that can lower blood pressure, and
their terminal half-life ranges from 4 to
18 hours. An intravenous form of sildenafil
with shorter half-life is also available.
The use of other currently available
pulmonary vasodilators, such as the
endothelin receptor antagonists and the
recently approved soluble guanylate cyclase
stimulator, riociguat, should probably be
avoided in acute RV failure. Endothelin
receptor antagonists have been associated
with increased mortality in left heart failure,
and riociguat may have significant systemic
vasodilator effects, especially under
conditions such as sepsis, where endogenous
nitric oxide production may be increased.
Calcium channel blockers should also be
avoided,
theyofhave
negative
Figure
3. because
The position
the interventricular
septum during the cardiac cycle is determined by the
inotropic between
effects, and
been (RV)
shown
difference
right have
ventricular
and left ventricular (LV) pressure. Under normal conditions,
LV
is greater
RV end-diastolic pressure, and the septum bows toward
to end-diastolic
increase RV pressure
stroke work
indexthan
(63).
the RV during diastole. As the RV fails, RV end-diastolic pressure begins to exceed that of the left
ventricle
(LV) and
septum bows toward the LV during diastole forming a “D”-shaped pattern and
Insufficient
RVthe
Contractility
impaired
LV
filling
(left
panel).
RV failure
Loss of RV contractile
forceWhen
in acute
RV occurs due to elevated pulmonary vascular resistance,
the combination of high RV systolic pressure and decreased LV filling may lead to near obliteration
failure is induced primarily by three
of the LV at end systole (right panel).
interrelated factors: (1) overstretching
of the RV free wall, placing the myocytes
at a mechanical disadvantage; (2)
Focused
Review
derangements in cellular metabolism, leading
to decreased myocardial contractile forces;
and (3) insufficient oxygen delivery due to
decreased coronary arterial perfusion. The
in RV free wall tens
systemic arterial pre
decrease RV perfusi
acute RV failure ass
pulmonary vascular
systolic pressures th
systemic pressure. I
goal of vasopressor
systemic blood pres
systolic pressure (70
increase myocardial
withheld until this fi
Vasopressors
Figure 6. Cycle of right ventricular (RV) decompensation. RV dysfunction begins with excessive
Several vasoactive dr
manage RV failure i
(Table 2). The ideal
acute RV failure wo
increases systemic a
contractility without
vascular resistance. N
primarily targets the
vasoconstriction wit
stimulation and card
However, the b1 eff
been shown to impro
coupling in animal m
(73–75). In a small
sepsis with right hea
use was associated w
myocardial oxygen d
in systemic vascular
pulmonary vascular
medium doses (5–10 mg kg21 min21), and a1
receptors at high doses (.10 mg kg21 min21).
pulmonary vascular resistance in patients
with left heart failure (73, 85). Dobutamine
Table 2. Vasoactive drugs for management of acute right ventricular failure and their
mechanism of action
Receptor Binding
Agent
a1
b1 b2
Norepinephrine
11 1
Phenylephrine
11
Epinephrine
Vasopressin
11 11 1
Dopamine
Low (,5 mg/kg/min)
Medium (.10 mg/kg/ 1
min)
High (.10 mg/kg/min) 11
Dobutamine
Milrinone
1
11
D
V1
Notes
Improves PA/RV coupling in animals
(73–75)
Increases PVR (71, 74, 77); may induce
reflex bradycardia
(79)
1 Dose dependent pulmonary vasodilatation
(0.01–0.03 U/min) and vasoconstriction
(24, 82, 83)
Risk of arrhythmias
11
11
11
11
11 1
b2-mediated drop in SVR (31); risk of
arrhythmias
Phosphodiesterase-3 inhibitor; inotropy and
pulmonary vasodilatation; drop in LVEDP
and SVR (72, 84, 89); risk of arrhythmias
Definition of abbreviations: D = dopaminergic receptor; LVEDP = left ventricular end-diastolic
pressure; PA = pulmonary artery; PVR = pulmonary vascular resistance; RV = right ventricle; SVR =
systemic vascular resistance; V1 = vasopressin receptor 1. 1 = low to moderate affinity, 11 =
moderate to high affinity.
818
is often a poor pr
failure. At the sam
to avoid increasin
normal levels, bec
pulmonary artery
increase RV workl
intensivists prefer
inotropic support,
of a chronotropic
Calcium sens
levosimendan, tha
contractility witho
calcium and oxyg
used to increase ca
failure. Randomiz
studies have show
systolic and diasto
with left heart fail
reports describe im
in response to lev
with RV failure as
thromboembolic p
and heart transpla
Mechanical S
When medical the
in the intensive ca
AnnalsATS Volume 11
sidered.
ifically
acorporeal
n used
failure due
chronic
ertension,
sion,
tomy or
Unlike
brane
ous
ump
h the
rial
nation
enous to
the RV
enation.
mbrane
on and
sed
usly
reports
nation
nitiation
y in a
Figure 8. Approach to management of acute right ventricular (RV) failure. Patients should be
assessed for acute cause of increased RV afterload or decreased contractility, such as pulmonary
embolism or right-sided infarction. If no readily reversible cause is identified, efforts should be directed
pices of the European Society of Cardiology—the EuroHeart Failure Surveys I
and II (6, 7). Data are also available from
national studies in Italy (8) and England
and Wales (9) and from a two-center
study in Helsinki (Finland) and Zurich
(Switzerland) (10). Two other published
studies care
are of unit:
interest Epidemiology
because they inAcute heart failure in the intensive
cluded a particular subset of patients hosDOI: 10.1097/01.CCM.0000296264.41365.80
pitalized
with acute heart failure: a mulOwais Dar, MB ChB, MRCP; Martin R. Cowie, MD,
MSc, FRCP
College, London, United Kingdom.
Dr. Cowie has disclosed consultancies with
ResMed, Takeda Pharmaceuticals, Medtronic, and
Stirling Medical; he also has received grants from
Takeda Pharmaceuticals and Medtronic. Dr. Dar has
Scientific
Reviews
not
disclosed any
potential conflicts of interest.
For information regarding this article, E-mail:
[email protected]
Copyright © 2007 by the Society of Critical Care
Medicine and Lippincott Williams & Wilkins
EuroHeart Failure Survey I. The first
EuroHeart Failure Survey enrolled 11,327
patients across Europe, with 115 hospitals
taking part in 24 European countries in
2000 –2001. The charts of patients dying or
discharged with a diagnosis of heart failure
were reviewed with follow-up data collected
from the survivors at 12 wks after discharge
(6).
Crit Care Med 2008 Vol. 36, No. 1 (Suppl.)
S3
More than a million patients are admitted annually to U.S.
hospitals with acute heart failure. Multicentered hospital-based
registries and surveys in the United States and Europe have
shown that the typical patient is >70 yrs of age, with a history of
heart failure, coronary artery disease, and hypertension. There are
an equal number of men and women. Patients typically spend
several days on the intensive care unit, with longer admissions in
Europe than the United States. The in-hospital mortality rate is
around 4% to 7%. The risk of subsequent hospital readmission is
high. The elderly, those with comorbidities, and those with cardiogenic shock or renal failure do particularly badly. Better treatment by those with expertise in the management of this syndrome and good follow-up care are likely to improve the
outcome for this large group of patients. (Crit Care Med 2008;
36[Suppl.]:S3–S8)
KEY WORDS: acute heart failure; registries; surveys
Right HF
Hypertensive HF
Cardiogenic
shock
Pulm edema
De novo AHF
Acute
decompensated
CHF
All
A
In-hospital mortality (%)
so similar for the
40
patients admitted
35
are units/coronary
30
chemic precipitant
cute heart failure poses a sig- ing heart (acute de novo heart failure) or ticentered New York study of heart failure
nificant burden on the health- can occur in patients with chronic heart with preserved systolic left ventricular
services within North failure, where the term25
acute decompen- function (11) and an intensive care/
n 25%, andcareinfecAmerica and Europe, largely sation is often applied. Cardiogenic shock coronary care unit survey from France
driven by
the costpreof the hospitalization is considered to be present when there (EFICA) (12).
patients
with
20 perfusion as ADHERE. The ADHERE registry in the
required to stabilize the syndrome. Hos- are symptoms of poor organ
pital discharges
in the United States rose a consequence of low cardiac output and United States has enrolled !100,000 par systolic
function,
by 174% from 399,000 in 1979 to low blood pressure.
tients since 2001 from 282 hospitals
15
in a
2003 less
(1). The total cost of
Multicentered hospital-based registries across the country. The charts of patients
ears to1,093,000
be
hospitalization in the United States was and surveys can provide much valuable in- with a primary or secondary discharge
in 2006,in
52% of the total formation about the syndrome,
10 although diagnosis of heart failure were reviewed
(10%$15.4
ofbillion
cases
direct cost of heart failure (2). European they may miss patients with milder presen- retrospectively (5). Acute heart failure
are similar, conwith !60% of the eco- tations who are managed in the doctor’s was defined as either new-onset heart
y), anddata
poorly
5 patients en- failure requiring hospitalization or denomic cost of heart failure related to hos- office or in primary care. The
pitalization
(3,
4).
Despite
this
enormous
rolled
in
registries
and
surveys
are likely to compensation of chronic established
re (13%
with prehealthcare activity, it is only recently that be more representative of all patients with heart failure with symptoms sufficient to
0 patients en- warrant hospitalization. ADHERE is a
the epidemiology
of acute heart failure acute heart failure than the
od pressure
!200
has become clearer, chiefly as the result rolled in randomized clinical trials of phar- commercially sponsored registry, with a
of several large-scale registries.
macologic treatment, where selection nonrandomized sampling frame of U.S.
compliance
with
forces biased inclusion toward younger hospitals. The registry relies on hospitalmale patients with fewer comorbidities.
Definition
of
Acute
Heart
Failure
based coding, and data collection on clinrtension or heart
ical features may not be complete as the
There is no universally agreed upon
study relies on retrospective chart review.
ommon
(11).
definition
of acute heart failure, but it is Heart Failure Registries and
However, comparison with a random
generally considered to represent the rel- Surveys
sample of Medicare patients suggests that
Mortality.
The
meatively abrupt
onset
of symptoms severe
The largest registry is ADHERE (Acute the data are representative of the general
enough to merit hospitalization. It can
markedly
shorter
occur as the
first manifestation of a fail- Decompensated Heart Failure National U.S. experience (13). In addition, the registry collects information on hospitalizain the United States
(5). Two in
FigureRegistry)
1. In-hospital
mortality
the EuroHeart Failure Survey II by history of heart failure (HF) and
tions, not individual patients, so some
shorter
term
surveys
of
heart
failure
have
s than in Europe
be represented several
timesNieminen et al (7). AHF, acute heart failure;
conducted in Europe under
the aus- patients
clinicalbeenpresentation.
Modified,
with may
permission,
from
From the National Heart & Lung Institute, Imperial pices of the European Society of Cardiol- in the data set.
ly related
the
College, London,to
United Kingdom.
EuroHeart
Failure Survey I. The first
ogy—the EuroHeart
Surveys
I
CHF,
heartFailure
failure;
Pulm,
pulmonary.
Dr. Cowie has disclosed consultancies
with chronic
and II (6, 7). Data are also available from EuroHeart Failure Survey enrolled 11,327
Takeda Pharmaceuticals,
Medtronic, and
hcare ResMed,
systems.
For
Stirling Medical; he also has received grants from national studies in Italy (8) and England patients across Europe, with 115 hospitals
Takeda Pharmaceuticals and Medtronic. Dr. Dar has and Wales (9) and from a two-center
takingin
partADHERE
in 24 European(5)
countries
the intensive
care
Table 4.
Medications
at and
admission
andorinEuroHeart Failure Survey II (7)
not disclosed any potential
conflicts of interest.
2000
–2001.
The
charts
of
patients
dying
study
in
Helsinki
(Finland)
Zurich
For information regarding this article, E-mail:
(Switzerland) (10). Two other published discharged with a diagnosis of heart failure
stay [email protected]
similar in
Copyright © 2007 by the Society of Critical Care studies are of interest because they in- were reviewed with follow-up data collected
and Lippincott Williams & Wilkins
Euro-HF II7
cluded a particular subset of patients hos- from the survivors at 12 wks after discharge
onger Medicine
duration
of
DOI: 10.1097/01.CCM.0000296264.41365.80
pitalized with acute heart failure: a mul- (6).