Download Death or Heart Failure Hospitalization

COPD or HF
A Clinical Challenge
Learning Session 3
www.pspbc.ca
Agenda
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Sharing success and lessons learned (65):
Optional co-morbid Patient Story: (10)
Comorbidity patients (60 - 40 didactic, 20 discussion
Break (15)
Planning for Sustainability (30, 15 didactic + 15 discussion):
Wrap up (30 – mostly evaluation)
2
Faculty/Presenter Disclosure
Speaker’s Name: Speaker’s Name
Relationships with commercial interests:
- Grants/Research Support: PharmaCorp ABC
- Speakers Bureau/Honoraria: XYZ Biopharmaceuticals Ltd
- Consulting Fees: MedX Group Inc.
- Other: Employee of XYZ Hospital Group
3
Disclosure of Commercial Support
This program has received financial support from [organization name] in the form
of [describe support here – e.g. educational grant].
This program has received in-kind support from [organization name] in the form
of [describe the support here – e.g. logistical support].
Potential for conflict(s) of interest:
- [Speaker/Faculty name] has received [payment/funding, etc.] from
[organization supporting this program AND/OR organization whose product(s) are
being discussed in this program].
- [Supporting organization name] [developed/licenses/distributes/benefits from
the sale of, etc.] a product that will be discussed in this program: [enter generic
and brand name here].
4
Mitigating Potential Bias
[Explain how potential sources of bias identified in slides 1 and 2 have been
mitigated].
Refer to “Quick Tips” document
5
Patients with Comorbidities
Objectives
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HF and COPD – a background
Epidemiology
Dealing with dyspnea
Approach to the patient with COPD & HF
The future …
7
Case
 65 year old woman with a thirty pack year hx. of smoking
presents with progressive dyspnoea.
 Five years previously there was a history of a AMI.
 There is a reported history of chronic cough and clear sputum.
 There is minimal peripheral edema.
 Salbutamol PRN gives some relief but the symptoms have
become progressive and more troublesome.
 What next …?
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Conclusions:
 COPD is common in HF
 and independently predicts mortality
 HF is common in COPD
 and independently predicts mortality
 Cardiovascular risk factors cluster in patients with COPD
 Many symptomatic, diagnostic and therapeutic challenges
14
Clinical Approach
 HF and COPD are common and they commonly co-exist in the
same patient
1. Diagnosis may be challenging due to similarities in clinical
presentation
2. Diagnostic tools exist which may help to differentiate these
disease entities in the dyspneic patient
3. In general, traditional pharmacological and non pharmacological therapies are well tolerated and may have
benefit across both disease states
15
Finding
Pooled
Sensitivity
Pooled
specificity
LR
LR
Positive
negative
0.61
0.86
4.4 (1.8-10.0)
0.45 (0.28-0.73)
Hx. of heart
failure
0.60
0.90
5.8 (4.1-8.0)
0.45 (0.38-0.53)
Myocardial
infarction
0.40
0.87
3.1(2.0-4.9)
0.69 (0.58-.82)
IHD
0.52
0.70
1.8 (1.1-2.8)
0.68(0.48-0.96)
COPD
0.34
0.57
0.81(0.60-1.1)
1.1 (0.95-1.4)
Initial clinical
judgment
16
Symptoms
Pooled
Sensitivity
Pooled
LR
LR
specificity Positive
negative
0.84
2.6 (1.5-4.5) .74 (0.540.91)
PND
0.41
Orthopnoea
0.51
0.74
2.2 (1.22.39)
.65 (0.450.92)
Edema
0.51
0.66
2.1 (0.925.0)
.64 (0.391.11)
17
Finding
Pooled
Sensitivity
Pooled
specificity
LR
LR
Positive
negative
Third heart sound
0.13
0.99
11 (4.9-25.0)
0.88(0.83-0.94)
Abdomino-jugular
reflex
0.24
0.96
6.4 (0.81-51.0)
0.79(0.62-1.0)
JVP elevated
0.39
0.92
5.1(3.2-7.9)
0.66(0.57-0.77)
Crackles
0.60
0.78
2.8(1.9-4.1)
0.51 (0.37-0.70)
Any murmur
0.27
0.90
2.6(1.74-4.1)
0.81(0.73-0.90)
Peripheral edema
0.50
0.78
2.3(1.5-3.7)
0.64(0.47-0.87)
Wheezing
0.22
0.58
0.52(0.38-0.71)
1.3 (1.1-1.7)
18
Differentiating COPD and HF Clinically
 These may be difficult to differentiate
› Overlap in signs
› Overlap in symptoms
› Overlap in investigations
 May be complicated in the face of an acute exacerbation of
either disease state
› Patient must have a ‘stable’ clinical status
19
Differentiating HF and COPD using diagnostics:
Echocardiography
 Helpful in patients when there is clear evidence of either systolic
or diastolic dysfunction
 This may be difficult in patients with COPD
 Poor visualization (10-30%) of patients
 Concomitant atrial fibrillation precludes accurate
assessment of diastolic function
 Evidence of impaired systolic/diastolic function doesn’t
necessarily imply that the patient has clinical HF
 Nuclear medicine testing with MUGA or MIBI may be a useful
alternate mechanism for assessing LVEF
20
Additional investigations to consider in the “stable”
patient
ECG
ECG
When “normal” HF < 10%
COPD
nT-pro-BNP
nT-pro-BNP
When “normal” HF < 10%
COPD
CXR
CXR
When “normal” HF < 12%
When “normal” HF < 9%
Low NPV and moderate PPV
COPD
Low NPV and low PPV
Davie et al., 1996; Rutten et al., 2005; Rutten et al., 2006; Fonseca et al., 2004; Fuat et al., 2006; Zaphiriou et al., 2005.
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Why Measure Spirometry?
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x COPD-6.
Diagnose COPD.
Confirm response to therapy.
Provide prognostic information for patients with HF!
Assess relative contributions of COPD versus HF to dyspnea.
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Differentiating HF and COPD using diagnostics:
Spirometry
 COPD (GOLD-criteria)
› Spirometry showing airflow obstruction: FEV1/FVC <70% (or
LLN) with or without complaints
 During HF exacerbations, FEV1 is more reduced than FVC
 In stable HF, both FEV1 and FVC are reduced to the same
extent
 HF can distort grading of severity (FEV1 % predicted) in COPD
 Fluid overload can cause a restrictive pattern in PFTs with
associated diffusion disturbances
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Key messages:
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BNP guided therapy:
Shorter length of stay: median of 8 versus 11 days
More cost effective $5.400 vs 7,200
Less likely to be admitted to ICU
Lower mortality
NEJM 200425
Non-Heart Failure Reasons for Elevation in BNP
ACUTE HF
CHRONIC HF
Alternate Diagnoses to Consider
Alternate Diagnoses to Consider
Acute Coronary Syndromes
Advanced age ( > 75 years)
Pulmonary Embolism
Atrial Fibrillation
Acute Renal Insufficiency
Renal Dysfunction (eGFR < 45)
PAH
LVH
Sepsis
COPD
nT-pro-BNP > 400 pg/mL or BNP > 125 pg/mL
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Conclusions - Diagnostics
 Consider BNP/nT-pro-BNP to rule out the presence of HF
› Has good negative predictive value (NPV)
 Spirometry is useful when the patient’s volume status is
optimized
› During acute HF exacerbations, diagnostic accuracy may be
limited
 Echo may be helpful to rule out the presence of systolic or
diastolic dysfunction
› Poor echo windows and the presence of concomitant atrial
fibrillation is a co-founder
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Therapeutic Considerations in HF and COPD
 HF drugs in COPD
› (1) ACE Inhibitors:
 Increases respiratory muscle strength and
decrease pulmonary artery pressures
› (2) Beta-Blockers:
 Choose cardio-selective agents (e.g. bisoprolol)
if there is a component of reactive airways
 BB use is associated with 22% reduction in
mortality and a decreased risk of AECOPD
› (3) Aldosterone Blockers:
 Improves exercise tolerance
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Common interventions:
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Smoking cessation.
Exercise prescription.
Action plans.
Co morbidities and over lap issues:
 Depression.
 End of life care.
 Control of dyspnea.
 Potential therapeutic overlap.
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What’s Happening in HF at the Provincial Level
 Development of new patient and provider resources for HF
through the Provincial HF Strategy
› Medications and Lifestyle Management
› Evaluation of existing resources with key stakeholder
feedback and continued development
› Standardized reporting of cardiac imaging
› Development of Nursing standards and medication titration
order sets for allied health
› End-of-life tools with HF focus in collaboration and alignment
with existing PSP
› ICD management
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What’s Happening in HF at the Provincial Level
PATIENT RESOURCES
PROVIDER RESOURCES
MEDICATIONS
REFERRAL FORMS
SODIUM
PATIENT ASSESMENT FORMS
FLUID
CARE MAPS & TX ALGORITHMS
EXERCISE
MEDICATION TITRATION
EXACERBATION PLAN
PATIENT SYMPTOM STATUS
HF 101
VISIT SNAP SHOT
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Conclusions:
 HF and COPD are common and they commonly co-exist in the
same patient:
› The presence of both is associated with worse outcomes
› Diagnosis may be challenging due to similarities in clinical
presentation
› Diagnostic tools exist which may help to differentiate these
disease entities in the dyspneic patient
› In general, traditional pharmacological and nonpharmacological therapies are well tolerated and may have
benefit across both disease states
32
Back to the Case
 BNP elevated at 600 confirming the diagnosis of HF associated
with volume overload
 Started on diuretics with some improvement in edema and
dyspnea, but persistent wheezing on exam
 Receives education regarding lifestyle management including
sodium and fluid restriction
 Subsequent echocardiogram confirms LVEF 30%
 Started on ACEi for LV dysfunction and HF
 Given history of CAD and previous MI, patient is also started on
statin
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Back to the Case
 Patient symptomatically better after diuresis but remains SOB.
 Spirometry shows an FEV1/FVC ratio of 65% predicted and an
absolute FEV1 of 58%. There is no evidence of reversibility.
 The patients was prescribed a SABA for symptom relief and
after two months using it frequently on a daily basis was started
on tiotropium with symptom improvement.
 The patient is also started on a beta blocker.
 Advised to ensure immunizations are up to date and also
referred to local cardio pulmonary rehab program.
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MR. B
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65-year old patient comes to your office with SOB
NYHA class II and stable
Major complain fatigue and lack of energy
Cough, mostly in am with some phlegm
Smoker
? MI 10 years ago
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PE and labs
 Jugular Venous Pressure (JVP) = 6 cm
 Rales, S3 and S4 heart sounds
 Lab values:
› – Troponin: negative
› – Serum creatinine: 132.6 µmol/L
› – Na = 141.1 mmol/L: K = 4.7 mmol/L
 No peripheral edema; chest x-ray suggests cardiomegaly, a bit
venous congestion
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Q1. What diagnosis would you give this patient?
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COPD
End-stage emphysema
Reactive airway disease
AHF
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Q 2: Which of the Historical Features is Most
Suggestive of HF as a Cause of his Dyspnea?
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Remote MI
Cough
Nocturnal cough
PND
Smoking
He does not have heart failure
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Q 3: Which Physical Exam Feature Best Supports
a Diagnosis of HF?
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High JVP
Presence of AF
S3
Holosystolic murmur
Quiet heart sounds
He does not have heart failure
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COPD and HF
 Prevalence of COPD ranges from 20 to 30% in patient with HF
 The prevalence of HF is 3 times greater among patient
discharge from the hospital with diagnosis of COPD
 They are comorbidity for each other
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COPD as a Cardiovascular Risk
 COPD patients are at increased risk of cardiovascular mortality
or morbidity independent of other risk factor including smoking
 The leading cause of death in COPD patients is Ischemic heart
disease not respiratory failure
 Low grade systemic inflammation causing atherosclerosis
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Signs of Heart Failure
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Elevated neck veins (jugular venous pressure)
Positive abdominojugular reflux
Rales or evidence of pleural effusion
S3
Ascites
Lower extremity edema
Arnold JMO et al. Can J Cardiol 2006;22(1):23-45.
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Clinical Presentation of AHF
Data from ADHERE database (Acute Decompensated Heart Failure National
Registry in the US)
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Dyspnea in 89% of patients at presentation
Rales in 68%
Peripheral edema in 66%
SBP <90 mm Hg in <3%
Adams KF et al; ADHERE Scientific Advisory
Committee and Investigators. Am Heart J 2005;149:209-16.
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Bedside Cardiovascular Examination in Patient
with HF
 Did careful physical exam on heart failure patients about to
undergo a right heart catheterization
 52 patients, mostly NYHA III, average EF 18%
Butman SM et al. J Am Coll Cardiol 1993;22(4):968-74.
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Bedside Cardiovascular Examination in Patient
with HF
 If rales were present, all had a wedge pressure >18, very
specific
 However, only 9 of 37 with a wedge pressure >18 had rales,
very insensitive
 So…clear lung fields tell you very little about the fluid status in
heart failure
Butman SM et al. J Am Coll Cardiol 1993;22(4):968-74.
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Bedside Cardiovascular Examination in Patient
with HF
 Only 3 of 15 with a low PCWP had a high JVP or positive
abdominojugular reflux test, spec of 80%
 30 of 37 with a high wedge had either a high JVP or positive
abdominojugular reflux test, sensitivity of 81%
 So a careful examination of the neck veins is the best physical
exam technique for determining the fluid status in heart failure
Butman SM et al. J Am Coll Cardiol 1993;22(4):968-74.
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Positive Likelihood Ratios for Heart Failure (in ER)
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Past history HF
PND
S3
CXR venous congestion
EKG AF
5.8
2.6
11
12
3.8
Wang CS et al. JAMA 2005;294:1944-56.
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Negative Likelihood Ratios for Heart Failure (in
ER)
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No rales (crackles)
No past HF
No SOB
CXR without cardiomegaly
EKG normal
0.51
0.45
0.48
0.33
0.64
Wang CS et al. JAMA 2005;294:1944-56.
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How Good are Existing Tools for Diagnosing Heart
Failure?
In ED, clinical misdiagnosis occurs in 25-50% of patients presenting with decompensating HF
(Agency for Health Care and Research 1994)
Dao Q et al. J Am Coll Cardiol 2001;37:379-85.
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Take home message in diagnosing “Heart Failure”
 Can be a wide range of presentations
 Many of the symptoms of heart failure overlap with other disease
states such as COPD, obesity, nephrotic syndrome, druginduced edema, cirrhosis and sleep apnea
Arnold JMO et al. Can J Cardiol 2006;22(1):23-45.
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Case Study 2 : Advanced age and SOB†
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85 year old female with SOBOE for 3 months
Flu (cough, SOB, fever, mild leg edema L>R)
Dx “viral pneumonia” in ER – antibiotics
CXR in ER ? nodule with subsequent CT 03/04 “fine interstitial
pattern”
 3 days ago: ER with progressive dyspnea NYD (seen and
discharged with antibiotic and puffer)
 Return to your office complaining of dyspnea
†Fictitious
patient profile. May not be representative of all patients with ADHF.
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Case 2: Old and SOB
 PMH
› Longstanding depression/ anxiety disorder
› ? MI 1973 (never hospitalized)
 Medication
› Elavil and Clonazepam
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Examination
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BP=162/96 mm Hg
HR=102 beats/min; T=36.2 C; RR=26 breaths/min
Mild respiratory distress
JVP “not sure”
Chest a “few creps”
Normal heart sounds
Mild asymmetric edema R>L
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Is this HF?
1.
2.
3.
4.
Definitely yes
Possibly
Probably not
Definitely not
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Elderly: Clinical Features HF
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Delirium
Falls
Functional decline
Sleep disturbance
Nocturia/ incontinence
Dyspnea uncommon if
sedentary
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•
•
•
Ankle edema
Other causes
Sacral edema
Pulmonary findings nonspecific
Arnold JMO et al. Can J Cardiol 2007;23(1):21-45.
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Investigations
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O2 sat 90% on RA
WBC 12 left shift, HB =110 NCNC
Cr 140 µmol/L
CK and Tn I normal
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EKG
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Further Investigations
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pH: 7.50
pCO2: 28
pO2: 82
Bicarb.: 22
Saturation: 3 litres
Leg dopplers negative
Spirometry: “poor effort”
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What is the Next Most Appropriate Investigation?
 Await response to clinical treatment (lasix, O2, antibiotics,
heparin, steroids)?
 BNP?
 Spiral CT to R/O PE?
 Echocardiogram?
 Cardiology consult?
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Diagnosis of HF
 Best clinician diagnosis is about 80%1
 Average time in ER before diuretic is 3 hours
 Most common drugs in ER: Salbutamol, antibiotics, furosemide
› Worsening renal function in hospital is associated with poor
prognosis2
› So we wish to avoid inappropriate diuretic while maximizing
use when indicated
 Better diagnostic methods needed
– BNP, NT- pro-BNP
 IMPROVE- HF CANADA Study3
1. Maisel A. Rev Card Med 2002;3(Suppl 4):S10-7. 2. Arnold et al. Can J Cardiol 2006:22(1):23-45.
3. Moe GW et al. Circulation 2007;115:3103-10.
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B-Type Natriuretic Peptide (BNP)
 32-amino acid peptide secreted primarily from the ventricles of
the heart
 Released in response to stretch and increased volume in the
ventricles
 BNP levels correlate with:
› Left ventricular end-diastolic pressure and volume
› New York Heart Association (NYHA) functional classification
› Extent of reversible ischemia
 Rapid, point-of-care assay for BNP now available to facilitate
diagnosis of HF and use as a prognostic marker
Moe GW. Heart Fail Monitor 2005;4(4):116-22.
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Processing of the Human BNP Gene
Hino J et al. Biochem Biophys Res Comm 1990;167:693-700.
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Physiology of BNP
1. Marcus LS, et al. Circulation 1996;94:3184-89. 2. Zellner C et al. Am J Physiol 1999;276(3 pt 2):H1049-57. 3. Tamura N et
al. Proc Natl Acad Sci USA. 2000;97:4239-44. 4. Abraham WT et al. J Card Fail 1998;4:37-44. 5. Clemens LE et al. J
Pharmacol Exp Ther 1998;287:67-71. 6. Rayburn BK, Bourge RC. Rev Cardiovasc Med 2001;2(Suppl 2):S25-31. 7.
Akerman MJ et al. Chest 2006;130:66-72.
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Causes of Increased BNP
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LV systolic dysfunction
LVH with diastolic abnormalities
ACS (increase mortality)
Stable angina (prognostic factor)
Valvular disease (aortic stenosis)
Constrictive pericarditis
Significant pulmonary embolism
Cor pulmonale
Pulmonary HTN
Aging (modest increases)
Renal insufficiency
Malignancy
Sepsis
Moe GW. Heart Fail Monitor 2005;4(4):116-22.
65
BNP and NT-proBNP In HF
Cut Points for HF Diagnosis
Arnold JMO et al. Can J Cardiol 2007;23(1):21-45.
66
BNP Concentration for the Prediction of Clinical
Events
Death or Heart Failure Hospitalization
Harrison A et al. Ann Emerg Med 2001;39(2);131-38.
67
Do BNP Levels Help Diagnose Those with Acute
Dyspnea?
Knudsen CW et al. Am J Med 2004;116(6):363-8.
.
70
BNP/NT-proBNP in Heart Failure
 Practical Tips
 Biomarkers such as BNP and NT-proBNP are complementary
to, but do not replace, good clinical evaluation
 No compelling factors favor the use of BNP versus NT-proBNP
 The choice of assay is dictated by
› availability
› clinician’s familiarity and ability to interpret the results
Arnold JMO et al. Can J Cardiol 2007;23(1):21-45.
71
What Does the CCS Say about BNP Testing?
 Recommendations:
 BNP or NT-proBNP should be measured to help confirm or rule
out a diagnosis of HF in the acute or ambulatory care setting in
patients in whom the clinical diagnosis is in doubt
(Class I, Level A)
 Measurement may also be considered in patients with known HF
for prognostic stratification
(Class IIa, Level A)
 Sequential measurement of BNP/NT-proBNP levels may be
considered to guide therapy in HF patients
(Class IIb, Level B)
Arnold JMO et al. Can J Cardiol 2007;23(1):21-45.
72
Acute SOB
73
Stable patient
 20 to 25% of ambulatory and stable HF patient have BNP less
than 100
 Echocardiography appears to be more reliable than BNP levels
to detect unsuspected LV systolic dysfunction in patient with
stable COPD
 Radionuclide ventriculography (MUGA) helps in patient with poor
LV window
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Conclusions
 Diagnosis of HF in multi-system disease is challenging.
 Co-morbidities are common, mask the diagnosis of HF, limit
therapeutic options, and negatively impact prognosis.
 BNP and ECHO may aid in the diagnosis of HF in this patient
population.
76
CASE MR C.
 70-Year old male
 PMHx of COPD
 Stable with no new SOB
 Echocardiogram shows EF of 38%
77
What medications will you consider?
 Beta blockers?
 Ace inhibitors?
 Statins?
78
Beta blockers
 Selective B1 receptor blockers
 Non selective beta blockers B1 and B2
79
 Selectives
› Metoprolol
› Bisoprolol
 Nonselectives
› Carvedilol
80
 Few reports of acute bronchospasm after initiation of BB lead to
exclusion of patients with coexistence HF and COPD from large
BB trails
 BB remains underprescribed for patient with COPD and HF
81
 Selective BB
› Do not change the symptoms and FEV1
› Do not attenuate beta 2 agonist effect
 Non selective BB
› May increase the symptoms
› Decrease beta agonist effect
82
Clinical Experience
 Both do not increase the exacerbation and hospitalization in
COPD patients
 Better to be controlled by a structured outpatient clinic
 Acute vs. chronic
 Using B agonists may change the response and it can increase
the risk of de compensated HF
83
 Non reversible COPD
› Can use both B1 selective and B2 non selective with alpha
blockers activity
 Reversible disease
› Selective B1 receptor
 Acute COPD or HF
› Do not use BB
84
ACE Inhibitors/ ARB
 ACE
› One of the first steps in HF treatment
› Also prevents cachexia and muscle atrophy in COPD patients
 ARB
› No evidence
85
Statins
 Some suggestions of clinical improvement and even reduction in
mortality
86
Sustaining Your Gains
Why Focus on Sustainability?
 Up to 70% of change initiatives fail, impacting:
› Best possible care
› Staff and provider
frustration
› Reluctance to engage in future
88
Why don’t changes sustain?
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Benefits for patients and staff are not clear
Changes are not credible
Changes are not part of the workflow
No one is monitoring over time
All staff have not be trained on changes
Key clinical leaders have not been engaged
The changes do not fit with the priorities of the clinic
89
What can you do?
1. Clarify what you are sustaining
2. Engage leaders
3. Involve and support front-line staff
4. Communicate the benefits of the improved process
5. Ensure the change is ready to be implemented and sustained
6. Embed the improved process in your electronic and human
processes.
7. Build ongoing measurement
90
What Are You Trying to Sustain?
With your community team discuss what you would like to
sustain in the practice and community, is it:
› A specific change?
› A measured outcome from your efforts?
› An underlying culture of improvement?
› Relationships established in the community?
› A combination?
› (5 min)
Source: NHS Improvement leader’s Guide: Sustainability, NHS Institute for Innovation and Improvement, 2007
91
Predictors of Sustainability
 Staff, providers and patients can describe why they like the
change and its impact
 Providers and staff are confident and can assist in explaining to
others
 Job descriptions reflect new roles
 Measurement is part of the practice and used to monitor
progress
 The change is no longer ‘new’, but ‘the way we do things around
here’
Adapted from: NHS Improvement leader’s Guide: Sustainability, NHS Institute for Innovation and Improvement, 2007
92
Group Reflection
 Using the PSP sustainability planner, reflect on the content of
each section and identify some actions you might need to take to
improve the chances of sustaining your changes.
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Thank you!