1. COPD or HF A Clinical Challenge Learning Session 3 Location here
Date here

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
Please fill out all applicable areas (highlighted in red). One slide per speaker.

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].
Please fill out all applicable areas (highlighted in red).

4. Mitigating Potential Bias
[Explain how potential sources of bias identified in slides 1 and 2 have been
mitigated].
Refer to the College of Family Physicians of Canada’s “Quick Tips” document.
Please fill out all applicable areas (highlighted in red).
Please visit the following link for the CFPC’s “Quick Tips” document:

5. Some info
A few housekeeping items: cells, washrooms. We know emergencies sometimes come up, please feel free to leave the room if you need to take a call
The agenda is on the table in front of you. Of importance you will note we are having a break for coffee around: (time)
Housekeeping
washrooms and nearest fire exist
Ground rules
Respect all ideas and opinions
Share experiences with your peers
On time back from break
Cell phones on mute or vibrate?

6. Agenda Sharing success and lessons learned (65 minutes):
Optional co-morbid Patient Story: (10 minutes)
Heart Failure Management ( didactic, 20 discussion)
Sharing the Care (15 minutes)
Break (15 minutes)
Planning for Sustainability (30 minutes, 15 didactic discussion):
Wrap up (15 minutes – mostly evaluation)

7. Sharing Successes and Lessons Learned

8. Patients with Comorbidities

9. 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 …?

15. Conclusions: COPD is common in HF:
and independently predicts mortality
HF is common in COPD:
Cardiovascular risk factors cluster in patients with COPD.
Many symptomatic, diagnostic and therapeutic challenges.

16. Clinical Approach
HF and COPD are common and they commonly co-exist in the same patient:
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 non - pharmacological therapies are well tolerated and may have benefit across both disease states.

17. 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

18. 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.

19. Additional investigations to consider in the “stable” patient
ECG
When “normal” HF < 10%
COPD
When “normal” HF < 12%
nT-pro-BNP
When “normal” HF < 9%
CXR
Low NPV and moderate PPV
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.

20. Why Measure Spirometry?
Screen with COPD-6.
Diagnose COPD.
Confirm response to therapy.
Provide prognostic information for patients with HF!
Assess relative contributions of COPD versus HF to dyspnea.

21. 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.

23. Key messages: 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 2004

24. Non-Heart Failure Reasons for Elevation in BNP
ACUTE HF
Alternate Diagnoses to Consider
Acute Coronary Syndromes
Pulmonary Embolism
Acute Renal Insufficiency
PAH
Sepsis
CHRONIC HF
Alternate Diagnoses to Consider
Advanced age ( > 75 years)
Atrial Fibrillation
Renal Dysfunction (eGFR < 45)
LVH
COPD
nT-pro-BNP > 400 pg/mL or BNP > 125 pg/mL

25. 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

26. 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

27. Common interventions:
Smoking cessation.
Exercise prescription.
Action plans.
Co morbidities and overlap issues:
Depression.
End of life care.
Control of dyspnea.
Potential therapeutic overlap.

28. 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 non- pharmacological therapies are well tolerated and may have benefit across both disease states.

29. Heart Failure

30. Evidence Based HF Therapies in BC

31. Principle of HF Management
Therapeutic Goals
1. prompt resolution of congestive symptoms.
2. initiate patient self management related to lifestyle and medication compliance.
3. initiate/enhance therapies direct to underlying disease process:
limit recurrent hospitalizations
improve mortality
4. prevent adverse events related to administered therapies.

32. Heart Failure Therapies
Therapy
Agent
Reduction in 1° Endpoint
Self Management
23%
Pharmacological
ACE-I
8% - 26%
Beta Blocker
23% - 65%
MRA
35%
ARB
15%
Device
ICD
23% - 31%
CRT
24% - 36%

33. Contemporary Management of HF
Pharmacological Therapies:
(1) Beta Blockers
(2) Inhibition of the RAAS
ACE-inhibitors (ACEi)
Angiotensin Receptor Blockers (ARB)
Mineralocorticoid Receptors Antagonists (MRA)
Device Therapies:
(1) ICD
(2) Cardiac Resynchronization Therapy (CRT)

34. Beta-Blockers Reduce Mortality and Decrease the Risk of Hospitalization

35. Impact of ACE Inhibitors on Mortality in HF

36. Benefits of ACE Inhibitors Persist

37. Spironolactone: EF<30 & Advanced Symptoms
10%
ARR

38. Combining Therapies Improves Outcomes

39. Cumulative Impact of Heart Failure Therapies: All Cause Mortality
Relative risk
2-yr Mortality
None 
---
35%
ACE Inhibitor
23%
27%
MRA (Spironolactone)
30%
19%
Carvedilol
25%
Cumulative risk reduction if all three therapies are used: 63%
Absolute risk reduction: 22%, NNT = 5
Fonarow GC. Rev Cardiovasc Med. 2003;4:8–17.

40. Important Therapeutic Considerations in HF Patients
Smoking cessation
Cardiac rehab
Action plans for acute decompensation
Addressing co-morbidities
COPD
CKD
Immunizations
Symptom management
End of life care
some synergies and therapeutic overlap

41. 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.

42. 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.

43. MR. B 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

44. PE and labs Jugular Venous Pressure (JVP) = 6 cm.
Rales, S3 and S4 heart sounds.
Lab values:
– Troponin: negative
– Serum creatinine: µmol/L
– Na = mmol/L: K = 4.7 mmol/L
No peripheral edema; chest x-ray suggests cardiomegaly, a bit venous congestion. 51

45. Q1. What diagnosis would you give this patient?
COPD
End-stage emphysema
Reactive airway disease
AHF 52

46. Q2. Which of the Historical Features is Most Suggestive of HF as a Cause of his Dyspnea?
Remote MI
Cough
Nocturnal cough
PND
Smoking
He does not have heart failure 53

47. Q 3: Which Physical Exam Feature Best Supports a Diagnosis of HF?
High JVP
Presence of AF S3
Holosystolic murmur
Quiet heart sounds
He does not have heart failure 54

48. 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.

49. 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.

50. Signs of Heart Failure 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. 57

51. Clinical Presentation of AHF
Data from ADHERE database (Acute Decompensated Heart Failure National Registry in the US)
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: 58 58

52. 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): 59

53. 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): 60

54. 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): 61

55. Positive Likelihood Ratios for Heart Failure (in ER)
Past history HF
PND S
CXR venous congestion 12
EKG AF
Wang CS et al. JAMA 2005;294: 62

56. Negative Likelihood Ratios for Heart Failure (in ER)
No rales (crackles)
No past HF
No SOB
CXR without cardiomegaly 0.33
EKG normal
Wang CS et al. JAMA 2005;294: 63

57. 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: 64

58. 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, drug- induced edema, cirrhosis and sleep apnea.
Arnold JMO et al. Can J Cardiol 2006;22(1):23-45. 65

59. Case Study 2 : Advanced age and SOB†
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. 66

60. Case 2: Old and SOB PMH Longstanding depression/ anxiety disorder
? MI 1973 (never hospitalized)
Medication
Elavil and Clonazepam 67

61. Examination
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. 68

62. Is this HF?
Definitely yes
Possibly
Probably not
Definitely not 69

63. Elderly: Clinical Features HF
Delirium
Falls
Functional decline
Sleep disturbance
Nocturia/ incontinence
Dyspnea uncommon if sedentary
Ankle edema
Other causes
Sacral edema
Pulmonary findings non- specific
Arnold JMO et al. Can J Cardiol 2007;23(1):21-45. 70

64. Investigations O2 sat 90% on RA. WBC 12 left shift, HB =110 NCNC.
Cr 140 µmol/L.
CK and Tn I normal. 71

66. ECG 73

67. Further Investigations
pH: 7.50
pCO2: 28
pO2: 82
Bicarb.: 22
Saturation: 3 litres
Leg dopplers negative
Spirometry: “poor effort” 74

68. 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? 75

69. 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):S Arnold et al. Can J Cardiol 2006:22(1):23-45.
3. Moe GW et al. Circulation 2007;115: 76

70. 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.
Natriuretic Peptides (NP) are hormones that are manufactured and released by the heart muscle cells, in response to extra fluid volume, which causes an increased stretch on the heart muscle and its chambers. B-type natriuretic peptide (BNP) is produced by the heart ventricles in response to ventricular volume expansion and pressure overload.
BNP is not secreted under normal circumstances, nor in response to routine activities of daily living, such as hydration status and physical activity. BNP is only generated and secreted in response to excess ventricular stretch and pressure as occurs in HF. In addition, it is not stored but is generated and secreted in direct response to the severity of the HF as it progresses or improves. Therefore, elevated levels are diagnostic for HF, under all circumstances and levels of severity of HF, for which a patient might present to a health care facility.
There is a positive relationship between disease severity and BNP levels. In addition, blood BNP levels correlate positively with left ventricular end diastolic pressure, and there is an inverse correlation to left ventricular function and BNP following acute myocardial infarction.
History:
It was demonstrated in 1979 that the density of secretory granules in the atria (“atrial granularity”) correlates to changes in water and electrolyte balance (de Bold et al. 1979)
It was later shown that atrial extracts injected into rats elicited an immediate natriuretic and diuretic effect (de Bold, et al 1981). In the early 1980s ANP was characterized by amino acid sequence and cDNA clones. (Atlas, et al and Greenberg et al. 1984)
BNP was then characterized by amino acid sequence and DNA clones (Maekawa, et al and Seilhamer, et al. 1989). Endogenous BNP levels were shown to be elevated in patients with heart failure and that BNP is the natural hormonal response of the heart to heart disease (Mukoyama, et al. 1990)
Atrial stretch receptors link blood volume to renal function
Distension of a balloon catheter in atria of dogs resulted in diuresis
Henry et al (1956)
Secretory granules discovered in the atria
Kisch (1956)
Jamieson and Palade (1964)
BNP was characterized by amino acid sequence and DNA clones
Maekawa, et al. (1988)
Seilhamer, et al. (1989)
Moe GW. Heart Fail Monitor 2005;4(4): 77 77

71. Causes of Increased BNP
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): 80

72. Cut Points for HF Diagnosis
BNP and NT-proBNP In HF
Cut Points for HF Diagnosis
Arnold JMO et al. Can J Cardiol 2007;23(1):21-45. 81 81

73. BNP Concentration for the Prediction of Clinical Events
Death or Heart Failure Hospitalization
In 325 patients presenting to the ED with dyspnea, BNP levels were determined. Patients were then followed for 6 months looking for the following endpoints: death (cardiac and non-cardiac), hospital admissions (cardiac), and repeat ED visits for HF. Using Kaplan-Meyer plots for all HF events, patients who left the emergency department with BNP levels >480 pg/ml had a 6-month cumulative probability of a HF event of (43%). On the other hand, patients who left the emergency department with BNP levels <230 pg/ml had an excellent prognosis with only 2.5% incidence of HF end-points. The odds ratio for 6-month HF death in patients with BNP levels > 230 was 46.
BNP levels measured in patients presenting with dyspnea to the ED are highly predictive of future cardiac events. Utilization of BNP levels in patients presenting with symptoms of HF should prove to be a cost-effective way to risk-stratify patients with HF.
Harrison A et al. Ann Emerg Med 2001;39(2); 82 82

74. 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. 86 86

75. 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. 87 87

76. Acute SOB

77. 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.

79. 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. 91

80. CASE MR C. 70-Year old male PMHx of COPD Stable with no new SOB
Echocardiogram shows EF of 38%

81. What medications will you consider?
Beta blockers?
Ace inhibitors?
Statins?

82. Beta blockers Selective B1 receptor blockers.
Non selective beta blockers B1 and B2.

83. Selectives:
Metoprolol
Bisoprolol
Nonselectives:
Carvedilol

84. 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 under-prescribed for patient with COPD and HF.

85. 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

86. 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.

87. 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

88. ACE Inhibitors/ ARB ACE: One of the first steps in HF treatment
Also prevents cachexia and muscle atrophy in COPD patients
ARB:
No evidence

89. Statins
Some suggestions of clinical improvement and even reduction in mortality.

90. Sustaining your goals
It’s never too early to consider how you are going to sustain your improvements. Implementing a change in practice does not guarantee it will sustain long term. In order to continue to reap the benefits from your hard work you need to focus on how to ensure your change will ‘stick’.
The risk of failing to sustain your changes is not just clinical, but can effect provider and staff satisfaction and future change efforts.
As we talk about sustainability of your changes, think about how you as a team can sustain the changes you have made.
Some strategies for holding the gains once initial improvements have been made (tested and implemented):
1. To work towards sustaining a change long term patients, staff and providers need to be clear what the benefits are in terms of patient care, workplace satisfaction, and personal practice. Using measurement to show the improvements will help to support the change. When each stakeholder can explain ‘what’s in it for me’ the change is more likely to sustain.
2. The permanence of the change should not depend on specific people, but should become embedded in the work processes. One of the ways to do this is to establish and document standard processes, so that even if there are staff changes everyone will know what the new process is and be able to follow it. Additionally, a plan for training new employees will help to ensure that the new responsibilities and new processes are understood and carried out correctly, and ensues continuity in practice over time.
3. Data collection continues so that the practice has information about whether the gains are being maintained. It may be that the data collection schedule can be reduced, with data collection occurring less frequently or with a smaller sample. The objective here is to monitor the new system, and guide improvements as they are tested and implemented.
4. One suggestion for embedding the change and making it permanent is to review job descriptions so that new personnel will know immediately what is involved in their responsibilities. Additionally, make sure that any documentations of policies and procedures reflect any change in process.
5. It is important to celebrate when an achievement has been reached, but also important to celebrate when that achievement has been sustained for a period of time. Keep focus and energy up by celebrating with your team your continued best practice and reminding yourselves of the good work you have done.

91. Why Focus on Sustainability?
Up to 70% of change initiatives fail, impacting:
Best possible care
Staff and provider frustration
Reluctance to engage in future
Implementing a change in practice does not guarantee it will sustain long term. In order to continue to reap the benefits from your hard work you need to focus on how to ensure your change will ‘stick’.
The risk of failing to sustain your changes is not just clinical, but can effect provider and staff satisfaction and future change efforts.

92. Why don’t changes sustain?
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.
The good news is that teams involved in this module have had a head start because of your community approach to care.
This helps by:
Having more partners in caring for patients and their families to insure best practice care is being provided in a patient centered way
Team mates to keep you accountable and encourage you to keep going with improvements
Using the ability and willingness of patients and families to be partners in their care

93. What can you do? Clarify what you are sustaining. Engage leaders.
Involve and support front-line staff.
Communicate the benefits of the improved process.
Ensure the change is ready to be implemented and sustained.
Embed the improved process in your electronic and human processes.
Build ongoing measurement.

94. 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)
Before you focus on specific strategies to sustain your changes over time, you need to be clear on what it is you are trying to sustain. You may be trying to sustain:
A specific change you implemented
An outcome you have achieved through your work
An underlying positive culture and attitude towards improvement
Relationships you have established that contribute to your success now and into the future
Or a combination of these
In your team, discuss what your group would like to sustain.
Source: NHS Improvement leader’s Guide: Sustainability, NHS Institute for Innovation and Improvement, 2007

95. 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’.
Once you have made some changes towards sustaining your gains, how will you know that your work is paying off? There are some simple ways to tell if your change is more likely to sustain over time.
When you ask staff, providers and patients about the changes you have made they will be able to describe to you why the change is a good one and the impact it will have on both patient care and staff/provider experience in the clinic.
Providers and staff are confident that they could explain the new way of working to others and help to train new staff or providers.
Any effected job description has been changed to reflect changes in roles
Measurement is ongoing even after the change has been implemented. The measures are reviewed regularly to monitor progress and any changes indicating a loss in gains results in a correction.
People effected by the change do not describe it as ‘new’ or ‘being tested’ but accept it as the ‘new way of working’.
Adapted from: NHS Improvement leader’s Guide: Sustainability, NHS Institute for Innovation and Improvement, 2007

96. 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.

97. Next Learning Session Date
Please make a note of the date of the next learning session – evening session, same format to be expected.
Thanks to the physician facilitators for their leadership in this module.
Again, we at PSP are here to support you and coach you each step of the way.

98. Practice Support Program
For more information
Practice Support Program
West Broadway
Vancouver, BC V6J 5A4
Tel: