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114
Table 9 New York Heart Association functional classication of heart failure
Class Patient symptoms
Class I No limitation of physical activity. Ordinary physical activity does not cause symptoms
of HF
Class IISlight limitation of physical activity. Comfortable at rest, but ordinary physical activity
results in symptoms of HF; can walk two blocks or climb two ights of stairs
Class
Marked limitation of physical activity. Comfortable at rest, but less than ordinary
III
activity causes symptoms of HF; e.g., walking two blocks
Class IVUnable to perform any physical activity (including ADLs) without symptoms of HF; or
symptoms of HF at rest
N. Pandya
examination should be performed in residents with shortness of breath, reduced exercise tolerance, edema, or other symptoms suggestive of HF.Review of prior records, current medications, use of alcohol, and/or illicit drugs and alternative therapies, as well as chemotherapy agents should be considered as contributing factors to HF.
The manifestations of heart failure may be atypical in long-term care residents with frailty, cognitive impairment, and multimorbidity. They may present with
fatigue, malaise, lethargy, declining function, neurological symptoms such as confusion, restlessness, sleep disturbance, orthopnea, dyspnea with exertion, cough, and edema. Gastrointestinal manifestations of HF can include anorexia, nausea, abdominal discomfort, and altered bowel function. Remember that exer­tional symptoms may be less prominent in older adults due to a more sedentary lifestyle.
Patients who have HFpEF are more often female, have a fourth heart sound, sustained PMI, absence of jugular venous distension, absence of peripheral edema, normal heart size on chest -ray, and left ventricular hypertrophy (LVH) on the elec­trocardiogram (EKG). By contrast, patients with HFrEF are more often male, have a third heart sound, displaced PMI, jugular venous distension, pitting edema, and Q waves on the EKG.There can be up to 8 lbs. of uid weight gain before a patient may develop peripheral edema.
Remember that peripheral edema may also be caused by venous insufciency, hepatic or renal failure, hypoalbuminemia, or medication such as calcium channel blockers, and should not be attributed to HF without a more detailed review of comorbidities and the medication regimen. The clinical and laboratory evaluation of HF is summarized in Table10.
Electrolytes and renal function should be measured regularly. Hypokalemia is a common adverse effect of diuretics and may increase the risk of fatal arrhythmias. Many residents with hypokalemia also have hypomagnesemia, which can result in an inadequate response to potassium supplementation. Hyperkalemia can be associ­ated with ACE inhibitors, angiotensin II receptor blockers, angiotensin receptor­neprilysin inhibitor (ARNI), and worsening renal function. The development of hyponatremia may be an indication of disease progression and is associated with
Common Clinical Conditions inPost-Acute andLong-Term Care
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Table 10 Initial evaluation of heart failure
Test Purpose
Physical examination; essential
CBC, CMP, magnesium, calcium
Lipid prole Evaluate for comorbidities TSH, free T4 Exclude hypothyroidism or hyperthyroidism Hemoglobin A1C Evaluate for presence of diabetes NT-proBNP or BNP Assist in the diagnosis of HF if cause of dyspnea is unclear (increase
Urine microalbumin Indicates risk for developing HF Chest X-ray Pulmonary congestion (may be absent in HF), effusion, exclude
EKG Evaluate LVH, ischemia, prior MI, atrial brillation (does not diagnose
Echocardiogram with doppler
Additional tests for selected patients
Ferritin, TIBC, transferring saturation
HIV Evaluate suitability for particular treatments and detect reversible/
Cardiac MRI- ordered by cardiologist
Stress test (echo or nuclear)
Assess weight, edema, jugular venous distension, cardiac rhythm, third heart sound, hepatojugular reux, crackles at lung bases, or diminished breath sounds due to pleural effusion
Evaluate underlying causes of HF, and suitability for treatment with certain medications
with age, in women, with renal impairment). For age >75years, NT-proBNP >1800pg/mL consistent with HF. If BNP <100pg/mL, HF is unlikely, but likely if BNP >500pg/mL.Serial measurements are not recommended
pneumonia or chronic lung disease; serial studies not recommended
HF) Determine EF, ventricular size and function, evaluate pericardium, and
valvular or other structural heart disease; may be repeated in 3–6months
Evaluate existing anemia, and exclude hemochromatosis
treatable causes of HF Evaluate for myocardial inltration (e.g., amyloid), or scar tissue from
previous cardiac event If patient has suspected CAD and is willing to undergo cardiac
catheterization and surgery for revascularization
115
reduced survival in the elderly with HF.The resident’s functional status should be monitored in addition to the physical examination to include the sitting and stand­ing BP when possible.
Common Precipitants ofHeart Failure
In addition to identifying the cause of heart failure, it is also important to assess for conditions that may precipitate an exacerbation of heart failure. Evidence-based medication management and the treatment of coexistent medical conditions can optimize treatment of HF (see Table11). Cardiologist consultation may be required in some instances.
116
Table 11 Common factors that precipitate HF
Cardiac
Myocardial infarction or ischemia Poorly controlled hypertension Excess of dietary sodium Medication nonadherence Excess uid intake (oral or IV) Arrhythmias—supraventricular (especially atrial brillation with rapid rate), bradycardia, sick
sinus syndrome Associated medical conditions—pulmonary embolism, hypoxia due to chronic lung disease,
infection (pneumonia, viral illness, sepsis), anemia, hyperthyroidism, chronic kidney disease (eGFR <30mL/min)
Medications—alcohol, -β adrenergic blockers (including ophthalmic agents), calcium channel- blockers, NSAIDS, glucocorticosteroids, mineralocorticoids, antiarrhythmic drugs
Provider/system problems (e.g., medication reconciliation errors)
N. Pandya
Disease Management andCare Considerations inHF
Close observation and early detection of symptoms and signs which may precede an acute HF episode by several days. Close follow-up may be required for days or months, with the risk of rehospitalization high. The following suggestions can improve patient outcomes of HF:
• Education of rst-line caregivers, and nurses to improve recognition, assessment,
and monitoring of HF patients.
• Timely intervention by the practitioner (with evaluation of weights, chest X-ray,
laboratory tests (see Table10), determine type of HF, initiation and adjustment
of therapy, determination of target weight.
• Determine a regular schedule of clinical follow-up (in person or virtual), weights
(3/week, before breakfast, on the same scale), and laboratory testing.
• Engage the interprofessional team (e.g., pharmacists, dietitians, physical thera-
pists) and nurse aides who are essential for care delivery.
• Establish an individualized care plan: Assess patient’s self-care ability, cogni-
tion, health literacy, and support system in order to plan for appropriate discharge
planning and subsequent follow-up.
• Consult a cardiologist or HF nurse specialist for patients who are responding
poorly, or experiencing repeated exacerbations and/or hospitalizations.
• Evaluate facility performance by developing team-based quality improvement
programs to track hospitalizations, rehospitalizations, symptom relief, physical
function, and strategies to improve outcomes
• Patients with both frailty and HF are likely to have higher morbidity so optimize
nutrition and rehabilitation.
>70
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117
Management
The following are guidelines and recommendations for the management of HF applicable to NH residents [13, 15]. The choice of pharmacologic and nonpharma­cologic therapy will depend on the patient’s clinical status, goals of care, comorbid conditions, and frailty. Current treatment recommendations are designed to opti­mize outcomes, reduce morbidity and mortality, and to break the vicious cycle of hospitalization, hospital discharge, and rehospitalization. Mortality signicantly increases with a cardiac ejection fraction <30–35%.
Nonpharmacologic therapy is essential:
• Promote smoking cessation.
• Moderate sodium restriction <3 g/day (unless hyponatremic; worse outcome
associated with low sodium diets.)
• Avoid excessive uid intake, but restriction is not usually necessary.
• Record daily weights especially in short stay patients in whom home discharge
is anticipated.
• Regular physical activity to the extent tolerated (combine strengthening and gait
training if possible).
• Evaluate for anemia and thyroid dysfunction.
In the last 4years, signicant evidence has emerged from large clinical trials on the use of angiotensin receptor-neprilysin inhibitors (ARNIs), sodium-glucose cotransporter-2 inhibitors (SGLT2 inhibitors), and ivabradine (an If calcium channel blocker highly specic for the sinoatrial pacemaker current), to improve HF symptoms, reduce hospitalizations, and prolong survival. The SGLT2 inhibi­tors are benecial in patients with and without diabetes. There is no new data on the use of loop diuretics and digoxin. Figure 1 illustrates a pharmacological approach to HFrEF.The indications, caveats for using medication classes, moni­toring, and potential adverse effects in older adults are summarized in Table12. After the initial diagnosis of HFrEF, it is recommended that medications be adjusted every 2weeks when indicated, in order to achieve guideline directed medical therapy.
HFrEF Stage C treatent
ARNI/ARB/ACEI (ARNI
preferred) and beta
blocker, with diurec if
needed
Add aldosterone
angonist
Add SGLT2 inhibitor
Titrate diurec agent if
fluid overload
Add hydralazine and
isosorbide dinitrate for
Black paents with
persistent symptoms
Add ivabradine if HR
on maximally tolerated
Fig. 1 Pharmacological approach to the management of HFrEF (adapted from the ACC Expert Consensus Decision Pathway for Optimization of Heart Failure Treatment, 2021 [15])
beta blockers
118
Check BP, renal function,
and K level weekly when
Adverse events in
older adults Caveats
Cough, mild renal
function impairment,
starting and titrating to
maximum tolerated dose
Eplerenone benecial in
HF following MI.Check
renal function and K level
2–3day after initiation, at
7th day, then monthly for
hypotension,
hyperkalemia,
angioedema (rare)
Mild renal function
impairment,
hyperkalemia
3months
Check BP, renal function,
and K level weekly when
starting and titrating to
maximum tolerated dose
Mild renal function
impairment,
hypotension,
hyperkalemia
Combining ACEI and ARB
not benecial and increases
adverse events
Hyperkalemia may be
managed by low
potassium diet or
Benet only demonstrated
with carvedilol, metoprolol
succinate and bisoprolol.
scheduled use of
potassium binders
Worsening of HF
(usually transient)
N. Pandya
Greatest impact when
resting HR <70/min, and
patients are “dry”
Medication
class Indication Outcomes in HF Contraindications
Table 12 Pharmacotherapeutic strategies and selection of treatments for older adults with HFrEF [13, 15, 16]
Hyperkalemia (K
>5.5mEq/L), hypotension
(syst BP <80 mm, estimated
Cr clearance <30mL/min
Serum creatinine >2.5mg/
dL, or K >5.0mEq/L
Reduced mortality and
Improved outcomes,
reduced mortality
whom use of ARNI is not
possible
ACE inhibitors Consider in patients in
hospitalizations
NYHA class III-IV and
low EF <35%
Aldosterone
antagonists
(MRA)
Hyperkalemia (K
>5.5mEq/L), hypotension
(syst BP <80mm, estimated
Cr clearance <30mL/min
Improved outcomes,
reduced mortality
Alternative to ACEI in
HF, consider in patients
in whom ARNI is not
possible
Angiotensin-
receptor
blockers
(ARBs)
Severe decompensated HF,
marked bradycardia (HR
<45–50/min), active
bronchospastic lung disease,
signicant heart block,
relative hypotension (SBP
<90–100mmHg)
Improved ventricular
function, reduced cardiac
deaths
Stage C
Beta-Blockers Newly diagnosed HFrEF,
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Valsartan plus sacubitril is
the rst in this class
Can be used instead of
ACEI, avoid starting within
36h of last ACEI dose
Serum levels of 0.5–0.9ng/
mL are optimal. Lower
doses 0.125mg/day
recommended
QOD dosing in patients
with renal impairment
50% dose reduction if on
verapamil, amidarone, or
quinidine
Check BP, renal function,
and K.If furosemide dose
exceeds 80md BID,
consider a different loop
Adverse events in
older adults Caveats
Mild renal function
impairment,
hypotension,
hyperkalemia,
angioedema (rare)
Nausea, visual
disturbances, cardiac
arrhythmias
(bradycardia and SVT
or VT)
“Therapeutic
concentrations” may
be associated with
toxicity and mortality
Hypotension,
orthostatic
hypotension,
hypokalemia
diuretic (e.g., bumetanide)
or add a thiazide diuretic
(e.g., metolazone)
nitrates (resolves with
continued use);
palpitations, nausea,
119
(continued)
and dizziness with
hydralazine
Hypotension before
treatment, history of
angioedema
Reduced mortality and
HF admissions
Newly diagnosed HFrEF,
Stage C, and NYHA
class II+III symptoms
Medication
class Indication Outcomes in HF Contraindications
ARB/
Neprilysin
inhibitors
Reduced HF
hospitalizations, but not
mortality
symptoms or recurrent
hospitalizations
Digoxin Persistent limiting HF
Improved survival Headaches with
edema
Diuretics HF with congestion and
For Black patients with
Hydralazine
persistent symptoms
despite use of ACEi/
ARBs and beta-blockers,
and in HF patients who
and ARBs
and nitrates
120
Initiate and titrate
beta-blockers to target
doses when possible
Adverse events in
older adults Caveats
Transient brightness in
some areas of the
visual elds
Monitor for bradycardia
Dapagliozin is the current
FDA-approved SGLT2
inhibitor for HFrEF
Uncommon but
potentially serious
genital infections,
Fournier gangrene,
lower extremity, and
For anticoagulation,
warfarin or one of the
acute kidney injury
newer oral anticoagulants
may be used
N. Pandya
(continued)
Medication
class Indication Outcomes in HF Contraindications
Table 12
Reduced hospitalizations
for HF in patients with
NYHA class II–III
HFrEF
HFrEF in sinus rhythm
with persistent HR >70/
min on maximally
Ivabradine NYHA class II–III
Improved hospitalization
and CV mortality in
tolerated beta-blocker
doses
Consider in patients with
HFrEF, NHHA class
SGLT2
inhibitors
patients with and without
diabetes. Reduced
decline in kidney
function in HFrEF and
CKD
Long-term
anticoagulation in
patients with HF and
II–IV
Routine anticoagulation
in HF patients without
atrial brillation is not
Antiplatelet or
Anticoagulant
therapy
comorbid atrial
brillation is indicated in
most patients
recommended
ACEi angiotensin-converting enzyme inhibitor, ARB angiotensin receptor blocker, ARNI angiotensin receptor neprilysin inhibitor, SGLT2i sodium glucose
transporter 2 inhibitor
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121
Rehospitalization forHF
Studies have shown that 20% of patients admitted to the SNF/NF with HF are read­mitted to the hospital within 30days, and up to 50% within 6months. Not all these rehospitalizations are due to HF; COPD, pneumonia, sepsis, other cardiac events and arrhythmias are contributing causes [17]. The percentage of short stay and long stay patients who are rehospitalized after nursing home admission are CMS nursing home quality measures. Contributing factors for rehospitalization due to HF include:
• Severity of HF and presence of comorbidities.
• Quality of care issues, and suboptimal use of evidence-based therapies for
chronic HF.
• Inconsistent availability of practitioners especially during night-time
exacerbations.
• Problems with medication administration and weight monitoring, use of NSAIDS.
• Nonadherence to sodium restriction and lack of food choices.
• Problems with care delivery, miscommunication, and with discharge procedures
(optimally should include medication reconciliation, transfer of information to
community providers, and follow-up appointments).
Refractory HF
HF can have an unpredictable course and a high incidence of sudden death despite intensive medical management. Older adults with HF who are discharged to skilled nursing facilities are known to have high mortality rates (14.4% within 30days and
53.5% within 1 year). Referral to an advanced heart failure specialist should be considered in patients who have required IV inotropes, had two or more emergency room visits or hospitalizations in the past 12months for HF exacerbations, persis­tent fatigue, edema with rising BNP or NT-proBNP, renal failure (creatinine >1.8 mg/dL or BUN >43 mg/dL), inability to tolerate appropriately dosed beta blockers, and/or ARB/ACEI/ARNI and/or aldosterone antagonists, development of atrial brillation, ventricular arrhythmias or repeated ICD shocks.
Palliative care and end-of-life care should be discussed and considered for those with refractory HF, recurrent hospitalization, and persistence of severe dis­abling symptoms such as dyspnea, fatigue, pain, sleep disturbance, and functional decline. Palliative care for HF patients has been shown to improve physical, psycho­social, and spiritual well-being. Palliative care consultation is appropriate before placement of an ICD or left ventricular assist device (LVAD) is considered. In addi­tion, an ICD should be inactivated upon admission to hospice if it is consistent with the goals of care [15, 18].
122
N. Pandya
Chronic Obstructive Pulmonary Disease
Chronic obstructive pulmonary disease (COPD) is an insidious, progressive lung disease characterized by airow obstruction that is not fully reversible. It is the third leading cause of death in older adults. COPD can be difcult to diagnose because persons gradually modify their lifestyle to compensate for progressive fatigue and dyspnea. The main symptoms are dyspnea, cough, and sputum pro­duction. COPD continues to be underdiagnosed and undertreated, and often dif­cult to differentiate from asthma, HF, and other conditions that limit physical activities. One in six patients admitted to a nursing facility may have COPD or emphysema. COPD is responsible for high utilization of acute health care and 34% probability of death in 180 days post hospital discharge to nursing facilities [18, 19].
Identication ofCOPD
Smoking (90% of cases), advanced age, repeated pulmonary infections, prior tuberculosis, exposure to biomass fuel, air pollution, and alpha-1 antitrypsin de­ciency are risk factors for COPD.Early identication of COPD is important since 50% of lung function is lost by the time mild exertional dyspnea occurs and only 30% of lung function remains when there is dyspnea at rest. Residents with dys­pnea and other recurrent pulmonary symptoms should be screened for COPD utilizing the clinical indicators listed in Table13 [18, 19]. A screening tool that uses caregivers to rate residents’ symptoms was validated by Zarrowitz etal. who reported that a history of asthma, shortness of breath at rest and shortness of breath on exertion, and smoking are likely to be consistent with a diagnosis of COPD [20].
Table 13 Clinical indicators of COPD in long-term care [18]
Dyspnea (progressive over time, worse with exertion) Abnormal pulse oximetry
Cough (may be intermittent and unproductive) Chronic sputum production (any pattern)
Wheezing and chest tightness Avoidance of activities that lead to dyspnea or impaired performance of ADLs History of smoking Recurrent pulmonary infections Occupational or environmental exposure to occupational dust and chemicals Weight loss, fatigue, anxiety, cognitive impairment, or sleep disorders
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123
Diagnosis ofCOPD
On examination, residents with advanced disease may be barrel-chested, have pro­longed expiration, use accessory muscles for inspiration, and have wheezing, rhon­chi, or distant heart sounds. The signs of cor pulmonale, i.e., right-sided HF, include jugular venous distension, hepatic congestion, and pedal edema.
The clinical indicators of COPD and the review of past medical records may help in the diagnose of COPD.Although the denitive method of diagnosis is spirome­try, which usually measures FEV1 (volume of air exhaled in 1s) to FVC (forced vital capacity or total volume of air able to be exhaled), this is usually not practical in the PALTC setting. The FEV1 to FVC ratio decreases with aging and hence can lead to overdiagnosis of COPD.Spirometry should be performed in symptomatic individuals when feasible. However, its use in frail or cognitively impaired residents is usually not feasible.
• Normal: FEV1/FVC≥70% or FEV1≥80% of predicted
• COPD: FEV1/FVC≤70%
• Restrictive lung disease: FEV1/FVC ≥ 90% (pulmonary brosis, severe
kyphosis)
Other tests may provide useful information when evaluating for the presence of COPD or other conditions with similar signs and symptoms.
• The CBC may have an abnormally high Hb level due to hypoxia
• The chemistry panel may show a high bicarbonate level (metabolic alkalosis)
due to hypercapnia
• Chest X-rays are not diagnostic, but may show HF, bullae, pneumonia, pulmo-
nary scarring, hyperination, and increased retrosternal airspace, to sug-
gest COPD
• An EKG may show atrial arrhythmias or right heart strain
Pulmonary consultation may be helpful if the cause of dyspnea is not clear or the resident exhibits a poor response to treatment. Clinical judgment is important since the differential diagnosis of COPD can include asthma, heart failure, bronchiectasis, recurrent aspiration, ACE-inhibitor induced cough, vocal cord dysfunction, pulmo­nary emboli, and respiratory tract tumors. The GOLD criteria classify the severity of COPD (Table14) [21].
The GOLD ABCD staging [20], may be clinically useful and guide referral to a pulmonologist.
• GOLD A—Fewer symptoms and <2 exacerbations a year
• GOLD B—More symptoms and <2 exacerbations a year
• GOLD C—Fewer symptoms and >2 exacerbations a year
• GOLD D—More symptoms and >2 exacerbations a year