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European Systolic Hypertension in the Elderly; Syst-China: Chinese Trial on Isolated Systolic Hypertension in Elderly) have shown a 32–47% reduction in stroke, a 13–30% reduction in coronary disease, and a 29–58% reduction in heart failure.

N. Pandya

Evaluation

The diagnosis of hypertension should be carefully determined. In addition to using an appropriate cuff size and measuring blood pressure in a seated position at rest, it is important that blood pressure be measured as the average of two readings and obtained on at least two occasions. This is especially important in older adults due to blood pressure variability. In the long-term care setting, BP may be highest in the morning and low after meals. Over 90% of elderly with an elevated BP will have essential hypertension, and the majority with new onset HTN will have systolic hypertension. As many drugs can increase blood pressure, a careful medication review should be performed. The pulse pressure (dened as SBP minus DBP) increases with age as does white coat hypertension. Nonsteroidal anti-inammatory drugs (NSAIDs) including COX-2 inhibitors, erythropoietin, alcohol, corticosteroids, and uncontrolled pain are often implicated in elevating BP.

A resident with HTN should be evaluated for the presence of comorbid conditions such as diabetes mellitus, chronic kidney disease (CKD), and sleep apnea that can contribute to HTN.If clinically appropriate, those who present with diastolic HTN or treatment-resistant HTN should be evaluated for a renovascular cause. Patients with unexplained hypokalemia accompanied by metabolic alkalosis may have hyperaldosteronism as a cause of HTN.Although the incidence of pheochromocytoma is low, it may warrant consideration if a resident’s BP is unusually labile and weight loss present [6].

Treatment Goals

• For non-institutionalized, mobile, community-dwelling older adults >65years,

the ACC/AHA [1] recommends a SBP goal of less than 130mmHg.

• For older adults >65years with a high disease burden and limited life expectancy

and who are unable to live independently, the goals of therapy may differ and

need to be determined within the context of patient preference and one’s overall

clinical status (especially functional and cognitive status, and risk for frequent

falls). Consider a discussion with family on the risks vs. benets of lowering the

blood pressure.

Cardiac risk factors should be modied to the extent possible. The elderly should be encouraged to increase physical activity if possible and to stop smoking. The treatment plan should include screening for diabetes and hyperlipidemia, and salt

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restriction if appropriate. The clinician should be aware that even a relatively simple intervention such as dietary sodium restriction could adversely affect nutritional status and contribute to weight loss. Clinical factors to consider when treating HTN in PALTC patients are reviewed in Table2. General management guidelines include:

Table 2 Advantages and disadvantages of class of antihypertensive medication

Antihypertensive class Advantages Disadvantages

Thiazide diuretics Loop diuretics

ACE inhibitors Angiotensin receptor blockers (ARB)

Calcium channel antagonists (CCA)

Beta adrenergic receptor blockers

Alpha adrenergic receptor blockers

Renin inhibitors Effective

Adapted from Geriatric Medicine and Gerontology, 7th edition. McGraw-Hill [7]

Reduction in mortality, stroke, coronary events Daily use Daily use

No CNS side effects Preserve renal function Reduce proteinuria Alternative agent if intolerant to ACE inhibitors

Effective in reducing stroke No CNS side effects No metabolic effects

None (not recommended as monotherapy)

Improved urinary symptoms in prostatic hypertrophy (BPH)

without dose-related adverse effects

Hypokalemia Urinary frequency Headaches, ototoxicity, electrolyte disturbances

Cough Hyperkalemia Hyperkalemia

Constipation Ankle edema Heart block (Nondihydropyridine CCAs) HF with amlodipine

CNS (Central Nervous System) side effects Increased glucose and lipids with cardio selective

Increased CHF hospitalization

No outcome data in the elderly Expensive

Recommended indications Cautions

Systolic hypertension Effective in HTN in HF and CKD

HF Diabetes ACEi ARBs Microalbuminuria

Systolic hypertension Angina

Prior MI Stable angina, ACS HF Atrial brillation with rapid rate (Benecial in

essential tremor, hyperthyroidism)

Prostatism Left ventricular

Systolic hypertension Diarrhea

Hyponatremia Gout Urinary frequency Use in am

Renal insufciency Renal artery stenosis Cough, altered taste, angioedema

Left ventricular dysfunction Avoid short-acting CCAs for HTN

COPD PAD Heart block Depression Hyperlipidemia Type 2 DM

dysfunction Not approved as rst-line treatment for HTN

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N. Pandya

• Initiate treatment with lower doses (half the usual dose) to minimize the risk of

side effects.

• A once daily regimen with a long-acting medication is preferred.

• In the absence of a hypertensive emergency or urgency, lower BP gradually over

weeks to months as the elderly have impaired baroreceptor and sympathetic neu-

ral responses, and impaired cerebral autoregulation.

• Measure supine and standing BP (if possible) prior to initiating treatment for

systolic HTN as 20% have orthostatic and/or postprandial hypotension, which

increase the risk of falls and hip fracture.

• The degree of blood pressure reduction is the major determinant of cardiovascu-

lar risk reduction, not the choice of antihypertensive drug.

• Diuretic therapy is effective in lowering systolic BP and decreases the prevalence

of orthostatic hypotension; monitor potassium levels.

• An alternative drug may be selected as the initial agent based on comorbid condi-

tions (DM, HF, CKD).

• If systolic blood pressure goals are not met, addition of a second drug from

another class depending on comorbidities is usually necessary

• In Stage 2 hypertension, usually two drugs are required, such as a thiazide

diuretic combined with an angiotensin converting enzyme (ACE) inhibitor.

• Combining an ACE inhibitor and an ARB increases the risk of hypotension, syn-

cope, hyperkalemia, and renal dysfunction without improving cardiovascular

outcomes [6].

• When control is poor, or deteriorating, consider evaluation for secondary causes.

Resistant Hypertension

Resistant hypertension is dened as poor control despite treatment with 3 antihypertensives that have complementary mechanisms of action (that includes a diuretic), or when control requires >4 or more medications. In addition to the contributing factors in Table3, renal artery stenosis is present in 25% of people with a serum

Table 3 Treatment approach resistant hypertension (ACC/AHA 2017 [1])

• Exclude pseudoresistance (inaccurate BP measurement or poor medication adherence)

• Identify and address contributing lifestyle factors (physical inactivity, uncontrolled pain, excessive alcohol, high salt intake)

• Discontinue or minimize potentially contributing medications (sympathomimetic agents, NSAIDs, erythropoietin, corticosteroids)

• Screen for secondary causes (CKD, primary hyperaldosteronism, obstructive sleep apnea, pheochromocytoma); screening for renal artery stenosis in PALTC with existing renal insufciency is not recommended

• Modify pharmacological treatment (increase diuretic therapy; addition of a mineralocorticoid receptor antagonist; adding other agents with a different mechanism of action; use a loop diuretic in patients with CKD)

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107

creatinine of >2mg/dL, and can contribute to heart failure, cardiac ischemia, and “ash” pulmonary edema, especially if bilateral renal stenosis is present. Despite the availability of diagnostic Doppler Ultrasonography, CT or MR angiography, two large studies in subjects >69years, failed to show benet of renal artery stenting on either cardiovascular or renal outcomes.

Implications forLong-Term Care

The benet of lowering blood pressure in the LTC population who are >85years, frail, or have multiple comorbidities is not clearly established as this population has not been included in clinical studies. Because this population often have a limited life expectancy and are prone to developing orthostatic and post-prandial hypotension, syncope, and falls, the risks of lowering blood pressure are increased and its potential benet reduced. Data is lacking to help practitioners determine how best to treat hypertension in residents with high-risk conditions such as recent stroke, functional impairment, and aortic aneurysm.

Anemia

Aging predisposes persons to decreased hematopoietic reserve (reduced ability of the pluripotent hematopoietic stem cells to replicate), reduced absorption of essential nutrients, decline in glomerular ltration (GFR) and erythropoietin (EPO) secretion, and increased concentrations of cytokines. The normal pattern of myeloidlymphoid precursor differentiation is also affected with aging, with a decline in lymphopoiesis and an increase in the differentiation of myeloid clones, which can mutate and cause myeloid neoplasms. However, anemia is not considered a normal part of aging. Anemia may have an insidious onset with nonspecic symptoms until it is becomes severe. Mild anemia is often assumed as being benign or attributed to the presence of chronic comorbidities. However, studies in community dwelling elders show that anemia may be an independent risk factor for adverse outcomes when DM, CKD, or cardiovascular disease is present. Anemia has been associated with signicant physiologic impairments and adverse clinical outcomes (Table4).

Table 4 Clinical impact of anemia

Physiological impairments Clinical outcomes

Reduced exercise tolerance Frailty Left ventricular hypertrophy Falls Decline in renal function Decline in physical function Dizziness, autonomic dysfunction Cognitive dysfunction Weakness, sarcopenia Hospitalizations, increased health care costs Osteoporosis Mortality

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N. Pandya

Denition andPrevalence ofAnemia

There is no uniform denition of anemia. The World Health Organization denes anemia as a hemoglobin (Hb) level less than 12g/dL in adult women and less than 13g/dL in adult men. These cutoffs are based on population data that did not include people >65years of age, and do not take into account the effect of race and ethnicity. The prevalence of anemia from the NHANES III study in US community-dwelling adults >65years was 11% in men and 10.2% in women. Anemia increases with each decade of age and is higher in black patients. In acute care, clinics for older adults, and in PALTC the prevalence of anemia is even higher.

From the NHANES III and the Scripps-Kaiser database, new lower limits of normal for men >59years and women >49years have been proposed that exclude confounding factors. These normal values were slightly higher for older white men and women (Hb 13.2 and 12.2g/dL, respectively) and slightly lower for older black men and women (Hb 12.7 and 11.5, respectively). However, these levels may not be optimal with regard to morbidity and mortality. For example, in the Women’s Health and Aging Study, a risk gradient for adverse outcomes (mortality, frailty, disability) was present with Hb in the “normal range” as was a rise in the erythropoietin level [8]. In nursing home studies in the USA and Turkey, 56% of residents were anemic, the risk even higher in those who were malnourished [9].

Signs andSymptoms

Signs and symptoms of anemia in long-term care residents may be nonspecic (Table5). Facility staff need to be aware of their signicance and, if present, to report them.

Table 5 Symptoms and signs of anemia

Anorexia, nausea Chest pain, dyspnea, palpitations, tachycardia Cold intolerance Decreased activity level or endurance

Depressive symptoms Ecchymoses

Gingival bleeding, petechiae Increase in falls Increased confusion, headache Jaundice Pallor (skin, conjunctivae)

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Causes ofAnemia

Anemia is generally due to an underlying clinical disorder and warrants an evaluation unless the resident has a reduced life expectancy, is receiving palliative care, or declines further evaluation. A systematic evaluation can help the practitioner make rational treatment decisions. However, using empiric iron replacement, for example, can potentially overlook a signicant underlying treatable condition. In community- dwelling adults >65years, about one-third of anemias are associated with nutrient deciencies, one-third related to disease without nutrient deciencies, and one-third are unexplained without nutrient deciencies. The causes of anemia may be classied by etiology, bearing in mind that more than one cause (such as blood loss, malnutrition or hemolysis) may be present in a given person.

A systematic approach to aide clinical decision-making can be useful in most clinical situations. This includes assessing the resident’s medical history, comorbidities, renal function, current and recent medication use, physical ndings, and review of laboratory tests. Anemia can then be classied as to whether there is

decreased production due to a hypoproliferative state or ineffective erythropoiesis, increased destruction due to hemolysis, or blood loss, and by red cell morphology

(see Table6). It is essential that the evaluation be directed by the most likely and clinically relevant cause, and by involving the patient and/or their health care surrogate in discussions especially if endoscopic studies or bone marrow biopsy would be indicated. Table7 lists suggested noninvasive diagnostic tests for the evaluation of anemia [10, 11].

Sometimes it can be difcult to differentiate iron deciency anemia from anemia of chronic inammation since the typical hematologic abnormalities of advanced iron deciency occur at a later stage and both types of anemia can coexist. Measurement of the soluble transferrin receptor in conjunction with iron studies and ferritin, may help in differentiating iron deciency anemia from anemia of chronic inammation.

Several additional tests are available but are usually not part of the routine evaluation of anemia. These include:

• Serum erythropoietin: Increases with severity of anemia but its response may

be blunted.

• Proinammatory markers: High sensitivity C-reactive protein, TNF, and IL-6

are established markers and may play a role in the future.

• Hepcidin: Increased in inammation and leads to dysregulation of iron metabo-

lism and systemic iron deciency or availability; standardized measurement

assay not available.

• Bone marrow biopsy: Indicated if morphological and laboratory evaluation of

anemia is not diagnostic and if multiple cell lines are abnormal (e.g.,

pancytopenia).

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Table 6 Causes of anemia and typical laboratory ndings [11]

Classication of anemia Causes

Hypoproliferative Iron deciency

Possible iron deciency

Erythropoietin deciency (CKD, endocrine causes)

Stem cell dysfunction Aplastic anemia MCV increased

Ineffective Erythropoiesis

Hemolytic Immunologic

B12 deciency Folate deciency

Myelodysplastic syndrome (refractory anemia)

Thalassemia Sideroblastic anemia

(idiopathic or secondary)

Intrinsic (abnormal hemoglobin, metabolic)

Extrinsic (mechanical)

Typical laboratory ndings Peripheral smear ndings

MCV decreased Serum ferritin <30ng/mL and/or TSAT <20% Serum ferritin 30–100ng/mL and/or TSAT <20%

eGFR <60 No abnormal cells

RDW normal MCV increased

RDW increased Low B12, increased homocysteine and methylmalonic acid Low folate, increased homocysteine

MCV increased Normal RDW B12 and folate normal

MCV low Hypochromic, microcytic

Increased reticulocyte count Increased LDH Increased bilirubin Decreased haptoglobin

N. Pandya

Microcytosis, hypochromia, anisopoikilocytosis

Oval macrocytes, spherocytes, hypersegmented neutrophils

Normocytic or macrocytic red cells, dysplastic neutrophils

cells with target cells and basophilic stippling

Schistocytes

Anemia ofCKD

As renal function declines in people with CKD, the Hb will also decline. This drop in Hb is especially noticeable as the GFR trends below 60mL/min per 1.73m2. The anemia of CKD is typically normochromic and normocytic primarily due to a deciency of erythropoietin production. These usually is no deciency of iron, B12, or folate, when the GFR is below 30mL/min per 1.73m2. About 50% of nursing facility residents have a GFR below 60mL/min per 1.73 m2 and in one recent study, 60 % of residents with Stage III CKD were anemic.

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Table 7 Noninvasive diagnostic tests [10, 11]

• Complete blood count (initial low Hb/Hct may not be evident in volume depletion) – Absolute reticulocyte count (conrms if appropriate marrow response)

• Peripheral blood smear (if reticulocytes are decient and if toxic, hormonal, or infectious causes have been excluded)

• Serum iron, ferritin, total iron-binding capacity, transferrin saturation (serum soluble transferring receptor)

• Serum folate and RBC folate

• Vitamin B12 (methylmalonic acid, and homocysteine more sensitive)

• Renal function (eGFR)

• Liver function

• Sedimentation rate

• Tests for hemolysis (serum LDH, bilirubin, and haptoglobin)

• Serum protein electrophoresis; and immunoxation

• Stool for occult blood (endoscopy if appropriate)

• Thyroid-stimulating hormone and free T4

• Total testosterone (if hypogonadism is suspected)

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Acute or Chronic Immune Activation (ACI)

Acute or chronic immune activation can cause a disturbance of iron homeostasis that limits the availability of iron for erythropoiesis due to the impaired release of iron from macrophages. Ferritin may be increased, while the other iron studies are low. This disturbance in iron homeostasis is mediated by proinammatory cytokines and the increased production of hepcidin in the liver. Hepcidin decreases duodenal absorption of iron. In addition, erythropoietic cell survival and erythropoietic cell response to EPO is decreased [12]. Some patients may respond to erythropoietin. Persons with chronic disease and hemoglobin levels below 10g/dL should be evaluated for additional causes of anemia such as blood loss, malnutrition, and hemolysis.

Blood Loss

This is a major concern in older adults with anemia. Loss of blood from the gastrointestinal or genitourinary tract should be investigated. In addition, malignancies, gastritis, angiodysplasia, and benign tumors may be responsible.

Treatment

Treatment of coexistent nutritional deciencies and hypothyroidism should be initiated. If anemia is related to medication, chronic bleeding, CKD, chronic inammation, malignancy, or hemolysis, then the underlying condition should be stabilized to the extent possible and any potentially offending drugs discontinued. Treatment options for specic types of anemia and cautions to consider are reviewed in Table8.

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Table 8 Treatment options for anemia based on etiology [11, 12]

Cause of anemia Treatment options Cautions

Iron deciency • Ferrous sulfate 325mg daily (65mg

elemental iron)

• Ferrous gluconate 300mg daily (36mg elemental iron)

• Parenteral iron (in cancer, CKD, or intolerance of oral)

Vitamin B12 deciency

Folate deciency • Folate 1mg orally, daily or 5mg daily if

Anemia of chronic inammation

Anemia of chronic kidney disease

Hemolytic anemia • Identify underlying cause

• Vitamin B12 1000μg IM weekly×1month, then monthly if malabsorption or neurological complications

• Oral B12 1000μg daily

severe malabsorption

• Treat or stabilize the underlying disease • Anemia may persist

• Epoetin alfa or darbepoetin alfa SC

• Control diabetes and HTN

• Discontinue any contributing medications

• Constipation

• GI distress

• Consider blood loss

• Vit C source if achlorhydria present

• Check for concurrent folate deciency

• Check for concurrent B12 deciency

• Erythropoietin use is not approved

• Maintain Hb 10–11g/ dL

• Weekly Hb till stable then monthly

• Monitor BP

N. Pandya

Blood transfusions are generally given for acute blood loss associated with hypotension and cardiovascular compromise. For chronic anemia, blood transfusion is recommended if the Hb drops below 7g/dL, the hematocrit decreases to 21%, or in the presence of angina, heart failure, dyspnea, tachycardia, or hypotension.

Heart Failure

Cardiovascular disease is often the primary diagnosis when persons are admitted to nursing facilities. Heart failure (HF) affects 20% of residents. Reduced cardiac function presents with signs and symptoms of reduced cardiac output that occur with exertion or at rest. Heart failure is responsible for signicant morbidity and mortality that includes acute care visits and hospital readmissions. The care of HF is complicated by frailty, multimorbidity, cognitive, and functional impairment. Hypertension is a major risk factor for the development of HF, especially HF with preserved ejection fraction (HFpEF). In one study HFpEF was present in 50% of nursing facility residents diagnosed with HF. Moreover, the incidence of HFpEF increases signicantly in older adults with diabetes, obesity, female gender, HTN, dyslipidemia, and atrial arrhythmias. Elderly with HF with a markedly high or low BP have a worse prognosis as do those with an abnormal LVEF [13]. SNF

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rehospitalization rates for HF range from 27 to 43%. Overall, 1-year mortality in LTC residents with HF exceeds 50%, and hospitalization exceeds 50% annually, although there are regional differences [14].

Causes ofHeart Failure

Causes of heart failure can be classied as intrinsic and extrinsic. Be aware that more than one cause may be present in an individual.

• Intrinsic causes: Myocardial infection, myocarditis, valvular heart disease, con-

genital heart disease, nonischemic dilated cardiomyopathy (due to viral disease,

alcohol excess, medication-related adverse effects, tachycardia -mediated thy-

roid disease), cardiac arrhythmias, hypertrophic cardiomyopathy, restrictive car-

diomyopathy (from amyloidosis), pericarditis, or cardiac tamponade

• Extrinsic causes: Systemic hypertension, chronic obstructive pulmonary dis-

ease, pulmonary embolism, anemia, thyrotoxicosis, drug toxicity, excess blood

volume/polycythemia

It is important to clarify ejection fraction terminology, and most of the recommendations in this section refer to HF with reduced EF (HFrEF). Three EF categories are currently dened as follows:

• HF with preserved ejection fraction (HFpEF): LV ejection fraction

(LVEF) >50%

• HF with mid-range ejection fraction (HFmEF): LVEF 41–49%

• HF with reduced ejection fraction (HFrEF): LVEF <40%

Evaluation

The American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the evaluation and management of HF have classied this condition in four stages (A–D) [15]. The rst two stages (A, B) are not symptomatic stages of heart failure but dened to help practitioners identify those at risk for developing HF.

Stage A: At risk for HF but without structural heart disease or symptoms of HF

Stage B: Structural heart disease but without signs or symptoms of HF

Stage C: Structural heart disease with prior or current symptoms of HF

Stage D: Refractory HF requiring specialized interventions

The NYHA functional classication can be used to clarify symptom severity (Table9).

The clinical differentiation between HF with preserved or reduced EF, although challenging, is helpful in decision-making. A complete history and physical

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