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Treatment of Congestive Heart Failure in Outpatient Physical Therapy Settings

James Carlson, MPT, CCS


• No Financial Disclosures

• No Non-Financial Disclosures

Disclosures


• Differentiate the pathophysiology between systolic and diastolic heart failure

• Understand medical management of systolic and diastolic heart failure

• Recognize signs, symptoms, and those at risk for decompensated heart failure

• Understand exercise hemodynamic considerations for clinical decision-making

• Utilize medical diagnostic testing to assist with clinical decision-making

• Demonstrate a stepwise approach for assessment and treatment of the heart failure patient

Learning Goals


Chapter One

Pathophysiology and Medical Management


Heart Failure Definition

Clinical syndrome that results when the heart cannot pump enough blood to adequately serve the body’s needs while at the same time maintaining normal pressures in the heart chambers lung vessels

Am Heart J. 2002;143(3):398


New York Heart Association Classification

Heart disease but no symptoms or limitations in ordinary physical activity

Mild symptoms with slight limitation during ordinary physical activity

Significant limitation in activity due to symptoms. Comfortable only at rest.

Severe activity limitations. Symptoms even while at rest.


Population Attributable Risk

Arch Intern Med. 2001;161(7):996

• Risk progressively increases with blood pressure over 150/90

• Controlled hypertension lowers heart failure risk by as much as 40%


Third heart sound

Dizziness

PND

Pulmonary rales

Edema

Orthopnea

JVD

Shortness of breath

Fatigue

Exercise intolerance

Adapted from: European Journal of Internal Medicine 57 (2018) 61–69

Signs and Symptoms


Normal Cardiac Function

• Determinants of cardiac output– Heart rate and rhythm– Contractility (stroke volume)– Preload (Frank–Starling)– Afterload (outflow

resistance)

• Determinants of venous return– Venous capacity– Skeletal muscle pump– Respiratory pump– Right and left ventricle

function


Left-Sided Heart Failure

Common etiologies– Myocardial infarction

– Nonischemic cardiomyopathy

– Severe aortic/mitral valve disease


Right-Sided Heart Failure

Most common etiologies– Right ventricle failure

– Primary pulmonary hypertension

– Secondary pulmonary hypertension (lung pathologies)


Systolic Heart Failure: Heart Failure With Reduced Ejection Fraction (HFrEF)

• Characteristics– Decreased contractility

– LVEF ≤ 35–40 percent• Eccentric hypertrophy

– Dilated chamber with normal or thin ventricle walls, typically thinned

Volume Overload


Systolic Failure Pathophysiology


RAAS System


Norepinephrine Renin Antidiuretichormone

Endothelin-1 Atrial natriureticpeptide

Normal Heart failure

Neurohumeral Response

↑ Heart rate, contractility, vasoconstriction,salt and water retention

Vasodilation


Systolic Failure Signs and Symptoms


Medical Management


Goals– Decreases peripheral congestion– Decreases pulmonary congestion– Improves preload mechanics

Optimize Blood Volume


• Under diuresis: hypervolemia– Hypotension

– Weakness

– Pulmonary congestion– Peripheral congestion

– Arrhythmia

• Over diuresis: hypovolemia; electrolyte imbalance – Hypotension

– Weakness

– Arrhythmia

Diuretics


Goal– Decreases outflow resistance to lower LV wall stress and improve contractility

– Decreases Ras activation and adrenergic stimulation

Decrease LV Wall Stress


• Dose too low: vascular resistance is too high– Hypotension

– Weakness/exercise intolerance

– Pulmonary congestion– Peripheral congestion

– Arrhythmia

• Dose too high: vascular resistance is too low– Hypotension

– Weakness/exercise intolerance

– Light-headedness

Afterload Reduction


• Lowers myocyte toxicity from beta stimulation• Restores beta receptor responsiveness• Lowers heart rate to improve diastolic filling• Afterload reduction through vasodilatory effects

Beta Blockade


• Angiotensin 2 receptor blockers• Vasodilators• Long-acting nitratesEnd-stage therapies

– Inotropic drugs• Dobutamine• Milrinone

– Pressors• Vasopressin

– Circulatory support• IABP• ECMO• Ventricular assist devices (VADs)

Adjunctive Therapies


• ACE inhibitors– Cough

– Renal dysfunction

– Hyperkalemia

• Angiotensin receptor blockers– Renal dysfunction

• Beta-blockers– Excessive bradycardia if over blocked

Important Side Effects


Diastolic Heart Failure: Heart Failure With Preserved Ejection Fraction (HFpEF)

• 70% of cases >70 years of age

• Characteristics– EF >50 percent

– Concentric hypertrophy• Thickened ventricle

wall• Normal to smaller

chamber size Impaired filling


Mechanisms not clearly understood (research studies lacking)

Diastolic Heart Failure Pathophysiology


Diastolic Failure Signs and Symptoms


Medical Management


• Etiologies that negatively effect LV filling– Tachycardia/tachyarrhythmias– Hypertension– Conditions that contribute to hypertension

• OSA • Renal disease• Obesity

• Blood pressure control– Target <130/80– Decreases outflow pressure to lower LV filling pressures– ACE/ARB commonly used, may also see calcium channel blockers

• Diuresis – Decreases peripheral and pulmonary congestion– May improve LV filling through decreased blood volume

• Beta blockade– May improve diastolic filling time via lowering heart rate– Target rates 60–80 bpm

Medical Management (cont.)


Mixed Systolic and Diastolic Heart Failure

• EF between 41% and 49%

• May also be referred to as borderline diastolic failure

• Has features of both HFrEF and HFpEF

• Impaired contractility and diastolic filling– LV hypertrophy

– LV dilation– Ventricle wall stiffness


Summary Points

HFrEF (<35%) HFpEF (>50%)

Left ventricle Dilated chamber and thin wall Normal to decreased chamber with thick ventricle wall

Contractility Impaired Normal

LV filling Impaired due to volume overload Impaired due to wall thickness and stiffness

Signs and symptoms Fatigue, weakness, hypotension, pulmonary and peripheral congestion

Medical management

DiureticsBeta-blockers

Afterload reducers (ACE, ARB)

DiureticsBeta-blockers

Afterload reducers (ACE, ARB)

Salt and fluid restrictions Strict Recommended

Mixed systolic and diastolic heart failure have features of bothManagement targeted toward HFrEF


Chapter Two

Decompensated Heart Failure


True or false? Decompensated heart failure typically presents rapidly, within 24–48 hours

a) True

b) False

Poll Questions


What percentage of patients have adequate health literacy to understand and manage their heart failure?

a) 12%

b) 22%

c) 32%

d) 42%

Poll Question (cont.)


• $30 billion annual cost to health care system

• Projected to grow to ~$50 billion by 2030

• One million hospital admissions annually

• Number one cause of hospital admissions for Medicare age group

• Between 25% and 50% have a readmission within six months

Hospital Admissions


• Acute to subacute (days to weeks)– Pulmonary symptoms dominant

– Arrhythmia signs (atrial or ventricular tachyarrhythmias)

– Palpitations with/without light-headedness

• Chronic (weeks to months)– Peripheral congestive symptoms dominate over

pulmonary

– Anorexia

– Low output signs (worsening fatigue/weakness)

Decompensation


Exertional dyspnea

Fatigue

Orthopnea

PND

Angina

DizzinessHFpEFHFrEF

PARAGON-HF trial. Circ Heart Fail 2018 European Journal of Internal Medicine 57 (2018)

Symptomology


Edema

JVD

Pulmonary rales

Orthostasis

Atrial fibrillationHFpEFHFrEF

PARAGON-HF trial. Circ Heart Fail 2018 European Journal of Internal Medicine 57 (2018)

Symptomology (cont.)


Eur Heart J. 2006;27(22):2725. Epub 2006 Sep 25.

Decompensated Heart Failure Clinical Presentations


Triggers

• Ischemic event• Progression of a

cardiomyopathy• Progression of valve

disease• Tachyarrhythmia• Worsening hypertension• Worsening renal function• Infection• Pulmonary dysfunction• Anemia


• Gradual development of symptoms over days to weeks

• Most likely presentation in OP PT settings

• Signs and symptoms– Gradual progressive dyspnea

– Diminished breath sounds, particularly in the lung bases

– Pulmonary rales

– Gradual and progressive weight gain and/or worsening edema

– JVD

– Abdominal congestion

Mild to Moderate ADHF


Importance of Recognition and Action


Patient-Related Factors for Hospitalizations


• Only 12% of US adults have adequate health literacy

• Health illiteracy is associated with – Higher rates of hospitalizations and emergency

department visits

– Higher use of services related to treating complications from their conditions

– Increased likelihood of hiding vocabulary, math, and reading difficulties

Health Literacy


At-Risk Populations

• Less than high school education

• Minority populations

• Older adults

• Non-English-speaking

• Low income

• Having to manage comorbid conditions


• Starts with recognizing decompensation early• Track weights

– Gradual increase is more common– Abdominal ascites is often present without changes in lower extremity

edema• Monitor vital signs

– Blood pressure changes– Resting and exertional HR changes– Heart rhythm changes– Pulse oximetry changes

• Assess for changes in pulmonary status– Increased work of breathing– Breath sounds– Orthopnea– PND

Decompensation/Hospitalization Prevention


• Understand medical management– Medications

– Sodium <2g/day– Fluid <1.5–2L/day

– ETOH to no more than one drink/day

– Medications to avoid (NSAIDs, etc.)• Maximize physical function

• Subtle declines in physical function/exercise tolerance often indicate a progression to decompensated failure

Decompensation/Hospitalization Prevention (cont.)


• Recognize domains where patients are struggling– Health care illiteracy contributes to medical management

nonadherence• Poor awareness of signs and symptoms• Understanding medical management• Taking medications

– Social support– Emotional health– Transportation

• Facilitate/advocate when necessary– Provider contacts– Social work referrals– Family– Telemedicine

Decompensation/Hospitalization Prevention (cont.)


• Each heart failure exacerbation results in disease progression• Gradual worsening of symptoms is most common clinical

presentation• Symptomology is comparable in both HFrEF and HFpEF• Majority of heart failure patients have poor health literacy and are

very likely hiding their understanding of medical management, etc.• Physical therapy role is multifactorial

– Recognizing decompensation– Communicating to providers– Treating physical debility– Education and problem-solving– Facilitating referrals

Summary


Chapter Three

Exercise Response in Heart Failure


True or false? Resistance exercise should be avoided due to the negative effects of elevated systemic vascular resistance.

a) True

b) False

Poll Questions


True or false? Exercise should be stopped when there is a greater than 20 mmHg drop in SBP.

a) True

b) False

Poll Questions (cont.)


Normal Exercise Response


• Achievement of >85% of maximal heart rate in absence of medications affecting heart rate response

• Linear rise in SBP ~10 mmHg per MET to a max of ~210 mmHg (M) and 190 mmHg (F)

• Unchanged or decreased DBP

• O2 saturations 93%–99%

Healthy Adult Responses to Maximal Exercise


• Heart rate recovery post exercise ≥12–18 bpm within first minute and ≥22–42 bpm within 2–5 minutes

• Unchanged or decreased DBP

• Ratio of SBP decline at three minutes to SBP decline at one minute <1 – Example

• Peak SBP 190, 180 mmHg at one minute• 160 mmHg at three minutes

• Ratio 160/180 of 0.88

Healthy Adult Recovery Responses


• Chronotropic incompetence

• Elevated HR post exercise

• Inotropic incompetence

• Failure to increase SBP or drop in SBP

• Increased susceptibility and presence of arrhythmia

• Clinical importance: is the degree of impairment adversely affecting patient stability or peripheral perfusion for a given workload

Heart Failure Exercise Responses


• VO2 >20 ml/kg/min (~6 METs) has best outcomes for morbidity and mortality

• Highest one-year mortality

– Peak VO2 of ≤10 ml/kg/min (3 METs)

– Inability to achieve SBP of >120 mmHg

– Combination of peak VO2 ≤3 METs with inability to achieve peak SBP of >120 mmHg has worst prognosis

• Severe ventricular ectopy post exercise (frequent couplets, triplets, nonsustained ventricular tachycardia)

• **Almost all studies completed on patients with HFrEF

Predictors of Poor Outcomes


• Chronotropic and inotropic incompetence

• Impaired ability to overcome elevated systemic vascular resistance

• Hypervolemia overloads the left ventricle

• Mitral regurgitation more common

• Impaired pulmonary diffusion

• Decreased respiratory muscle endurance

• Pulmonary congestion and/or pulmonary hypertension resulting in RV failure

Exercise Impairment (HFrEF)


Myocardial and Vascular Dysfunction (HFrEF)

Myocardial dysfunction – Decreased

responsiveness to circulating catecholamines

– Decreased inotropy

– Chronotropic incompetence

– Impaired preload mechanics

Vascular dysfunction– Increased sympathetic

tone

– Sodium and water retention producing vascular congestion

– Decreased responsiveness to local skeletal muscle vasodilators


Skeletal and Respiratory Muscle Dysfunction (HFrEF)

LV failure

Decreased perfusion

Skeletal and respiratory muscle changes

Disuse atrophy

Weakness/fatigueBreathlessness

Sympathetic activation


Skeletal and Respiratory Muscle Dysfunction (cont.)

Skeletal muscle– Myocyte death

– Decreased capillary density

– Mitochondrial dysfunction

– Muscle fiber atrophy biased towards slow twitch fibers resulting in a relative increase in Type IIb fast twitch highly fatigable fibers

Respiratory muscle

– Myopathy

– Shift from fast to slow twitch fibers

– Minute ventilation out of proportion to C02 production

– Hyperactivity of skeletal muscle metaboreceptors producing excessive ventilatory response relative to workload


General Exercise Impairment (HFpEF)

• Chronotropic incompetence (57%–77%)

• Supraventricular tachycardias (rates >130–150) exacerbate diastolic filling impairment

• Atrial fibrillation more common. Elevated LV filling pressures further reducing diastolic filling.

• High prevalence of pulmonary hypertension (70–80%), increasing presence of right-sided heart failure


Myocardial and Vascular Dysfunction

Myocardial dysfunction – Decreased diastolic filling

rate– Increased wall stiffness,

reducing distensibility of ventricle wall

– Slowed, delayed ventricle relaxation, worsening with exercise

– Decreased suction/recoil during early filling

– Increased dependence on left atrial kick for filling

Vascular dysfunction – Aortic stiffness

– Peripheral arterial stiffness

– Impaired endothelium-dependent vasodilatory exercise response

– Decreased oxidative metabolism capability

– Decreased microvascular density


Major society guidelines recommend cardiac rehabilitation

– Stable class II to III heart failure (HF)

– No advanced arrhythmias

– No other limitations to exercise

– Aerobic and resistance training recommended

Rehabilitation (HFrEF)


↑Respiratory muscle strength

↓Sympathetic tone

↓Neurohumeralactivation

↑Endothelial function

Lower heart rates and minute ventilation at given workload

Lower systemic vascular resistance during exercise

Improved skeletal muscle oxidative capacity

Aerobic Training (HFrEF)


• Meta-analysis– Three days per week (home based, hospital or OP clinic)– 30–60 minutes in duration– 13 to 23 weeks– Intensity: 30%–95% of one-repetition max– High variability in muscle groups and modes of resistance

training (free weights, bands, machines, body weight, etc.)• Key outcomes

– Safe: no study demonstrated any adverse effects on preload, afterload, or ejection fraction or reported any adverse events

– Effective: equivalent improvement in peak VO2 when compared to aerobic training and combined aerobic and resistance training

Resistance Training (HFrEF)


Afterload reduction

Improved O2 extraction

Resistance Training Effects (HFrEF)

• Heart-specific– Reduces neurohumeral

activity– Reduces autonomic

activity– Lowers vascular resistance

• Skeletal muscle– Attenuates skeletal muscle

atrophy– Increases muscle mass – Decreases vascular

resistance– Improves endothelial

response


• Abnormal responses to exercise stress are to be expected, especially with higher NYHA class

• Red flags– Persistent elevation in heart rate with reduction in

workload/recovery– Ventricular/atrial irritability and/or arrhythmia with

exercise/recovery– Failure to maintain blood pressure adequate for peripheral

perfusion• Aerobic and resistance training improve VO2 and reduce central

and peripheral maladaptations• Resistance training safe and effective and directly targets skeletal

muscle dysfunction (may be a more effective use of clinical time)

Summary Points


Chapter Four

Clinical Assessment and Treatment


Patient history: clinically stable? Yes No

Anginal symptoms or equivalents

Pulmonary and peripheral congestion

Cardiac output changes

Arrhythmia signs

Decline in exercise/ADL ability

Evaluation


Video

Subjective Interview


Objective exam: clinically stable? Yes No

Vital signs• ECG (when able)• Pulse• Blood pressure• Oxygen saturationsVolume status• Weight• Auscultation• Abdominal congestion• Peripheral edema• JVD

Perfusion• Capillary refill• Temp/color

Objective Assessment


Video

Objective Assessment


Consider potential etiologies?– Worsening ischemia

– Arrhythmia

– Medication/diet adherence

– Relative hypertension

– Worsening renal function

– Poorly controlled DM

Decompensation

Yes No

Patient history: clinically stable?

Objective exam: clinically stable?


• The more objective information you provide, the better• What?

– Change in volume– Pulmonary congestive signs– Change in vital signs (ECG changes when able)– Changes in exertional tolerance

• To whom?– The patient– Nurse case manager– PCP cardiology– Emergency department

Communicating Suspected Decompensation


Yes No



Vital sign stability

Assessing exercise capacity vs. functional capacity?

Clinical Assessment of Stable Patients


National Heart Disease Protocol for Poorly Fit SubjectsStage Time Speed Grade METs

1 3 min 2 mph 0% 2.5

2 3 min 2 mph 3.5% 3.5

3 3 min 2 mph 7% 4.5

Exercise Stress Test

Stage Time Speed Grade METs

1 1–2 min 3 mph 2.5% 4.3

2 1–2 min 3 mph 5% 5.4

3 1–2 min 3 mph 7.5% 6.4

4 1–2 min 3 mph 10% 7.4

Standardized Balke Protocol

National Heart Disease Protocol for Poorly Fit Subjects


Treadmill MET calculator link: http://www.fedel.com/mets/

Alternate Balke Protocol

Stage Time Speed Grade METs (3.3 mph)1 1 min 1.5 0 2.1 2 1 min 3.3 mph (M), 3.0 (F) or self

paced brisk walk pace0 3.5

3 1 min 2% 4.44 1 min 3% 4.95 1 min 4% 5.36 1 min 5% 5.87 1 min 6% 6.28 1 min 7% 6.79 1 min 8% 7.1

10 1 min 9% 7.6For submaximal test, terminate at Borg RPE 12–13 or when patient achieves

symptom-limited threshold


• Peak HR of 120–130 bpm or 70% of age-predicted maximum

• RPE 12–13

• Peak workload of >5 METS

• Mild angina or moderate dyspnea

• Hypotension/hypotensive signs

• New or worsening ventricular ectopy

• New-onset arrhythmia or bundle branch block

• Other symptom-limited threshold

Submaximal Testing Endpoints


• Direct assessment of hemodynamic response from rest through exercise and recovery– Heart rate and blood pressure – O2 saturations– ECG

• Ventricular ectopy• Atrial ectopy• Arrhythmia• Pacemaker responsiveness

– Borg scale (13–14 target)

• Establishes MET threshold to gauge starting exercise intensities

Clinical Benefit


Which distance on a 6-Minute Walk Test represents the minimum threshold for predicting frailty and hospitalization risk in heart failure patients?

a) 200 meters

b) 250 meters

c) 300 meters

d) 350 meters

Poll Question


• Comorbidities prohibit stress test

• Lack confidence or capability to perform a stress test

• Higher NYHA class

• Lower-functioning frail individuals

• Hemodynamic assessment remains important– Baseline values

– Response to stress

– Response in recovery

When to Use Functional Tests and Measures


• 81% one-year mortality if unable to complete test; 33% if able to complete test

• Distance <300 meters predicts increased risk for frailty, mortality, and hospitalization– 3.7-fold increased one-year mortality risk– 60% hospitalized by six months, compared to 12% >300 meters

• Each 100-meter increase lowers mortality and hospitalization

6-Minute Walk Test


10-Meter Gait Speed

• Frailty– <0.8 meters/second (M)

– <0.7 meters/second (F)

• Falls risk– <0.65 meters/second

– Dependency with ADLs

• Survival (one and six years)– 1 meter/second (90%)– <0.65 meters/second

(65%)• Hospitalization (one year)

– >1 meter/second (20%)– <0.65 meters/second

(50%)


FrailGait speed: 0.48 meters/secondGrip strength: 18 kg6MWT distance: 170 metersCreatine clearance (ml/min): 60

At risk for frailtyGait speed: 0.75 meters/secondGrip strength: 22 kg6MWT distance: 210 metersCreatine clearance (ml/min): 73

A cutoff distance of <300 meters predictive of identifying at-risk individuals with heart failure

Non-frailGait speed: 1.09 meters/secondGrip strength: 30 kg6MWT distance: 401 metersCreatine clearance (ml/min): 31

Frailty Risk in Heart Failure


Four-Square step test

Neuromuscular Screen

• Start by standing in square 1, facing square 2

• Begin in a clockwise direction, then immediately move counterclockwise

• Times >15 seconds predictive of falls risk


Age 20–29 30–39 40–49 50–59 60–69 70–79 80–85

Averagetime (sec)

6.0 6.1 7.6 7.7 7.8 9.3 10.8

• Normative data based on 17- to 18-inch chair height, no arm use; mean value for all adults >60 years: 12.1 seconds; >50 years: 8.7 seconds

• >15 seconds predictive of falls• >16.7 seconds independent predictor of injurious falls

• Healthy adult norms

5-Times Sit-to-Stand

**Not tested on heart failure patients


Age 60–64 65–69 70–74 75–79 80–84 85–89 90–94

Male 17 16 15 14 13 11 9

Female 15 15 14 13 12 11 9

Age 60–64 65–69 70–74 75–79 80–84 85–89 90–94

Male 14–19 12–18 12–17 11–17 10–15 8–14 7–12

Female 12–17 11–16 10–15 10–15 9–14 8–13 4–11

Norms for community dwelling adults (mean reps)

30-Second Chair Stand

High and low range of normal (reps)

Minimal clinically important change: 2 reps**Not tested on heart failure patients


Summary

Yes No



Vital sign stability

Exercise stress test or functional tests

Impairments

Rehab interventions

??


Chapter Five

Using Diagnostic Testing for Clinical Decision-Making


Which diagnostic test will give you information on systolic function, diastolic function, valve function, and pulmonary artery pressure?

a) Nuclear stress test

b) Echocardiogram

c) Left heart catheterization

d) Right heart catheterization

Poll Question


Transthoracic (TTE) or transesophageal (TEE)

• Identifies left ventricular chamber size, wall thickness and contractility (EF)

• Quantifies left ventricle diastolic filling impairment

• Identifies atrial chamber dilation

• Identifies right ventricular chamber size and systolic function

• Identifies and quantifies severity of valve disease

• Provides an estimation of pulmonary artery pressure

• Provides an estimation of central venous pressures

Echocardiogram


• Present in both HFrEF and HFpEF– Grade 1: slowed and incomplete LV relaxation – Grade 2: higher dependence on LA to push blood into the LV– Grade 3: noncompliant LV. High LA pressures. May be reversed with

diuretics– Grade 4: noncompliant LV. High LA pressures. Not reversed with

diuretics

• HFpEF– LV hypertrophy, LA enlargement and increased PA pressures

• HFrEF – LV dilation and LA enlargement with or without increased PA

pressures

• Dyspnea from pulmonary congestion is often the first clinical symptom with more severe diastolic dysfunction

Diastolic Filling Impairment


Pulmonary Hypertension • Etiologies

– Left heart failure

– Lung disease

– Primary to pulmonary arterial hypertension

– Severe aortic/mitral valve disease

• Severity (leads to right ventricle failure)

– Mild: 30-40 mmHg

– Moderate: 40-70 mmHg

– Severe: >70 mmHg


• Arrhythmia’s associated with heart failure– PVC’s, bigeminy, trigeminy, couplets

– Ventricular tachycardia (sustained, non-sustained)

– Right and left bundle branch blocks

– 2nd and 3rd degree AV block

– Supraventricular tachycardias

– Atrial fibrillation/flutter

• Ventricular ectopy >10% of total heart beats in a 30 second period or stage of stress test or develops in recovery is associated with higher risk of V-tach

• ICD’s common when ejection fraction <35%• Pacemakers common with more severe AV blocks

Electrocardiogram (ECG)


• Establishes MET capacity• Establishes symptom threshold• Identifies ischemia• Identifies prior or current arrhythmia presence/burden• Provides a baseline hemodynamic response for both exercise and

recovery to use in intensity of rehab intervention• Bruce protocol is most common

Stress Testing

Stage METs Speed (mph) % Grade1 5 1.7 102 7 2.5 123 9.5 3.4 144 13 4.2 165 16 5.0 18


• Identifies areas of viable myocardium• Identifies arrhythmia presence/burden• Quantifies ventricular contractility (ejection fraction)• Quantifies location and severity of ventricular wall motion impairment• May be done pharmacologically or as part of exercise stress test

Nuclear Stress Testing


• Establishes presence of intervened and nonintervened coronary artery disease

• Identifies territories susceptible to further ischemic damage

Coronary Angiography

RCA LAD LCX

SA and AV nodes, RV Purkinje His bundle, LV Purkinje LV Purkinje

RV, septum (inferior wall) LV, septum, (anterior wall) LV (lateral wall)


Right Heart Catheterization

• Common test for patients with more severe stages of heart failure (LVAD/transplantation)

• Most accurate assessment of chamber pressures, cardiac output, and pulmonary artery pressure

• Elevated pulmonary artery and elevated PCWP are predictors of poor exercise capacity, morbidity, and mortality

• PCWP >18 highly associated with pulmonary vascular congestion


Establishes severity or presence of comorbid obstructive or restrictive lung disease

Pulmonary Function Testing

Obstructive Lung DiseaseGold 1 Mild FEV1/FVC <0.7 FEV1 ≥80% predictedGold 2 Moderate FEV1/FVC <0.7 FEV1 50%–79% predictedGold 3 Severe FEV1/FVC <0.7 FEV1 30%–49% predictedGold 4 Very severe FEV1/FVC <0.7 FEV1 <30% predicted

Restrictive Lung DiseaseStage 1 Mild FEV1/FVC >0.7 FVC 60%–80% predicted

Stage 2 Moderate FEV1/FVC >0.7 FVC 50%–59% predicted

Stage 3 Severe FEV1/FVC >0.7 FVC <50% predicted


• Quantifies– Pulmonary vascular congestion (edema)

– Pericardial effusion

– Clearing of vascular congestion reflects responsiveness to diuretic therapy

• Identifies any infectious comorbidity

Chest X-ray


Troponin

Labs

BNP

0.0–0.2 ng/ml Normal (rules out MI)2–10 ng/ml Small MI

>20–30 ng/ml Large MI

< 200 pg/ml Normal (rules out CHF)200–400 pg/ml Compensated CHF

400–2000 pg/ml Moderate CHF

>2000 pg/ml Severe CHF


• Diuretic use can affect electrolyte levels

Electrolytes

• Sodium and potassium depleting diuretics (thiazide, loop)

• Hypokalemia: skeletal and respiratory muscle weakness, tachyarrhythmias

• Hyponatremia: confusion, abdominal symptoms, gait disturbances

• Potassium-sparing diuretics (aldosterone antagonists)

• Hyperkalemia: weakness, bradycardia, heart block

Sodium 136–146 mmol/LPotassium 3.5–4.7 mmol/L

Calcium 8.5–10.1 mg/dLMagnesium 1.7–2.4 mg/dL


• Fluid overload: RBC, Hgb, HCT will be low• Dehydration: RBC, Hgb, HCT, and creatinine will be high

• Anemia can produce tachycardias, leading to decompensated heart failure

• Infection increases systemic burden, resulting in cardiac overload

RBC 4.2–5.7 K/uLWBC 4–11 K/uLHCT 40%–51%HGB 13–17 g/dL

CBC


• Creatinine (0.7-1–17 mg/dL)– Renal failure common cause of decompensation

– Renal failure common cause of elevated BP

– Electrolyte levels may also be affected

• INR (0.9–1.1 normal; target: 2–3 for A-fib, PE and mechanical valve/circulatory support device)

• A1C (90-day avg blood sugar levels 4%–6% normal; target of <7% for DM)– Poor diabetic control can be a trigger for decompensated

heart failure

Additional Labs


• 71-year-old male with HFpEF referred to PT for deconditioning• Cardiac history: three-vessel CABG 2007, NSTEMI 2017, chronic atrial

fibrillation and hypertension. CHF-related hospitalizations: 2017 and 2018• Additional PMH: CKD, carotid artery disease• Echo: (technically limited study due to A-fib)

– EF 45%–50%, moderate concentric hypertrophy– Biatrial dilation – Moderate mitral regurgitation– Moderate tricuspid regurgitation– Estimated pulmonary artery pressure 43 mmHg

• Medications: furosemide, lisinopril, spironolactone, metoprolol and warfarin• Dry weight: 205 lb. (three-month history consistently at 195 lb.)• Blood pressure history (six months): 120s/60s• ECG history (six months): 50s–70s, atrial fibrillation

Case Study


Labs– RBC: 4.2 (4.2–5.7 K/uL)

– HGB: 13 (13–17 g/dL)

– HCT: 40 (40%–51%)– Sodium: 128 (136–146 mmol/L)

– Potassium: 4.6 (3.5–4.7 mmol/L)

– Calcium: 9.4 (8.5–1.0 mg/dL)

– Creatinine: 1.47 (0.7–1.17 mg/dL)

– INR: 2.55 (2–3 target for chronic A-fib)

Case Study (cont.)


• Vital sign history– Weight and BP have been stable

• Echo – Moderate LVH– Reduced contractility (EF 45%–50%)– Biatrial enlargement– Moderate PH (43 mmHg)

• Atrial fibrillation– Ventricular rate has been well controlled

• Labs– Elevated creatinine may indicate renal dysfunction– Potassium stable, sodium is low– INR is therapeutic for A-fib

Clinical Application


• Good probability of stable initial clinical presentation given history of vital sign stability, arrhythmia stability and stable weights

• Sources of potential exercise intolerance – Intolerance due to LV filling impairment

• Moderate LVH

• Moderate MR

• Worsening atrial fibrillation

– Predictors of intolerance to increased in blood volume

• Biatrial enlargement

• Moderate MR

– Intolerance d/t RV failure

• Moderate PH (43 mmHg)

Clinical Implications


• Atrial fibrillation with rapid ventricular rate will decrease diastolic filling time further exacerbating loss of atrial kick

• Diuretic considerations: worsening hyponatremia could result in acute gait disturbances/muscle weakness

• Hypervolemia could reflect worsening renal function; dietary indiscretion/diuretic noncompliance also considerations

• Elevated BP could exceed afterload threshold and may be due to beta-blocker/ACE inhibitor noncompliance or worsening renal function

Additional Considerations


• Identifies susceptibilities to changes in clinical stability and exercise intolerance

• Identifies pre-existing arrhythmias that can affect clinical stability

• Establishes prior MET capacity and hemodynamic response• Identifies severity of pulmonary comorbidities that may impact

cardiac burden

• Identifies severity of ischemic disease• Labs assist in identifying electrolyte abnormalities, anemia,

infection, renal dysfunction, diabetic control and anticoagulation all of which can impact clinical presentation and decision making

Benefits of Reviewing Diagnostic Testing and Labs


Chapter Six

Case Studies


Case One


• 68-year-old obese (BMI 32) male with HFpEF on long-term anticoagulation reports worsening unsteadiness over the past two years with frequent near falls in the past six months

• Cardiac history– MI in 1990 and 2004– 1990, s/p 3-vessel CABG (LIMA-LAD, SVG-PDA, SVG-D1) – PCI/DES to mid-LAD, 11/2004 – PCI/DES to LCx, 4/2005 – PCI/DES OM1 2006 – PCI/DES to SVG → D1, 1/2012

• Arrhythmia history– Atrial fibrillation (successful DCCV) – Complete heart block: permanent pacemaker: -100% ventricular

pacing

History


History (cont.)

PMH– Anemia

– Lumbar spinal stenosis– Chronic kidney disease

– Hyperlipidemia

– Diabetes mellitus type II with neuropathy and retinopathy

– Obstructive sleep apnea

Labs– RBC: 4.0 (4.2-5.7)

– WBC: 8.0 (4-11)– HCT: 44 (40-51)

– HGB: 11.5 (13-17)

– Sodium: 130 (136-146)– Potassium: 3.9 (3.5-4.7)

– Calcium: 8.9 (8.7-10.1)– Magnesium: 2.0 (1.7-2.4)

– INR: 2.2 (0.9-1.1)


• Current TTE– Normal LV size with mild concentric hypertrophy– Low normal LV systolic function, EF: 55%– Grade 3 diastolic dysfunction– Severe biatrial enlargement– Mild MR– Mild TR– Mild-moderate pulmonary hypertension with estimated PASP

40–45 mmHg

• Current coronary angiography– Three bypass grafts, including PCI, are patent– Stents in the mid portion of the LAD beyond the LIMA all patent

History (cont.)


Medications

• Aspirin• Atorvastatin • Carvedilol• Cholecalciferol (vit D3) • Clopidogrel bisulfate• Docusate NA • Ferrous sulfate • Furosemide • Gabapentin • Insulin• Isosorbide mononitrate• Lisinopril• Nitroglycerin• Warfarin• Omeprazole

Heart failure

– Diuretic

– Vasodilator

– Beta-blocker

Anemia

Anticoagulation


• Home– Three-bedroom ranch, mainly carpeted, throw rugs kitchen and living room

threshold (not nonskid), three in kitchen by sink, fridge, and entrance

• Stairs– Entering home: three entrances, three to four STE with railing (all concrete)

• Home DME/assistive device– Cane: in home, shorter distances <50 feet – 4WW: uses outside of home

• Social support– Spouse

• Activity level – Sedentary

Psychosocial


• Dyspnea: none at rest, moderate to severe with walking 100 yards• Orthopnea: denies• PND: occasional • Lower extremity edema: stable• Anginal baseline: chest pain one time a week• Nitro use: one to two times a month• Cardiac symptoms with ADLs: none• Cardiac symptoms with mobility: gait 100 yards before

dizziness/sob• Falls: two in the past six months, multiple near falls due to

dizziness• NYHA class: III/IV

Cardiac Signs and Symptoms


• Auscultation– Heart: S1, S2, no murmur, rub, or gallop

– Lungs: clear throughout all fields• Extremities

– 2+ mid tibial edema bilateral; skin intact

Cardiovascular and Pulmonary Assessment

Orthostatic Blood pressure Heart rate RA

Supine 106/52 60 97%

Sitting 102/55 65 96%

Standing 98/50 63 96%


• Gait speed: 0.63 m/sec (with walker and SPC)• 6-minute Walk Test: 217 meters with 4ww, reported leg

fatigue at three minutes– RPE: 13– Max HR: 80; 100% paced– BP: 84/50– SpO2: 95%– FiO2: RA

• 30-Second Chair Stand Test: 9 reps with use of hands• Dynamic gait index: 12/24

Tests and Measures


• 6-Minute Walk Test – Our patient: 217 meters– Heart failure poor prognostic indicator: <300 meters

• Gait speed– Our patient: 0.63 m/sec (40% impaired)– Household ambulation: 0.4 m/sec– Heart failure: <0.8 increased risk for frailty, 0.65 falls risk predictor,

increased risk of mortality, hospitalization, and dependency with ADLs• 30-Second Chair Stand Test

– Our patient: 9 reps– Moderately active male 65–69: 16– Community-dwelling male 65–69: 12–18

• Dynamic gait index– Our patient: 12/24– Community-dwelling adult: scores ≤19 indicated increased risk of falls

Rehab Prognosis?


0102030405060708090

1 2 3 4 5 6

Rest Aerobic Resistance

Key findings– Very minimal heart rate change from rest reflecting chronotropic incompetence

(patient is not atrial paced)

– Resistance exercise often produced a better heart rate response

HR Trend: Visits 1–6


Key findings• Within the first four to five visits, exertional blood pressure dropped below

resting blood pressure

• Blood pressure drop was often more pronounced with aerobic exercise training

60

70

80

90

100

110

120

130

140

1 2 3 4 5 6

Rest Aerobic Resistance

SBP Trends: Visits 1–6


Based on the patient’s initial evaluation and current treatment response, is continuing physical therapy appropriate?

a) Yes

b) No

Poll Question


High-intensity interval training vs. moderate-intensity continuous exercise training in heart failure with preserved ejection fraction: a pilot study

Angadi, SS, Mockadam F. Journal of Applied Physiology, Sept. 2014

Clinical Decision: Add Higher-Intensity Interval Training


Key results– Improvement in chronotropic exercise response for both

aerobic and resistance exercise

– Resistance exercise again tends to outperform aerobic

HR Trend Visits 7–25


94

125

101100

123116

91

11098

122122108

116117116

95

125130

1 3 5 7 9 11 13 15 17

Rest SBP: Visits 7–25

106

88104 104

77

99

1 2 3 4 5 6

Rest SBP: Visits 1–6

Key results– Reversal of the falling trend seen in the first six visits

BP Stability Pre/Post Intervention


100

117104108108114

90

115105

112112112112114106

87102

130

1 2 3 4 5 6 7 8 9 101112131415161718

Aerobic SBP: Visits 7–25

9886 92 97

90 96

1 2 3 4 5 6

Aerobic SBP: Visits 1–6

Key results– Upward shift in SBP with aerobic exercise from a level of

~ 95 mmHg to 104 mmHg

Exercise BP Response Pre/Post Intervention


9888

101 10897 101

1 2 3 4 5 6

Resistance SBP: Visits 1–6

10191

102116112104103103 101101

120

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

Resistance SBP: Visits 7–25

Key results– Upward trend in SBP response with resistance exercise from

beginning– Steady improvement of blood pressure responsiveness throughout

duration of therapy, consistently achieving SBP >100 mmHg

Exercise BP Response Pre/Post Intervention


050

100150200250300350

6MWT (m)0

0.2

0.4

0.6

0.8

1

Gait Speed(m/sec)

02468

1012

30-Sec Sit-to-Stand (reps)

• Initial: 0.6 m/sec• Discharge: 0.85

m/sec (SPC)

Change in Outcome Measures

• Initial: 207 meters• Discharge: 307

meters (4ww)

• Initial: 9 reps (with arm use)

• Discharge: 11 reps (with intermittent arm use)


By improving hemodynamic stability and peripheral skeletal muscle function, have we reduced falls risk?

– The measurable improvements in chronotropic response and blood pressure stability would indicate yes

– The meaningful improvements in functional tests would also indicate yes

– Reality? (unknown: patient never returned to physical therapy following completion of his rehab)

Have We Reduced Falls Risk


Case Two

Deconditioning


• Patient is a 71-year-old male referred to PT for weakness post recent hospitalization for decompensated HFrEF

• PMH– Nonischemic cardiomyopathy– COPD– DM2 with neuropathy – Depression– Chronic A-fib– OSA– Enlarged prostate

• Hospitalizations– 10/2018: decompensated HFrEF, admission weight 322 lb., discharge weight

284 lb.– 11/2018: decompensated HFrEF, admission weight 291 lb., discharge weight

286 lb.– Target dry weight: 284 lb.

History


• Present status

– Reports since left hospital that he has been regaining about 1 pound a day, mostly in the belly. Denies any change in edema in his legs. Does not feel diuretic is working despite taking it as prescribed. Breathing is still very limited, but does feel that he is able to walk farther than before he was admitted. Denies chest pressure or equivalents, orthopnea, or PND. Occasionally feels palpitations, but denies change in frequency or intensity pre/post hospitalizations. Has never felt racing.

• Psychosocial

– Patient lives alone with four cats; home has 4STE with railing. Uses a cane for ambulation. Retired factory worker. Reports one fall a couple months ago trying to carry an old computer while walking on the ice.

Initial PT Appointment One and a Half Months Following Last Hospitalization


Medications

• Albuterol• Atorvastatin• Bupropion• Finasteride• Furosemide• Gabapentin• Metformin• Metoprolol• Omeprazole• Spironolactone• Tiotropium• Warfarin

Heart failure

– Diuretic

– Beta-blocker

– Patient unable to tolerate ACE or ARB

COPD

Anticoagulation


• TTE: April 2018– The left ventricular chamber size is moderately dilated. Mild eccentric left

ventricular hypertrophy is observed. The estimated ejection fraction is 35%.– Diastolic function could not be evaluated secondary to atrial fibrillation– The right ventricle is not well visualized but appears mildly dilated with normal

global systolic function– There is severe biatrial enlargement– The right ventricular systolic pressure is mildly elevated: 35 mmHg– CVP is mildly elevated (estimated at 8 mmHg)– Compared to the previous echo from 2017, LV and RV size has increased.

RVSP has increased.• PFT: April 2018 (Stage II COPD)

– FVC: 3.53%–77% pred– FEV1: 1.96%–58% pred– FEV1/FVC: 0.56

Diagnostic Studies


• The patient tolerated without significant adverse effects. Normal hemodynamic response.

• There are no definitive ST segment changes to suggest ischemia. No arrhythmias are seen outside of the baseline atrial fibrillation.

• Myocardial perfusion imaging demonstrates no evidence of ischemia

• Overall left ventricular function is mild to moderately decreased, LVEF is calculated at 38% post stress; apical/inferoapical regional wall motion abnormalities are noted

• The size of the left ventricle is moderately increased both at rest and stress

Regadenoson Nuclear Stress Test: April 2018


A1C: current 6.2 History 6.1–6.4% <7% for good diabetic control

Creatinine: current 1.4 History 1.2–1.4 Normal 0.7–1.17

INR: current 2.1 History 1.3–2.7 2–3 target for A-fib

Lab History

BNP: 1100 and 900 at October and November admissions

Current electrolytes

Sodium 141 mmol/L 136–145

Potassium 3.5 mmol/L 3.5–4.7

Calcium 8.1 L mg/dL 8.5–10.1

Magnesium 2.1 mg/dL 1.7–2.4


• Resting vital signs– HR: 85–98– ECG: A-fib– BP: 89/65– SpO2: 97%– FiO2: room air– Weight: 292 lb.

• Auscultation: diffuse inspiratory wheezing in all lung fields, greater at the apices, crackles in both bases

• Extremities: 2–3+ in both lower extremities and firm, right > left

• Abdomen: + ascites

Cardiovascular and Pulmonary


Is the patient stable for assessment?


• 10-Meter Gait Speed: 0.69 meters/second with single-point cane

• 6-Minute Walk Test: not stable to assess• 2-Minute Walk Test: 50 meters with single-point cane

– Vital sign response• HR: 100–115• ECG: A-fib• BP: 100/71• Spo2: 98%• FiO2: RA• Normative data: 172 meters for healthy age-matched adult

Tests and Measures


• Symptomology– Edema/ascites: (+) – dry weight: 284 lb., current weight 292 lb. (+ 8 lb.) – Dyspnea: (+) – exertional dyspnea remains problematic – Orthopnea: (-) – stable– PND: (-) – stable – Anginal symptoms: (-) – stable– Arrhythmia signs: (-) – unknown, has preexisting A-fib, not reporting

perception of racing, fluttering, or palpitations• Examination

– Lungs: (+/-) – inspiratory wheezing, greatest in apices and diminished in bases, wheezing also a common finding in COPD, crackles a common finding in both HF and COPD

– Edema: (+/-) – present in both legs, unknown what baseline is as this is first PT appt.

– Ascites: (+) – present, and patient feels more weight gain in belly

Clinical Decision-Making


• Vital signs– Arrhythmia: (+/-); has history of known A-fib and currently rate controlled– BP: (+/-); low at rest, but this may reflect patient baseline. Would be useful

to review the chart for patient’s measured blood pressures– O2 saturations: (-); 97% on room air, reflecting adequate gas exchange (as

best we can assess in therapy)

• Functional testing– Gait speed: 0.69 meters/second with SPC

– Heart failure: <0.8 increased risk for frailty, 0.65 falls risk predictor, increased risk of mortality, hospitalization, and dependency with ADLs

– 6MWT: Not stable for assessment

– 2MWT: 50 meters (29% of predicted value for healthy age-matched adult); patient demonstrated HR and BP stability with this test

Clinical Decision-Making (cont.)


• Two prior hospitalizations one month apart

– 8-pound weight gain in two weeks

– Symptomatic exertional dyspnea

– Subjective report of abdominal distention with positive clinical finding

– Wheezing and crackles in lung fields

– Gait speed at threshold for frailty, falls, and hospitalization risk

– Unable to complete a 6-Minute Walk Test

– Poor performance on 2-Minute Walk Test

• Indicative of mild to moderate acute decompensated heart failure clinical presentation

• Decision to contact provider via Skype messaging and communicate exam findings. Patient was ultimately sent to ED and admitted for abdominal tap.

Decompensation and Hospitalization Risk


245250255260265270275280285290295

Visit 1 Visit 2 Visit 3 Visit 4 Visit 5 Visit 6 Visit 7 Visit 8 Visit 9 Visit 10

Rehab WeightsPatient's Weight Dry Weight

Future PT Visits


0

20

40

60

80

100

120

140

Visit 1 Visit 2 Visit 3 Visit 4 Visit 5 Visit 6 Visit 7 Visit 8 Visit 9 Visit 10

Systolic Blood Pressure

Rest Activity

Future PT Visits (cont.)


• Three subsequent hospitalizations requiring abdominal paracentesis

• Unable to achieve any rehab consistency, and the patient was discharged with palliative approach to mobility and home safety

• DME Issues– Grab bars– Elevated toilet seat– 4WW– Discussion regarding potential future power mobility needs if

unable to stabilize heart failure

• Patient has not returned to physical therapy

Outcome


• Each heart failure patient is their own case study

• Assessment of clinical stability is important at each visit

• Monitoring vital signs is important for tracking exercise response and changes to treatment interventions

• Use of higher-intensity exercise and resistance training should not be avoided for stable patients

• Many patients require a decision to not to treat until clinical stability is achieved

Summary Points


• Systolic and diastolic heart failure have nearly the same clinical presentations but differing etiologies

• Medical management for both involve optimizing blood volume, afterload reduction, beta blockade and controlling arrhythmias

• Poor health literacy significantly contributes to adherence to medical management

• Understanding medical management is important for clinical decision making and recognizing areas to support, educate and facilitate for patients with poor health literacy

• Diligent clinical assessment each visit is important for both treatment planning and recognizing decompensation

Course Summary Points


• Understanding pathophysiology of exercise intolerance for systolic and diastolic heart failure is important for determining intensity and type of rehab intervention

• Reviewing diagnostic tests and labs is useful in predicting where cardiac dysfunction and clinical instability is likely

• Poor prognostic indicators include a six-minute walk distance less than 300 meters and a ten-meter gait speed <0.65 meters/second

• Resistance training is an effective intervention for systolic and diastolic heart failure and is likely a more effective use of clinical time

• There is no protocol in treating heart failure patients as each is unique and has potential for complexity in medical management, comorbidities and functional impairments

Course Summary Points (cont.)


PAGE 1

Abbreviations ListJames Carlson, MPT, CCS

Activities of daily living (ADL): things we normally do in daily living. Includes any daily activity we perform for self-care such as feeding ourselves, bathing, dressing, grooming, work, homemaking, and leisure.

Adrenergic system: a group of organs and nerves that regulate the neurotransmitters adrenaline and/or noradrenaline. It is one of the main neurohumeral systems that regulate heart rate, stroke volume and vascular tone.

Angiotensin receptor blocker (ARB): medications that block the action of angiotensin II by preventing angiotensin II from binding to angiotensin II receptors on the muscles surrounding blood vessels. As a result, blood vessels enlarge (dilate) and blood pressure is reduced.

Angiotensin-converting enzyme (ACE): a central component of the renin-angiotensin system. It converts the hormone angiotensin I to the active vasoconstrictor angiotensin II. ACE Inhibitors block this enzyme causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart.

Antidiuretic hormone (ADH): a hormone which helps regulate blood pressure, blood volume and tissue water content by controlling the amount of water and hence the concentration of urine excreted by the kidney.

Ascites: accumulation of protein-containing fluid within the abdomen.

Atrioventricular (AV): relating to the atrial and ventricular chambers of the heart, or the connection or coordination between them.

Beats per minute (bpm): number of contractions of the heart per minute.

Blood pressure (BP): pressure of circulating blood on the walls of blood vessels.

Brain natriuretic peptide (BNP): a blood test that measures levels of a protein called BPN that is made by your heart and blood vessels. BNP levels are higher than normal when you have heart failure.

Central venous pressure (CVP): blood pressure in the vena cava.

Chronic kidney disease (CKD): chronic impairment in the kidneys ability to filter blood.

Chronic obstructive lung disease (COPD): a group of lung diseases where airflow obstruction occurs during exhalation.


PAGE 2

Coronary artery bypass graft (CABG): form of bypass surgery that can create new routes around narrowed and blocked coronary arteries, permitting increased blood flow to deliver oxygen and nutrients to the heart muscle.

Diabetes mellitus (DM): a chronic disease associated with abnormally high levels of the sugar glucose in the blood.

Diastolic blood pressure (DBP): blood pressure in your arteries between contractions.

Direct current cardioversion (DCCV): procedure used to treat irregular heart rhythms (commonly atrial fibrillation). The procedure involves a general anesthetic and placement of electrodes on the chest. An electrical impulse is passed across the electrodes to return the heart rhythm to normal.

Drug eluding stent (DES): a peripheral or coronary stent (a scaffold) placed into narrowed, diseased peripheral or coronary arteries that slowly releases a drug to block cell proliferation.

Durable medical equipment (DME): any equipment that provides therapeutic benefits to a patient in need because of certain medical conditions and/or illnesses.

Electrocardiogram (ECG): a recording of the electrical activity of the heart.

Emergency department (ED): department of a hospital responsible for the provision of medical and surgical care to patients arriving at the hospital in need of immediate care.

Ethyl alcohol or ethanol (ETOH): medical synonym for alcohol.

Extracorporeal membrane oxygenation (ECMO): a heart and lung bypass pump providing prolonged cardiac and respiratory support to persons whose heart and lungs are unable to provide an adequate amount of gas exchange or perfusion to sustain life.

FEV1/FVC: ratio of the air expired in the first second relative to the total volume of expired during a maximal forceful exhalation.

First Diagonal (D1): branch of the left anterior descending artery.

First Obtuse Marginal (OM1): branch of the circumflex artery.

Forced expiratory volume in 1 second (FEV1): volume of air that can be forced out in one second after taking a deep breath.

Forced vital capacity (FVC): the amount of air that can be forcibly exhaled from your lungs after taking the deepest breath possible.

Four wheeled walker (FWW): type of assistive device used to aide walking that has four wheels.


PAGE 3

Fraction of inspired oxygen (Fi02): concentration of oxygen that a person inhales, room air is 21% oxygen at sea level.

Heart failure (HF): clinical syndrome that results when the heart cannot pump enough blood to adequately serve the body’s needs while at the same time maintaining normal pressures in the heart chambers lung vessels.

Heart failure with preserved ejection fraction (HFpEF): heart failure where the ejection fraction is normal. It is also referred to as diastolic heart failure.

Heart failure with reduced ejection fraction (HFrEF): also known as systolic heart failure. A loss of contractility causing left ventricular ejection fraction to drop below 35%.

Heart rate (HR): number of times the heart beats per minute.

Hematocrit (Hct): measurement of the percentage of red blood cells relative to the total blood volume.

Hemoglobin (Hgb): oxygen carrying component of red blood cells.

Intraortic balloon pump (IABP): a mechanical device implanted in the aorta that increases myocardial oxygen perfusion and indirectly increases cardiac output through afterload reduction.

Jugular venous distension (JVD): distension of the jugular vein on the right side of the neck caused by elevation of central venous pressure.

Left anterior descending artery (LAD): main coronary artery supplies blood to the left ventricle, septum and bundle of his and purkinje fibers.

Left atrium (LA): chamber of the heart where blood enters from the superior and inferior vena cava.

Left circumflex artery (LCX): heart artery that supplies blood to the left atrium, side and back of the left ventricle, papillary muscles and purkinje fibers.

Left internal mammary artery (LIMA): common artery that is harvested during coronary artery bypass surgery.

Left ventricle (LV): heart chamber below the left atrium responsible for pumping blood to the body.

Left ventricle hypertrophy (LVH): pathological thickening of left ventricular muscle.

Left ventricular ejection fraction (LVEF): percentage of blood pumped out of the left ventricle during ventricular systole. Normal is 55–75%.

Metabolic equivalent of task (MET): amount of oxygen consumed relative to a physical task in milliliters of O2 per kg body weight per minute.


PAGE 4

Mitral regurgitation (MR): leakage of blood across the mitral valve into the left atrium during ventricular systole.

Myocardial infarction (MI): blockage of blood flow to heart muscle.

New York Heart Association (NYHA): functional classification for heart failure stratified by severity of heart failure patient-reported symptoms.

Non-ST segment elevation MI (NSTEMI): a type of heart attack where the ST segment does not elevate on electrocardiogram.

Non-steroidal anti-inflammatory drugs (NSAIDS): medications commonly prescribed or purchased over the counter to treat the inflammation associated with conditions such as arthritis, tendonitis, and bursitis.

Obstructive sleep apnea (OSA): potentially serious sleep disorder where breathing repeatedly stops and starts during sleep.

Orthopnea: shortness of breath that occurs when lying flat often requiring a person to elevate their upper body to alleviated the symptoms.

Outpatient (OP): clinical setting the healthcare system where patients receive care outside of the hospital.

Paroxysmal nocturnal dyspnea (PND): attacks of shortness of breath and coughing during the night that commonly awake a person from sleep.

Percutaneous coronary intervention (PCI): non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup.

Peripheral capillary oxygen saturation (Spo2): estimate of the amount of oxygen in the blood.

Physical therapy (PT): movement experts who optimize quality of life through prescribed exercise, hands-on care, and patient education.

Posterior descending artery (PDA): an artery running in the posterior interventricular sulcus to the apex of the heart where it meets with the left anterior descending artery.

Premature ventricular contraction (PVC): extra heartbeats that begin in one of your heart’s two lower pumping chambers (ventricles).

Pulmonary artery (PA): artery delivering blood from the right ventricle to the lungs.

Pulmonary artery systolic pressure (PASP): pressure within the pulmonary arteries during right ventricular systole.


PAGE 5

Pulmonary capillary wedge pressure (PCWP): indirect estimate of left atrial pressure (LAP) measured by wedging a pulmonary catheter with an inflated balloon into a small pulmonary arterial branch.

Pulmonary embolism (PE): blockage of one of the pulmonary arteries in your lungs.

Pulmonary function testing (PFT): noninvasive tests that measure lung volume, capacity, rates of flow, and gas exchange.

Pulmonary rales: also referred to as crackles, popping or rattling sounds caused by the “popping” open of collapsed alveoli from fluid or poorly ventilated areas of lung tissue.

Rating of perceived exertion (RPE): scale used to measure the intensity of exercise, either 0–10 or 6–20

Red blood cells (RBC): cells that carry oxygen and carbon dioxide in the blood.

Renin angiotensin-aldosterone system (RAS or RAAS): a hormone system that regulates blood pressure, fluid, electrolyte balance as well as systemic vascular resistance in response to central nervous system stimulation or low blood pressure.

Restrictive lung disease (RLD): a group of lung diseases which prevent the lungs from fully expanding during inhalation.

Right coronary artery (RCA): heart artery that supplies blood to the right ventricle, the right atrium, and the SA (sinoatrial) and AV (atrioventricular) nodes.

Right ventricle (RV): heart chamber below the right atrium responsible for pumping blood to the lungs.

Right ventricle systolic pressure (RSVP): pressure created in the right ventricle during right ventricular. systole.

Room air (RA): medical acronym for room air.

S1: normal heart sound heard during chest auscultation that reflects closure of the mitral valve and marks the end of ventricular diastole.

S2: normal heart sound heard during chest auscultation that reflects closure of the aortic valve and marks the end of ventricular systole.

Saphenous vein graft (SVG): bypass graft derived from harvesting a portion of the saphenous vein.

Single point cane (SPC): cane that has only one tip.

Sinoatrial node (SA): small body of specialized muscle tissue in the wall of the right atrium of the heart that acts as a pacemaker by producing a contractile signal at regular intervals.


PAGE 6

6-Minute Walk Test (6MWT): assesses distance walked over 6 minutes as a sub-maximal test of aerobic capacity/endurance.

ST segment: section of the ECG between the end of the S wave (the J point) and the beginning of the T wave.

Stair to enter (STE): number of stairs to enter a home.

Systolic blood pressure (SBP): pressure in your arteries during the contraction of your heart muscle.

The international normalized ratio (INR): blood test that measures how well the body forms clots.

Transesophageal echocardiogram (TEE): alternative way to perform an echocardiogram. A specialized probe containing an ultrasound transducer at its tip is passed into the patient’s esophagus.

Transthoracic echocardiogram (TTE): most common type of echocardiogram, which is a still or moving image of the internal parts of the heart using ultrasound. In this case, the probe is placed on the chest or abdomen of the subject to get various views of the heart.

Tricuspid regurgitation: leakage of blood through the tricuspid valve into the right atrium during right ventricular systole.

2-Minute Walk Test (2MWT): assesses distance walked over two minutes as a sub-maximal test of aerobic capacity/endurance.

Ventricular assist device (VAD): also known as a mechanical circulatory support device — is an implantable mechanical pump that helps pump blood from ventricles to the rest of the body. It can support the left ventricle (LVAD), right ventricle (RVAD) or both ventricles (BiVAD).

Volume of oxygen (VO2): measurement of the amount of oxygen a person can utilize during intense exercise.

White blood cells (WBC): also called leukocytes, are an important part of the immune system. These cells help fight infections.


1

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MedBridge Treatment of Congestive Heart Failure in Outpatient Physical Therapy Settings

James Carlson, MPT, CCS

1. Ahmad FS, et. al. Incorporating patient centered factors into heart failure re-admission

risk prediction: a mixed methods study. American Heart Journal 2018 (200): 75-82. 2. Ahlund, K, et. al. Physical Performance Impairments and Limitations in Hospitalized

Frail Older Adults. J Geriatr Phys Ther. 2018 Oct/Dec;41(4):230-235. 3. Alexander KP. Walking as a Window to Risk and Resiliency. 2017 Aug; 136 (7): 644-

645. 4. Doletsky A, et. al. Interval training early after heart failure decompensation is safe and

improves exercise tolerance and quality of life in selected patients. European Journal of Preventive Cardiology 2018, 25 (1): 9-18.

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6. Lo AX, et. al. Impact of Gait Speed and Instrumental Activities of Daily Living on All-Cause Mortality in Adults ≥65 Years of Age with Heart Failure. Am J Cardiol. 2015 March; 115(6): 797–801.

7. Park CS, et. al. Characteristics, Outcomes, and Treatment of Heart Failure With Improved Ejection Fraction. J Am Heart Assoc. 2019 Mar 19;8(6):e011077. doi: 10.1161/JAHA.118.011077.

8. Pulignano G, et. al. Incremental Value of Gait Speed in Predicting Prognosis of Older Adults with Heart Failure. Insights from the IMAGE-HF Study. JACC: HEART FAILURE. 2016 April; 4 (4): 289-298.

9. Santos FV, et. al. Resistance Exercise enhances oxygen uptake without worsening cardiac function in patients with systolic heart failure: a systematic review and meta-analysis. Heart Fail Rev (2018) 23:73–89.

10. Shah AM, et. al. Heart Failure Stages Among Older Adults in the Community: The Atherosclerosis Risk in Communities Study. Circulation. 2017 January 17; 135(3): 224–240.

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12. Solomon SD, et al. Baseline characteristics of patients with heart failure and preserved ejection fraction in the PARAGON-HF trial. Circ Heart Fail. 2018 Jul;11(7): 1-10.

13. Taylor RS, et. al. Exercise-based rehabilitation for heart failure (review). Cochrane Database of Systematic Reviews 2014, Issue 4. Art. No.: CD003331. DOI: 10.1002/14651858.CD003331.pub4.


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14. Upadhya B, Haykowsky MJ, Eggebeen J, Kitzman DW. Exercise intolerance in heart failure with preserved ejection fraction: more than a heart problem. Journal of Geriatric Cardiology (2015) 12: 294−304.

15. Ward, RE, et. al. Functional Performance As a Predictor of Injurious Falls Among Older Adults. J Am Geriatr Soc. 2015 February ; 63(2): 315–320.

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