Reducing Heart Failure Hospital Readmissions: Are You Prepared?

REDUCING HEART FAILURE HOSPITAL READMISSIONS:

ARE YOU PREPARED?Lois Ustanko, RN, MHA

Director of Health Ministries, Sanford Health Fargo

Victoria Teske, MS GNP-BCAssistant Professor

Minnesota State University MoorheadNurse Practitioner Long Term Care

Sanford Health

GERO Nursing ConferenceApril 11, 2014

Behavioral Objectives1. Describe a community-based approach to improve

coordination between care settings.2. Identify best practices that can be implemented to reduce

avoidable hospital readmissions.3. Describe the physiology and pathophysiology of heart failure.4. Discuss the clinical assessment and classifications of the

patient with heart failure.5. Discuss the indications, dosing, adverse effects, and

monitoring of drugs used to manage heart failure.6. Formulate effective teaching plans for patients with heart

failure and their family members.

Why is this important?

HospitalTransitional

SNF

ER

Home

Assisted Living

Nursing Home

Death

23%

35% 19%

20%

Source: AHCA

Boomers fear a medically intrusive dying process Communication among patients, their families,

and health care providers is often lacking Nurses have continuous contact with patients

and families during the last phase of life so have the potential to shift the focus

With the growing number of aging in the U.S. the need for competent end-of-life care increases

Experts Report “Burdensome” CareRetrospective Study of Medicare Beneficiaries Who Died, Mean Age of 82.3 Years

Series1404142434445

% with NH Stay in Last 90 Days of Life

200020052009

Series102468

10

% with Hospice Stay of < 3 Days

200020052009

Series155

60

65

70

% with Hospitalization in Last 90 Days of Life

200020052009

ICU Ventilator0

10

20

30

% with ICU & Ventilation in Last 30 Days of Life

200020052009

Transitions• Mean of 3.1

transitions in last 90 days

• 14.2% experienced a transition in the last 3 days of life

• 11.5% had > 3 hospital stays in last 90 days

Source: Teno et al, 2013

$400

$4500

77 yrs.

Higher Per Capita Spending Doesn’t Translate into Higher Life Expectancy

Hospital Readmissions Reduction Program (HRRP)

Source: 2006 CIA Fact Bookhttp://www.santarosaconsulting.com/santarosateamblog/post/2012/03/29/an-early-look-at-hospital-readmissions-reduction-program

United States

Cuba

It Takes a Village Being an active team member is required

in this era of pay for performance.

Changing ParadigmsTraditional Focus Transformational Focus

Immediate clinical needs Comprehensive needs of the whole person

Patients as recipients of care Patients and families as essential, active members of the care team

Varity of different teams based on setting of care

Cross continuum teams with a focus on the patient plan over time

Key Areas:1. Patient education with Teach Back2. Multidisciplinary rounds (bedside is best)3. Post discharge follow up-medical homes4. Early follow up-timely appointments5. Medication reconciliation6. Proactive thinking-treat symptoms early

Cross-Continuum Team Collaboration

Key Elements

Health Information Exchange & Shared Care Plans

Patient and Family Engagement

Identify those at risk Case reviewsNursing competencies

Medication reconciliation S-BAR for status change reportsNursing home capabilities Access to the EMRTelehealth Shared CHF patient education materials

Advance care planning Medical homes

INTERACT

Communication Tools

Decision Support

Tools

Advance Care

Planning Tools

Quality Improvemen

t Tools

Go tohttp://www.interact2.net/tools.html

Signs of Transition to End-Stage HFEnd-of-life care should be considered in patients who have symptoms at rest despite repeated attempts to optimize pharmacologic, cardiac device, and other therapies, as evidenced by 1 or more of the following: Multiple hospital admissions. Chronic poor quality of life with minimal or

no ability to accomplish activities of daily living.

Multiple implantable defibrillator shocks. Inability to control the heart failure with

standard medications. Need for continuous intravenous inotropic

therapy support to increase myocardial contractility.

Heart Failure Society of America

Heart Failure is a Chronic, Progressive Illness

Patients with heart failure report high symptom burden, including• Pain• Anxiety• Shortness of breath

Mortality rates can be as high as 30% once the patient presents to the ER multiple times.

MAR 2011 JUN 2011 SEP 2011 DEC 2011 MAR 2012 JUN 2012 SEP 2012 DEC 2012 MAR 2013 JUN 201310%

12%

14%

16%

18%

20%

22%

14.7%

15.3%15.7% 15.9% 15.9% 15.7%

15.0% 15.1%14.5%

14.2%

15.9% 15.9% 15.9% 16.2% 16.0% 16.2% 16.1%15.9%

15.6%15.1%

18.6% 18.6% 18.6% 18.5% 18.4% 18.3% 18.2% 18.1% 17.9% 17.7%

30 Day Readmission Rate-Trends from SNFs

SANFORD MEDICAL CENTER FARGO North Dakota United States

1-Year Period Ending

So how are we doing?

What does the future hold?

• Trained facilitators across the community for Advance Care Planning

• Increased use of technology used to complete assessments

• SNFists—physicians and/or Advance Practice Nurses whose whole practice focuses on SNF patients

• Shared competency training sessions with use of simulation and other approaches.

Reducing Heart Failure Admissions

Clinical syndrome of:◦Decreased exercise tolerance

◦Fluid retentionDue to structural heart disease

What is Heart Failure?

Cardiac output = the amount of blood the heart is able to pump in 1 minute (Normal range approximately 5 liters)

Stroke volume = the amount of blood the heart pumps with each contraction

Peripheral vascular resistance (PVR) = resistance encountered in all vessels◦ Affected by: ◦ Radius of arteries◦ Blood viscosity ◦ Blood volume◦ Aortic valve ◦ Pulmonic valve

Factors That Affect Blood Pressure

Cardiac Output = Stroke Volume x Heart Rate

Mean Arterial Blood Pressure = Cardiac Output x Peripheral Vascular Resistance (PVR)

Cardiac Output and Blood Pressure

Systole Diastole

Alteration in pressures of the vascular system

◦ Hemodynamics Perception of decreased

blood volume◦ Neurohumoral mechanisms

Pathophysiology of CHF

HemodynamicsNot just for the ICU nurse anymore!

Forces that affect circulating blood throughout the body and in and out of chambers of the heart

Relationship between: ◦Preload (volume, stretch) ◦Afterload (resistance)

Blood pressure measurement and palpating a pulse reflect degree of stability

Basically getting the blood where it needs to go!

Hemodynamics

Force that stretches muscle fibers of a restingheart – how much they are stretched justprior to contraction• What determines stretch?

1. The amount of blood present in R & L atria2. Condition of the myocardium

• The greater the volume of blood in the heartthe greater the preload• Blood volume ↑→ muscle stretches → strokevolume ↑……….up to a point!

Preload

Relationship between fiber stretch and contractile force

The more it is stretched in diastole (filling or resting) the harder it contracts in systole

If stretches too much, output decreases

Frank Starling Law of the Heart

Tension that ventricle must generate to overcome resistance to ejection

To open aortic valve and eject blood, left heart needs to overcome resistance of:◦ Peripheral vascular resistance (PVR)

(HTN)◦ Aortic Valve (Aortic stenosis)

Right heart must overcome resistance of:◦ Pulmonary vascular system (Hypoxemia)

Afterload

Affected by:

◦PreloadStretchVolume

◦AfterloadResistance

Cardiac Contractility

Cover-up this

“Perception of Decreased Blood

Volume”

Hypotension (doesn’t occur initially) Tachycardia Cool, clammy skin Decreased urine output Alteration in mental status

Symptoms of Shock

Heart (pump) failure→ cardiogenic shock• Increased preload, increased stretch

• Compensatory initially but if pressure increases too much stretch goes too far and stroke volume decreases

• CO = SV x HR• Overstretched LV → ↓ contractility → ↓SV → ↓ cardiac output → perception ofdecreased blood volume

Cardiogenic Shock

Occurs secondary to perception of decreased blood volume

Norepinephrine - vasoconstriction, increased contractility

Epinephrine – increased heart rate and increased contractility

Stimulates secretion of renin → activation of renin angiotensin aldosterone system

Activation of Sympathetic Nervous System (SNS) in Heart Failure

Renin excreted by kidney in response to 1. decrease in BP2. sympathetic stimulation

3. decreased serum sodium (Na+)4. decreased renal blood flow

Renin Angiotensin Aldosterone System

Renin Angiotensin Aldosterone System

Norepinephrine → Vasoconstriction ↑ BP (afterload), stimulates production of renin

Angiotensin II → ↑ BP (afterload)

Aldosterone (saves water and sodium, wastes potassium) → ↑ preload and afterload

↑ afterload → ↑ SVR (resistance the heart has to pump against)

↑ preload → ↑ stretch of ventricles (stretch too much)

WHOOPS → Cardiac Output even more

Perception of Decreased Blood Volume

Increases the blood pressure and heart rate Increases the resistance that the heart has

to pump against Increases the work of the heart Increases the volume that the heart has to

pump through the system

Perception of Decreased Blood Volume

Manifestations and Assessment of Heart

Failure

Cardiac◦ Increased workload leads to increased O2

consumption and angina◦ Decreased contractility leads to low output ◦ Tachycardia, dysrhythmias◦ Low output leads to low BP and decreased tissue

perfusion, lowered exercise tolerance◦ Jugular vein distention, increased CVP, systemic

edema

Clinical Picture of Heart Failure

Right Heart Failure Left Heart FailureCauses

Left HF, COPD (cor pulmonale), PE, RV infarction, pulmonary HTN

PathophysiologyOutput of RV < venous return → venous congestion and decreased output to lungs

Causes MI, HTN, AR, AS, cardiomyopathy

PathophysiologyDecreased cardiac output

Right and Left Heart Failure Symptoms

Decreased cardiac output from left ventricle →

Increased preload left heart →

Increased pressure in pulmonary vascular system →

Fluid moves from pulmonary capillaries into lung tissue → impaired diffusion of oxygen and carbon dioxide

Pathophysiology of Respiratory Manifestations

Dyspnea◦ Ask many questions◦ Any activities you’ve stopped doing? Any

modifications by caregiver? Cough Orthopnea Paroxysmal Nocturnal Dyspnea Dyspnea on exertion (DOE)

Respiratory Symptoms

Class Patient SymptomsClass I (Mild) No limitation of physical activity.

Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea

Class II (Mild) Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation or dyspnea

Class III (Moderate) Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea

Class IV (Severe) Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.

NYHA Classification of Heart Failure

Inspection◦ Respiratory rate◦ Use of accessory muscles

Auscultation Percussion O2 saturation Mentation Decline in function/self compensation

Respiratory Assessment

Crackles

Crackle 1 Crackle 2 Crackle 3

Continuous, high pitched, musical sound, almost a whistle

During inspiration or expiration Caused by high velocity air flow through

narrowed airway

Wheezes

Wheezes 1 Wheezes 2

Heart Failure- bibasilar crackles (can disappear with continuous exaggerated respiration), sounds with pleural effusion, wheezing

Lobar Pneumonia –crackles over one involved lobe, breath sounds

Asthma – scattered wheezes Pneumothorax – decreased or absent

breath sounds COPD – generally decreased or absent,

wheezes

Common Pulmonary Auscultation Abnormalities

Assesses underlying tissue◦ Bilaterally◦ Superior to inferior

Normal is resonance

Hyperresonance – hyperinflation (emphysema, pneumothorax, asthma)

Dullness or flatness- (atelectasis, pleural effusion, pneumothorax, consolidation)

Percussion of the Lungs

Cardiac Cycle: Normal S1S2Abnormal S3 & S4 Systole-diastole-systole-diastole Lub-dub-lub-dub S1-S2-S1-S2 (Normal) S1-S2S3-S1-S2S3 (S3) S1-S2-S4S1-S2-S4S1-S2 (S4)

S3 S4Normal

Extra Heart Sounds

S3 S4

Occurs during diastole

◦ Reflects ventricular filling

◦ Heard immediately after S2

◦ Heard best with bell Ventricular gallop Myocardial failure, volume

overload

Occurs During Diastole◦ Marks atrial contraction◦ Immediately precedes

S1◦ Heard best with the bell

Etiology – increased resistance to ventricular filling following atrial contraction

Hypertensive heart disease, CAD, cardiomyopathy

Produced by turbulent blood flow◦ Across partial obstruction◦ Increased blood flow through normal

structure◦ Flow into dilated chamber◦ Across stenotic or regurgitant valves◦ Shunting through abnormal passage

A systolic murmur of aortic stenosis

Cardiac Murmurs

Jugular Venous Pressure (Distension)

Jugular Venous Distension (JVD) Identify external

(center of clavicle to angle of jaw) and internal (below sternocleidomastoid) jugular veins

Identify sternal angle Elevate head @30-45

degrees Measure in cm distance

from sternal angle to top of distended vein (vertically)

Add to 5. Normal is 0-9 cm

Measurement of R CHF or fluid overload Bed at 30 degrees Press firmly on RUQ for 30-60 seconds Observe for increase in JVP > 1 cm rise is abnormal as heart can not

handle increase in venous return

Hepatojugular Reflux HJR)

Decreased blood supply leads to anorexia, N/V, slow digestion

Increased filtration pressure from increased preload, fluid volume overload → Abdominal distention, ascites, hepatosplenomegaly

Tenderness Protuberant abdomen Dullness to percussion Fluid wave

Gastrointesinal Assessment

Increase in capillary pressure Other causes include ↓ serum albumin, renal

disease, dependent position (resolves during the night)

Peripheral, sacral, scrotal, gastrointestinal tract Associated color changes Bilateral or unilateral

◦ 1+ Slight Pitting, no distortion◦ 2+ Somewhat deeper pit, no readily detectable distortion◦ 3+ Pit is noticeably deep, extremity looks fuller and swollen◦ 4+ Pit is very deep, lasts a while, extremity is grossly

distorted *Mosby, 2002

EDEMA

Peripheral Pulses Color, Capillary Refill Skin Temperature Renal Output Mentation

Assessment of Perfusion

Vasoconstriction leads to: ◦ Cool, clammy or dry skin ◦ Cyanosis ◦ Slow capillary refill ◦ Decreased peripheral pulses

Pulse Amplitude0=Absent

1+=Thready/Weak 2+=Normal 3+=Increased 4+=Bounding

Peripheral Vascular Assessment

Decreased oxygenation of brain◦Lethargy◦Confusion◦Restlessness ◦Insomnia ◦Poor mental concentration

Neurological Changes With Heart Failure

Decreased perfusion leads to:◦ Activation of renin angiotensin aldosterone

system◦ Antidiuretic hormone release◦ Decreased urine output◦ Fluid retention◦ Dark, concentrated urine◦ Increased BUN, creatinine

Renal System in Heart Failure

Same time Same clothes Monitor trends Reweigh PRN Concern for symptomatic weight loss –

HYPOVOLEMIA (dehydration) Changes in body weight not routinely associated

with dyspnea or edema, may not occur! ◦ Failure to monitor◦ Weight loss from cachexia◦ Diminished appetite due to ascites

Weights

Orthostatic hypotension Falls Dry lips, mouth Tachycardia Hypotension Thirst (blunted in elderly) Weight loss Increased BUN creatinine ratio (>20:1)

Fluid Volume Deficit

Brain natrurietic peptide (BNP) –? correlation with ↑ heart failure, better for long term monitoring

Sodium ◦ ↑in fluid volume deficit◦ ↓In fluid volume excess

Potassium◦ Loss associated with diuretics, aldosterone release◦ Spironolactone, ACE inhibitors ↑

BUN/Creatinine ◦ Affected by medications, fluid volume status, ↓ cardiac output

Hemoglobin/hematocrit◦ ↑in fluid volume deficit◦ ↓In fluid volume excess

Key Laboratory Results

Blood pressure◦ Goal is to reduce afterload and preload◦ Systolic “lowest tolerated” as low as 90 systolic◦ Need to maintain perfusion (head and kidneys)◦ Decreased BP

Hypovolemia?◦ Increased BP

Nonadherence? ↑SNS activity?

Heart rate◦ Stroke volume x heart rate = Cardiac output◦ Too low cardiac output drops◦ Too high, ventricular filling time decreases → ↓ stroke

volume Respiratory rate

Vital Signs

DyspneaCracklesPeripheral Edema

Most Common Clinical Features of Hospitalized Patients in Order (ADHERE, OPTIMIZE-HF)

Signs of hypervolemia may be absent in patients with worsening heart failure Miller, Frana, Rodriquez, Laule-Kilian, Perruchoud (2005)

Increased filling and intravascular pressures may be present before clinical manifestations Stevenson, Perloff (1989)

Volume overload frequently present in nonedematous patients Androne, Hryniewicz, Hudaihed, Mancini, Lamanca, Katz (2004)

Consider This…..

Need multiple assessment approaches

BOTTOM LINE………

Pharmacological Management of Heart

FailureAngiotensin Converting Enzyme InhibitorsAngiotensin Receptor BlockersBeta BlockersDiureticsOthers……….

Inhibit ACE → prevents angiotensin I from converting to angiotensin II

Angiotensin II is a potent vasoconstrictor (Blocked = total peripheral resistance)

Angiotensin II blocks release of nitric oxide (Blocked = total peripheral resistance)

Angiotensin II stimulates aldosterone production → sodium and water retention and potassium elimination (Blocked = ECF, hyperkalemia)

Angiotensin Converting Enzyme (ACE) Inhibitors

Decreases total peripheral resistance and extracellular fluid volume, also glomerular filtration pressure (renal protective)

Decreases preload and afterload Side effects – first dose hypotension,

(especially if on diuretics), hyperkalemia, cough, rash, angioedema

Captopril (Capoten), benazepril (Lotensin), enalapril (Vasotec), quinnapril (Accupril), lisinopril (Prinivil), quinapril (Accupril), others

Angiotensin Converting Enzyme Inhibitors

Block angiotensin II receptors Decreased preload and afterload Similar effects No cough, less hyperkalemia Angiotensin II also produced by pathways

that don’t involve ACE i.e. lungs- ARBs can completely block ALL activity.

Candesartan (Atacand), losartan (Cozaar), valsartan (Diovan) others

Angiotensin II Receptor Blockers

SNS activation → effects of norepinephrine and epinephrine → increase heart rate, vasoconstriction, contractility and renin release

Block that response Non selective

Propanolol (Inderal) Carvedilol (Coreg) (also alpha 1 blocker) Labetalol (Normodyne, Trandate) also alpha 1

Selective Metoprolol (Lopressor, Toprol) Sustained release metoprolol (Toprol XL) Atenolol (Tenormin) Bisoprolol (Zebeta)

*Approved for use in heart failure

Beta Blockers

Heart failure, asthmatics, and diabetics

5 classes Loop diuretics Thiazides Osmotics Potassium sparing Carbonic anhydrase inhibitor (weak)

Block reabsorption of sodium and water ↑ urine output extracellular fluid volume Decreased preload

Amount of solute as filtrate flows through nephron

The earlier the site of action the greater the diuresis (more solute to work with so they make more of an impact)

Diuretics

Loop diuretics

ThiazidesPotassium sparing

Loop diuretics Most effective even when renal blood flow and creatinine

clearance Block reabsorption of sodium and chloride in loop of Henle Furosemide (Lasix), bumetanide (Bumex), torsemide

(Demadex) Also increases urinary excretion of potassium, magnesium,

calcium If not responding to high dose Lasix (400 mg) GI absorption

may be impaired due to congestion, torsemide better absorbed.

Adverse Effects Dehydration Hypotension Hypokalemia, hypomagnesemia, hypocalcemia,

hyponatremia Otoxtoxicity

Loop Diuretics

Thiazides Block reabsorption of sodium and water in

the early segment of the distal convoluted tubule

Questionably effective if creatinine clearance <30 ml/min

Side effects similar to loop diuretics except for one thing…they urinary excretion of calcium

Hydrochlorathiazide (HydroDIURIL) Thiazide types – metolazone, others

Aldosterone antagonist Looses sodium and water, saves

potassium Works in the distal nephron Delayed response, up to 48 hours Advanced heart failure Decreased preload

Adverse effects Hyperkalemia – caution with other

drugs that save potassium (ACE inhibitors)

Spironolactone (Aldactone)

Dilation of arterioles (not veins) Decrease afterload Very little orthostatic hypotension Side effects reflex tachycardia, renin release

and fluid retention Beta blocker for tachycardia Diuretic for fluid retention

Hydralazine (Apresoline) Minoxidil Nitroprusside (arterial and venous dilation)

Direct Arterial Vasodilators

Isosorbide, nitroglycerine Decrease oxygen demand by dilating veins,

which decreases preload Used for angina Combined with hydralazine for advanced

heart failure, ACEI intolerance (BiDil) Side effects headache, reflex tachycardia,

hypotension Tolerance

Nitrates

Digoxin Actions

Positive inotrope (stronger contractions) Lowers heart rate

Adverse Effects Dysrhythmias (risk ↑ with hypokalemia) Bradycardia (pulse monitoring) GI symptoms (N & V, anorexia) Renal elimination Narrow margin of safety

Follow levels

Amiodarone (Cordarone, Pacerone) Increased risk of arrhythmias and sudden death

◦ Underlying structural disease◦ Mechanical factors◦ Neurohormonal factors◦ Electrolyte abnormalities◦ Ischemia◦ Drugs

AntiarrhythmicEffective for both atrial and ventricular dysrhythmiasSerious toxicities

Half life 25-110 days Highly lipid soluble, accumulates in liver and lungs Pulmonary toxicity (10% risk mortality), heart failure, AV

Block, corneal microdepositis, hepatitis, neurological changes

Multiple drugs Other comorbidities Interactions Diuretics $$$$$$$$$

Challenges of Medication Adherence

Final ThoughtsTeaching PlanEnd of Life

Change in eating habits, environment New cook Medication adherence Increased thirst (fluid intake) Use of NSAIDS Worsening comorbidities

◦ COPD, renal disease, DM Economic issues Cognition Depression Anxiety Health literacy Number of providers

Assess Factors Contributing to Exacerbation

INDIVIDUALIZED APPROACH TO CARE AND TEACHING PLAN

Individualized approach◦ Consider exacerbation history, what went wrong?◦ Consider support system◦ Plans for follow up

Parameters for weights, blood pressures, pulse Fluid restriction? Diet Information about medications Consider medication taking behaviors

◦ Daily routine◦ Missed medication

Assess understanding

Effective Teaching Plan

Patients with any 3 (orthopnea, edema, weight gain, need for ↑ diuretic dose and JVD) 4-6 weeks post discharge → ◦ 2 year mortality ↑ x 3

Lucas, Johnson, Hamilton, et al. (2000) Number of clinical exacerbations (two or

more of ↑ edema, dyspnea, orthopnea, PND, JVD, weight) → ◦ Poor quality of life, decreased function and

exercise tolerance, increased mortality 2 yearsSayers, Riegel, Goldberg, Coyne, Samaha (2008)

Prognosis

Multiple hospitalizations for exacerbations risk for ↑ mortality

Medications limited by side effects (*renal function)

Consider quality of life Education of client and support system Plan in place

End of Life

Heart failure is a syndrome that presents with alterations in hemodynamics and maladaptive responses of the sympathetic nervous system

Signs and symptoms include those of diminished cardiac output and tissue congestion

Multiple approaches to assessment are necessary to accurately identify acute decompensation

The medication regimens for heart failure patients are effective but adherence is crucial

Teaching plans should be holistic, consider each clients specific situation

Heart failure exacerbations associated with decreased quality of life, increased mortality therefore addressing palliative and end of life care needs to be addressed following multiple hospitalizations

Summary