reducing heart failure hospital readmissions: are you prepared?
DESCRIPTION
Reducing Heart Failure Hospital Readmissions: Are You Prepared?. Lois Ustanko , RN, MHA Director of Health Ministries, Sanford Health Fargo Victoria Teske, MS GNP-BC Assistant Professor Minnesota State University Moorhead Nurse Practitioner Long Term Care Sanford Health - PowerPoint PPT PresentationTRANSCRIPT
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