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
GERO Nursing Conference
April 11, 2014
Behavioral Objectives
1. 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?
Source: AHCA
35%
Home
19%
Transitional
Hospital
SNF
Assisted
Living
23%
ER
Nursing
Home
Death
20%
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” Care
Retrospective Study of Medicare Beneficiaries Who Died, Mean Age of 82.3 Years
% with Hospitalization
in Last 90 Days of Life
70
2000
65
2005
60
2009
55
% with ICU & Ventilation
in Last 30 Days of Life
40
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
2000
% with Hospice Stay of
< 3 Days
10
5
2000
2005
2009
0
% with NH Stay in Last
90 Days of Life
45
2000
20
2005
2005
0
2009
2009
ICU
Ventilator
40
Source: Teno et al, 2013
Higher Per Capita Spending Doesn’t
Translate into Higher Life Expectancy
Hospital Readmissions Reduction Program (HRRP)
$4500
United States
77 yrs.
Cuba
$400
Source: 2006 CIA Fact Book
http://www.santarosaconsulting.com/santarosateamblog/post/2012/03/29/an-early-look-at-hospitalreadmissions-reduction-program
It Takes a Village
Being an active team member is required
in this era of pay for performance.
Key Areas:
1. Patient education with Teach Back
2. Multidisciplinary rounds (bedside is best)
3. Post discharge follow up-medical homes
4. Early follow up-timely appointments
5. Medication reconciliation
6. Proactive thinking-treat symptoms early
Changing Paradigms
Traditional 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 Elements
Cross-Continuum Team Collaboration
Identify those at risk
Nursing competencies
Case reviews
Health Information Exchange & Shared Care Plans
Medication reconciliation
Nursing home capabilities
Telehealth
S-BAR for status change reports
Access to the EMR
Shared CHF patient education materials
Patient and Family Engagement
Advance care planning
Medical homes
INTERACT
Communication
Tools
Decision
Support
Tools
Go tohttp://www.interact2.net/tools.html
Advance Care
Planning
Tools
Quality
Improvement
Tools
Heart Failure is a Chronic, Progressive Illness
Signs of Transition to End-Stage HF
End-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:


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.



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
So how are we doing?
22%
30 Day Readmission Rate-Trends from SNFs
20%
18.6%
18.6%
18.6%
18.5%
18.4%
18.3%
18.2%
18.1%
17.9%
18%
15.9%
15.9%
15.9%
16.2%
16.0%
16.2%
16.1%
15.9%
15.6%
16%
15.3%
14%
15.7%
15.9%
15.9%
17.7%
15.1%
15.7%
15.0%
14.7%
15.1%
14.5%
14.2%
12%
10%
MAR 2011
JUN 2011
SEP 2011
DEC 2011
MAR 2012
JUN 2012
SEP 2012
DEC 2012
MAR 2013
1-Year Period Ending
SANFORD MEDICAL CENTER FARGO
North Dakota
United States
JUN 2013
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.
 Clinical
syndrome of:
◦ Decreased exercise
tolerance
◦ Fluid retention
 Due to structural heart
disease

Cardiac output = the amount of blood the heart is

Stroke volume = the amount of blood the heart

Peripheral vascular resistance (PVR) = resistance
able to pump in 1 minute (Normal range
approximately 5 liters)
pumps with each contraction
encountered in all vessels
◦
◦
◦
◦
◦
◦
Affected by:
Radius of arteries
Blood viscosity
Blood volume
Aortic valve
Pulmonic valve
 Cardiac
Output = Stroke Volume x
Heart Rate
 Mean
Arterial Blood Pressure =
Cardiac Output x Peripheral Vascular
Resistance (PVR)
Systole
Diastole

Alteration in pressures of the
vascular system
◦ Hemodynamics

Perception of decreased
blood volume
◦ Neurohumoral mechanisms
Not 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:

Blood pressure measurement and palpating a pulse
reflect degree of stability

Basically getting the blood where it needs to go!
◦ Preload (volume, stretch)
◦ Afterload (resistance)
Force that stretches muscle fibers of a resting
heart – how much they are stretched just
prior to contraction
• What determines stretch?

1. The amount of blood present in R & L atria
2. Condition of the myocardium
• The greater the volume of blood in the heart
the greater the preload
• Blood volume ↑→ muscle stretches → stroke
volume ↑……….up to a point!
 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


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)
 Affected
by:
◦ Preload
 Stretch
 Volume
◦ Afterload
 Resistance
Cove
r-up
this





Hypotension (doesn’t occur initially)
Tachycardia
Cool, clammy skin
Decreased urine output
Alteration in mental status
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 of
decreased blood volume




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
Renin excreted by kidney in response to
1.
2.
3.
4.
decrease in BP
sympathetic stimulation
decreased serum sodium (Na+)
decreased renal blood flow






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




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

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
Right Heart Failure
Causes
Left HF, COPD (cor
pulmonale), PE, RV
infarction, pulmonary
HTN
Pathophysiology
Output of RV <
venous return →
venous congestion
and decreased output
to lungs
Left Heart Failure
Causes
MI, HTN, AR, AS,
cardiomyopathy
Pathophysiology
Decreased cardiac output

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

Dyspnea
◦ Ask many questions
◦ Any activities you’ve stopped doing? Any modifications
by caregiver?




Cough
Orthopnea
Paroxysmal Nocturnal Dyspnea
Dyspnea on exertion (DOE)
Class
Patient Symptoms
Class 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.

Inspection
◦ Respiratory rate
◦ Use of accessory muscles





Auscultation
Percussion
O2 saturation
Mentation
Decline in function/self compensation
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 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

Assesses underlying tissue

Normal is resonance

Hyperresonance –
hyperinflation (emphysema,
pneumothorax, asthma)

Dullness or flatness(atelectasis, pleural
effusion, pneumothorax,
consolidation)
◦ Bilaterally
◦ Superior to inferior





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)
Normal
S3
S4



Occurs during diastole
◦ Reflects ventricular filling
◦ Heard immediately after S2
◦ Heard best with bell
Ventricular gallop
Myocardial failure, volume
overload



S3
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
S4


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
Jugular Venous Pressure
(Distension)





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






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
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





Peripheral Pulses
Color, Capillary Refill
Skin Temperature
Renal Output
Mentation

Vasoconstriction leads to:
◦
◦
◦
◦

Cool, clammy or dry skin
Cyanosis
Slow capillary refill
Decreased peripheral pulses
Pulse Amplitude
0=Absent
1+=Thready/Weak
2+=Normal
3+=Increased
4+=Bounding
 Decreased
oxygenation of brain
◦ Lethargy
◦ Confusion
◦ Restlessness
◦ Insomnia
◦ Poor mental concentration

Decreased perfusion leads to:
◦
◦
◦
◦
◦
◦
Activation of renin angiotensin aldosterone system
Antidiuretic hormone release
Decreased urine output
Fluid retention
Dark, concentrated urine
Increased BUN, creatinine






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








Orthostatic hypotension
Falls
Dry lips, mouth
Tachycardia
Hypotension
Thirst (blunted in elderly)
Weight loss
Increased BUN creatinine ratio (>20:1)


Brain natrurietic peptide (BNP) –? correlation with ↑
heart failure, better for long term monitoring
Sodium
◦ ↑in fluid volume deficit
◦ ↓In fluid volume excess

Potassium

BUN/Creatinine

Hemoglobin/hematocrit
◦ Loss associated with diuretics, aldosterone release
◦ Spironolactone, ACE inhibitors ↑
◦ Affected by medications, fluid volume status, ↓ cardiac
output
◦ ↑in fluid volume deficit
◦ ↓In fluid volume excess

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

Respiratory rate
◦ Stroke volume x heart rate = Cardiac output
◦ Too low cardiac output drops
◦ Too high, ventricular filling time decreases → ↓
stroke volume
 Dyspnea
 Crackles
 Peripheral
Edema

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)
Need multiple
assessment approaches
Angiotensin Converting Enzyme Inhibitors
Angiotensin Receptor Blockers
Beta Blockers
Diuretics
Others……….




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)
 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






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



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
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)
Potassium
sparing
Loop diuretics
Thiazides
 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





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)
 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)






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

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

Increased risk of arrhythmias and sudden death
◦
◦
◦
◦
◦
◦

Underlying structural disease
Mechanical factors
Neurohormonal factors
Electrolyte abnormalities
Ischemia
Drugs
Antiarrhythmic
 Effective for both atrial and ventricular dysrhythmias
 Serious 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
$$$$$$$$$
Teaching Plan
End 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
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

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 years
Sayers, Riegel, Goldberg, Coyne, Samaha (2008)





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
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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