Heart Failure in the Transplant Patient

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Transcript Heart Failure in the Transplant Patient

Presented by:
Bethany Westerfeldt RN, CCRN, MSN, NP-C, ANP,
BC
For WITNS
October 13, 2012
Objectives
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 1. Discuss types of Heart Failure
 LV systolic dysfunction
 HF with preserved LV systolic function (HFpEF) aka diastolic
dysfunction
 2. Discuss brief pathophysiology of Heart Failure
 3. Assessment of Heart Failure
 4. Treatments of Heart Failure
Types of Heart Failure:
Systolic Dysfunction

 Many etiologies:
 Most common etiologies: CAD, HTN, DM, substance
abuse(cocaine, alcohol), chemo, peripartum, uncontrolled
tachycardia, viral, valvular heart disease, severe illness
 Affects cardiac output or quantity of blood pumped to rest
of body
 Can be improved or controlled with medication and
lifestyle changes
 Frequency of diagnosis increases with age, more prevalent
after age 65 though affects pts at any age point
 Syndrome of neurohormonal activation affecting many
body systems
Types of Heart Failure:
Diastolic dysfunction
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 Defined as HF with preserved LV systolic function (normal
LVEF) or EF more than 40%
 LV often with hypertrophy, concentric remodeling with
increased extracellular matrix, abnormal relaxation and
filling, decreased diastolic dispensability
 Shares activation of neurohormonal activation with systolic
dysfunction
 Prevalence: 40-50% of all pts diagnosed with HF, often
seen in conjunction with systolic dysfunction
 More commonly in elderly, females and pts with
hypertension
Heart Failure
Classifications:
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1.
2.
3.
4.
New York Heart Association (NYHA) functional
classification of HF:
No limitations of physical activity, no symptoms with
ordinary activity
Slight limitation, symptoms with ordinary activities
Marked limitation, symptoms with less than ordinary
activities
Severe limitation, symptoms of HF at rest
ACC/AHA classification
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Therapeutic Goals:
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 Prolong life
 Slow/reverse cardiac remodeling
 Reduce visits and admissions to hospital
 Improve overall functional capacity and quality of life
 Reduce dyspnea and fatigue
 Control/minimize edema and fluid retention
Transplant population:
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 At risk for conditions the increase HF risk (both types):
 Hypertensive disease, DM, sleep apnea and CAD
 Antirejection meds that increase BP, renal disease, risk DM
 Solid weight gain: risk for DM, HTN, sleep apnea, atrial
arrhythmias
 Preexisting conditions:
 Limiting activity: Gout, arthritis/DJD, other musculoskeletal
disorders, obesity
 Structural heart disease: valve disorders, storage diseases
(amyloid, hemochromatosis, saroidosis)
CKD and CV disease:

 Known high risk of development of CVD in pt. with HTN
 Systolic BP more significant than DBP on CV all cause
mortality
 Pulse pressure (SBP minus DBP)
 Independent predictor of MI, HF and CV death
 Reflects stiffness larger arteries
 Increases with advancing age from 50 yr. on up
 Reliable prognostic factor for mortality CKD
 Pts on HD or renal transplant patients
Neurohormonal effects of
Heart Failure

 SNS activity: “whipping a dying horse”-the catecholamine
stimulation
 Stimulation of Alpha 1 & Beta 1&2 receptors
 Increases cardiac output by increasing heart rate& stroke
volume
 Prolonged stimulation leads to myocyte hypertrophy, dilation,
ischemia, arrhythmias, deterioration and death of cardiac
cells
 Activates Renin-Angiotensin-Aldosterone System (RAAS)->
(further) vasoconstriction & sodium retention
Prevalence of specific signs &
symptoms in systolic & diastolic HF

Signs & Symptoms
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 Dyspnea & fatigue
 Limitation of exercise
tolerance
 Fluid retention-may lead
to pulmonary edema
 PND & orthopnea
 Cough, can be primarily
nocturnal
 Poor appetite
 Early satiety & bloating
 Chest pain: not always in
pts with CAD
 Palpitations
 Lightheadedness
 Especially positional
 Edema, ascites, anasarca
 Poor sleep quality
 Difficulty thinking clearly,
or concentrating
 These abnormalities can
impair functional capacity
& quality of life
Clinical signs:
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 Increased adrenergic activity
 peripheral vasoconstriction (cool extremities)
 pallor &/or cyanosis of digits
 diaphoresis
 tachycardia
 loss of normal sinus rhythm
 distention (obvious) of peripheral veins due to
vasoconstriction (prominent JVD)
 narrowed pulse pressure
Clinical signs
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 Pulmonary rales & /or wheezes:
 usually an acute heart failure finding
 Chronic HF pts mobilize pulm fluid into lymph nodes:
 are enlarged on x-ray & CT
 JVD: indication of right atrial pressure (preload)
 Normal JVD is under 10 cm
 HJR: compression over liver causes distention of JVD further
 Indicates congested abdomen/liver and/or inability of right
heart to accept or eject the transiently increased volume
LV systolic dysfunction

 Ischemic: CAD is the cause of approximately 2/3 of
pts LV dysfunction
 Remodeling: change in tissue & geometry of LV
 Neurohormonal changes:
 affect endothelium of vessels as well as cardiac muscle with
deposition of fibrinous material
 alters contraction and electrical pathways of myocardium
 Neurohormonal activation of Renin-Angiotensin-Aldosterone
system & Norepinephrine
 Down-regulation of alpha, beta 1 & beta 2 adrenergic
receptors
Treatment of Systolic HF

Diuretics, ACE-Inhibitors, Beta blockers, Digoxin,
Aldosterone blockers, Vasodilators & IV Inotropic
agents
 Value of these agents shown in multiple clinical trials
 Shown to decrease symptoms & increase length/quality of
life
Diastolic Dysfunction

 Abstracted charts from 37,500 Medicare pts from
National Heart Failure Project database
 Only 57% of pts had LV fxn assessed
 Of 19,710 pts with documented EF, 1/3 had EF> 50%
 This group was 79% women with mean age of 79.7 yrs
Characteristics of Outpatient
Diastolic HF
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 Overwhelmingly female (85%) & elderly(70 yo)
 Marked increase in LV mass/volume ratio
 Higher BMI
 More likely to have HTN
 Exercise limitation similar to systolic HF pts
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Diastolic Dysfunction
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Increased myocardial stiffness
Ventricular interaction or pericardial restraint
Abbreviated LV filling time
Multifactorial: thyrotoxicosis, AV fistula, beriberi
Volume overload stress
Obesity
Impaired LV relaxation
Myocardial ischemia
Hypertrophy
Systolic dysfunction
DM
Hypothyroidism
Diastolic Dysfunction
Diagnostic Criteria
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 Required criteria:
 Normal EF (> 50%)
 Clinical Evidence of Heart Failure
 Framingham of Boston Criteria
 Plasma BNP &/or chest x-ray
 Cardiopulmonary exercise testing
 Confirmatory Criteria:
 LVH or Concentric Remodeling
 Left Atrial Enlargement (in absence of AF)
 Echo Doppler or Cath Evidence of Diastolic Dysfunction
 Exclusions: Non-Myocardial Disease
Treatment of Diastolic HF
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 Class I
 Control systolic & diastolic BP
 Control ventricular rate in AF
 Use diuretics to control edema
 Class IIA
 Coronary revascularization
 Class IIB
 Restore & maintain NSR
 Beta blocker, ACE-I, ARB, Calcium antagonists, digitalis
Treatment of DHF
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General approach:
Symptom reduction
 Control blood pressure
 Decrease circulating volume
 Salt & fluid restriction
 Diuretics
 Nitrates
 Neurohormonal blockade (ACEI/ARB)
 Treat tachycardia
 Increase duration of diastole (slow HR) in select pts
 Maintain synchronous atrial contraction
Treatment DHF
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Lifestyle modification & education
Salt & fluid restriction
Exercise program
Other dietary concerns
Weight control
Target underlying mechanisms
Drugs:
 that improve calcium homeostasis
 blunt hormonal activation
 prevent & regress fibrosis are in existence or
development
Treatment of DHF
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 Look at underlying disease processes contributing to DHF &
choose drug combinations to combat them
 Eg: Diabetic elderly female
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Angiotensin blocking drug
Diuretic
beta blocker
CCB if resting HR>70.
 Most often requires antihypertensive
 Lots of trial & error to finding right combination of meds
that minimize symptoms & side effects
Patient self care at home:
systolic & diastolic HF
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 Weigh daily
 same time
 same clothing amount
 Report daily gain of >3 lbs. or overall >5 lbs.
 Low salt diet (2 grams)
 Take all meds as prescribed
 Report any side-effects or problems with meds
 Know symptoms of HF & report worsening:
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SOB or decreased activity tolerance
Increased fatigue, unable to sleep lying down
Swelling of ankles or abdomen
Frequent colds
Decreased urination, increase in weight
Pt. care at home:
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 Participate in regular exercise & stress reduction
 Plan daily activities in advance to conserve energy
 Plan strategies to help reduce fatigue:
 delegate jobs
 take naps or rest periods
 Withdrawal of meds known to affect clinical status:
 NSAIDS
 antiarrhythmic
 most calcium channel blockers
Lifestyle & monitoring
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OTC medications to stay away from:
NSAIDS:
 ASA (high dose)
 ibuprofen
 naproxen
Decongestants:
 Sudafed
 anything with ephedrine
Most diet pills
Case Study
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 44 yo male, previous hx DM and DD renal tx ‘05, no
known CAD (negative stress prior to tx)
 Presents with 4-6 wk hx progressive DOE, weight gain,
decreased appetite, cough that worsens at night
 States he’s having hard time at work, carries 60 lb. bags &
other equipment road construction
 Believes he has “bad cold”, treated by PCP for
bronchitis/pneumonia without relief of symptoms
Case study
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 Sx not improved after steroidsabx
 History reveals change in appetite, bloating, PND-wakes
up after 2 hrs coughing, sits on side of bed or walks
around
 Reports chest “soreness”, mid sternal area, no radiation, no
palpitations, no diaphoresis, n/v
 What would you suspect?
 What would you do next?
Case study
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 CXR shows cardiomegaly,
pulmonary congestion
 12 lead ecg shows NSR
 no evidence of acute MI
 normal voltage
 TTE shows
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LV systolic dysfunction
LVEF 25%
moderately dilated RA & LA
normal RV function
LVEDD 65 mm (nl= 56)
no thrombus
 Labs: lytes wnl, bun/cr:35/1.8, t
bili 1.6, ast 66, alt 94, TSH 8.7
with normal fT4, TT3.
Treatment
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 If possible:
 Start or increase ACE inhibitor or ARB
 Diurese
 Once near euvolemic
 Start or increase beta blocker (preferably carvedilol or
metoprolol succinate)
6 months later…
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 Calls with SOB without weight gain
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Appetite poor
Decreased activity tolerance
Increased fatigue
PND and orthopnea
What to do next?
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 Assess over the phone:
 What brings on SOB/activity limitations
 Assess for edema
 Other symptoms:
 chest discomfort
 palpitations
 Early satiety, bloating, nausea…
 Labs:
 Creatinine rise from 1.4 to 1.8
 BUN rise from 28 to 36
 Serum potassium 3.6, sodium 130
What do you do next?
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 Most likely, increased renal indices from volume overload
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Diurese, based on symptoms and labs
Leave ACE-I unchanged
F/u labs in 3-7 days
If equivocal, get pt to be assessed in clinic
TTE can be done in pts difficult to assess volume status
Can always schedule for RH cath (may need anticoag
management in pts on warfarin)
Case study 2
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 78 yo female s/p OH Tx ‘02 presents with progressive SOB,
weight gain
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longstanding hx htn
obesity
swelling of her legs
bloating over past couple of months
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poorly controlled BP for past 45 yrs
sedentary lifestyle
no DM
hypothyroid
 Hx reveals:
 States she’s been sleeping in her husband’s recliner for past 3
weeks
 sleep quality poor r/t fatigue
 poor quality of life “unable to do anything”
What do you suspect?
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What questions do you want to ask her?
What do you want to do with her?
Case Study 2
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Physical exam:
JVP elevated to 15 cm above RA
No scleral icterus
Oropharynx pink, moist
Lungs with few basilar crackles & wheezes
Abdomen soft, obese; Liver WNL
Extremities +2 to knees bilaterally
Blood pressure: 178/92
Findings
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 CXR shows pulmonary congestion
 TTE shows:
 concentric LV hypertrophy
 abnormal E/a ratio (diastolic filling)
 LVEF 75%
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BNP elevated to 528
lytes normal
creatinine 2.4
LFT’s normal
12 lead ecg shows:
 increased voltage in precordial leads ( LV hypertrophy)
 NSR
 Left heart cath with minor luminal irregs
 RHC with elevated PCWP, RA,RV and PA pressures
CXR
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What do you do next?
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 Diurese
 Helps relieve symptoms
 Labs to evaluate lytes and renal function
 Can schedule for clinic visit
 Trend home monitoring data
Thank you!
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