1. Heart Failure in the Transplant Patient
Presented by:
Bethany Westerfeldt RN, CCRN, MSN, NP-C, ANP, BC
For WITNS
October 13, 2012

2. Objectives 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

4. 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

5. Types of Heart Failure: Diastolic dysfunction
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

6. Heart Failure Classifications:
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

7. ACC/AHA classification

8. Therapeutic Goals: 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

9. Transplant population:
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)

14. 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

17. 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

20. Prevalence of specific signs & symptoms in systolic & diastolic HF

21. Signs & Symptoms 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

22. Clinical signs: 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

23. Clinical signs 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

24. 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

25. 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

27. 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

28. Characteristics of Outpatient Diastolic HF
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

29. Diastolic Dysfunction
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

30. Diastolic Dysfunction Diagnostic Criteria
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

31. Treatment of Diastolic HF
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

32. Treatment of DHF 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

33. Treatment DHF 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

34. Treatment of DHF
Look at underlying disease processes contributing to DHF & choose drug combinations to combat them
Eg: Diabetic elderly female
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

35. Patient self care at home: systolic & diastolic HF
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:
SOB or decreased activity tolerance
Increased fatigue, unable to sleep lying down
Swelling of ankles or abdomen
Frequent colds
Decreased urination, increase in weight

36. Pt. care at home: 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

37. Lifestyle & monitoring
OTC medications to stay away from:
NSAIDS:
ASA (high dose)
ibuprofen
naproxen
Decongestants:
Sudafed
anything with ephedrine
Most diet pills

38. Case Study
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

39. Case study 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?

40. Case study CXR shows cardiomegaly, pulmonary congestion
12 lead ecg shows NSR
no evidence of acute MI
normal voltage
TTE shows
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.

41. Treatment If possible: Start or increase ACE inhibitor or ARB Diurese
Once near euvolemic
Start or increase beta blocker (preferably carvedilol or metoprolol succinate)

42. 6 months later… Calls with SOB without weight gain Appetite poor
Decreased activity tolerance
Increased fatigue
PND and orthopnea

43. What to do next? Assess over the phone: Labs:
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

44. What do you do next?
Most likely, increased renal indices from volume overload
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)

45. Case study 2
78 yo female s/p OH Tx ‘02 presents with progressive SOB, weight gain
longstanding hx htn
obesity
swelling of her legs
bloating over past couple of months
Hx reveals:
poorly controlled BP for past 45 yrs
sedentary lifestyle
no DM
hypothyroid
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”

46. What do you suspect? What questions do you want to ask her?
What do you want to do with her?

47. Case Study 2 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

48. Findings CXR shows pulmonary congestion TTE shows: BNP elevated to 528
concentric LV hypertrophy
abnormal E/a ratio (diastolic filling)
LVEF 75%
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

49. CXR

50. What do you do next? Diurese Labs to evaluate lytes and renal function
Helps relieve symptoms
Labs to evaluate lytes and renal function
Can schedule for clinic visit
Trend home monitoring data

51. Thank you!