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Presented by: Bethany Westerfeldt RN, CCRN, MSN, NP-C, ANP, BC For WITNS October 13, 2012 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 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 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: 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 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 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) 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 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: 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 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 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 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 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 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 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 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 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 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 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 Lifestyle & monitoring OTC medications to stay away from: NSAIDS: ASA (high dose) ibuprofen naproxen Decongestants: Sudafed anything with ephedrine Most diet pills 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 Case study Sx not improved after steroidsabx 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 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. Treatment 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… Calls with SOB without weight gain Appetite poor Decreased activity tolerance Increased fatigue PND and orthopnea What to do next? 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? 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) 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 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? What questions do you want to ask her? What do you want to do with her? 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 Findings CXR shows pulmonary congestion TTE shows: 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 CXR What do you do next? Diurese Helps relieve symptoms Labs to evaluate lytes and renal function Can schedule for clinic visit Trend home monitoring data Thank you!
