R EDUCING H EART F AILURE H OSPITAL R EADMISSIONS : A RE Y OU P REPARED ? 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? Hospital Transitional 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” Care Retrospective Study of Medicare Beneficiaries Who Died, Mean Age of 82.3 Years 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 $ yrs. Higher Per Capita Spending Doesn’t Translate into Higher Life Expectancy Hospital Readmissions Reduction Program (HRRP) Source: 2006 CIA Fact Book 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 Paradigms Traditional FocusTransformational Focus Immediate clinical needsComprehensive needs of the whole person Patients as recipients of carePatients 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 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

Cross-Continuum Team Collaboration Key Elements Health Information Exchange & Shared Care Plans Patient and Family Engagement Identify those at riskCase reviews Nursing competencies Medication reconciliationS-BAR for status change reports Nursing home capabilitiesAccess to the EMR Telehealth Shared CHF patient education materials Advance care planningMedical homes

I NTERACT Communicatio n Tools Decision Support Tools Advance Care Planning Tools Quality Improveme nt Tools Go tohttp://

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:  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.

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.

 Clinical syndrome of: ◦ Decreased exercise tolerance ◦ Fluid retention  Due to structural heart disease

 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

 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: ◦ 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!

 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.decrease in BP 2.sympathetic stimulation 3.decreased serum sodium (Na+) 4.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 FailureLeft 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 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)

ClassPatient 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 1Crackle 2Crackle 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 ◦ Bilaterally ◦ Superior to inferior  Normal is resonance  Hyperresonance – hyperinflation (emphysema, pneumothorax, asthma)  Dullness or flatness- (atelectasis, pleural effusion, pneumothorax, consolidation)

 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 S4 Normal

S3S4  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

Jugular Venous Pressure (Distension)

 Identify external (center of clavicle to angle of jaw) and internal (below sternocleidomastoid) jugular veins  Identify sternal angle  Elevate 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 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 ◦ 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

 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

 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)

Loop diuretics Thiazides Potassium 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

 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 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

 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