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 • Describe a community-based approach to improve coordination between care settings. • Identify best practices that can be implemented to reduce avoidable hospital readmissions. • Describe the physiology and pathophysiology of heart failure. • Discuss the clinical assessment and classifications of the patient with heart failure. • Discuss the indications, dosing, adverse effects, and monitoring of drugs used to manage heart failure. • Formulate effective teaching plans for patients with heart failure and their family members.
Why is this important? Source: AHCA 35% Home 19% Hospital Transitional SNF Assisted Living 23% ER Nursing Home 20% Death
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” CareRetrospective 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
Higher Per Capita Spending Doesn’t Translate into Higher Life ExpectancyHospital 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-hospital-readmissions-reduction-program
It Takes a Village Being an active team member is required in this era of pay for performance. Key Areas: • Patient education with Teach Back • Multidisciplinary rounds (bedside is best) • Post discharge follow up-medical homes • Early follow up-timely appointments • Medication reconciliation • Proactive thinking-treat symptoms early
Key Elements Cross-Continuum Team Collaboration Identify those at risk Case reviews Nursing competencies Health Information Exchange & Shared Care Plans Medication reconciliation S-BAR for status change reports Nursing home capabilities Access to the EMR Telehealth Shared CHF patient education materials Patient and Family Engagement Advance care planning Medical homes
Interact Go tohttp://www.interact2.net/tools.html
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: • 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 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.
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.
What is Heart Failure? • Clinical syndrome of: • Decreased exercise tolerance • Fluid retention • Due to structural heart disease
Factors That Affect Blood Pressure • 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 and Blood Pressure • Cardiac Output = Stroke Volume x Heart Rate • Mean Arterial Blood Pressure = Cardiac Output x Peripheral Vascular Resistance (PVR)
Pathophysiology of CHF • Alteration in pressures of the vascular system • Hemodynamics • Perception of decreased blood volume • Neurohumoral mechanisms
Hemodynamics Not just for the ICU nurse anymore!
Hemodynamics • 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!
Preload • 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!
Frank Starling Law of the Heart • 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
Afterload • 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)
Cardiac Contractility • Affected by: • Preload • Stretch • Volume • Afterload • Resistance Cover-up this
Symptoms of Shock • Hypotension (doesn’t occur initially) • Tachycardia • Cool, clammy skin • Decreased urine output • Alteration in mental status
Cardiogenic Shock 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
Activation of Sympathetic Nervous System (SNS) in Heart Failure • 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 Angiotensin Aldosterone System Renin excreted by kidney in response to • decrease in BP • sympathetic stimulation • decreased serum sodium (Na+) • decreased renal blood flow
Perception of Decreased Blood Volume • 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
Perception of Decreased Blood Volume • 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
Clinical Picture of Heart Failure • 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
Causes Left HF, COPD (corpulmonale), 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 Right Heart Failure Left Heart Failure
Pathophysiology of Respiratory Manifestations • 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
Respiratory Symptoms • Dyspnea • Ask many questions • Any activities you’ve stopped doing? Any modifications by caregiver? • Cough • Orthopnea • Paroxysmal Nocturnal Dyspnea • Dyspnea on exertion (DOE)
Respiratory Assessment • Inspection • Respiratory rate • Use of accessory muscles • Auscultation • Percussion • O2 saturation • Mentation • Decline in function/self compensation
Crackles Crackle 1 Crackle 2 Crackle 3
Wheezes • 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
Common Pulmonary Auscultation Abnormalities • 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
Percussion of the Lungs • Assesses underlying tissue • Bilaterally • Superior to inferior • Normal is resonance • Hyperresonance – hyperinflation (emphysema, pneumothorax, asthma) • Dullness or flatness- (atelectasis, pleural effusion, pneumothorax, consolidation)
Cardiac Cycle: Normal S1S2Abnormal S3 & S4 • 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
Extra Heart Sounds • 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 S3 S4
Cardiac Murmurs • 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 Distension (JVD) • 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
Hepatojugular Reflux HJR) • 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