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Heart Failure Learning Objectives Students will be able to: Discuss epidemiology of heart failure in NZ • Define heart failure – acute and chronic Compare the pathophysiology of systolic and diastolic ventricular heart failure. Describe compensatory mechanisms associated with heart failure Describe Left and Right ventricular failure and link to clinical manifestation of Heart Failure Describe nursing interventions and multidisciplinary management of heart failure including pharmacological therapy. New Zealand Epidemiology • Major public health problem. > 1.3% of population • Admission rates increased by 10.6% over last 5 years (National • • • • • • Heart Foundation of New Zealand) Average of about 850 deaths per year =2% Mortality = 20% at 6months and 30% at 12 months Approximately 8 times higher among Maori males aged 45-65 Hospital admissions about 5,500 per year with a mean duration of stay 5-16 days (Maori 8-9 times higher) Accounts for 1.5 -2% of health budget (>$NZ60m) Occurs on average 10 -15 yrs earlier amongst Maori than nonMaori Definition of Heart Failure Heart failure (HF) is caused by any structural or functional cardiac abnormality that impairs the ability of the left ventricle to fill with or eject sufficient blood to meet the metabolic needs of the body. HF is not a specific anatomic abnormality but a clinical syndrome characterized by specific symptoms http://merck.praxis.md/bpm/bpm.asp?page=BPM01CA06§ion=report&ss=1&hilight=cong estive+heart+failure Pathology Cycle of Heart Failure: Not enough blood is pumped out of the ventricles causing the body to stimulate the heart to work harder. The failing heart muscle is unable to respond and the pathology of heart failure becomes worse. Pathology of Heart Failure • Classified as systolic or diastolic failure • Systolic – inability to pump or eject blood - EF • Diastolic – inability of ventricles to relax and fill resulting in decreased stroke volume and cardiac output – EF • Mixed systolic and diastolic – EF • Ejection fraction (EF) –blood ejected from left ventricle with each contraction. (normal =55% -60%) Heart Failure Systolic Heart Failure- decreased ventricle contraction (most common) - decreased CO, decreased blood ejected Diastolic Heart Failure- decreased ventricle filling during diastole (older adults and woman) - hypertension continued increased workload - decreased relaxation SDL– Compare the pathophysiology and clinical manof causes of the above. Aetiology of Heart Failure Causative factors CAD MI Chronic hypertension Pulmonary hypertension Valvular heart disease Cardiomyopathy- disease of myocardium (viral) Hyperthyroidism (thyrotoxicosis) Congenital Heart Disease Aetiology of Heart Failure Exacerbating/Precipitating Factors Anaemia Infection Arrhythmias (especially AF) Some drugs (NSAIDs, Ca2+ blockers, corticosteroids) Renal dysfunction Pulmonary embolus Silent MI /MI ( Affect Contractility ) Excess sodium intake Transfusions or infusions increasing preload Poor compliance with current management regime Pregnancy Lewis pg 776/895 ( view mechanisms of above) Definitions Cardiac Output = HR (heart rate) X SV (stroke volume) Stroke Volume = amount of blood ejected with each heart beat Preload: end diastolic filling volume of the left ventricle (EDV) reflects stretch of the cardiac muscle cells Afterload: resistance to ventricular emptying during systole. (amount of pressure the left ventricle must generate to squeeze blood into the aorta) • Myocardial Contractility: the squeezing contractile force that the heart can develop at a given preload Ejection Fraction: indication of the amount of blood ejected with the contraction Frank/Starling Law of the Heart - the heart will contract with greater force when preload (EDV) is increased Clinical Cardiovascular Anatomy & Physiology Concepts, Definitions, & Principles Green, J. 2003, Texas A&M university 2003 (+ next 2 slides) Cardiac Output Cardiac output http://www.youtube.com/watch?v=0v8-O8P7kw8 Preload and afterload End Diastolic Volume (EDV) Volume at the end of diastole (end of ventricular filling) End Systolic Volume (ESV) Volume at the end of systole (end of ventricular contraction) Stroke Volume (SV) = EDV - ESV Ejection Fraction (EF) = SV EDV Left ventricular norm: 62% Ejection Fraction is the best indicator of heart performance and disease prognosis Starlings Law Force of heart contraction normal contractility SV left ventricular performance d contractility (heart failure) preload (EDV) The heart will contract with greater force when preload (End Diastolic Volume) is increased What is happening? • Dilation – enlargement of heart chambers due to • • • • • elevated pressure over a long time Hypertrophy – increase in cardiac wall thickness due to increased workload and CO. Contractility decreased SNS stimulation : due to decrease in CO. Neurohormonal response: renin-angiotensin response – sodium retention- increased peripheral vasoconstriction – increased arterial BP ADH secreted due to low CO (Lewis 777/896) Endothelin production from endothelial cells results in vasoconstriction Ventricular remodeling Counter regulation Body’s ability to maintain balance. Natriuretic peptides ANP (Atrial) and Btype NP are hormones produced by heart muscle promoting venous and arterial vasodilation Antagonists of endothelin and aldosterone and enhance diuresis Prolonged distension as in HF leads to a depletion of these peptides and increased Myocardial workload Lewis 778/896 Neurohormonal effect Cardiac Remodeling Eccentric hypertrophy • Volume overload • Increased CO for prolonged period • Cavity dilatation with an increase in muscle mass • Ratio between wall thickness and cavity remains relatively constant Cardiac remodeling Concentric Hypertrophy Chronic pressure overload (untreated hypertension) or AS Ratio between wall thickness and cavity size increases Heart failure Heart Failure (Types) Left Sided Right sided Acute/ Chronic ??? SDL Compare left and right sided heart failure with reference to pathophysiology and clinical manifestations. Right and left heart failure Left and/or Right Sided Failure Left Ventricular Failure Poor LV function Leads to pulmonary congestion Right Ventricular Failure - Left ventricular failure - Pulmonary Hypertension - right sided hypertrophy and failure Poor RV function Leads to increased systemic venous pressure Bi-ventricular failure Acute Decompensated Heart Failure (ADHF) ( Pulmonary oedema) Acute and Chronic Failure Acute MI Valvular rupture PE Drug induced (cocaine) Chronic Typically dilated cardiomyopathy Downloaded 20 May 07 from http://www.sciosinc.com/img/heartfailure_image.gif Congestive Heart Failure Tests CXR ECG Echocardiography FBC – to exclude anaemia Urinalysis BUN Creatinine Liver function tests Albumin ABG Transthoracic Doppler studies BNP Downloaded 20 May 07 from http://sprojects.mmi.mcgill.ca/icm_c/Chest/case1/pic1.jpg NYHA Classification Class I: patients with no limitation of ordinary activities ( ADL’s) - they suffer no symptoms. Class II: patients with slight, mild limitation of activity; they are comfortable with rest or with mild exertion. Class III: patients with marked limitation of activity; they are comfortable only at rest. Class IV: patients who should be at complete rest, confined to bed or chair; any physical activity brings on discomfort and symptoms occur at rest. http://www.hcoa.org/hcoacme/chf-cme/chf00070.htm Clinical Manifestations Shortness of breath with or without activity. Orthopnea, difficulty breathing while lying flat, often pillows are required to sleep. Low BP- Hypotension Rapid or irregular pulse. Edema or swelling of legs, feet and ankles, abdomen, liver, spleen and lungs. A chronic dry or frothy cough that may be bloodtinged or resemble foam. Nocturia, or an increase in urination at night. Unexplained or unintentional rapid weight gain. Distended or swollen neck veins. Clinical Manifestations Palpitations, or feeling the heart beat. Loss of appetite or indigestion. Cold, diaphoretic (sweaty) dusky colored skin. Oliguria, or decreased urine output. Changes in behavior such as restlessness, confusion, decreased attention span and memory. Heart Failure Treatment Strategies for ADHF Improving left ventricular function by: • Decreasing intravascular volume • Decreasing venous return (preload) • Decreasing afterload Improving Gas exchange and oxygenation Improving cardiac function /CO, HR & rhythm Reducing anxiety Decreasing progression of disease Lewis : 901 Management Non pharmacological General Counselling Smoking cessation Vaccination Prognosis discussion Activity recommendations Dietary recommendations > sodium restrictions Medication counselling Management General Counselling Explanation of heart failure and reasons for symptoms Cause of heart failure Expected symptoms Action plan if symptoms worsen Self-monitoring Treatment plan Clarification of responsibilities and compliance with medical plan Management Activity recommendations Recreation, leisure and work activity Sex, sexual difficulties and coping strategies Dietary recommendations • Sodium restriction • Avoid excessive fluid intake • Fluid restriction if required • Alcohol restriction Management Medication Counselling Effects of medications on quality of life and survival Dosing Likely side effects and what to do if they occur Coping mechanisms for complicated regimens Financial assistance/lower cost meds Management Pharmacological management ACE inhibitors > reduce venous pressure Diuretics > Reduce veous pressure and fluid ß-blockers > prevent tachycardia Calcium channel blockers Others Spironolactone Digoxin Angiotensin II antagonists Anticoagulation Aspirin Nitrates – prevent ischaemiaM Management Prognosis Life expectancy Advance Directives Advice for family in the event of sudden death Continuing care and controlling oxygenation Physical comfort and psychological suport Abdominal -Paracentesis Case study (Lewis 793/912) LDL Read through case study and answer questions which follow.
