Presentation on theme: "Maintaining Fluid Balance In Patients with Heart Failure Sarah Carek, RN, MSN Student Alverno College Spring 2010."— Presentation transcript:
Maintaining Fluid Balance In Patients with Heart Failure Sarah Carek, RN, MSN Student Alverno College Spring 2010
What should I know by the end of this tutorial? Understand the basic physiology of the heart. Develop a clear picture as to how Heart Failure is a pathological process. Recognize how excess fluid volume can result from Heart Failure. Apply nursing interventions to patients with Heart Failure. Examine how aging, stress, inflammation and genetics play in the development of Heart Failure.
Tutorial Navigation Click to advance to the next slide. Click to go to the previous slide All buttons will be on the bottom of each page. Begin the tutorial by clicking on the first topic on the home page.
Slides with Animation FYI..many slides contain animation. Keep clicking the mouse to advance through the entire animation. If you hover your cursor over areas and it changes from an arrow to a hand…click and animation will occur. Any underlined words have definitions available. Hover your cursor over the word and the definition will appear.
Home Page Pathophysiology of Heart Failure Causes of Heart Failure Important Nursing Interventions Cardiac Physiology Fresh and New: Aging, Stress, Inflammation & Genetics References Contact Information
CARDIAC PHYSIOLOGY Microsoft Clipart (manually altered)
Let’s see what you know already! Right Ventricle Right Atrium Left Ventricle Left Atrium Hover your mouse cursor over each section of the heart until the cursor turns from an arrow to a hand. Then click to reveal its label. **If the mouse has not turned from an arrow to a hand..Do Not Click*** Aorta Superior Vena Cava Inferior Vena Cava Pulmonary Arteries Pulmonary Veins Microsoft Clipart (manually altered)
What do the areas of the heart do? Click on the boxes to the left to find their function. Right Ventricle Left Atrium Left Ventricle Right Atrium Pumps deoxygenated blood from the body into the right ventricle. Pumps deoxygenated blood to the lungs to get oxygenated. Receives oxygenated blood from the lungs and pumps it to the left ventricle. Pumps oxygenated blood to the body to get used for energy
Normal Blood Flow Microsoft Clipart (manually altered)
What about the valves? The valves of the heart assure that blood flows in the right direction. Click on the diagram to find the four valves. They are half-moon shaped. Again when the cursor turns into a hand, it means you can click on it. Tricuspid Valve Pulmonic Valve Aortic Valve Mitral (Bicuspid) Valve Microsoft Clipart (manually altered)
The Cardiac Cycle Systole Diastole The period during the cardiac cycle where the ventricles are contracting and moving the blood forward. The period during the cardiac cycle where the ventricles are relaxed and filling with new blood. (Porth & Matfin, 2009) Microsoft Clipart (manually altered) Microsoft Clipart Click on the boxes on the left to find their definition.
The Heart as a Pump Cardiac output measures how well the heart is doing its job of pumping blood to the body. The heart has the ability to adjust cardiac output based on the body’s needs (i.e. exercise, sleep, illness). This depends on preload, afterload, cardiac contractility and heart rate. preloadafterloadcardiac contractility Average cardiac output = 3.5 – 8 Liters/minute Cardiac Ouput Stroke Volume Heart Rate (Porth & Matfin, 2009)
Starling’s Law End-Diastolic Volume The more blood in the heart at the end of diastole… Stretching of Cardiac Muscle The more the cardiac muscle fibers stretch… Force of Contraction The greater the force of the contraction. FYI: The fibers only stretch so far. There is a maximum force of contraction that can be achieved. (Porth & Matfin, 2009) Keep clicking to advance through the animation of the slide.
Let’s Review Try Again! Close! Excellent! No…but you are on the right track. Right Atrium Left Atrium Left Ventricle Right Ventricle
Try Again! You’re Right! Nope. Keep Trying! To prevent blood from moving forward. To keep blood moving forward. To let air escape preventing an air embolus. To prevent blood from leaking out of the heart.
A. CO = HR x AV Incorrect B. CO = SV x HR Good Job! C. CO = AV x SV Try Again! D. CO = HR x EF Nope
A. Blood Viscosity B. Cardiac Contractility C. Heart Rate D. Preload E. Afterload Blood Viscosity does not help the heart increase cardiac output. Correct! In order to increase cardiac output the heart must be able to change the force of contraction. Yes! The heart can change its rate in order to increase or decrease cardiac output. Good Job! According to Starling’s Law, if End-Diastolic Volume (preload) increases, the force of contraction will as well. Excellent! Cardiac output can be adjusted based on systemic arterial pressure (afterload).
PATHOPHYSIOLOGY OF HEART FAILURE Microsoft Clipart (manually altered)
Cardiac Function is Impaired Remember the heart is a pump… CO SV HR Cardiac Output is a reflection of how well the heart is doing its job of being a pump. HR either speeds up or slows down depending of what the sympathetic or parasympathetic nervous system tells the heart what to do. SV is determined by our friends preload, afterload and cardiac contractility. Heart Failure happens when there is one or more alterations in preload, afterload or cardiac contractility leading to decreased Cardiac Output. Preload A stiffer heart will decrease the amount of blood at the end of diastole AFTERLOAD If vascular resistance is elevated, the heart has to pump harder to overcome it, putting stress on it which can wear it out CONTRACTILITY Decreased ATP production and availability of Calcium ions causes the heart to become less able to contract effectively (Porth & Matfin, 2009)
These Malfunctions can be Classified into Systolic and Diastolic Dysfunction Impaired contractility leads to a decrease in Ejection Fraction and Cardiac Output. Preload, ventricular wall dilation and pressure subsequently increase.Ejection Fraction The ventricles are unable to relax and expand, leading to a decrease in preload, stroke volume and cardiac output. SYSTOLIC DYSFUNCTION DIASTOLIC DYSFUNCTION (Porth & Matfin, 2009) Click on each box to find the definition. Remember the arrow should turn to a hand before you click.
Heart Failure can also be classified as either Left Sided Heart Failure or Right Sided Heart failure.
Right Heart FailureLeft Heart Failure Blood cannot reach the lungs to get oxygenated. Oxygenized blood from the lungs cannot get to the body. Blood begins to pool in the venous system and tissues. Cardiac Output decreases and blood pools in the lungs. (Porth & Matfin, 2009) Dependent Edema Jugular Vein Distension Ascites Pooling of Blood in GI Tract Pooling of Blood in Hepatic Veins Decrease in Tissue Perfusion Activity Intolerance Cough, Orthopnea Hypoxia, PNDPND Pumonary Edema Are you starting to see how excess fluid balance contributes to heart failure?
Before learning about what causes these malfunctions to occur….Let’s Review Yes! Good Job. That’s Right! Excellent! Try Again. This is the thickness of the blood. Afterload Cardiac Contractility Preload Blood Viscosity
Try Again! No. We didn’t talk about this one. Sorry I made this one up! Great! Diastolic Dysfunction Right Ventricular Dysfunction Priastolic Dysfunction Systolic Dysfuction
CAUSES OF HEART FAILURE ***Remember to place your cursor over the underline words to get the definition*** Microsoft Clipart (manually altered)
Acute Coronary Syndrome Myocardial Infarction and Unstable Angina Decreased blood flow to the myocardium caused by a clot in the coronary arteries. Myocardial Damage (Infarction): evidenced by serum cardiac markers (CK-MB, Troponin). Ventricular Remodeling: the area of the ventricle that is damaged undergoes changes in size, shape and thickness (hypertrophy and dilation). Damage to the ventricle can lead to alterations in preload, afterload and cardiac contractility leading to a decrease in cardiac output. Blood begins to pool leading to fluid volume overload!!! (Porth & Matfin, 2009)
Ischemic Heart Disease Coronary Artery Disease Decreased blood flow to the myocardium from the coronary arteries caused by plaque buildup.plaque buildup Myocardial Damage (Infarction): evidenced by serum cardiac markers (CK-MB, Troponin). Ventricular Remodeling: the area of the ventricle that is damaged undergoes changes in size, shape and thickness (hypertrophy and dilation). Damage to the ventricle can lead to alterations in preload, afterload and cardiac contractility leading to a decrease in cardiac output. Blood begins to pool leading to fluid volume overload!!! (Porth & Matfin, 2009)
Cardiomyopathy Hypertrophic Cardiomyopathy Left Ventricle thickens through genetic predisposition.genetic predisposition The heart is unable to fill properly during diastole – Altered Preload. Stroke volume is decreased. Cardiac Output is decreased. Blood begins to pool leading to fluid volume overload!!! (Porth & Matfin, 2009)
Cardiomyopathy cont… Dilated Cardiomyopathy The ventricle is enlarged and wall thickness is decreased due to genetic predisposition, infection, alcohol or unknown cause.genetic predispositioninfectionunknown cause Preload and pressure increase. Cardiac Output decreases. Blood begins to pool leading to fluid volume overload!!! (Porth & Matfin, 2009)
Valvular Heart Disease Mitral Valve Disorders StenosisRegurgitation Because the valve is unable to open fully, the left atrium becomes distended leading to impaired filling during diastole. This leads to decreased cardiac output. Because the valve does not open and close completely, it becomes leaky. Stroke volume is reduced leading to decreased cardiac output. Blood begins to pool leading to fluid volume overload!!! (Porth & Matfin, 2009)
Valvular Heart Disease Cont… Aortic Valve Disorder StenosisRegurgitation Because the valve is unable to open fully, blood is unable to exit the left ventricle properly and begins to pool. This decreases cardiac output. Because the valve allows blood to flow back into the left ventricle during diastole, cardiac output is decreased. Blood begins to pool leading to fluid volume overload!!! (Porth & Matfin, 2009)
Let’s see if you understand causes of heart failure… Try Again! This is a cause of chronic heart failure. Nope. Keep thinking! This is a chronic cause of HF. Excellent! Ischemia to the heart can cause it to not pump blood like it should resulting in heart failure. This is a cause of chronic heart failure. Dilated Cardiomyopathy Aortic Stenosis Myocardial Infarction Mitral Valve Prolapse
Now you’re thinking! Now that’s just crazy talk. Yay! Good Job! Blood cannot fill properly during diastole. Blood will spill out of the heart everywhere. Cardiac Output is decreased. Blood pools creating edema.
Let’s take a look at how you fit into taking care of heart failure patients… Take a minute to think of nursing interventions you do on a daily basis that might apply to a patient with heart failure.
Remember the nursing process…? Assess Diagnose Plan Implement Evaluate
Fluid Volume Excess Assessment – Lung sounds – Daily weights – Vital signs – I & O’s – Behavior – Drug side effects Interventions – Restricted sodium diet – Fluid restrictions – Diuretics – Turning patients with edema – Promoting positive self image – Consult with physician Things You Would Find On Assessment (Ackley & Ladwig, 2006) Keep clicking to advance the animation.
The Stats ¾ of the 5 million Americans suffering with heart failure are over the age of 65 and ½ are over the age of 75. Heart failure is the leading cause of hospitalization among the elderly. 1 million older adults are hospitalized annually with heart failure. You can see that older adults with heart failure are a huge population for us as healthcare providers. As America ages, the population will only grow larger. (AHA, 2010)
Changes Related to Aging Arteries stiffen creating resistance against which the heart has to pump. Heart muscle stiffens, creating filling difficulty. Cardiac Output declines due to a decline in the maximum rate the heart can reach. The aged are less able to increase the force of their contractions as is needed during stress, illness and exercise. (Thomas & Rich, 2006)
Remember Starling’s Law… End-Diastolic Volume The more blood in the heart at the end of diastole… Stretching of Cardiac Muscle The more the cardiac muscle fibers stretch… Force of Contraction The greater the force of the contraction. With age the heart muscles stiffens, limiting the amount of blood that can fill during diastole. Thus the fibers cannot stretch as far, creating a decreased force of contraction. (Thomas & Rich, 2006)
Remember the equation for cardiac output… CO SV HR If the heart rate is under sympathetic nervous system (SNS) and parasympathetic nervous system (PSNS) control….think about what chronic stress would do to the heart rate and subsequently cardiac output…. Stress Activation of SNS Release of Epinephrine and Norepinephrine Increased heart rate and blood pressure In a diseased heart, cardiac output would not increase as it should during the normal stress response. The heart would not be capable of pumping blood efficiently. Therefore a prolonged stress response would only exacerbate the signs and symptoms of heart failure. (Porth & Matfin, 2009)
Heart Failure and Inflammation Inflammatory mediators (such as nitric oxide) are activated in a patient with heart failure in an effort to improve cardiac function. These mediators can damage the endothelium in blood vessels supplying the heart with blood. Ventricular and vascular remodeling of the myocardium may be a result of this damage. Ventricular remodeling of the myocardium can result in heart failure because the ventricular cannot pump blood efficiently. Blood begins to pool leading to fluid volume overload!!! (Brunini, et.al., 2009)
Genetics and Heart Failure Some patients are believed to be at high risk for heart failure due to their genetic make-up. In a small population, mutations have been found in single genes that trigger the development of heart failure. Gene mutations have been found in the people with ventricular remodeling and cardiomyopathies Some mutation examples are – Genes encoding for protein components of the sarcomere which leads to hypertrophy of the myocardium. – Gene mutations resulting in altered dystrophin which normally gives stability to the sarcomere. Blood begins to pool leading to fluid volume overload!!! (Morita, Seidman & Seidman, 2005)
References Ackley, B.J. & Ladwig, G.B (2006). Nursing diagnosis handbook: a guide to planning care (7 th Ed.). St. Louis, MO: Mosby Elsevier. American Heart Association (2010). Statistics retrieved from http://www.americanheart.org/presenter.jhtml?identifier=1200026. http://www.americanheart.org/presenter.jhtml?identifier=1200026 Brunini, T.M., Mann, G.E., Matsuura, C., Meirelles, L.R., Menden-Ribeiro,A.C., & Moss, M.B. (2009). The role of exercise on l-arginine nitric oxide pathway in chronic heart failure. The Open Biochemistry Journal, 3, 55-65. Morita, H., Seidman, C.E., & Seidman, J. (2005). Genetic causes of human heart failure. The Journal of Clinical Investigation, 115(3), 518-526. Porth, C.M. & Matfin, G. (2009). Pathophysiology: concepts of altered health status (8 th Ed.). Philadelphia, PA: Lippincott Williams & Wilkins. Thomas, S. & Rich, M.W. (2006). Heart failure in older people. Generations (Fall 2006), pp. 25-32.
Contact Information Questions, Comments, Concerns? Sarah Carek, RN, MSN student email@example.com (608) 577-7866