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CONGESTIVE CARDIAC FAILURE.pptx
- 1. CONGESTIVE CARDIAC FAILURE PRESENTED BY: SHIVANI S. SHRIVASTAVA MSC NURSING 1ST YEAR KASTURBA NURSING COLLEGE, SEWAGRAM
- 2. GENERAL OBJECTIVE At the end of the seminar group will be able to gain knowledge regarding congestive cardiac failure and apply that knowledge in educational and clinical area.
- 3. SPECIFIC OBJECTIVE At the end of the seminar the group will be able to : 1.Define Congestive Cardiac Failure. 2.Enumerate the aetiology and risk factors of congestive cardiac failure. 3.Explain the Anatomy and Physiology of congestive cardiac failure. 4.Depict the pathophysiology of congestive cardiac failure.
- 4. 5.Enlist the clinical manifestation of congestive cardiac failure on the basis of its types. 6.Explain the diagnostic evaluation of congestive cardiac failure. 7.Describe the medical management of congestive cardiac failure. 8.Explain the surgical management of congestive cardiac failure.
- 5. 9.Describe the nursing management of congestive cardiac failure. 10.Enlist the complications of congestive cardiac failure. 11.Explain the current trends and issues in congestive cardiac failure.
- 6. INTRODUCTION Congestive cardiac failure (heart failure) refers to a clinical syndrome caused by inherited or acquired abnormalities of heart structure and function, causing a constellation of symptoms that lead to decrease quality and quantity of life. It is referred to as congestive cardiac failure as many patients experience pulmonary or peripheral congestion.
- 7. DEFINITION Congestive Cardiac failure is a clinical syndrome that results from the progressive process of remodelling, in which mechanical and biomechanical forces alter the size, shape, and function of the ventricle’s ability to fill with or pump enough oxygenated blood to meet the metabolic demands of the body.
- 8. ETIOLOGY AND RISK FACTORS Heart failure is caused by increased workload on the heart which causes increase in an effort to move blood. The workload on the heart is of two types. WORKLOAD PRELOAD AFTERLOAD
- 10. The etiology of CCF is divided into three major categories: 1.Abnormal loading conditions 2.Abnormal muscle function 3.Limited ventricular filling
- 15. MUSCULATURE OF THE HEART
- 16. PHYSIOLOGY The actions of heart are classified into four types: Actions Chronotropic action Inotropic action Dromotropic action Bathmotropic action
- 17. PROPERTIES OF CARDIAC MUSCLES PROPERTIES All-or-none law Staircase phenomenon Summation of Subliminal Stimuli Refractory period
- 19. Summation of Subliminal Stimuli Refractory period
- 21. CARDIAC OUTPUT •Cardiac output is the amount of blood pumped from each ventricle. It is expressed in three ways: 1.Stroke volume: 70 mL (60 – 80 mL) when the heart rate is normal (72/minute). 2.Minute volume: 5L/ventricle/minute. 3.Cardiac index: 2.8 ± 0.3 L/square meter of body surface area/minute
- 22. EJECTION FRACTION • Ejection fraction is the fraction of end diastolic volume that is ejected out by each ventricle. Normal ejection fraction is 60% to 65%. It is calculated as: E1 = 𝑺𝑽 𝑬𝑫𝑽 = 𝑬𝑫𝑽−𝑬𝑺𝑽 𝑬𝑫𝑽 Where, E1 = Ejection fraction SV = Stroke Volume EDV = End diastolic-volume ESV = End systolic-volume
- 23. PATHOPHYSIOLOGY The categorization of heart failure is further done into: 1.Heart Failure with Preserved Ejection Fraction (HFpEF), LVEF ≥ 40% to 50% to define HFpEF also referred to as systolic failure. 2.Heart Failure with Reduced Ejection Fraction (HFrEF), LVEF ≤ 35% to 40% to define HFrEF also referred to as diastolic failure.
- 24. PATHPHYSIOLOGIC CONCEPTS IN HEART FAILURE Mechanism of cardiovascular injury and progression: •Altered cellular protein •Metabolic adaptations and mal adaptations •Neurohormonal activation •Inflammatory response and remodeling •Myocyte regeneration and apoptosis
- 25. PATHOPHYSIOLOGY OF HEART FAILURE WITH PRESERVED EJECTION FRACTION
- 26. PATHOPHYSIOLOGY OF HEART FAILURE WITH REDUCED EJECTION FRACTION (OTHER ORGAN SYSTEMS) •Inflammation:
- 28. CARDIAC REMODELLING Cardiac remodelling is defined as cardiac structural changes and happen in response to conditions. Although initially adaptive, when sustained, remodelling can contribute to the development and progression of heart failure.
- 29. The Frank-Starling Law and Heart Failure Hemodynamics: The Frank-Starling Law describes the increase in SV when EDV is increased and is critical for the response to left ventricular systolic dysfunction. For any given amount of Ca2+ released into monocyte, there is increase in cross- bridge formation and enhanced sensitivity of myofilament to Ca2+ as the sarcomere lengthen.
- 31. CLINICAL MANIFESTATIONS The manifestations of heart failure depend on: Specific ventricle involved Precipitating cause of failure Degree of impairment Rate of progression Duration of failure Clients underlying conditions
- 32. TYPES OF HEART FAILURE Heart failure has been classified into several stages based on the client’s functional ability and clinical manifestations. TYPES 1.LVF vs RVF 1.Backward vs Forward 1.High output vs Low output
- 33. Left ventricular failure vs right ventricular failure
- 34. Backward Versus Forward Failure Backward failure focuses on the ventricle’s inability to eject completely. Forward failure is a problem of inadequate perfusion. This causes: omental confusion omuscular weakness orenal retention of sodium and water
- 35. High-Output Versus Low-Output Failure High-output failure occurs when the heart, despite normal-output to high-output levels, is simply not able to meet the accelerated needs of the body. Low-output failure is related not to increased metabolic needs of the tissues but to poor ventricular pumping action and a low cardiac output.
- 37. MANAGEMENT MEDICAL MANAGEMENT The goals of the management are: • To reduce myocardial workload • Improve ventricular pump performance • Perfuse essential organs • Prevent further heart failure by affecting the process of cardiac remodelling • Reduce myocardial workload
- 38. The management of heart failure is divided into two situations: I.The treatment of decompensated heart failure: 1.Reduce Myocardial Workload •Diuretics •Vasodilators
- 39. 2.Elevate the Client’s Head: •High Fowler position •The legs are maintained in a dependent position
- 40. 3.Reduce Fluid Retention •Diets with 2 to 4 g of sodium are usually prescribed. •It is usually not necessary to restrict fluid intake in clients with mild or moderate heart failure. In more advanced cases, however, it is beneficial to limit water to 1000 ml/day (1 L/day).
- 41. 4. Improve Ventricular Pump Performance •Use of adrenergic agonist, or inotropic medications.
- 42. 5.Supplement Oxygen High concentrations of oxygen by mask or cannula are provided. For hypoxemia, partial rebreather masks with a flow rate of 8 to 10 L/min can be used to deliver oxygen concentrations of 40% to 70%.
- 43. A non-rebreathing mask can achieve even higher oxygen concentrations. If these methods do not raise the arterial oxygen tension (PaO,) above 60mm Hg, the client may need intubation and ventilatory management. Intubation also provides a route for removing secretions from the bronchi.
- 44. 6.Control Dysrhythmias Atrial fibrillation with a rapid ventricular response is the most common dysrhythmia seen in heart failure clients. Atrial fibrillation can lead to embolic stroke, so clients are given anticoagulants. The rhythm is often controlled with medications such as amiodarone.
- 45. 7.Reduce Myocardial Remodeling ACE inhibitors reduce afterload by blocking the production of angiotensin, a potent vasoconstrictor. They also increase renal blood flow and decrease renal vascular resistance, which enhances diuresis.
- 46. 8.Reduce Stress and Risk of Injury The proper use of rest as the initial step in management offers many benefits. Rest can promote diuresis, slow the heart rate, and relieve dyspnea, all of which allow more conservative use of pharmacologic agents.
- 47. II.Treatment of chronic heart failure: Chronic heart failure has been classified according to severity. •Adhere to dietary restrictions •Monitor blood pressure •Modify activity •Adhere to medications
- 48. Digoxin: Digoxin is often added to the medication regimen in chronic heart failure.
- 53. NURSING MANAGEMENT 1.Decreased cardiac output related to heart failure or dysrhythmias or both. 2.Excess fluid volume related to reduced glomerular filtration, decreased cardiac output, increase antidiuretic hormone (ADH), and aldosterone production and sodium and water retention. 3.Ineffective tissue perfusion related to decreased cardiac output. 4.Risk for impaired skin integrity related to decreased tissue perfusion and activities.
- 56. 3.Kidney failure
- 57. 4.Anemia
- 58. 5.Stroke
- 60. 7.Leg venous stasis and ulcers
- 61. CURRENT TRENDS AND ISSUES Heart failure is the leading cause of death worldwide. The inability of the adult mammalian heart to regenerate following injury results in the development of systolic heart failure. Thus, identifying novel approaches toward regenerating the adult heart has enormous therapeutic potential for adult heart failure.
- 62. SUMMARY Heart failure (HF) is a complex clinical syndrome associated with increased mortality and morbidity. It is also common and becoming more prevalent with the aging population and improvement in survival of patients with cardiovascular diseases such as coronary artery disease. Several fundamental concepts and principles have evolved and are described here.
- 63. CONCLUSION We now know that most coronary heart disease, the number one cause of HF, can be prevented by control of coronary risk factors. More precise understanding of varying pathophysiologic mechanisms is needed in order to identify 2 more precise, targeted therapy for HF phenotypes, thus allowing for a rational, aggressive, and cost-effective prevention strategy before patients reach the late stages of the syndrome.
- 64. BIBLIOGRAPHY 1. FUSTER VALENTIN, HARRINGTON A. ROBERT, NARULA JAGAT, EAPEN J. ZUBIN, “HURST’S THE HEART”, VOLUME-2, LIBRARY OF CONGRESS CATALOGING-IN-PUBLICATION DATA, 14TH EDITION, PAGE NO: 1651-1768. 2. BLACK M. JOYCE, HAWKS HOKANSON JANE, “BLACK’S MEDICAL-SURGICAL NURSING CLINICAL MANGEMENT FOR POSITIVE OUTCOMES”, ELSEVIER PUBLICATIONS, 1ST EDITION, 2019, PAGE NO:1437-1445. 3. CHAURASIA D B, “B D CHAURASIA’S HUMAN ANATOMY VLOUME-1”, CBS PUBLISHERS AND DISTRIBUTORS, 6TH EDITION, PAGE NO: 252-261. 4. SEMBULINGAM K, SEMBULINGAM PREMA, “ESSENTIALS OF MEDICAL PHYSIOLOGY”, JAYPEE PUBLICATIONS, 6TH EDITION, 525-532. 5. https://www.google.com/search?q=anatomical+structure+of+heart+anterior+surface&tbm=isch&ved=2ahUK EwipzIyy7c_0AhXFm0sFHaigCOwQ2- cCegQIABAA&oq=anatomical+structure+of+heart+anterior+surface&gs_lcp=CgNpbWcQAzoHCCMQ7w MQJzoGCAAQCBAeOgQIABAeULMMWOtgYMZnaANwAHgAgAHSAYgBmBqSAQYwLjE5LjKYAQ CgAQGqAQtnd3Mtd2l6LWltZ8ABAQ&sclient=img&ei=PV2uYem5PMW3rtoPqMGi4A4&rlz=1C1CHZN _enIN980IN980 6. https://pubmed.ncbi.nlm.nih.gov/32311026/
Editor's Notes
- Preload – can be defined as the initial stretching of cardiac muscle fiber length before contraction. The force generated by cardiac muscle by shortening them and its ability to pump forward Afterload – The amount of tension the heart must generate to overcome systemic pressure and allow adequate ventricular emptying. It is the opposing generated by peripheral vessel pressure
- LEAFLETS
- The heart is a conical hollow muscular organ situated in the mediastinum and is eenclosed in pericardium. Placed obliquiley behinf the body of sternum and adjoining parts of costal cartilage. Measure – 12*9 cm Weight – 300 gm in male and 250 gm in female
- The right atrium is the right upper chamber of the heart. It receives venous blood from the whole body, pumps it to the right ventricle through the right atrioventricular or tricuspid opening. It forms the right border, the sternocostal surface and base of heart. Tributaries or inlets of the Right Atrium: Superior vena cava. Inferior vena cava. Coronary sinus. Anterior cardiac veins. Venae cordis minimi (thebesian veins). Sometimes the right marginal vein. The right ventricle is a triangular chamber which receives blood from the right atrium and pumps it to the lungs through the pulmonary trunk and pulmonary arteries. It forms the inferior border and a large part of the sternocostal surface of the heart.
- The left atrium is a quadrangular chamber situated posteriorly. Its appendage, the left auricle projects anteriorly to overlap the infundibulum of the right ventricle. The left atrium forms the left two-thirds of the base of the heart, the greater part of the upper border, parts of the sternocostal and left surfaces and of the left border. It receives oxygenated blood from the lungs through four pulmonary veins, and pumps it to the left ventricle through the left atrioventricular or bicuspid or mitral orifice which is guarded by the valve of the same name. The left ventricle receives oxygenated blood from the left atrium and pumps it into the aorta. It forms the apex of the heart, a part of the sternocostal surface, most of the left border and left surface, and the left two-thirds of the diaphragmatic surface.
- The valves of the heart maintain unidirectional flow of the blood and prevent its regurgitation in the opposite direction. There are two pairs of valves in the heart, a pair of atrioventricular valves and a pair of semilunar valves. The right atrioventricular valve is known as the tricuspid valve because it has three cusps. The left atrioventricular valve is known as the bicuspid valve because it has two cusps. It is also called the mitral valve. The semilunar valves include the aortic and pulmonary valves, each having three semilunar cusps. The cusps are folds of endocardium, strengthened by an intervening layer of fibrous tissue. FIBROUS SKELETON: The fibrous rings surrounding the atrioventricular and arterial orifices, along with some adjoining masses of fibrous tissue, constitute the fibrous skeleton of the heart. It provides attachment to the cardiac muscle and keeps the cardiac valve competent. The atrioventricular fibrous rings are in the form of the figure of 8.
- Cardiac muscle fibres form long loops which are attached to the fibrous skeleton. Upon contraction of the muscular loops, the blood from the cardiac chambers is wrung out like water from a wet cloth. The atrial fibres are arranged in a superficial transverse layer and a deep anteroposterior (vertical) layer. The ventricular fibres are arranged in superficial and deep layers.
- Chronotropic action: Chronotropic action is the frequency of heartbeat or heartrate. It is of two types: Tachycardia Bradycardia 2. Inotropic action: Force of contraction is called as inotropic action. It is of two types: Positive inotropic action or increase in the force of contraction. Negative inotropic action or decrease in force of contraction. 3. Dromotropic action: Dromotropic action is the conduction of impulse through heart. It is of two types: Positive dromotropic action or increase in the velocity of conduction. Negative dromotropic action or decrease in the velocity of conduction. 4. Bathmotropic action: Bathmotropic action is the excitability of cardiac muscles. It is of two types: Positive bathmotropic action or increase in the excitability of cardiac muscles. Negative bathmotropic action or decrease in the excitability of cardiac muscles.
- All-or-None law: According to this law , when a stimulus is applied, whatever may be the strength, the whole cardiac muscle gives maximum response or it does not give response at all. Below the threshold level, that is if the strength of stimulus is not adequate, the muscle does not give response. Staircase phenomenon: When the ventricle of quiescent heart is stimulated at a short interval of 2 seconds, without changing the strength, the force of contraction increases gradually for the first few contractions and then it remains same. Gradual increase in the force of contraction is called staircase phenomenon.
- Summation of Subliminal Stimuli: When a stimulus with a subliminal strength is applied, the quiescent heart does not show any response. When few stimuli with same subliminal strength are applied in succession, the heart shows response by contraction, due to summation of stimuli. Refractory period: Refractory period is the period in which the muscle does not show any response to stimulus. It is of two types: Absolute refractive period: It is the period during which the muscle does not show any response at all, whatever maybe the strength of stimulus. It is because depolarization occur in this period. Relative refractory period: It is period during which the muscle shows response if the strength of stimulus is increased to its maximum. It is the stage at which the muscle is in repolarising state.
- More than half of the volume of cardiac myocytes is comprised of contractile protein which helps in cardiac functioning. A myocardial cell contains bundles of myofibril, which is made up of functional units of sarcomere. A sarcomere contains myosin (thick), Actin (thin) filaments. Hydrolysis of Adenosine Triphosphate (ATP) Cause actin and myosin to slide past each other, shortening the myofibrils and ultimately producing myocyte contraction which is foundation of power of myocardium.
- Stroke volume is the amount of blood pumped out by each ventricle during each beat. Minute volume is the volume of blood pumped out by each ventricle in one minute. It is the product of stroke volume and heart rate. Cardiac index is the minute volume expressed in relation to square meter of body surface area. It is defined as the amount of blood pumped out per ventricle/minute/square meter of the body surface area.
- From 130 to 150 mL of end-diastolic volume, 70 mL is ejected out by each ventricle (stroke volume). EDV – The volume of blood in left ventricle at the end of ventricular filling. ESV – The volume of blood remaining in the heart at the end of systole or contraction.
- CHART 1
- CHART 2
- The volume of blood that moves forward can be described as cardiac output, which depends on stroke volume (SV), and heartrate and stroke volume mainly depends on three major factors whish preload, contractility and afterload, and preload describes the End diastolic volume contractility describes the force generated by shortening of sarcomere and ability to pump blood forward. Afterload is the opposing force as such as peripheral arterial pressure, that the moving blood encounters once it is pumped out of the heart.
- DIAGRAM
- FLASH CARD
- Diuretics – First line therapy, loop diuretics eg, furosemide inhibits sodium chloride resorption in ascending loop of henle, d blood volume, d preload, d syatemic and pulmonary congestion Nitroglycerine – d myocardial oxygen demand , d preload and afterload given IV Morphine – Anxiolytic and analgesic causes vasodilation d preload, also causes atrial dilation, d systemic vascular resistance and I co Nesiritide – vasodilation Betablockers
- Even though the legs are oedematous, they should not be elevated. To reduce the venous return
- It improves the cardiac performance an to prevent , control and eliminate edema
- Dobutamine Dopamine Milrinone Dopexamine Digoxin
- to relieve hypoxia and dyspnea and to improve oxygen-carbon dioxide exchange.
- Digoxin is a positive inotrope, often taught to clients as a medication that “slows and strengthens the heartbeat.” Improved cardiac output enhances kidney perfusion which may create a mild diuresis of sodium and water.
- The goal of mechanical circulatory support is to decompress the hypokinetic ventricle, decrease myocardial workload, reduce oxygen demands, and maintain adequate systemic perfusion to sustain end-organ function.
- systems are widely used for short-term hemodynamic stabilization. These devices remove blood from the inferior vena cava to a centrifugal pump that pumps the blood to an oxygenator. The oxygenated blood is returned to the client via the femoral artery.
- When the heart is irreversibly damaged and no longer functions adequately and when the client is at risk of dying, cardiac transplantation and the use of an artificial heart to assist or replace the failing heart are measures of last resort. One-year survival rates as transplantation are greater than 85%, Although transplantation may not be appropriate for all clients, it maybe only option available to some.
- For clients with low cardiac output who are not candidates: for cardiac transplantation, a procedure called cardiomyoplasty may support the failing heart. This procedure involves wrapping the latissimus dorsi muscle ground the heart and electrostimulating it in synchrony with ventricular systole.
- heart failure can actually stretch your atria and cause tissue in your heart to thicken and scar. Those changes throw off the electrical signals, and that messes up the heart's rhythm and can cause AFib.
- V-fib most commonly occurs during an acute heart attack or shortly thereafter. When heart muscle does not get enough blood flow, it can become electrically unstable and cause dangerous heart rhythms. A heart that has been damaged by a heart attack or other heart muscle damage is vulnerable to V-fib.
- Heart failure can reduce the blood flow to your kidneys, which can eventually cause kidney failure if left untreated.
- Anemia in heart failure is considered to develop due to a complex interaction of iron deficiency, kidney disease, and cytokine production, although micronutrient insufficiency and blood loss may contribute.
- Heart failure may increase the risk of ischemic stroke because of thromboembolic complications and increased activity of procoagulant factors.
- Cachexia is a well-known problem in patients with end-stage chronic HF, and it is a risk factor of death for the patients at this stage of the disease. Patients with cardiac cachexia suffer from generalised loss of lean tissue, fat tissue, as well as bone tissue. Cachectic CHF patients are weaker and fatigue earlier. This is due to both reduced skeletal muscle mass and impaired skeletal muscle quality.
- Poor circulation can cause skin to thicken, change color and look shiny. Hair may fall out and ulcers can develop if you sustain an injury.
- Mitochondrial metabolism is an essential homeostatic process for maintaining growth and survival. The emerging role of mitochondrial metabolism in controlling cell fate and function is beginning to be appreciated. Recent evidence suggests that metabolism controls biological processes including cell proliferation and differentiation, which has profound implications during development and regeneration. The regenerative potential of the mammalian heart is lost by the first week of postnatal development when cardiomyocytes exit the cell cycle and become terminally differentiated. This inability to regenerate following injury is correlated with the metabolic shift from glycolysis to fatty acid oxidation that occurs during heart maturation in the postnatal heart. Thus, understanding the mechanisms that regulate cardiac metabolism is key to unlocking metabolic interventions during development, disease, and regeneration.