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Caring for patient in acute heart failure

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IntroductionHeart failure it the term used to describe state where the heart fails to maintain an adequate circulation for the needs of the body despitean adequate venous return. Acute heart failure occurs as a result of a sudden decrease in ventricular function and may be associated withan acute event such as a viral illness, valvular dysfunction or an acute myocardial infarction. Chronic heart failure develops over time andis often the result of inability of auto regulatory mechanisms to compensate for decreased ventricular function. Acute heart failurefrequently occurs in patients with chronic, long standing impairment of ventricular function.Learning OutcomesUpon successful completion of this section, you should be able to:describe the pathophysiology and classifications of heart failureidentify the risk factors and conditions that contribute towards heart failureidentify the neuro-hormonal compensatory mechanisms which occur in heart failurerelate the clinical manifestations of heart failure to the relevant pathophysiological processesidentify rationales for the investigations that aid in the diagnosis of heart failuredescribe how the pathophysiology of heart failure impacts upon patient care, particularly in relation to pharmacological regimesdiscuss the nursing care required for a patient in acute pulmonary oedemadiscuss the psychosocial issues surrounding the patient with heart failure.4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failurehttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 4/13ReviewHeart failure is associated with a failure of the normal body mechanisms which regulate blood flow. It is importantthat you understand the role of the following compensatory mechanisms in the pathophysiology of heart failure.You may need to consult a pathophysiology text to review the following.Note the definitions of stroke volume, preload, afterload and contractility.Describe the Frank Starling mechanism and its effect on cardiac output.Describe the role of the following compensatory mechanisms for decreased cardiac output.Include both the short and long term effects of stimulation of these systemsthe sympathetic and parasympathetic nervous systemsthe rennin angiotensin systemmyocardial hypertrophy or remodelingthe naturetic peptides.Define the following terms:positive and negative inotropespositive and negative chronotropesdromotrophyadrenergic receptor.Lecture Notes – Click HereAcute Heart Failure physiology and CP…4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failurehttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 5/13Core text readingCore text readingAitken, A, Marshall, A, & Chaboyer, W., 2015, ACCCN’s critical care nursing, 3nd edn, Elsevier, Australia, Chapter 10, pp 285-304.Optional ReadingLaurent, D 2010, chapter 24 ‘Heart failure and cardiogenic shock’, in Wood, S, Froelicher, M & Motzer, S (eds),Bridges cardiac nursing, 6th edn, Lippincott,Williams and Wilkins, Philadelphia, pp. 555-578. (Also available onJournals at Ovid (Books) database.)4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failurehttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 6/13Heart and lung interactionUnderstanding the interaction between the heart and lung in spontaneous breathing is important for understanding some of the clinicalsigns and symptoms related to heart failure.Blood flows through the right side of the heart to the lungs, and then back to the left side of the heart through the aortic valve and root tothe systemic circulation. This flow is mainly dependent on differences in pressure between circulation compartments with blood flowingfrom high pressure to low pressure. These pressures are affected by gravity and movement of the chest wall for breathing and thecontraction of the heart muscle. The compartments are the venous bed (mainly the abdominal and splanchnic circulation) the right atrium,the right ventricle, the pulmonary circulation, the left atrium, the left ventricle, the aortic root and the arterial bed. The pressures are higherin the thicker walled elastic arterial and left ventricle compartments than the thin walled, easily collapsible venous compartments.Blood returns to the heart during inspiration when the pleural pressure becomes more negative from chest wall moving out causing theright atrium to dilate—lowering its pressure hence the gradient between the venous bed (in the abdomen and muscle) is increased to apoint that blood flows from a higher to a lower pressure into the right atrium. The right ventricle dilates to receive the incoming blood asdoes the pulmonary bed from the release of atrial naturetic peptide that the dilating right atrium releases. The larger the breath volumesduring inspiration the greater the diaphragm and intercostals movement and hence the lower the pleural pressures. The pulmonary beddilates and constricts in response to the lung volumes and compliance and oxygen concentration which is varied throughout the lung. Thispulmonary blood once oxygenated flows into the left atrium and left ventricle during diastole from a high to a low pressure with someassistance from gravity.The term transmural pressure (PTM) or the difference in pressure across the walls of each of the compartments or vessel or organ(Transmural pressure = internal surface pressure—external surface pressure) is referred to in literature you will read. There is a transmuralpressure of the heart, the aortic root and the lung—but the lung is explained in terms of transpulmonary pressure (pressure differencebetween blood vessels and alveolar) and intrathoracic pressure as the large vessels in the thoracic as well as the pleural space have alarger impact on pressure than just the lung and lung tissue.As ventricular afterload is defined as the force opposing ejection, ventricular afterload is represented by the level of transmural pressure,in the course of systole, within either the aortic root (LV afterload) or the pulmonary artery trunk (RV afterload). In terms of the LV; at theonset of spontaneous inspiration, the intraluminal pressure in the aortic root decreases less than does intrathoracic pressure, due to theconnection of this vessel with extrathoracic arteries. As a result, aortic transmural pressure increases.Spontaneous deep breathing places the acute failing heart under stress as it increases preload and afterloadWith spontaneous breathing therefore, LV afterload is greater in inspiration than in expiration. Respiration has a profound effect on LVafterload in pathologic conditions, such as when negative intrathoracic pressures (from large spontaneous breaths and increased work ofbreathing) are exaggerated (e.g. in sleep apnoea, acute pulmonary oedema or respiratory failure) or when LV systolic function is impaired.This concept is exampled in sleep apnoea where large breath volumes after periods of apnoea increase the aortic root pressure henceincreasing the LV afterload, causing the left ventricle to dilate to work harder to contract and over time leading to systolic heart failure(large dilated LV) similar to those with chronic hypertension.Heart Lung interactions in spont breath…4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failurehttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 7/13Pathophysiology of heart failureeReadingsThompson, PL (ed.) 2011, Coronary care manual, 2nd edn, Elsevier, Australia. Chapter 12 ‘Pathophysiology of cardiac failure’, pp.88-95 – Click hereHeart failure is frequently classified according to the section of the heart, or the aspect of cardiac function which is affected. In this waydefinitions of forward and backward failure have been used as well as left and right sided, and systolic and diastolic failure. It is importantthat you understand these definitions and can distinguish between different types of heart failure according to their pathophysiologicalprocesses.Systolic and Diastolic Heart FailureThe distinction between systolic (enlarged floppy ventricle) and diastolic heart failure (smaller, tighter and less elastic ventricle) is animportant one to understand as it impacts greatly on critical care nursing practice. Both systolic and diastolic heart failure result in aninability of the heart to provide adequate blood flow to meet perfusion demand. While systolic heart failure results from impaired cardiaccontractility, diastolic heart failure results from impaired ventricular compliance resulting in impaired filling. Both systolic and diastolic heartfailure can occur simultaneously.ActivityUse your resources to find the answers to the following questions.Distinguish between the pathophysiology of left and right sided heart failure.Describe the pathophysiology of systolic and diastolic heart failure.Describe the effects of systolic and diastolic heart failure on preload, afterload and contractility of the heart.What is meant by the term Left Ventricular Ejection Fraction (LVEF). How is this measured and what is thenormal value.Distinguish between the clinical manifestations of left and right sides heart failure and systolic and diastolicdysfunction.Diastolic Heart Failure diagnoisis and t…Medical School – Heart Failure with Re…4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failurehttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 8/13Lifespan considerationsPaediatricAs with adults, heart failure is a associated with a cardiac output that is inadequate to meet the metabolic needs of the body. In children,congenital heart disease is the most common cause of heart failure. A congenital heart defect must be considered in any neonate or infantwho presents with circulatory or respiratory compromise.Heart failure in children can be placed in 3 categoriesVentricular pump dysfunction – this will result in reduced contractility therefore imparing ventricular ejection. Causes may includecardiomyopathy, myocarditis, arrhythmias and congenital heart disease.Volume overload with preserved ventricular contractility – Increased preload may occur where there is a left to right shunt of bloodfrom the systemic to the pulmonary circulation. This may be due to septal defects, patent ductus arteriosus and aortapulmonary windows.Pressure overload with preserved ventricular contractility – An increase in afterload may occur when there is a ventricular outflowobstruction that impedes blood ejection, e.g, aortic and pulmonary stenosis.Heart failure in children can also be caused by severe, chronic anaemia or inflammatory cardiac disease. The clinical signs of heart failuremay include lethargy, weakness and fatigue, tachycardia, decreased urine output and increasing peripheral vasoconstriction.The link will provide you with a more detailed view of heart failure in the paediatric population. – Click Here (Singh, R.K(2014). www.uptodate.com.Older AdultSeveral specific changes in cardiac structure and function are associated with cardiac ageing, and they may explain a number ofpathophysiological and phenotypic features typical of the elderly. Particularly important is the greater predisposition of the elderly todevelop HF, particularly HF with preserved ejection fraction.Figure 1: Pathophysiological mechanisms predisposing to the development of diastolic dysfunction and heart failure in otherwise healthy ageing hearts. European Journal ofHeart Failure Volume 15, Issue 7,page 717.4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failurehttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 9/13Pharmacological management of heart failureManagement of heart failure focuses on relief of symptoms and enhancement of cardiac performance. This includes correcting anyprecipitating causes such as coronary artery disease hypertension and arrhythmias. In the critical care environment support of more thanone body system is frequently required in the patient with acute heart failure who presents with cardio-respiratory failure.Cardiac performance is optimised in heart failure by correction of any precipitating causes such as coronary artery disease, hypertensionand arrhythmias. Preload, afterload and contractility are optimised using fluid and medication therapy. (Note that cardiogenic shock andcardiac assist devices are covered in semester 2 )eReadingThompson, PL, (ed.) 2011, Coronary care manual, 2nd edn, Elsevier, Australia. – Click HereChapter 31 ‘Beta-blockers’, pp. 241-245.Chapter 32 ‘Ace-inhibitors and angiotensin receptor blockers’, pp. 247-52.Chapter 33 ‘Aldosterone blockade’, pp. 253-257.Chapter 34 ‘Calcium channel blockers’, pp. 258-261.Chapter 35 ‘Nitrate therapy’, pp. 263-266.ActivityReview the actions of the following major pharmacological groups on cardiovascular function. Give and example ofeach. Give consideration as to if they have an effect on preload, afterload, or contractility in heart failure.Beta blockers.Angiotensin-Converting Enzyme (ACE) inhibitors.Angiotensin II receptors blockers.Calcium channel blockers.Cardiac glycoside, i.e. digoxin.Define the terms agonist and antagonist.4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failurehttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 10/13Inotropes in acute heart failureInotropes are used extensively for patients with heart failure to maintain blood pressure and improve cardiac output. Sympathemometic(catecholamine) inotropic agents include agents such as adrenaline, adrenaline and dopamine which are naturally occurring as well asothers such as dobutamine which is not. These agents act on the adrenergic receptors of the sympathetic nervous system. There are alsotwo major types of adrenergic receptors, alpha receptors and beta receptors. The beta receptors in turn are divided into beta and betareceptors. Also, there is a division of alpha receptors into alpha and alpha receptors. The actions of these receptors are detailed in thereading below.Other positive inotropes fall into the category of phosphodiesterase inhibitors. The most commonly used of these in the Australian clinicalsetting is milrinone.Vasopressin often used in conjunction with noradrenaline, is often considered to be an inotrope as it increases blood pressure; however, itis one of the most important endogenously released stress hormones, especially during shock. Vasopressin acts on vasopressin receptorsand not only vasoconstricts but also vasodilates some vascular beds making its action different to other vasoconstricting agents.ActivityThe drugs mentioned below can be used in acute heart failure. Organise them into a table defining them by groupand describe their action including any activation of adrenergic receptors where applicable. State whether eachdrug is used for reduction in preload or afterload or both, or whether they are used for inotropic or chronotropicsupport. Include the effect of different dose rates.Glycerol Trinitrate (GTN)MorphineAdrenalineNoradrenalineDopamineSodium NitroprussideDobutamineIsoprenalineAramineHydrallazineMilrinoneLevosimendan1 21 2eReadingThompson, PL, (ed.) 2011, Coronary care manual, 2nd edn, Elsevier, Australia. – Click HereChapter 38 ‘Inotropic and vasoactive agents’, pp. 284-289.4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failurehttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 11/13Acute pulmonary oedemaPatients with acute heart failure often present with symptoms of acute pulmonary oedema due to the influx of fluid from the circulationacross the alveolar capillary membrane and into the alveolar space. This causes a reduction in gas exchange, alveolar collapse and poorventilation perfusion relationship. Acute pulmonary oedema can be associated with both systolic and diastolic failure but leading to anincrease in hydrostatic pressure within the pulmonary capillaries. In acute heart failure diastolic heart failure (cramped heart) frommyocardial ischaemia is very common.eReadingsThompson, PL (ed.) 2011, Coronary care manual, 2nd edn, Elsevier, Australia. Chapter 66 ‘Cardiac failure and acut pulmonaryoedema after acute coronary syndromes’, pp. 503 -508 – Click hereThe typical patient with acute cardiogenic pulmonary oedema is pale; cool to touch and sweaty, reflecting intense sympathetic nervoussystem activation, obviously breathless and sitting upright. Coughing up pink frothy sputum is relatively uncommon. Patients may have acentral or peripheral cyanosis and reduced oxygen saturations. The venous pressure is often clinically normal and the jugular venouspressure hard to estimate but elevated in well hydrated patients (but most often they are dehydrated). Most patients do not haveperipheral oedema. Auscultation of the chest often reveals bilateral fine basal pulmonary crepitations that do not clear on coughing andthere may be high-pitched expiratory rhonchi.Acute pulmonary oedema (APO) usually occurs in those with a history of hypertension. Hypertensive patients have a very sensitivesympathetic nervous system (and accompanying neurohormonal compensation) so when chest pain or myocardial ischaemia stimulatesthe sympathetic drive; there is extremely sudden and massive shunting of peripheral blood to the pulmonary bed causing fluid overloadthat diffuses through to the alveolar hilum and space causing pulmonary oedema. One of the reasons for success of non-invasiveventilation (NIV) in APO is that because NIV increases the positive pressure in the thorax; blood return to the thorax is impeded therebytransferring blood to the systemic veins. Diuretics such as Frusemide which are commonly prescribed for APO are effective because theyvasodilate the venous bed also moving blood from the pulmonary bed to the peripheral venous bed. They also have a diuretic affect; oftennot desired in a dehydrated APO patient without peripheral oedema who has blood in the wrong (pulmonary bed) compartment.Cardiogenic Pulmonary oedema4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failurehttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 12/13The use of continuous positive airway pressure in acute heart failureContinuous Positive Airway Pressure, (CPAP) has been used successfully to treat patients with a sudden onset of acute pulmonaryoedema, as has other forms of non invasive ventilation such as bi level positive airway pressure (BiPAP). Both of these therapies improvepulmonary gas exchange and reduce work of breathing as well as improving cardiovascular performance in the failing heart. This sectionfocuses on the cardiovascular effect of these therapies in acute pulmonary oedema. The nursing care of patients undergoing NIV iscovered in subsequent sections.Positive pressure ventilation reduces preload and afterload in the failing heartDuring systole, NIV increases the intrathoracic pressure (and the pleural pressure is much less negative)and reduces venous return, thusdecreasing the right and left ventricular preload; in diastole, NIV increases the pericardial pressure, reduces PTM, and thus decreasesafterload in the left ventricle wall as well as in the aortic root.NIV also causes a decrease in the heart rate secondary to lung inflation and resultant increased parasympathetic tone (remember theincreased sympathetic tone that caused the sudden shift in fluid—this parasympathetic tone counteracts that). Recent evidence suggeststhat the use of CPAP in patients with AHF decreases intubation rate and improves survival.Flash Pulmonary Edema Emergency4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failurehttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585804 13/13ReferencesAcute heart failure and cardiogenic shock: a multidisciplinary practical guidance. Intensive Care Med 2015;42:147-63. – Click HereKee, K & Naughton, MT 2010, ‘Heart failure and the lung’, Circulation, vol. 74, no. 12, pp. 2507-2516.
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