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Heart failure
Heart failure is the inability of the heart to pump sufficient blood to meet the needs of tissues. It results in fluid overload and poor tissue perfusion. It has multiple causes including reduced contractility, valve disorders, coronary artery disease, and hypertension. Symptoms vary between acute pulmonary edema with respiratory distress, and chronic fatigue and edema. Treatment involves reducing preload and afterload through medications like ACE inhibitors, ARBs, beta-blockers, vasodilators, and diuretics.
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Heart failure
- 1. Heart failure Suchithra .p.v 1styear Msc Nursing College of Nursing
- 2. Heart failure • HeartFailure is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients. • It is otherwise known as Congestive Cardiac Failure. • Heart failure results in intravascular and interstitial volume overload and poor tissue perfusion.
- 4. causes • Reduced ventricularcontractility • Ventricular outflow obstruction (pressure overload ) • Ventricular inflow obstruction • Ventricular volume overload • Arrhythmia • Diastolic dysfunction
- 5. Acute causes • Acutemyocardial infarction • Dysrrhythmias • Pulmonary emboli • Thyrotoxicosis • Hypertensive crisis • Rupture of papillary muscle( eg: mitral valve) • Ventricular septal defect • Myocarditis
- 6. Chronic causes • Coronaryartery disease • Hypertension • Rheumatic heart disease • Congenital heart disease • Cor pulmonale • Cardiomyopathy • Anemia • Bacterial endocarditis • Valvular disorders •
- 7. RISK FACTORS • Advancingage • Hypertension • Diabetes • Obesity • High serum cholesterol • Cigarette smoking
- 8. PRECIPITATING CAUSES • Anemia •Infection • Hypothyroidism • Bacterial endocarditis • Paget’s disease • Nutritional deficiencies • Hypervolemia
- 9. PATHO PHYSIOLOGY Compensatory mechanism •1. Hemodynamic alterations • 2. Neurohormonal responses • 3. Ventricular dilation • 4. Ventricular hypertrophy
- 10. Alterations in Beta-adrenergicReceptor pathway • Increased NE concentration cause down regulation of beta-1 adrenergic receptors in the ventricles. • Beta- adrenergic receptor kinase(BARK) enzyme level increases.
- 11. Role of ArginineVasopressin (AVP) • Circulating AVP is elevated. This leads to salt and water retention and systemic vasoconstriction.
- 12. Role of cytokinine •They have crucial roles in mediating the changes in myocardial structure and function in CHF.
- 13. Cellular and MolecularMechanisms • Role of calcium • Calcium plays a central role in myocardial contraction and relaxation. In CHF, there is prolonged elevation of intracellular calcium during relaxation
- 14. • Role offree radicals and apoptosis • Altered mitochondrial oxygen metabolism results in formation of free radicals. • Free radicals produced by various mechanisms have been shown to result in apoptosis of cardiac myocytes in CHF.
- 15. DECOMPENSATED HEART FAILURE •Ventricular remodeling • Sustained neurohumoral activation
- 16. Counter regulatory mechanism •ANP and BNP are hormones produced by the heart muscle . • ANP is released in response to stretch or increased volume in the chambers. • Levels of circulating ANP can be correlate with functional class prognosis and hemodynamic state.
- 17. • Inhibit renin,aldosterone and ADH secretion and results in excretion of sodium and water • Promotes venous and arterial vasodilatation. • BNP is released in response to an increase in wall stress or triggered by pressure.
- 18. TYPES OF HEARTFAILURE • Left –sided heart failure or left ventricular dysfunction • Right sided heart failure or right ventricular failure • Biventricular heart failure • Diastolic and systolic dysfunction
- 19. High output versuslow 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 tissues Low output failure occurs in most forms of heart disease resulting in hypoperfusion of tissue cells .
- 20. Backward versus forwardfailure • Backward failure focuses on the ventricles inability to eject completely ,which increases ventricular filling pressures ,causing venous and pulmonary congestion . • Forward failure is a problem of inadequate perfusion. It results when reduced contractility produces a decrease in stroke volume and cardiac output
- 21. • Acute versuschronic heart failure
- 23. CLINICAL MANIFESTATIONS • LeftSided HeartFailure • Acute LVF presents with a sudden onset of dyspnoea at rest. • progresses to acute respiratory distress, orthopnoea and prostration. • appears agitated ,pale and clammy • Rapid pulse
- 24. • Cool periphery •High BP • Elevated JVP if associated with RVF. • Auscultaition – crepitations,triple gallop rhythm. • Displaced apex beat.
- 25. Respiratory system • Tachypnea •Capillary refill > 3 seconds • Orthopnea • Dyspnea on exertion • Nocturnal dyspnea • Cough with frothy sputum (indicative of pulmonary edema)
- 26. • Basilar cracklesor rhonchi • Cyanosis • Hypoxia (respiratory acidosis) • Kussmaul’s sign • Cheyne stokes respiration
- 27. Cardiovascular system • Diaphoresis •Audible S3 and S4 heart tones • Murmur or mitral insufficiency • Enlarged left ventricle on X-ray • Enlarged left atrium on X-ray • Narrowing pulse pressure • Pulses alternans (alteration of weak and strong beats)
- 28. • Basilar cracklesor rhonchi • Cyanosis • Hypoxia (respiratory acidosis) • Kussmaul’s sign • Cheyne stokes respiration • Elevated pulmonary artery pressures • Elevate pulmonary artery occlusive pressures
- 29. Central nervous system •Mental confusion Generalized symptoms • Weight gain. • Fatigue/weakness/lethargy
- 30. Right sided heartfailure Gastrointestinal system • Hepatomegaly • Splenomegaly • Hepatojugular reflux • Ascites
- 31. • Weight gain •Weight loss and emaciation as a result of inadequate intake of food and wasting of tissues. This picture is termed as cardiac cachexia
- 32. Cardiovascular system • Arrhythmias •Elevated CVP • Elevated right atrial pressure • Elevated right ventricular pressure • Narrowing pulse pressure • Murmur or tricuspid insufficiency
- 33. • Audible S3and S4 heart tones • Enlarged right atrium on X-ray • Enlarged right ventricle on X-ray • Dependant pitting edema • Venous distention
- 34. • Urinary system •Oliguria • Nocturia
- 35. Chronic heart failure •Fatigue • Dyspnea • Orthopnea • Paroxysmal nocturnal dyspnea • Tachycardia • Edema
- 36. • Nocturia • Skinchanges Chronic swelling result in pigment changes causing the skin to appear brown • cool and damp to the touch • Behavioral changes • Chest pain • Weight changes
- 37. COMPLICATIONS • Pleural effusion •Dysrhythmias EF less than 35%have a high risk of fatal dysrhythmias and sudden cardiac death. • Renal failure • Impaired liver function & Cardiac cirrhosis • Thromboembolism Hypokalemia & Hyperkalemia
- 38. DIAGNOSTIC STUDIES • History •Physical Examination
- 40. • Electrocardiogram • Laboratorydata(cardiac enzymes, BNP,serum chemistries ,liver function studies ,thyroid function studies and complete blood count). In severe CHF dilutional hyponatremia occurs. BUN and creatinine are moderately elevated.
- 41. • BNP levelsare used to assess the HF. • BNP<100pg/ml - heart failure very improbable • BNP100-500pg/ml -HF probable • BNP>500pg/ml -HF very probabl
- 42. • Echocardiogram :EF less than 40% accepted as evidence of systolic dysfunction. • Asessment of myocardial viability This can be done by using dobutamine or dipyridamole stress echocardiography, nuclear imaging using thallium or sestamibi and positron emission tomography
- 43. Identify patients whowill benefit from long term therapy with drugs such as ACE inhibitors • Stress testing,(treadmill test, stress echocardiography and nuclear perfusion studies) • Cardiac catheterization and coronary angiography:
- 44. • Endomyocardial biopsy Thisis indicated in patients with clinical indication of myocarditis and systemic disease with possible cardiac involvement such as hemochromatosis, amyloidosis, sarcoidosis and those who have received adriamycin chemotherapy.
- 45. MANAGEMENT OF ACUTE PULMONARYEDEMA • Sit the patient up • Give oxygen(high flow ,high concentration ). non invasive positive pressure ventilation (CPAP-5-10 mmhg) • IV glceryl trinitrate 10-200 microgram /minute until clinical improvement occurs or systolic blood pressure falls to ˂110mmHg. • loop diuretic such as frusemide 50-100mg IV
- 46. • continuous monitoring •Ionotropic agents • Intra aortic balloon pump
- 47. Management • General measures •Pharmacologic therapy • Devices • Surgery • Newer evolving therapies
- 48. General measures • Rest •Correction of aggravating factors • Salt restriction – sodium intake should be limited to ˂ 2g/day • Fluid restriction- to 1-2l/day is advisable in patients with dilutional hyponatremia. • Smoking cessation • Avoid alcohol • Management of co morbidities
- 49. Pharmacologic therapy To Reduceworkload • Angiotensin converting enzyme inhibitors • Angiotensin II receptor blockers • Vasodilators • Diuretics • Beta blockers
- 50. ACE inhibitors • Interruptsthe vicious cycle of neurohumoral activation • Prevents salt and water retension ,peripheral arterial and venous vasoconstriction • Also increase the concentrations of the vasodilator bradykinin. • Decreases SVR and improves myocardial performance.
- 51. • Enalapril: 2.5mg 12 hrly • Lisinopril 2.5 mg daily • Ramipril :1.25 mg daily • Captopril :50 mg tds
- 52. Adverse effects • Persistantcough • Hypotension • Hyperkalemia • deteriorating renal function • Loss of taste
- 53. Angiiotensin II receptorblockers • Similar hemodynamic effects to ACE inhibitors • Do not affect bradykinin metabolism • Losartan, Valsartan, Irbesartan and Eprosartan • Losartan :25 mg daily • Candesartan:4 mg daily • Valsartan : 40 mg daily
- 54. Vasodialators • Venous dialationblood is trapped in the veins ,and venous return to the heart is decreased .This reduces preload • eg: nitroglycerin and isosorbide dinitrate • Dilation of arterioles: arteriolar vasodilators decreases peripheral vascular resistance and afterload • Eg:ACE inhibitors
- 55. Combined action onveins and arterioles • decrease both preload and afterload • sodium nitroprusside relaxes the smooth muscle of both veins and arterioles.it does not directly affect the heart muscle or heart rate
- 56. Beta blockers • Directlyblock the direct effects of the SNS • Cardio selective agents block beta 1 adrenergic receptors.non selective agents block beta 1 and beta 2 adrenergic receptors. • Eg: atenolol,metoprolol , bisoprolol, bucindolol, labetalol,carvedilol,esmolol (25-50 mg bd)
- 57. Diuretics • To mobilizeedematous fluid , reduce pulmonary venous pressure ,and reduce preload • Thiazide diuretics may be the first choice in chronic HF • Eg;benzthiazide,chlorothiazide,chlorthalidone, metolazone
- 58. • Loop diuretics •eg.Frusimide ,torsemide • Spironolactone is an inexpensive ,potassium sparing diuretic.
- 59. Human b-type natriureticpeptide Nesiritide is a synthetic form of human BN
- 60. Beta adrenergic agonists •short term treatment • E.g.:-dopamine, dobutamine
- 61. Cardiac glycosides • Eg; Digoxin • Slow the ventricular rate, improves cardiac function • Optimum therapeutic level os digoxin in serum is 1-1.5 ng/ml • Toxic level is above 2ng/ml
- 62. Calcium channel blockers •Vasodilator • Anti ischemic effects • Eg: Verapamil, diltiazem, amlodipine
- 63. • Phosphodiesterase inhibitors:- Eg:amrinone,milrinone • Antidysrhythmic drugs e.g.adenosine, digoxin, ibutilide, magnesium
- 64. Devices • Implantable cardiacdefibrillators and resynchronization therapy
- 65.
- 66.
- 67. Surgery • Heart transplantation •Coronary revascularization • Dynamic cardiomyoplasty • Partial left ventriculectomy( Batista procedure) • Aneurysmectomy • Mitral annuloplasty and mitral valve repair
- 68. Newer evolving therapies •Gene therapy • To increase the myocardial contractility at molecular level • Genes expressing SERCA2a are increased by using adenovirus transfection of myocytes
- 69.
- 70. Nursing diagnosis Decreased cardiacoutput r/t heart failure ,dysrhythmia or both • Assess blood pressure for hypotension or hypertension • Assess heart rate and rhythm • Document rhythm strips q8h • Auscultate heart rate q2h • Monitor lung sounds
- 71. • Monitor intakeand output • Assess for change in mental status • Administer prescribed medications • Encourage physical and mental support • Encourage client to eat small frequent feeds
- 72. • Excess fluidvolume related to cardiac failure as evidenced by edema ,dyspnea on exertion ,increased weight gain • Monitor intake and output chart • Assess for presence of peripheral edema • Assess for jugular vein distention • Follow low sodium or fluid restriction • Auscultate breath sounds • Administer diuretic therapy
- 73. Impaired gas exchangerelated to increased preload, mechanical failure or immobility as evidenced by increased respiratory rate, shortness of breath, and dyspnea on exertion • Auscultate breath sounds q2h • Assess respiratory rate • Asses for cyanosis • Monitor pulse oximetry • Position the client to facilitate breathing • Administer diuretic therapy
- 74. Ineffective tissue perfusionrelated to decreased cardiac output • Note colour and temperature of the skin q4h • Monitor peripheral pulsesq4h • Provide a warm environment • Encourage active rang of motion • Monitor urine output
- 75. • Activity intolerancerelated to fatigue secondary to cardiac insufficiency and pulmonary congestion as evidenced by dyspnea,shortness of breath ,weakness, increased in heart rate on exertion • space nursing activities • Schedule rest periods • Monitor the clients response to activities • Instruct the client to avoid activities that increase cardiac workload
- 76. • Anxiety r/tto dyspnea or perceived threat of death as evidenced by restlessness, irritability • Deficient knowledge related to disease process as evidenced by questions about the disease and prognosis
- 77. References • KV Krishnadas.Text book of Medicine. 5th edition.Jaypee publications.New Delhi.2008 • Marscall S. Runge. Georege A.Netter’s Cardiology .2nd ed. USA .2014 • Nicki R.Colledge,Brian R. Walker,Stuart H.Ralston.Davidson’s Principles and Practice of Medicine 21st edition 2010 Churchil Living stoneElsevier page no 542-550 • Richard Hatchett, David R Thompson. Cardiac Nursing. Elsevier publications. USA.2007