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A brief synopsis of acute decompensated heart failure

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A brief synopsis of acute decompensated heart failure

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A brief synopsis of acute decompensated heart failure

  1. 1. A Brief Synopsis of acute decompensated heart failure Dr. Emad Efat Shebin El kom Chest hospital June 2017
  2. 2. Definition Acute decompensated heart failure (ADHF): a common and potentially fatal cause of acute respiratory distress. 1. The clinical syndrome is characterized by the development of dyspnea, generally associated with rapid accumulation of fluid within the lung's interstitial and alveolar spaces, which is the result of acutely elevated cardiac filling pressures (cardiogenic pulmonary edema). 2. ADHF can also present as elevated left ventricular filling pressures and dyspnea without pulmonary edema.
  3. 3. Definition CHF can be categorized into: Systolic versus diastolic Left-sided versus right –sided Left lungs Right peripheral Acute versus chronic Acute- MI Chronic-cardiomyopathy High output hypermetabolic state
  4. 4. Definition 1.Systolic heart failure: Diagnosed when the ejection fraction has decreased below the threshold of 55%. The ejection fraction is a calculation of how much blood is ejected out of the left ventricle (stroke volume) divided by the maximum volume remaining in the left ventricle at the end of diastole 2. Diastolic heart failure:  This condition occurs when the heart can contract normally but is stiff, or less compliant  More common in patients older than 75 years of age, especially in patients with high blood pressure, and it is also more common in women.
  5. 5. Definition
  6. 6. Definition 1.Left-sided heart failure: Fluid collects in the lungs makes it more difficult for the airways to expand as a person inhales. Breathing becomes more difficult and the person may feel short of breath, particularly with activity or when lying down. 2.Right-sided heart failure: Fluid begins to collect in the feet and lower legs (pitting edema). With pitting edema, a finger pressed on the swollen leg leaves an imprint. Non-pitting edema is not caused by heart failure. As the right heart failure worsens, the upper legs swell and eventually the abdomen collects fluid (ascites). Weight gain accompanies the fluid retention.
  7. 7. The American College of Cardiology/American Heart Association stages patients according to the progression of their heart failure. The stages are as follows: Stage A: High risk for developing heart failure – Patient has one or more risk factors for developing heart failure. Stage B: Asymptomatic heart failure – This stage includes patients who have an enlarged or dysfunctional left ventricle from any cause, but are asymptomatic. Stage C: Symptomatic heart failure – Patient experiences heart failure symptoms shortness of breath, fatigue, inability to exercise, etc. Classification
  8. 8. Stage D: Refractory end stage heart failure – Patient has heart failure symptoms at rest in spite of medical treatment. – Cardiac transplantation, mechanical devices, more aggressive medical therapy, or end of life care may be necessary. New York Heart Association's functional classification :  Class I No limitation of physical activity.  Class II Slight limitation of physical activity.  Class III Marked limitation of physical activity.  Class IV Symptoms occur even at rest; discomfort with any physical activity. Classification
  9. 9. Symptoms  Dyspnea with progressively increasing severity as the following:  Exertional dyspnea: The most sensitive symptom  Orthopnea: dyspnea that develops in the recumbent position and is relieved with elevation of the head with pillows.  Paroxysmal nocturnal dyspnea (PND): sudden awakening of the patient, after a couple of hours of sleep, with a feeling of severe anxiety, breathlessness, and suffocation  Dyspnea at rest  Acute pulmonary edema  Cough: Cough that produces pink, frothy sputum is highly suggestive of congestive heart failure (CHF).  Wheezing
  10. 10. Symptoms  Chest pain/pressure  Palpitations: are the sensation a patient has when the heart is racing.  Common non-cardiac signs and symptoms of heart failure include: fatigue, weakness anorexia, nausea, weight loss, bloating oliguria, nocturia cerebral symptoms: confusion, memory impairment, anxiety, headaches, insomnia, nightmares.
  11. 11. Orthopnea
  12. 12. Paroxysmal nocturnal dyspnea
  13. 13. Left-sided heart failure
  14. 14. Physical Examination  Cardiac cachexia  The pulse may be weak, rapid, and thread  Systolic arterial pressure may be reduced  The proportional pulse pressure (pulse pressure/systolic pressure) may be markedly reduced  Fever may be present  Diaphoresis, pallor, peripheral cyanosis and coldness of the extremities  Rales heard over the lung bases  With acute pulmonary edema, rales are frequently accompanied by wheezing.
  15. 15. The Signs And Symptoms Physical Examination
  16. 16. Physical Examination  Predominant Right-Sided Heart Failure:  Jugular venous distention  Kussmaul sign: Increase jugular venous pressure with respiration  Hepatojugular reflux is the distention of the jugular vein induced by applying manual pressure over the liver  Hydrothorax: usually bilateral, or on the right side  Congestive hepatomegaly and ascites.  Peripheral edema  Edema may be severe (anasarca) in severe right heart failure.
  17. 17. The Signs And Symptoms Physical Examination
  18. 18. Physical Examination Hepatojugular reflux Pitting edema
  19. 19. Physical Examination  Cardiac findings:  Protodiastolic (S3) gallop  Cardiomegaly: Notable exceptions include heart failure from acute MI, constrictive pericarditis, restrictive cardiomyopathy, valve or chordae tendineae rupture, or heart failure due to tachyarrhythmias or bradyarrhythmias.  Pulsus alternans (alternation of 1 strong and 1 weak beat)  Accentuation of P2 heart sound in pulmonary arterial hypertension  Mitral and tricuspid regurgitation murmurs: due to ventricular dilatation.
  20. 20. Causes  The most common cause is coronary artery disease,  Hypertension  Valvular heart disease  Congenital heart disease  Cardiomyopathies  Myocarditis  Infectious endocarditis.  Prolonged, serious arrhythmias  Toxic exposures, such as alcohol or cocaine  Endocrine disorders (including thyroid disorders)  Exposures (such as radiation or chemotherapy)
  21. 21. Causes
  22. 22. Risk factors  Age  Hypertension  Physical inactivity  Diabetes  Obesity  Smoking  Metabolic syndrome  Enlargement of the left ventricle  Infection of the heart muscle (usually viral)  Pheochromocytoma  Thyroid disease  Valvular heart disease  familial heart disease  Coronary artery disease  Dyslipidemia  Alcohol use  Substance abuse  Prior heart attack  History of chemotherapy/radiation to the chest  Sleep disorders  Collagen vascular disease, rheumatic fever
  23. 23. Risk factors
  24. 24. Congestive heart failure may be exacerbated by: 1. lifestyle habits:  Unhealthy habits, such as smoking and excessive use of alcohol  Obesity and lack of exercise  High salt intake, which may cause more fluid retention  Noncompliance with medications and other therapies 2. Cardiac ischemia 3. Dysrhythmias 4. Cardiac or extracardiac infection 5. Pulmonary embolus 6. Physical or environmental stresses 7. Iatrogenic volume overload. 8. Pregnancy 9. Hyperthyroidism Precipitating factors
  25. 25.  Acute Respiratory Distress Syndrome  Altitude Illness - Pulmonary Syndromes  Anaphylaxis  Chronic Obstructive Pulmonary Disease and Emphysema  Anemia  Acute Bronchitis  Hyperventilation Syndrome  Myopathies  Pericarditis and Cardiac Tamponade  Pneumonia  Pneumothorax and Pneumomediastinum  Pulmonary Embolism  Shock, Septic  Venous Air Embolism Differentials
  26. 26. Other Problems to be Considered  The cardiac conditions combined with asthma or symptoms of chronic obstructive pulmonary disease (COPD) are difficult clinical challenges.  The standard of care has been shotgun therapy, namely treating patients for both congestive heart failure (CHF) and an acute pulmonary process such as asthma, with both diuretics and beta-agonists.
  27. 27. Investigations Lab Studies: 1. Serum levels of beta-natriuretic peptide (BNP) and the BNP precursor, Pro-BNP: Serum levels of BNP lower than 100 pg/mL are unlikely to be from CHF. BNP levels more than 500 pg/mL are most consistent with CHF. 1. Complete blood count (CBC), which may indicate anemia or infection as potential causes of heart failure 2. Urinalysis (UA), which may reveal proteinuria, which is associated with cardiovascular disease 3. Serum electrolyte levels, which may be abnormal owing to causes such as fluid retention or renal dysfunction 4. Blood urea nitrogen (BUN) and creatinine levels, which may indicate decreased renal blood flow
  28. 28. Investigations Lab Studies: 5. Fasting blood glucose levels, because elevated levels indicate a significantly increased risk for heart failure (diabetic and nondiabetic patients) 6. Elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), or bilirubin levels, which is suggestive of a congestive hepatopathy. 7. Cardiac enzymes and other serum markers for ischemia or infarction may also be useful. 8. ABG levels may be of benefit (i.e. evaluation of hypoxemia, Hypercapnia, acidosis, dilutional hyponatremia).
  29. 29. Investigations Imaging Studies: Chest radiography: – Chest radiography is the most useful tool. – Cardiomegaly with a cardiothoracic ratio greater than 50%. – Pleural effusions may be present bilaterally or if they are unilateral more commonly observed on the right. – Early CHF may manifest as cephalization of pulmonary vessels, generally reflecting a pulmonary capillary wedge pressure (PCWP) of 12-18 mm Hg. As the interstitial fluid accumulates, more advanced CHF may be demonstrated by Kerley B lines (PCWP is 18-25 mm Hg). – Pulmonary edema is observed as perihilar infiltrates often in the classic butterfly pattern, reflecting a PCWP of more than 25 mm Hg.
  30. 30. Stage I CHF - Redistribution  Redistribution of the pulmonary veins. This is know as cephalization (blue arrow) because the pulmonary veins of the superior zone dilate due to increased pressure.  An increase in width of the vascular pedicle (red arrows) Cardiogenic pulmonary edema
  31. 31. The vascular pedicle is bordered on the right by the superior vena cava and on the left by the left subclavian artery origin Cardiogenic pulmonary edema
  32. 32. Stage II CHF - Interstitial edema Characterized by: 1. Kerley’s A lines: extend radially from the hilum to the upper lobes; represent thickening of the interlobular septa that contain lymphatic connections. Cardiogenic pulmonary edema
  33. 33. 2. Kerley’s B lines are short horizontal lines situated perpendicularly to the pleural surface at the lung base; they represent edema of the interlobular septa. Cardiogenic pulmonary edema
  34. 34. 3. Thickening of the bronchial walls (peribronchial cuffing) and as loss of definition of these vessels (perihilar haze). Cardiogenic pulmonary edema
  35. 35. 4. Fluid in the major or minor fissure (shown here) produces thickening of the fissure beyond the pencil-point thickness it can normally attain Cardiogenic pulmonary edema
  36. 36. Stage III CHF - Alveolar edema Characterized by: Alveolar edema with perihilar consolidations and air bronchograms ( Bat's wing or butterfly pulmonary opacities ) (yellow arrows) pleural fluid (blue arrow) prominent azygos vein and increased width of the vascular pedicle (red arrow) an enlarged cardiac silhouette (arrow heads). Cardiogenic pulmonary edema
  37. 37.  Echocardiography :  Evaluation of patients with known or suspected congestive heart failure.  Establishing the diagnosis of diastolic HF  Regional wall motion abnormalities.  Globally depressed or myopathic left ventricular function  Cardiac tamponade and pericardial constriction.  Pulmonary embolus.  Valvular heart disease as mitral or aortic stenosis or regurgitation.  Cardiac output (ejection fraction)  Pulmonary artery and ventricular filling pressures. Investigations
  38. 38.  ECG: It is a nonspecific tool but may be useful in diagnosing concomitant:  Cardiac ischemia.  Prior myocardial infarction (MI).  Cardiac dysrhythmias.  Chronic hypertension.  Left ventricular hypertrophy. Investigations
  39. 39.  Nuclear Imaging Nuclear imaging can be used in the assessment of heart function and damage in CHF.  Angiography: Cardiac catheterization and coronary angiography are indicated in the following situations: CHF caused by systolic dysfunction in association with angina or regional wall motion abnormalities Before cardiac transplantation CHF secondary to post-infarction ventricular aneurysm or other mechanical complications of MI Investigations
  40. 40. Investigations High-resolution computed tomography (HRCT): Stage I CHF – Redistribution:  Redistribution of blood flow from the lower to the upper. This is know as cephalization because the pulmonary veins of the superior zone dilate due to increased pressure.  Increased artery-to-bronchus ratio at hilar level (normally they are equal)  Cardiomegally Significant enlargement of segmental / subsegmental pulmonary arteries (NB pulmonary artery-to- bronchus ratio >1) and Mosaic attenuation pattern
  41. 41. Investigations - HRCT Stage II CHF - Interstitial edema Characterized by: 1. Thickened interlobular septa : Septal lines, also known as Kerley lines, become prominent. They usually occur when pulmonary capillary wedge pressure reaches 20-25 mmHg. Smooth septal thickening (red arrow) in the lower right lobe, increased vascular diameter ( yellow arrow) and bilateral pleural effusion (black arrow) in a patient with congestive heart failure. Please observe the aneurysm on the descending aorta
  42. 42. Investigations - HRCT 2. Bronchial wall thickening will also be seen, and is the basis of peribronchial cuffing seen on chest x-rays. Interstitial pulmonary edema. (A) Axial chest CT demonstrates smooth thickening of interlobular septae (white arrow). This is the CT equivalent of Kerley B lines seen on chest x-rays. (B) Magnified view from the RLL in the same patient demonstrates bronchial wall thickening (green arrow), which is the CT equivalent of peribronchial cuffing seen on radiographs. Also, note that the adjacent pulmonary artery branch (red arrow) is slightly larger than the bronchus.
  43. 43. Investigations - HRCT 3. Fluid in the major or minor fissure produces thickening of the fissure 4. Peribronchovascular interstitial thickening 5. ground-glass opacities 6. mosaic pattern of attenuation 7. pleural effusion 8. lymph nodes may be enlarged congestive heart failure presenting ground-glass opacities and smooth interlobular septa thickening, a mosaic pattern of attenuation and bilateral pleural effusion Thickening of the right major fissure from subpleural edema
  44. 44. Investigations - HRCT Stage III CHF - Alveolar edema Characterized by:  Peribronchial nodules  Alveolar edema with perihilar consolidations and air bronchograms ( Bat's wing or butterfly pulmonary opacities )  Pleural effusion  An enlarged cardiac silhouette High-resolution computed tomography scans, showing slices acquired at the aortic arch level, using a pulmonary window, in a patient with acute myocardial infarction and Cardiogenic pulmonary edema presenting consolidations, ground-glass opacities, smooth interlobular septal thickening and bilateral pleural effusion.
  45. 45. Investigations - HRCT Cardiomegaly: The heart is enlarged if the cardiothoracic ratio (CTR) is greater than 50% in the axial plane. If the heart is enlarged, check for other signs of heart failure such as pulmonary oedema, septal lines (or Kerley B lines), and pleural effusions. Transverse CTR=T/C T (superior white arrows) : the maximum transverse cardiac diameter. C (inferior white horizontal arrows): The transverse thoracic diameter, would normally be taken at the level of the dome of the left hemidiaphragm
  46. 46.  Central venous catheter (CVC) placement  Pulmonary artery catheters  Cardiac catheterization may be necessary for a complete evaluation and assessment of prognosis.  Maximal exercise testing with/without respiratory gas exchange and/or blood oxygen saturation, which assesses cardiac and pulmonary function with activity  Screening for sleep-disturbed breathing, which affects neurohormonal activation  Holter monitoring, which may reveal arrhythmias or abnormal electrical activity Procedures to be done
  47. 47.  Prehospital Care: 1. Begin treatment with the ABCs (Airway, Breathing, Circulation). 2. Administer supplemental oxygen. 3. Use cardiac monitoring and continuous pulse oximetry. 4. Obtain intravenous access 5. A prehospital ECG, if available. 6. Provide nitroglycerin sublingual or spray for active chest pain in the patient without severe hypotension 7. Intravenous furosemide. Treatment
  48. 48. Treatment  Emergency Department Care: 1. The ABCs. 2. Administer supplemental oxygen, initially 100% nonrebreather facemask. 3. Use cardiac monitoring and continuous pulse oximetry. 4. Obtain intravenous access. 5. To reduce venous return, elevate the head of the bed. 6. Start with nitrates and diuretics if patients are hemodynamically stable.. 7. Treat the underlying cause as well, if identified. 8. Eliminate contributing factors when possible. 9. Restrict fluid and sodium. 10. Urine output monitoring (perhaps with urethral catheter placement)
  49. 49. 11. Prophylaxis against venous thromboembolism (deep vein thrombosis and pulmonary embolism) with low dose unfractionated heparin or low molecular weight heparin, or fondaparinux, or by mechanical device (e.g., intermittent pneumatic compression device) 12. Noninvasive ventilation [NIV]: Nasal continuous positive airway pressure (CPAP) therapy and facemask ventilation therapy. BiPAP therapy may improve ventilation and vital signs more rapidly than CPAP, a higher incidence of MI associated with BiPAP has been reported. 13. Patients with respiratory failure who fail to improve with NIV (within one half to two hours) or do not tolerate or have contraindications to NIV should be intubated for conventional mechanical ventilation Treatment
  50. 50. CPAP
  51. 51. The airways are kept open using a BiPAP machine. BiPAP machines are adjusted to dual settings so that the pressure of the air coming in on inspiration can be different from the pressure of the air being exhaled. BiPAP (Bi-level Positive Airway Pressure)
  52. 52.  Diuretics: First-line therapy, Preload reduction, for acute heart failure. Given by bolus or continuous infusion and in high or low doses Generally includes a loop diuretic (ie, furosemide, bumetanide, torsemide) In patients with hypertensive heart failure who have mild fluid retention, thiazide diuretics may be preferred because of their more persistent antihypertensive effects. Addition of a second diuretic to potentiate the effects of the loop diuretic. For patients in whom the diuretic response is inadequate, intravenous chlorothiazide or oral metolazone or spironolactone are reasonable choices for a second diuretic. Other agents, such as vasopressin antagonists and adenosine receptor blockers, can be used to assist diuretics. Medication
  53. 53.  Diuretics: Spironolactone improves survival. In addition, the associated reduction in collecting tubule sodium reabsorption and potassium secretion can both enhance the diuresis and minimize the degree of potassium wasting. Transition to oral diuretic therapy is made when the patient reaches a near euvolemic state. Hemodialysis or ultrafiltration, may be used alternative strategies, if diuretic resistance occurs. Ultrafiltration is an effective method of fluid removal that provides adjustable fluid removal volumes and rates and no effect on serum electrolytes. However, studies have not found a clinical benefit over diuretic therapy and it does not preserve renal function compared to diuresis. Medication
  54. 54.  Vasodilators: Vasodilators (eg, nitroprusside, nitroglycerin, or nesiritide) will decrease preload and/or afterload. These agents reduce myocardial oxygen demand by lowering preload and afterload. Nitroprusside:  Early vasodilator therapy, in patients with severe hypertension, acute mitral regurgitation, or acute aortic regurgitation. It causes balanced arterial and venous dilation like Nesiritide Nitroglycerin — Nitrates, the most commonly used vasodilators in ADHF, cause greater venous than arterial vasodilation Nitrate administration is contraindicated after use of phosphodiesterase type 5 inhibitors (e.g., sildenafil) Medication
  55. 55.  Inotropic agents: Principal inotropic agents include dopamine, dobutamine, inamrinone (formerly amrinone), milrinone, dopexamine, and digoxin. In patients with severe left ventricular systolic dysfunction and low output syndrome (diminished peripheral perfusion and endorgan dysfunction), dopamine and dobutamine are usually used. Dobutamine is probably the current agent of choice These agents augment both coronary and renal blood flow. Patients receiving intravenous inotropes require continuous blood pressure and cardiac rhythm monitoring. Medication
  56. 56.  Vasopressors: In patients with ADHF and marked hypotension Vasopressors used in this setting include norepinephrine, high dose dopamine (>5 micrograms/kg/min), and vasopressin They can be used as a temporizing measure to preserve systemic blood pressure and endorgan perfusion They increase afterload and decrease cardiac output Analgesics:  Intravenous morphine may be considered in some patients with acute pulmonary edema as an ungraded recommendation  They reduce anxiety and distress associated with dyspnea but also induce nausea and depress respiratory drive. Medication
  57. 57.  Digoxin : Has no role in the emergency management of CHF due to delayed absorption and diminished efficacy. Limit use of digoxin to chronic CHF, in which its role has been well established. Digoxin is mainly used as an antiarrhythmic to control the rate of the heart in atrial fibrillation and flutter. In contrast, excessive digoxin in the blood can cause life threatening arrhythmias. Although commonly used in the past, digoxin has moved far down the list of recommended drugs for treatment of heart failure. It is still considered for patients who are taking ACE inhibitors, angiotensin receptor blockers (ARBs), beta blockers and/or diuretics and are still experiencing heart failure symptoms. Medication
  58. 58.  ACE inhibitors: Initiation of therapy For patients who are not already taking an ACE inhibitor, single agent angiotensin receptor blocker (ARB), or angiotensin receptor-neprilysin inhibitor, we suggest that such therapy not be initiated at the time of presentation with an episode of ADHF. An oral ACE inhibitor or ARB can usually be started within 24 to 48 hours, once the patient is hemodynamically stable. Initiation of these therapies known to improve outcomes is recommended prior to hospital discharge. Continued therapy For patients who are already taking an ACE inhibitor, single agent ARB, or ARNI, we suggest that maintenance of oral therapy be cautiously continued. However, the dose should be decreased or the drug discontinued if hypotension, worsening renal function, or hyperkalemia is present. Medication
  59. 59.  Beta-blockers:  Beta blockers reduce mortality when used in the long term management of patients with HF with reduced ejection fraction,  but must be used cautiously in patients with decompensated HF with reduced ejection fraction because of the potential to worsen acute HF.  Initiation of therapy prior to discharge is recommended in stable patients Medication
  60. 60. Applying the shotgun approach:  Aerosolized more selective beta-2 agonists , Terbutaline as well as albuterol, isoetharine, and bitolterol, decrease tachycardia, dysrhythmias, and cardiac work while transiently enhancing cardiac function.  Steroids:  Not administered by intravenous or oral route, due to systemic sodium retention and volume expansion, hypokalemia, and occasional hypertension.  Inhaled steroids, may be used but because their delayed onset of action, they remain an area in need of further study. Patient with CHF and asthma exacerbations
  61. 61.  Diuretics  Theophylline and aminophylline: Limit roles in the acute setting. They are positive inotropic agents mediated by an increase in catecholamines, and they dilate coronaries and exert mild diuretic effects. they can exacerbate dysrhythmias (eg, multifocal atrial tachycardia [MAT], ischemia) by increasing cardiac work. Patient with CHF and asthma exacerbations
  62. 62. Further Inpatient Care:  Patients presenting with acute symptoms of congestive heart failure (CHF) or pulmonary edema require hospital admission with few exceptions: – gradual onset of shortness of breath – rapid response to therapy – oxygen saturation greater than 90% – No acute coronary syndromes and MI.  Critical care unit admission for patients who require intubation or remain with significant respiratory, hemodynamic, and/or cardiovascular compromise. Further Outpatient Care: Patient education with specific instructions regarding dietary restrictions and compliance with medical therapy. Follow-up
  63. 63. In/Out Patient Medications:  ACE inhibitors are indicated in patients with ejection fractions of 35% or less.  Digoxin may also be helpful in patients with ejection fractions of 35% or less.  Diuretics, such as furosemide, may be helpful regardless of ejection fraction.  Carvedilol are indicated as therapy for patients with diastolic dysfunction or for patients with coronary insufficiency.  Calcium channel blockers, Amlodipine are useful in patients with diastolic dysfunction and heart failure. Follow-up
  64. 64. 1. Electrophysiologic intervention:  Cardiac resynchronization therapy (CRT)  Pacemakers  Implantable cardioverter-defibrillators (ICDs) 2. Revascularization procedures :  Coronary artery bypass grafting (CABG)  Percutaneous coronary intervention (PCI)  Valve replacement or repair  Ventricular restoration. 3. Mechanical cardiac support:  Intraaortic balloon pump counterpulsation,  Extracorporeal membrane oxygenation (ECMO), or  Short term left ventricular assist devices Invasive therapies
  65. 65. 1. A permanent pacemaker: A permanent pacemaker is a small device implanted in the chest just under the collarbone. A pacemaker may be used if the heart's natural pacemaker (the SA node) is not working properly causing a slow heart rate or rhythm, or if the electrical pathways are blocked. Electrophysiologic intervention
  66. 66. 1. Cardiac resynchronization therapy (CRT) also known as biventricular pacing: It is used for ventricles that don't contract at the same time. This can worsen heart failure. A biventricular pacemaker paces both ventricles at the same time, increasing the amount of blood pumped by the heart. Electrophysiologic intervention
  67. 67. 1. Implantable cardioverter-defibrillators (ICDs): It looks similar to a pacemaker, though slightly larger. It works very much like a pacemaker. However, the ICD can send an energy shock that resets an abnormal heartbeat back to a normal. Many devices combine a pacemaker and ICD in one unit. Electrophysiologic intervention
  68. 68. 1. Percutaneous coronary intervention (PCI) The cardiologist places a small, hollow metal (mesh) tube called a "stent" in the artery to keep it open following a balloon angioplasty. The stent prevents constriction or closing of the artery during and after the procedure. Drug-eluding stents are now used. These stents are coated with medication that helps prevent narrowing of the artery. Revascularization procedures
  69. 69. 2. Coronary artery bypass grafting (CABG): It is a type of surgery that improves blood flow to the heart. It's used for people who have severe coronary heart disease (CHD), also called coronary artery disease. CABG surgery creates new routes around narrowed and blocked arteries, allowing sufficient blood flow to deliver oxygen and nutrients to the heart muscle. Revascularization procedures
  70. 70. 3. Valve replacement or repair:  The ACC/AHA recommends that valve repair or replacement in patients with hemodynamically significant valvular stenosis or regurgitation and asymptomatic heart failure should be based on contemporary guidelines.  The ACC/AHA indicates that such surgery should be considered for patients with severe aortic or mitral valve stenosis or regurgitation, even when ventricular function is impaired. Revascularization procedures
  71. 71. 4. Surgical ventricular restoration: Revascularization procedures a | The geometric effects of cardiac dilatation change the normal elliptical architecture of the heart into b | a spherical form (myocardial infarction scar shown by the white area). c | Surgical ventricular restoration reduces ventricular volume and rebuilds the elliptical shape. In very dilated hearts, the site of patch placement is either located at the scar or placed just beneath the aortic valve to rebuild form.
  72. 72.  Mechanical cardiac support:  For selected patients with severe HF with reduced ejection fraction (generally with left ventricular ejection fraction <25 percent) with acute, severe hemodynamic compromise (cardiogenic pulmonary edema with cardiogenic shock)  Nondurable mechanical support is an option as a “bridge to decision” or “bridge to recovery”  Mechanical modalities used in this setting include Intraaortic balloon pump counterpulsation, extracorporeal membrane oxygenation (ECMO), or short term left ventricular assist devices Mechanical cardiac support
  73. 73. Mechanical cardiac support Intraaortic balloon pump counterpulsation, during systole, the balloon is deflated actively (by facilitating the outflow of blood from the left ventricle to the aorta) and during diastole the balloon inflates to improve the heart’s perfusion with increased blood flow to the level of the coronary arteries level, improving overall cardiac function.
  74. 74. Mechanical cardiac support ECMO involves an extracorporeal circuit that directly oxygenates and removes carbon dioxide from the blood using an oxygenator, a gas exchange device that uses a semipermeable membrane to separate a blood compartment from a gas compartment.
  75. 75. Mechanical cardiac support Ventricular assist devices support the ventricular function of the heart. The ventricles push blood out of the heart. Depending upon the site of implantation, it may help to assist the heart with pushing the blood to the lungs (right side), to the entire body (left side) or sometimes it may be used in both ventricles (biventricular).
  76. 76.  Selected patients with severe heart failure, debilitating refractory angina, ventricular arrhythmia, or congenital heart disease that cannot be controlled despite pharmacologic, medical device, or alternative surgical therapy should be evaluated for heart transplantation.  The patient must be well informed, motivated, and emotionally stable; have a good social support network; and be capable of complying with intensive medical treatment.  Total Artificial Heart (TAH): Despite more than 40 years of effort, the clinical application of artificial heart technology is still immature. However, with the approval of the SynCardia device and with new efforts to create small pumps, TAHs will ultimately be routine components of heart failure surgery for very sick patients with heart failure and biventricular failure. Heart Transplantation
  77. 77. Heart Transplantation The SynCardia device : Originally used as a permanent replacement heart, the Total Artificial Heart is currently approved as a bridge to human heart transplant for transplant-eligible candidates at risk of imminent death from biventricular failure. It is the world’s first and only Food and Drug Administration (FDA), Health Canada and Conformité Européene (CE) approved Total Artificial Heart
  78. 78.  Close monitoring of blood pressure.  Patient should modify diet as follows:  Sodium restriction.  Weight reduction .  Appropriate fluid restriction .  Modify activity as follows:  During severe stage, bed rest with elevation of head of bed and anti-embolism stockings to help control leg edema.  Gradual increase in activity with walking to help increase strength. Prevention
  79. 79.  Acute MI  Cardiogenic shock  Arrhythmias (most commonly atrial fibrillation)  Ventricular arrhythmias, such as ventricular tachycardia,  Electrolyte disturbances  Mesenteric insufficiency  Protein enteropathy  Digitalis intoxication Complications
  80. 80. Thank you

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