Heart failure management


Published on

Published in: Health & Medicine
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Heart failure management

  1. 1. Dr. Himanshu Jangid Heart Failure and Management
  2. 2. Definition   Heart failure is a complex pathophysiologic state described by the inability of the heart to fill with or eject blood at a rate appropriate to meet tissue requirements.  The clinical syndrome is characterized by symptoms of dyspnea and fatigue and signs of circulatory congestion or hypoperfusion.
  3. 3. Etiology  The principal pathophysiology of heart failure is the inability of the heart to fill or empty the ventricle.  The most common cause of right ventricular failure is left ventricular (LV) failure.
  4. 4. Etiology  Heart failure is most often due to  (1) impaired myocardial contractility secondary to ischemic heart disease or cardiomyopathy;  (2) cardiac valve abnormalities;  (3) systemic hypertension;  (4) diseases of the pericardium; or  (5) pulmonary hypertension (cor pulmonale).
  5. 5. FORMS OF VENTRICULAR DYSFUNCTION  Heart failure may be described in various ways:  systolic or diastolic,  acute or chronic,  left sided or right sided,  high output or low output.
  6. 6. Left ventricular dysfunction regardless of cause, results in progressive remodeling of the ventricular chamber leading to dilation and a low ejection fraction.
  7. 7. Systolic Heart Failure  Causes of SHF  CAD,  Dilated cardiomyopathy (DCM),  Chronic pressure overload (aortic stenosis and chronic hypertension),  Chronic volume overload (regurgitant valvular lesions and high output cardiac failure).
  8. 8. Systolic Heart Failure  CAD typically results in regional defects in ventricular contraction, which may become global over time  All other causes of SHF produce global ventricular dysfunction  Ventricular dysrhythmias are common in patients with LV dysfunction.  Patients with left bundle branch block and SHF are at high risk of sudden death.
  9. 9. Diastolic Heart Failure  DHF can be classified into four stages.  Class I DHF is characterized by an abnormal LV relaxation pattern with normal left atrial pressure.  Classes II, III, and IV are characterized by abnormal relaxation as well as reduced LV compliance resulting in an increase in LV end- diastolic pressure (LVEDP)  As a compensatory mechanism, the pressure in the left atrium increases so that LV filling can occur despite the increase in LVEDP.
  10. 10. Diastolic Heart Failure  Ischemic heart disease, long-standing essential hypertension, and progressive aortic stenosis are the most common causes of DHF.  In contrast to SHF, DHF affects women more than men.  Hospitalization and mortality rates are similar in patients with SHF and DHF.
  11. 11. ACUTE AND CHRONIC HEART FAILURE  Acute heart failure is defined as  a change in the signs and symptoms of heart failure requiring emergency therapy.  In acute heart failure due to a sudden decrease in cardiac output,  systemic hypotension is typically present without signs of peripheral edema.
  12. 12. ACUTE AND CHRONIC HEART FAILURE  Acute heart failure encompasses three clinical entities:  (1) worsening chronic heart failure;  (2) new-onset heart failure such as with cardiac valve rupture, large myocardial infarction, or severe hypertensive crisis; and  (3) terminal heart failure, which is refractory to therapy.
  13. 13. ACUTE AND CHRONIC HEART FAILURE  Chronic heart failure is present in patients with long-standing cardiac disease.  Typically, chronic heart failure is accompanied by venous congestion, but blood pressure is maintained.
  14. 14. LEFT-SIDED AND RIGHT-SIDED HEART FAILURE  In left-sided heart failure high LVEDP promotes pulmonary venous congestion.  The patient complains of  dyspnea  orthopnea  and paroxysmal nocturnal dyspnea  which can evolve to pulmonary edema.
  15. 15. LEFT-SIDED AND RIGHT-SIDED HEART FAILURE  Right-sided heart failure systemic venous congestion.  Peripheral edema and congestive hepatomegaly are the most prominent clinical manifestations.  Right-sided heart failure may be caused by pulmonary hypertension or right ventricular myocardial infarction,  but the most common cause is left-sided heart failure.
  16. 16. LOW-OUTPUT AND HIGH-OUTPUT HEART FAILURE  The normal cardiac index varies between 2.2 and 3.5 L/min/m2.  The most common causes of low-output heart failure are CAD,  cardiomyopathy,  hypertension,  valvular disease,  pericardial disease.  It may be difficult to diagnose low-output heart failure because a patient may have a cardiac index that is nearly normal in the resting state but does not respond adequately to stress or exercise.
  17. 17. LOW-OUTPUT AND HIGH-OUTPUT HEART FAILURE  Causes of high cardiac output include  anemia,  pregnancy,  arteriovenous fistulas,  severe hyperthyroidism,  beriberi,  Paget's disease.
  18. 18. LOW-OUTPUT AND HIGH-OUTPUT HEART FAILURE  The ventricle fails not only because of the increased hemodynamic burden placed on it but also because of direct myocardial toxicity as caused by thyrotoxicosis and beriberi and myocardial anoxia caused by severe and prolonged anemia.
  19. 19. PATHOPHYSIOLOGY OF HEART FAILURE  The initiating mechanisms of heart failure are  pressure overload (aortic stenosis, essential hypertension),  volume overload (mitral or aortic regurgitation),  myocardial ischemia/infarction,  myocardial inflammatory disease,  restricted diastolic filling (constrictive pericarditis, restrictive myocarditis).
  20. 20. PATHOPHYSIOLOGY OF HEART FAILURE  In the failing ventricle, various adaptive mechanisms  These include  (1) the Frank-Starling relationship;  (2) activation of the sympathetic nervous system (SNS);  (3) alterations in the inotropic state, heart rate, and afterload; and  (4) humoral-mediated responses.  In advanced stages of heart failure mechanisms become maladaptive myocardial remodeling, the key pathophysiologic change responsible for the development and progression of heart failure.
  21. 21. Frank-Starling Relationship  The Frank-Starling relationship  The increase in stroke volume that accompanies an increase in LV end-diastolic volume and pressure  Stroke volume increases because the tension developed by contracting muscle is greater when the resting length of that muscle is increased.  The magnitude of the increase in stroke volume produced by changing the tension of ventricular muscle fibers depends on myocardial contractility.
  22. 22. Frank-Starling Relationship  For example, when myocardial contractility is decreased, as in the presence of heart failure, a lesser increase in stroke volume is achieved relative to any given increase in LV end-diastolic pressure.  Constriction of venous capacitance vessel shifts blood centrally, increases preload, and helps maintain cardiac output by the Frank- Starling relationship.
  23. 23. Activation of Sympathetic Nervous System  Activation of the SNS promotes arteriolar and venous constriction.  Arteriolar constriction serves to maintain systemic blood pressure despite a decrease in cardiac output.  Increased venous tone shifts blood from peripheral sites to the central circulation, thereby enhancing venous return and maintaining cardiac output by the Frank-Starling relationship.
  24. 24. Activation of Sympathetic Nervous System  Arteriolar constriction  redistribution of blood from the kidneys, splanchnic organs, skeletal muscles, and skin  to maintain coronary and cerebral blood flow despite overall decreases in cardiac output.  The decrease in renal blood flow  activates the renin-angiotensin-aldosterone system (RAAS)  which increases renal tubular reabsorption of sodium and water,  increase in blood volume and ultimately cardiac output
  25. 25. Alterations in the Inotropic State, Heart Rate, and Afterload  The inotropic state describes myocardial contractility as reflected by the velocity of contraction developed by cardiac muscle.  The maximum velocity of contraction is referred to asVmax.  When the inotropic state of the heart is increased, as in the presence of catecholamines,Vmax is increased.  Conversely,Vmax is decreased when myocardial contractility is impaired as in heart failure.
  26. 26. Alterations in the Inotropic State, Heart Rate, and Afterload  Afterload is the tension the ventricular muscle must develop to open the aortic or pulmonic valve.  The afterload presented to the left ventricle is increased in the presence of systemic arteriolar constriction and hypertension.  can be decreased by administering vasodilating drugs.
  27. 27. Alterations in the Inotropic State, Heart Rate, and Afterload  In the presence of SHF and low cardiac output,  The stroke volume is relatively fixed with any increase in CO being dependent on an increase in heart rate.  Tachycardia is an expected finding in the presence of SHF with a low ejection fraction and reflects activation of the sympathetic nervous system.  However, in the presence of DHF, tachycardia can produce a decrease in CO due to inadequate ventricular filling time.  Therefore, heart rate control is a target for therapy of DHF.
  28. 28. Humoral-Mediated Responses and Biochemical Pathways  As heart failure progresses, various neurohumoral pathways are activated  to maintain adequate cardiac output during exercise and ultimately even at rest.  Generalized vasoconstriction is initiated via several mechanisms including increased activity of the SNS and RAAS,  parasympathetic withdrawal,  high levels of circulating vasopressin,  endothelial dysfunction,  and release of inflammatory mediators.
  29. 29. Humoral-Mediated Responses and Biochemical Pathways  Heart as a “an endocrine organ.”  Atrial natriuretic peptide  is stored in atrial muscle and released in response to increases in atrial pressures, such as produced by tachycardia or hypervolemia.
  30. 30. Humoral-Mediated Responses and Biochemical Pathways  B-type natriuretic peptide (BNP)  It is secreted by both the atrial and ventricular myocardium.  In the failing heart, the ventricle becomes the principal site for BNP production.  The natriuretic peptides promote blood pressure control and protect the cardiovascular system from the effects of volume and pressure overload.  Physiologic effects of the natriuretic peptides include diuresis, natriuresis, vasodilation, antihypertrophy, anti-inflammation, and inhibition of the RAAS and SNS
  31. 31. Myocardial Remodeling  It is the process by which mechanical, neurohormonal, and genetic factors change the LV size, shape, and function.  The process includes  myocardial hypertrophy,  myocardial dilation and wall thinning,  increased interstitial collagen deposition,  myocardial fibrosis, and scar formation due to myocyte death.
  32. 32. Myocardial Remodeling  Myocardial hypertrophy compensatory mechanism to chronic pressure overload.  Cardiac dilation to volume overload and increases the CO.  also associated with increased myocardial oxygen requirements and decreased cardiac efficiency.  most common cause of myocardial remodeling is ischemic injury.  both hypertrophy and dilation of the left ventricle.
  33. 33. SIGNS AND SYMPTOMS OF HEART FAILURE  LV failure results in signs and symptoms of pulmonary edema,  right ventricular failure results in systemic venous hypertension and peripheral edema.  Patient fatigue and organ system dysfunction are related to inadequate CO.
  34. 34. Symptoms of Heart Failure  Dyspnea reflects increased work of breathing due to stiffness of the lungs produced by interstitial pulmonary edema.  Patients experiencing angina pectoris may interpret substernal discomfort as breathlessness.  Dyspnea related to heart failure will be linked to other supporting evidence  history of orthopnea,  paroxysmal nocturnal dyspnea,  third heart sound,  rales on physical examination,  elevated BNP levels.
  35. 35. Symptoms of Heart Failure  Orthopnea reflects the inability of the failing left ventricle to handle the increased venous return associated with the recumbent position.  manifested as a dry, nonproductive cough that develops when in the supine position and that is relieved by sitting up.  Paroxysmal nocturnal dyspnea is shortness of breath that awakens a patient from sleep.  Paroxysmal nocturnal dyspnea and wheezing caused by pulmonary congestion (“cardiac asthma”) are accompanied by radiographic evidence of pulmonary congestion.
  36. 36. Symptoms of Heart Failure  Fatigue and weakness at rest or with minimal exertion.  Anorexia, nausea, or abdominal pain related to increased liver congestion and prerenal azotemia.  Decreases in cerebral blood flow may produce confusion, difficulty concentrating, insomnia, anxiety, or memory deficits.  Nocturia may contribute to insomnia.
  37. 37. Physical Examination  tachypnea and the presence of moist rales.  resting tachycardia and a third heart sound (S3 gallop or ventricular diastolic gallop).  This heart sound is produced by blood entering and distending a relatively noncompliant left ventricle.
  38. 38. Physical Examination  Systemic hypotension with cool and pale extremities.  Lip and nail bed cyanosis  A narrow pulse pressure with a high diastolic pressure  Marked weight loss  Increase in the metabolic rate, anorexia and nausea, decreased intestinal absorption of food caused by splanchnic venous congestion.
  39. 39. Physical Examination  In the presence of right heart or biventricular failure,  jugular venous distention  may be present or inducible by pressing on the liver (hepatojugular reflux).  The liver is typically the first organ to become engorged with blood in the presence of right or biventricular failure.
  40. 40. Physical Examination  Right upper quadrant pain and tenderness or even jaundice in severe cases.  Pleural effusions (usually right sided) may be present.  Bilateral pitting pretibial leg edema is typically present with right ventricular failure and reflects both venous congestion and sodium and water retention.
  41. 41. DIAGNOSIS OF HEART FAILURE  The diagnosis of heart failure is based on the  History,  Physical examination,  Interpretation of laboratory and diagnostic tests.
  42. 42. Laboratory Diagnosis  Plasma BNP levels  Below 100 pg/mL indicate that heart failure is unlikely (90% negative predictive value);  BNP in the range of 100 to 500 pg/mL suggests an intermediate probability for heart failure;  Levels above 500 pg/mL are consistent with the diagnosis of heart failure (90% positive predictive value).  Plasma levels of BNP may be affected by other factors such as sex, advanced age, renal clearance, obesity, pulmonary embolism, atrial fibrillation, and/or other cardiac tachydysrhythmias.
  43. 43. Laboratory Diagnosis  Decreases in renal blood flow may lead to prerenal azotemia characterized by a disproportionate increase in blood urea nitrogen concentration relative to the serum creatinine concentration.  When moderate liver congestion is present, LFT may be mildly elevated, and when liver engorgement is severe, the prothrombin time may be prolonged.  Hyponatremia, hypomagnesemia, and hypokalemia may be present.
  44. 44. Electrocardiography  Patients with heart failure usually have an abnormal 12-lead electrocardiogram (ECG).  Low predictive value for the diagnosis of heart failure.  The ECG may show evidence of  A previous myocardial infarction,  LV hypertrophy,  Conduction abnormalities (left bundle branch block, widened QRS), or various cardiac dysrhythmias, especially atrial fibrillation and ventricular dysrhythmias.
  45. 45. Chest Radiography  Detecting the presence of pulmonary disease, cardiomegaly, pulmonary venous congestion, and interstitial or alveolar pulmonary edema.  Distention of the pulmonary veins in the upper lobes of the lungs.  Perivascular edema appears as hilar or perihilar haze.  The hilus appears large with ill-defined margins.
  46. 46. Chest Radiography  Kerley lines, reflecting edematous interlobular septae in the upper lung fields (KerleyA lines),  lower lung fields (Kerley B lines),  or basilar regions of the lungs producing a honeycomb pattern (Kerley C lines) may also be present.
  47. 47. Chest Radiography  Alveolar edema produces homogeneous densities in the lung fields, typically in a butterfly pattern.  Pleural effusion and pericardial effusion may be observed.  Radiographic evidence of pulmonary edema may lag behind the clinical evidence of pulmonary edema by up to 12 hours.  Likewise, radiographic patterns of pulmonary congestion may persist for several days after normalization of cardiac filling pressures and resolution of symptoms.
  48. 48. Echocardiography  The most useful test.  assess whether any abnormalities of the myocardium, cardiac valves, or pericardium are present.  This examination addresses the following topics:  ejection fraction, LV structure and functionality,  the presence of other structural abnormalities such as valvular and pericardial disease  and the presence of diastolic dysfunction and right ventricular function.  A preoperative echocardiographic evaluation can serve as a baseline for comparison with perioperative echocardiography if a patient's condition deteriorates.
  49. 49. CLASSIFICATION OF HEART FAILURE  There are four functional classes:  Class I: Ordinary physical activity does not cause symptoms  Class II: Symptoms occur with ordinary exertion  Class III: Symptoms occur with less than ordinary exertion  Class IV: Symptoms occur at rest
  50. 50. CLASSIFICATION OF HEART FAILURE  American HeartAssociation published the 2005 Guideline Update  Stage A: Patients at high risk of heart failure but without structural heart disease or symptoms of heart failure  Stage B: Patients with structural heart disease but without symptoms of heart failure  Stage C: Patients with structural heart disease with previous or current symptoms of heart failure  Stage D: Patients with refractory heart failure requiring specialized interventions
  51. 51. Management of Chronic Heart Failure  lifestyle modification,  patient and family education,  medical therapy,  corrective surgery,  implantable devices,  and cardiac transplantation
  52. 52. Lifestyle Modifications  Lifestyle modifications are aimed at decreasing the risk of heart disease and include  smoking cessation,  a healthy diet with moderate sodium restriction,  weight control,  exercise,  moderate alcohol consumption,  and adequate glycemic control.
  53. 53. Management of Systolic Heart Failure  Angiotensin-Converting Enzyme Inhibitors  Beneficial effects include promoting vasodilation, reducing water and sodium reabsorption, and supporting potassium conservation.  decrease ventricular remodeling and even to potentiate the “reverse-remodeling” phenomenon.  For this reason, they are considered the first line of treatment in heart failure.  Side effects ofACEIs include hypotension, syncope, renal dysfunction, hyperkalemia, and development of a nonproductive cough and angioedema.
  54. 54. Management of Systolic Heart Failure  Angiotensin II Receptor Blockers  These drugs have similar but not superior efficacy compared to ACEIs.  only recommended for patients who cannot tolerateACEIs.  In some patients treated with ACEIs, angiotensin levels may return to normal due to alternative pathways of angiotensin production.  Such patients may benefit from the addition of an angiotensin receptor blocker to the medical therapy.
  55. 55. Management of Systolic Heart Failure  AldosteroneAntagonists  In advanced stages of heart failure, there are high circulating levels of aldosterone.  Aldosterone stimulates sodium and water retention, hypokalemia, and ventricular remodeling.  Spironolactone, an aldosterone antagonist, may reverse all these effects.  During therapy with spironolactone, patients should have renal function and potassium levels monitored and the dose of spironolactone adjusted accordingly.
  56. 56. Management of Systolic Heart Failure  β-Blockers  β-Blockers are used to reverse the harmful effects of SNS activation in heart failure.  reduce morbidity and the number of hospitalizations and improve both quality of life and survival.  β-Blockers improve the ejection fraction and decrease ventricular remodeling.  Caution should be used when administering β-blockers to patients with  reactive airway disease,  diabetics with frequent hypoglycemic episodes,  and patients with bradydysrhythmias or heart block.
  57. 57. Management of Systolic Heart Failure  Diuretics  Diuretics can relieve circulatory congestion and the accompanying pulmonary and peripheral edema more rapidly than any other drugs.  Diuretic-induced decreases in ventricular diastolic pressure will decrease diastolic ventricular wall stress and prevent the persistent cardiac distention  Thiazide and/or loop diuretics are recommended as an essential part of the therapy of heart failure.  Potassium and magnesium supplementation may be needed  Excessive doses of diuretics may cause hypovolemia, prerenal azotemia, or an undesirably low cardiac output and are associated with worse clinical outcomes.
  58. 58. Management of Systolic Heart Failure  Digitalis  Digitalis enhances the inotropy of cardiac muscle and decreases activation of the SNS and the RAAS.  may impede the worsening of heart failure and result in fewer hospitalizations.  Digitalis can be added to standard therapy when patients are still symptomatic despite treatments with diuretics,ACEIs, and β-blockers.  Patients with the combination of atrial fibrillation and heart failure present another subgroup that may benefit from digoxin therapy.
  59. 59. Management of Systolic Heart Failure  Caution in elderly patients or to those with impaired renal function  Manifestations of digitalis toxicity include anorexia, nausea, blurred vision, and cardiac dysrhythmias.  Treatment of toxicity may include reversing hypokalemia, treating cardiac dysrhythmias, administering antidigoxin antibodies, and/or placing a temporary cardiac pacemaker.
  60. 60. Management of Systolic Heart Failure  Vasodilators  Vasodilator therapy relaxes vascular smooth muscle, decreases resistance to LV ejection, and increases venous capacitance.   In patients with dilated left ventricles, administration of vasodilators results in increased stroke volume and decreased ventricular filling pressures.
  61. 61. Management of Systolic Heart Failure  Statins  By their anti-inflammatory and lipid-lowering effects  decrease morbidity and mortality in patients with SHF.  Promising studies suggest that DHF patients could derive similar benefits from statin therapy.
  62. 62. Surgical Management of Heart Failure  LV ischemia may be treated with  Percutaneous coronary interventions  or coronary artery bypass surgery.  Correctable cardiac valve lesions may be alleviated surgically.  Ventricular aneurysmectomy may be useful in patients with large ventricular scars after myocardial infarction.  The definitive treatment for heart failure is heart transplantation.
  63. 63. Surgical Management of Heart Failure  Cardiac resynchronization therapy (CRT) is aimed at patients  with advanced stages of heart failure who have a ventricular conduction delay (QRS prolongation on the ECG).  CRT, also known as biventricular pacing, consists of  the placement of a dual-chamber cardiac pacemaker but with an additional lead introduced into the coronary sinus/coronary vein until it reaches the dyssynchronous LV wall.
  64. 64. Surgical Management of Heart Failure  CRT is recommended for  NYHA Class II/IV patients with an LV ejection fraction less than 35% and a QRS duration between 120 and 150 milliseconds.  Patients undergoing CRT may have  fewer symptoms,  better exercise tolerance,  and improved ventricular function  The reverse remodeling induced by CRT may also improve survival in these patients.
  65. 65. Management of Acute Heart Failure  Acute heart failure therapy has three phases:  the emergency phase,  the in-hospital management phase,  and the predischarge phase.  For the anesthesiologist, the emergency phase is of most interest
  66. 66. Management of Acute Heart Failure  Diuretics andVasodilators  Loop diuretics can improve symptoms rapidly, but in high doses, they may have deleterious effects  Use a combination of a low dose of loop diuretic with an intravenous vasodilator.  Nitroglycerin and nitroprusside reduce LV filling pressure and SVR and increase stroke volume.  However, nitroprusside may have a negative impact in patients with acute myocardial infarction.
  67. 67. Management of Acute Heart Failure  Inotropic Support  Positive inotropic drugs have been the mainstay of treatment for patients in cardiogenic shock.  via an increase in cyclic adenosine monophosphate, which promotes an increase in intracellular calcium levels  Catecholamines (epinephrine, norepinephrine, dopamine, and dobutamine) do so by direct β-receptor stimulation,  whereas phosphodiesterase inhibitors (amrinone, milrinone) block the degradation of cyclic adenosine monophosphate.
  68. 68. Management of Acute Heart Failure  Side effects of inotropic drugs include  tachycardia,  increased myocardial energy demand and oxygen consumption,  dysrhythmias,  worsening of DHF,  and down-regulation of β-receptors.  Long-term use of these drugs may result in cardiotoxicity and accelerate myocardial cell death.
  69. 69. Management of Acute Heart Failure  Calcium Sensitizers  increase contractility without increasing intracellular levels of calcium.  Therefore, there is no significant increase in myocardial oxygen consumption or heart rate and no propensity for dysrhythmias.  The most widely used medication in this class is levosemindan.  It is an inodilator increasing myocardial contractile strength and promoting dilation of systemic, pulmonary, and coronary arteries.  It does not worsen diastolic function.
  70. 70. Management of Acute Heart Failure  Exogenous B-Type Natriuretic Peptide  Nesiritide (Natrecor) is recombinant BNP that binds to both the A- and B-type natriuretic receptors.  It promotes arterial, venous, and coronary vasodilation, thereby decreasing LVEDP and improving dyspnea.  Nesiritide induces diuresis and natriuresis.  It has many effects similar to nitroglycerin but generally produces  less hypotension  and more diuresis than nitroglycerin.
  71. 71. Management of Acute Heart Failure  Nitric Oxide Synthase Inhibitors  The inflammatory cascade results in production of a large amount of nitric oxide in the heart and vascular endothelium.  These high levels of nitric oxide have a negative inotropic and profound vasodilatory effect leading to cardiogenic shock and vascular collapse.  Inhibition of nitric oxide synthase should decrease these harmful effects.  L-NAME (N-nitro-L-arginine methyl ester) is the principal drug in this class under investigation.
  72. 72. Management of Acute Heart Failure  Mechanical Devices  If the etiology of acute heart failure is a large myocardial infarction,  the insertion of an intra-aortic balloon pump should be considered.  The intra-aortic balloon pump is a mechanical device inserted via the femoral artery and positioned just below the left subclavian artery.
  73. 73. Management of Acute Heart Failure  Its balloon inflates in diastole increasing aortic diastolic blood pressure and coronary perfusion pressure.  The balloon deflates in systole creating a “suction” effect that enhances LV ejection.  Complications of intra-aortic balloon pump placement include femoral artery or aortic dissection, bleeding, thrombosis, and infection.
  74. 74. Prognosis  The mortality rate during the first 4 years following the diagnosis of heart failure approaches 40%.  Certain factors have been associated with a poor prognosis and include  increased urea and creatinine levels,  hyponatremia, hypokalemia,  severely depressed ejection fraction,  high levels of endogenous BNP,  very limited exercise tolerance,  and the presence of multifocal premature ventricular contractions.
  75. 75. MANAGEMENT OF ANESTHESIA Preoperative Evaluation and Management  Patients treated for heart failure are usually on several medications that may affect anesthetic management.  It is generally accepted that diuretics may be discontinued on the day of surgery.  Maintaining β-blocker therapy is essential since many studies have shown that β-blockers reduce perioperative morbidity and mortality.
  76. 76. Preoperative Evaluation and Management  Due to inhibition of the RAAS,ACEIs may put patients at increased risk of intraoperative hypotension.  This hypotension can be treated with a sympathomimetic drug such as ephedrine, an α-agonist such as phenylephrine, or vasopressin or one of its analogues.
  77. 77. Preoperative Evaluation and Management  If ACEIs are being used to prevent ventricular remodeling in heart failure patients and kidney dysfunction in diabetic patients, then stopping the medication for 1 day will not significantly alter these effects.  However, ifACEIs are used to treat hypertension, then discontinuing therapy the day of or the day before surgery may result in significant hypertension.
  78. 78. Preoperative Evaluation and Management  Angiotensin receptor blockers produce profound RAAS blockade and should be discontinued the day before surgery.  Digoxin therapy can be continued until the day of surgery.  Results of recent electrolyte, renal function, and liver function tests and the most recent ECG and echocardiogram should be evaluated
  79. 79. Intraoperative Management  All types of general anesthetics have been successfully used in patients with heart failure.  However, drug doses may need to be adjusted.  Opioids seem to have a particularly beneficial effect in heart failure patients because of their effect on the δ-receptor, which inhibits adrenergic activation.  PPV and PEEP may be beneficial in decreasing pulmonary congestion and improving arterial oxygenation.
  80. 80. Intraoperative Management  Intra-arterial pressure monitoring in a major operation is required  Fluid overload is avoided.  Intraoperative use of a pulmonary artery catheter  Transesophageal echocardiography may be a better alternative, allowing not only monitoring of ventricular filling but also ventricular wall motion and valvular function. 
  81. 81. Regional anesthesia  Regional anesthesia is acceptable for suitable operations  In fact, the modest decrease in systemic vascular resistance secondary to peripheral SNS blockade may increase cardiac output.  However, the decreased systemic vascular resistance produced by epidural or spinal anesthesia is not always predictable or easy to control.
  82. 82. Intraoperative Management  Special consideration  cardiac transplanted pts requiring other surgeries.  These patients are on long-term immunosuppressive therapy and are at high risk of infection.  Strict aseptic technique is necessary when performing any invasive procedure such as central line placement or neuraxial block.
  83. 83. Intraoperative Management  The transplanted heart is denervated.  An increase in heart rate can only be achieved by administering direct acting β-adrenergic agonists such as isoproterenol and epinephrine.  An increase in heart rate will not occur with administration of atropine or pancuronium.
  84. 84.  A blunted response to α-adrenergic agonists may also be observed.  The transplanted heart increases cardiac output by increasing stroke volume.  Therefore, these patients are preload dependent and require adequate intravascular volume.
  85. 85. Postoperative Management  Patients who have evidence of acute heart failure during surgery should be transferred to ICU where invasive monitoring can be continued postoperatively.  Pain should be aggressively treated since its presence and hemodynamic consequences may worsen heart failure.  Patients should have their usual medications restarted as soon as possible.
  86. 86. . THANKYOU