Valvularheartdisease 101005111315-phpapp01


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anaesthetic management during non cardiac surgeries in patients suffering from valvular heart disease and cardiomyopathies

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Valvularheartdisease 101005111315-phpapp01

  1. 1. DR CHANDRA SEKHAR BEHERA PG FINAL YEAR ANAESTHESIOLOGY Valvular Heart Disease cardiomyopathy and Anaesthesia
  2. 2. Valvular Heart Disease & anaesthesia
  3. 3. Definition : <ul><li>An acquired or congenital disorder of a cardiac valve characterized by stenosis (obstruction) or regurgitation (backward flow) of blood </li></ul>
  4. 6. Incidence <ul><li>Valvular heart disease is found in 4% of patients over the age of 65 in the developed world. </li></ul>
  5. 7. Valvular Heart Disease <ul><ul><li>Mitral stenosis </li></ul></ul><ul><ul><li>Mitral insufficiency </li></ul></ul><ul><ul><li>Mitral valve prolapse </li></ul></ul><ul><ul><li>Aortic insufficiency </li></ul></ul><ul><ul><li>Aortic stenosis </li></ul></ul><ul><ul><li>Pulmonary stenosis </li></ul></ul><ul><ul><li>Pulmonary insufficency. </li></ul></ul><ul><ul><li>Tricuspid Stenosis. </li></ul></ul><ul><ul><li>Tricuspid insufficency. </li></ul></ul>
  6. 8. What Information is Required? <ul><li>Clinical history </li></ul><ul><li>Physical exam </li></ul><ul><li>Investigations </li></ul>
  7. 9. Common findings of the history and physical exam in patients with valvular disease: <ul><ul><li>A history of rheumatic fever, IV drug abuse, or heart murmur </li></ul></ul><ul><ul><li>Decreased exercise tolerance </li></ul></ul><ul><ul><li>May exhibit S/S of CHF (dyspnea, orthopnea, fatigue, pulmonary rales, JVD, hepatic congestion, and dependent edema) </li></ul></ul><ul><ul><li>Compensatory increases in SNS tone manifest as resting tachycardia, anxiety, and diaphoresis </li></ul></ul>
  8. 10. Mitral Stenosis <ul><ul><li>Normal: 4 - 6 cm 2 </li></ul></ul><ul><ul><li>Mildly stenotic: 1.5 - 2.5 cm 2 </li></ul></ul><ul><ul><li>Moderately stenotic: 1.1 - 1.5 cm 2 </li></ul></ul><ul><ul><li>Severely stenotic: < 1 cm 2 </li></ul></ul><ul><ul><li>Usually have symptoms when area is decreased by 50% </li></ul></ul>
  9. 12. PICTURE
  10. 13. Etiology <ul><ul><li>Delayed complication of rheumatic fever </li></ul></ul><ul><ul><li>66% of patients are female </li></ul></ul>
  11. 14. Pathophysiology <ul><ul><li>Valve leaflets thicken, calcify and become funnel-shaped </li></ul></ul><ul><ul><li>Left atrium dilates (pressure) </li></ul></ul>
  12. 15. Signs and symptoms: <ul><ul><li>90% of patients present with CHF and Atrial fibrillation </li></ul></ul><ul><ul><li>10-15% develop chest pain </li></ul></ul><ul><ul><li>Hoarseness caused by enlarged left atrium putting pressure on left recurrent laryngeal nerve </li></ul></ul><ul><ul><li>Pulmonary hypertension from chronic increased pulmonary vascular resistance </li></ul></ul><ul><ul><ul><li>Hemoptysis often occurs </li></ul></ul></ul>
  13. 16. Treatment: <ul><ul><li>Anticoagulation </li></ul></ul><ul><ul><li>Sodium restriction </li></ul></ul><ul><ul><li>Diuretics </li></ul></ul><ul><ul><li>Valve replacement </li></ul></ul><ul><ul><ul><li>Onset to incapacitation averages 5-10 years and most patients die within 2-5 years of onset </li></ul></ul></ul>
  14. 17. Anesthesia concerns <ul><ul><li>Maintain sinus rhythm </li></ul></ul><ul><ul><li>Avoid tachycardia, large increases in CO </li></ul></ul><ul><ul><li>Avoid both hypovolemia and fluid overload </li></ul></ul><ul><ul><li>Avoid increases in pulmonary vascular resistance </li></ul></ul><ul><ul><li>Phenylephrine is preferred over ephedrine </li></ul></ul><ul><ul><li>Epidural is preferred over spinal due to gradual onset of sympathetic block with epidural </li></ul></ul>
  15. 18. Management <ul><ul><li>HR - keep slow to allow for diastolic filling; avoid sinus tachycardia </li></ul></ul><ul><ul><li>Rhythm - sinus rhythm; if A-fib, control rate </li></ul></ul><ul><ul><li>Preload - Maintain or slightly increase to help with left ventricular filling; excess preload may cause pulmonary edema </li></ul></ul><ul><ul><li>Afterload - SVR should be maintained; avoid decreases in SVR; avoid increases in PVR </li></ul></ul><ul><ul><li>Contractility - Maintain to provide adequate cardiac output </li></ul></ul><ul><ul><li>** epidural preferred over spinal </li></ul></ul>
  16. 19. Pregnancy Considerations <ul><li>Vaginal delivery: Early admission/invasive blood pressure monitoring/ Small top-ups for epidural/avoid iv fluids. </li></ul><ul><li>Caesarean delivery : </li></ul><ul><li>Spinal anaesthesia is best avoided. </li></ul><ul><li>Careful epidural anaesthesia in class 1 and 2 patients </li></ul><ul><li>General anaesthesia NYHA class 3 and 4 patients . Specific pharmacotherapy to obtund the intubation response. </li></ul><ul><li>Bolus oxytocin is contraindicated in view of the risk of precipitous systemic hypotension and pulmonary hypertension. </li></ul><ul><li>A brief period of postoperative ventilation may be required in some cases. </li></ul>
  17. 20. Mitral Regurgitation <ul><li>A portion of the LV volume is ejected back into LA during systole because of an incompetent valve. This leads to: </li></ul><ul><ul><li>Increased left atrial pressure, **but the atrium usually does not enlarge </li></ul></ul><ul><ul><li>Increased pulmonary artery pressure </li></ul></ul><ul><ul><li>Pulmonary edema/HTN </li></ul></ul><ul><ul><li>Left ventricular hypertrophy occurs due to the increased workload required to maintain volume output </li></ul></ul>
  18. 22. Etiology <ul><ul><li>ACUTE </li></ul></ul><ul><ul><li>Myocardial ischemia or infarctions </li></ul></ul><ul><ul><li>Infective endocarditis </li></ul></ul><ul><ul><li>Chest trauma </li></ul></ul><ul><li>CHRONIC </li></ul><ul><ul><li>Rheumatic fever </li></ul></ul><ul><ul><li>Incompetent valve </li></ul></ul><ul><ul><li>Destruction of mitral valve annulus </li></ul></ul>
  19. 23. Pathophysiology <ul><ul><li>Reduction in forward SV due to backward flow of blood into left atrium during systole (can be as much as 50% of SV) </li></ul></ul><ul><ul><li>Left ventricle compensates by dilating and increasing end-diastolic volume </li></ul></ul><ul><ul><li>Regurgitation reduces left ventricular afterload, but may enhance contractility </li></ul></ul><ul><ul><li>End-systolic volume remains normal, but eventually increases as disease progresses </li></ul></ul>
  20. 24. MECHANISM
  21. 25. Signs and symptoms <ul><ul><li>Degree of atrial compliance will determine the clinical manifestations </li></ul></ul><ul><ul><ul><li>Normal or reduced atrial compliance (acute MR) will result in pulmonary vascular congestion and edema </li></ul></ul></ul><ul><ul><ul><li>Increased atrial compliance (chronic MR) will demonstrate signs of decreased cardiac output </li></ul></ul></ul><ul><ul><li>Chronic weakness and fatigue </li></ul></ul><ul><ul><li>“ Blowing pansystolic murmur” best heard at the cardiac apex and often radiating to left axilla </li></ul></ul>
  22. 26. Treatment <ul><ul><li>Medical Tx: digoxin, diuretics and vasodilators </li></ul></ul><ul><ul><li>Surgical valvuloplasty </li></ul></ul><ul><ul><ul><li>Usually reserved for those with moderate to severe symptoms (regurgitant volume 30-60% or >60%, respectively, of SV) </li></ul></ul></ul>
  23. 27. Management <ul><ul><li>HR - maintain or increase; avoid bradycardia which worsens regurgitant flow </li></ul></ul><ul><ul><li>Rhythm - sinus rhythm </li></ul></ul><ul><ul><li>Preload - Maintain or slightly increase ; an elevated preload will cause an increase in regurgitant flow, and low preload causes inadequate cardiac output </li></ul></ul><ul><ul><li>Afterload - Decrease to improve forward cardiac output; avoid sudden increases in SVR </li></ul></ul><ul><ul><li>Contractility - Maintain or increase to decrease left ventricular volume </li></ul></ul><ul><ul><li>**spinal & epidurals well tolerated, but bradycardia must be avoided** </li></ul></ul>
  24. 28. Anesthesia concerns <ul><ul><li>Avoid slow heart rate (ideally 80-100 bpm) </li></ul></ul><ul><ul><li>Avoid increase in afterload </li></ul></ul><ul><ul><li>WATCH IV FLUIDS </li></ul></ul><ul><ul><ul><li>excess fluids will dilate the LV and worsen regurgitation </li></ul></ul></ul><ul><ul><ul><li>Need adequate volume to maintain forward SV </li></ul></ul></ul><ul><ul><li>Preload reduction with vasodilators and diuretics </li></ul></ul><ul><ul><li>Minimize drug-induced myocardial depression </li></ul></ul><ul><ul><li>Spinal and epidural are well tolerated (avoid bradycardia) </li></ul></ul><ul><ul><li>Give prophylactic antibiotics </li></ul></ul>
  25. 29. Anesthetic Considerations <ul><li>Prevent peripheral vasoconstriction </li></ul><ul><li>Avoid myocardial depressants </li></ul><ul><li>Treat acute atrial fibrillation immediately </li></ul><ul><li>Maintain a normal or slightly elevated heart rate </li></ul><ul><li>Monitor PCW pressure or intensity of murmur </li></ul>
  26. 30. Pregnancy Considerations <ul><li>No specific recommendations for the management of mitral regurgitation during labour and delivery. </li></ul><ul><li>Prior to labour symptoms may be managed with diuretics and vasodilators. </li></ul><ul><li>During labour, regional anaesthesia is usually well tolerated. However, in complicated NYHA class 3-4 cases, general anaesthesia may be required. </li></ul>
  27. 31. Mitral Valve Prolapse Anesthetic Considerations <ul><li>Avoid decreases in preload </li></ul><ul><li>Continue antiarrhythmic therapy </li></ul><ul><li>With MVP and moderate to severe mitral insufficiency the same considerations as listed for mitral insufficiency alone apply </li></ul>
  28. 32. Aortic Stenosis <ul><li>Aortic Valve Area </li></ul><ul><li>Normal 2.6 - 3.5 cm2 </li></ul><ul><li>Mild 1.2 – 1.8 cm2 </li></ul><ul><li>Moderate 0.8 – 1.2 cm2 </li></ul><ul><li>Significant 0.6 .0.8 cm2 </li></ul><ul><li>Critical < 0.6 cm2 </li></ul><ul><li>LV-Aortic Gradient </li></ul><ul><li>Mild 12 – 25 mmHg </li></ul><ul><li>Moderate 25 – 40 mmHg </li></ul><ul><li>Significant 40-50 mmHg </li></ul><ul><li>Critical > 50 mmHg </li></ul>
  29. 33. Etiology <ul><li>congenital bicuspid aortic valve (2%). </li></ul><ul><li>Rheumatic heart disease. </li></ul><ul><li>Valve Calcification. </li></ul>
  30. 35. Pathophysiology <ul><li>Obstruction of left ventricular ejection. </li></ul><ul><li>Concentric hypertrophy of left ventricular muscle. </li></ul><ul><li>Decreased compliance of left ventricle making it difficult to fill. </li></ul>
  31. 36. Anesthesia concerns: <ul><ul><li>Maintain normal sinus rhythm, heart rate and intravascular volume </li></ul></ul><ul><ul><ul><li>Optimal heart rate 70-80 bpm </li></ul></ul></ul><ul><ul><li>WATCH OUT FOR VASODILATION </li></ul></ul><ul><ul><li>Treat hypotension with phenylephrine </li></ul></ul><ul><ul><li>Mild to moderate AS may tolerate spinal or epidural (epidural preferred) </li></ul></ul><ul><ul><li>Spinal and epidural contraindicated in severe AS </li></ul></ul><ul><ul><li>High risk of myocardial ischaemia </li></ul></ul>
  32. 37. Peri-operative Care. <ul><li>Symptomatic patients for elective non-cardiac surgery should have aortic valve replacement first as they are at great risk of sudden death perioperatively (untreated severe symptomatic stenosis has a 50% one year survival). </li></ul><ul><li>Asymptomatic patients for major elective surgery associated with marked fluid shifts (thoracic, abdominal, major orthopaedic) with gradients across the valve > 50 mmHg should have valve replacement considered prior to surgery. </li></ul><ul><li>Asymptomatic patients for intermediate or minor surgery generally do well if managed carefully. </li></ul>
  33. 38. Haemodynamic goals <ul><li>(Low) normal heart rate </li></ul><ul><li>Maintain sinus rhythm </li></ul><ul><li>Adequate volume loading </li></ul><ul><li>High normal systemic vascular resistance </li></ul><ul><li>(Phenylepherine / Metarminol) </li></ul><ul><li>Effective analgesia. </li></ul>
  34. 39. Postoperative Management <ul><li>Have a low threshold for admission to ICU / HDU </li></ul><ul><li>Meticulous attention must be paid to fluid balance and post operative pain management </li></ul><ul><li>Infusions of vasoconstrictors may be required to maintain haemodynamic stability </li></ul>
  35. 40. Pregnancy considerations <ul><ul><li>Caesarean section: </li></ul></ul><ul><ul><li>General anaesthesia with the aid of invasive haemodynamic monitoring. Aggressive maintenance of systemic blood pressure with vasopressors (e.g. phenylephrine). </li></ul></ul><ul><li>Spinal anaesthesia is generally contraindicated. </li></ul><ul><li>There are reports of the successful management of </li></ul><ul><li>vaginal delivery under carefully introduced and limited </li></ul><ul><li>epidural analgesia, but this should be restricted to very </li></ul><ul><li>experienced hands. </li></ul>
  36. 41. Aortic regurgitation <ul><li>Etiology: </li></ul><ul><li>Rheumatic heart disease. </li></ul><ul><li>Endocarditis. </li></ul><ul><li>Aortic dissection </li></ul><ul><li>Connective tissue disorders </li></ul>
  37. 42. Management <ul><li>HR - Avoid sudden decreases; an increase (10-15 beats) causes shortening of diastolic phase which decreases the regurgitant fraction and increases cardiac output </li></ul><ul><ul><li>Rhythm - sinus rhythm preferred </li></ul></ul><ul><ul><li>Preload - increase to maximize forward cardiac output and maintain blood pressure </li></ul></ul><ul><ul><li>Afterload - decrease afterload to favor forward cardiac output (keep moving forward); avoid sudden increase in afterload </li></ul></ul><ul><ul><li>Contractility - maintain </li></ul></ul><ul><ul><li>** most patients tolerate spinal or epidural provided intravascular volume is maintained </li></ul></ul>
  38. 43. Treatment <ul><ul><li>Once symptomatic, death can occur within 5 years unless lesion is surgically repaired </li></ul></ul><ul><ul><li>Digitalis, diuretics and afterload reduction (ACE inhibitors) for chronic (eventual surgical repair) </li></ul></ul><ul><ul><li>Inotropes (dopamine, dobutamine) and vasodilator for severe, chronic aortic regurgitation (requires surgery) </li></ul></ul>
  39. 44. Anesthetic considerations <ul><ul><li>Maintain normal heart rate </li></ul></ul><ul><ul><ul><li>Increased frequency of conduction abnormalities, consider pacing </li></ul></ul></ul><ul><ul><li>Keep SVR low </li></ul></ul><ul><ul><li>Avoid myocardial depression </li></ul></ul><ul><li>Maintain or slightly increase preload </li></ul><ul><ul><li>Give prophylactic antibiotics </li></ul></ul><ul><ul><li>Most patients will tolerate spinal or epidural, provided intravascular volume is maintained </li></ul></ul>
  40. 45. Peri-operative Care <ul><li>Asymptomatic Patients- tolerate surgery well. </li></ul><ul><li>Patients with low functional capacity- Consider valve replacement surgery first. </li></ul><ul><li>Haemodynamic goals </li></ul><ul><li>High normal heart rate – around 90 bpm </li></ul><ul><li>Adequate volume loading </li></ul><ul><li>Low systemic vascular resistance </li></ul><ul><li>Maintain contractility </li></ul><ul><li>Spinal/Epidural well tolerated. </li></ul>
  41. 46. Pregnancy considerations <ul><li>During labour, epidural analgesia improves forward flow, and is therefore the anaesthetic of choice in patient’s requiring an operative delivery. </li></ul>
  42. 47. Pulmonary Stenosis <ul><ul><li>Haemodynamic management: Maintain right ventricular preload, left ventricular afterload and right ventricular contractility. </li></ul></ul><ul><ul><li>Avoid hypothermia, hypercarbia, acidosis, </li></ul></ul><ul><ul><li>hypoxia and high ventilatory pressures. </li></ul></ul><ul><ul><li>Spinal anaesthesia may be associated with an uncontrolled reduction in right ventricular preload and should therefore be avoided in severe cases. </li></ul></ul>
  43. 48. Pregnancy Considerations <ul><li>Spinal anaesthesia may be associated with an uncontrolled reduction in right ventricular preload and should therefore be avoided in severe cases. </li></ul>
  44. 49. Endocarditis prophylaxis <ul><li>Consider prophylaxis for all patients with valvular lesions. </li></ul><ul><li>Three main questions: </li></ul><ul><li>Which patients have a high risk? </li></ul><ul><li>Which procedures cause &quot;significant&quot; </li></ul><ul><li>bacteraemia? </li></ul><ul><li>Which antibiotics are active against </li></ul><ul><li>these bacteria? </li></ul>
  45. 50. Prophylaxis for valvular heart disease. <ul><li>Prophylaxis against infective endocarditis is recommended for the following patients: </li></ul><ul><li>Patients with prosthetic heart valves and patients with a history of infective endocarditis. (Level of Evidence: C) </li></ul><ul><li>Patients with congenital cardiac valve malformations, particularly those with bicuspid aortic valves, and patients with acquired valvular dysfunction (e.g., rheumatic heart disease). (Level of Evidence: C) </li></ul><ul><li>Patients who have undergone valve repair. (Level of Evidence: C) </li></ul><ul><li>Patients who have hypertrophic cardiomyopathy when there is latent or resting obstruction. (Level of Evidence:C) </li></ul><ul><li>Patients with MV prolapse (MVP) and auscultatory evidence of valvular regurgitation and/or thickened leaflets on echocardiography.* (Level of Evidence: C) </li></ul>
  46. 51. No prophylaxis required <ul><li>Prophylaxis against infective endocarditis is not recommended for the following patients: </li></ul><ul><li>Patients with MVP without MR or thickened leaflets on echocardiography.* (Level of Evidence: C) </li></ul><ul><li>Patients with physiological, functional, or innocent heart murmurs, including patients with aortic valve sclerosis as defined by focal areas of increased echogenicity and thickening of the leaflets without restriction of motion and a peak velocity less than 2.0 m per second. (Level of Evidence: C) </li></ul><ul><li>Patients with echocardiographic evidence of physiologic MR in the absence of a murmur and with structurally normal valves. (Level of Evidence: C) </li></ul><ul><li>Patients with echocardiographic evidence of physiological tricuspid regurgitation (TR) and/or pulmonary regurgitation in the absence of a murmur and with structurally normal valves. (Level of Evidence: C) </li></ul>
  47. 52. <ul><li>Prophylaxis recommended Prophylaxis not recommended </li></ul><ul><li>Dental procedures </li></ul><ul><li>with mucosal bleeding without mucosal bleeding </li></ul><ul><li>Respiratory tract </li></ul><ul><li>tonsillectomy / adenoidectomy intubation of the trachea </li></ul><ul><li>flexible bronchoscopy </li></ul><ul><li>Gastrointestinal tract </li></ul><ul><li>procedures damaging the intestinal mucosa endoscopy </li></ul><ul><li>surgery or endoscopy of the biliary tract </li></ul><ul><li>sclerotherapy of oesophageal varices </li></ul><ul><li>Urogenital tract </li></ul><ul><li>surgery of the prostate hysterectomy* </li></ul><ul><li>cystoscopy vaginal delivery*, Caesarean section </li></ul><ul><li>dilatation of the urethra bladder catheterization (in the </li></ul><ul><li>absence of infection) </li></ul><ul><li>* consider prophylaxis in high risk </li></ul><ul><li>patients </li></ul>
  48. 53. Antibiotic regimens <ul><li>1. Dental, Oral, Respiratory Tract, or Oesophageal Procedure </li></ul><ul><li>Standard: Amoxicillin 2.0 g (child: 50 mg/kg) per os 1 h preoperatively </li></ul><ul><li>Ampicillin 2.0 g (child 50 mg/kg) iv 30 min preoperatively </li></ul><ul><li>* Alternative: Clindamycin 600 mg (child 20 mg/kg) per os </li></ul><ul><li>or Cefalexin per os or Cefazolin iv or Erythromycin per os </li></ul><ul><li>2. Gastrointestinal or Genitourinary Procedure </li></ul><ul><li>High-risk patient: </li></ul><ul><li>Standard: Ampicillin + Gentamicin (2.0 g + 1.5 mg/kg) iv, </li></ul><ul><li>after 6 h, Ampicillin 1.0 g iv or Amoxicillin 1.0 g per os </li></ul><ul><li>* Alternative: Vancomycin + Gentamicin (1.0 g+ 1.5 mg/kg, </li></ul><ul><li>infuse over 1-2 h directly preoperatively, child: 20 mg/kg + 1.5 mg/kg) </li></ul><ul><li>Moderate-risk patient: </li></ul><ul><li>Standard: Amoxicillin per os or Ampicillin iv </li></ul><ul><li>* Alternative: Vancomycin (1.0 g) iv infuse over 1-2 h directly preoperatively </li></ul>
  49. 54. CONCLUSION <ul><li>Anaesthesia for a patient with valvular heart disease can be challenging. </li></ul><ul><li>The aim of anaesthesia is to keep the diseased heart within its &quot;optimal working conditions&quot; </li></ul>
  50. 55. Cardiomyopathies and anaesthetic implications
  51. 56. Definition <ul><li>“ A primary disorder of the heart muscle that causes abnormal myocardial performance and is not the result of disease or dysfunction of other cardiac structures … myocardial infarction, systemic hypertension, valvular stenosis or regurgitation” </li></ul>
  52. 57. Classification <ul><li>etiology </li></ul><ul><li>gross anatomy </li></ul><ul><li>histology </li></ul><ul><li>genetics </li></ul><ul><li>biochemistry </li></ul><ul><li>immunology </li></ul><ul><li>hemodynamics </li></ul><ul><li>functional </li></ul><ul><li>prognosis </li></ul><ul><li>treatment </li></ul>
  53. 58. WHO Classification <ul><li>Unknown cause (primary) </li></ul><ul><ul><li>Dilated </li></ul></ul><ul><ul><li>Hypertrophic </li></ul></ul><ul><ul><li>Restrictive </li></ul></ul><ul><ul><li>unclassified </li></ul></ul><ul><li>Specific heart muscle disease (secondary) </li></ul><ul><ul><li>Infective </li></ul></ul><ul><ul><li>Metabolic </li></ul></ul><ul><ul><li>Systemic disease </li></ul></ul><ul><ul><li>Heredofamilial </li></ul></ul><ul><ul><li>Sensitivity </li></ul></ul><ul><ul><li>Toxic </li></ul></ul>Br Heart J 1980; 44:672-673
  54. 59. Functional Classification <ul><li>Dilatated (congestive, DCM, IDC) </li></ul><ul><ul><li>ventricular enlargement and syst dysfunction </li></ul></ul><ul><li>Hypertrophic (IHSS, HCM, HOCM) </li></ul><ul><ul><li>inappropriate myocardial hypertrophy in the absence of HTN or aortic stenosis </li></ul></ul><ul><li>Restrictive (infiltrative) </li></ul><ul><ul><li>abnormal filling and diastolic function </li></ul></ul>
  55. 60. Idiopathic Dilated Cardiomyopathy
  56. 61. Dilated cardiomyopathy <ul><li>DCM is a syndrome characterized by cardiac enlargement and impaired systolic function of one or both ventricles. Although it was formerly called congestive cardiomyopathy, the term dilated cardiomyopathy is now preferred because the earliest abnormality usually is ventricular enlargement and systolic contractile function, with the sign and symptoms of congestive heart failure often (but not invariably) developing </li></ul>
  57. 62. Clinical findings <ul><li>The key hemodynamic features of the DCM are elevated filling pressures, failure of myocardial contractile strength, and a marked inverse relationship between afterload and stroke volume. </li></ul><ul><li>Clinical picture of DCM may vary from asymptomatic with only cardiomegaly to severe CHF. </li></ul><ul><li>Apart from CHF, dysrhythmias and embolism (systemic or pulmonary) are also common features of DCM patients. </li></ul>
  58. 63. History and Physical Examination <ul><li>Symptoms of heart failure </li></ul><ul><ul><li>pulmonary congestion (left HF) dyspnea (rest, exertional, nocturnal), orthpnea </li></ul></ul><ul><ul><li>systemic congestion (right HF) edema, nausea, abdominal pain, nocturia </li></ul></ul><ul><ul><li>low cardiac output fatigue and weakness </li></ul></ul><ul><li>hypotension, tachycardia, tachypnea, JVD </li></ul>
  59. 64. Cardiac Imaging <ul><li>Chest radiogram </li></ul><ul><li>Electrocardiogram </li></ul><ul><li>24-hour ambulatory ECG (Holter) </li></ul><ul><ul><li>lightheadedness, palpitation, syncope </li></ul></ul><ul><li>Two-dimensional echocardiogram </li></ul><ul><li>Radionuclide ventriculography </li></ul><ul><li>Cardiac catheterization </li></ul><ul><ul><li>age >40, ischemic history, high risk profile, abnormal ECG </li></ul></ul>
  60. 65. management <ul><li>Recent management of chronic cardiac failure include medical therapy with drugs for example vasodilators, diuretics or beta-blockers and atrio-biventricular pacemakers for patients with incordinate movements of heart chambers </li></ul>
  61. 66. Anaesthetic concern <ul><li>GA carries a high risk as these patients may develop CHF or arrhythmias during intraoperative period. </li></ul>
  62. 67. Concern…….. <ul><li>Patients with atrio-biventricular pacemaker are having significant morbidity and increased anaesthetic risk as compare to patients with conventional single and dual chamber pacemakers. </li></ul><ul><li>It is equally important, however, to ensure that pacemakers are programmed optimally. </li></ul>
  63. 68. Concern………….. <ul><li>This is particularly important for biventricular pacemaker as it delivers a therapy with each ventricular pace beat. In contrast, conventional single and dual chamber pacemakers pace only when required. 4 </li></ul>
  64. 69. <ul><li>two major problems, DCM with progressive severe cardiac dysfunction and permanent pacemaker at the site of surgery </li></ul>
  65. 70. <ul><li>Preoperatively cardiologist was consulted for optimal medical management of cardiomyopathy and evaluation of pacemaker functioning. Central venous catheter placement and arterial cannulation were performed under local anaesthesia before induction. </li></ul><ul><li>Anaesthesia was induced with vecuronium bromide as myogenic electrical activity associated with muscle fasciculation induced by succinylcholine may result in EMI (myopotential inhibition). </li></ul>
  66. 71. <ul><li>Inhibition of pacemaker function may occur in presence of electromechanical interference (EMI) leading to pacemaker failure at the time of surgery. </li></ul><ul><li>EMI can also lead to inappropriate inhibition or triggering of a paced output, asynchronous pacing, reprogramming, damage to device circuitry and triggering a defibrillator discharge. </li></ul><ul><li>Continuous invasive hemodynamic monitoring is essential as EKG is not reliable in the presence of EM </li></ul>
  67. 72. <ul><li>Bipolar cautery is less hazardous than unipolar, although EMI may still occur. The cardiologist and the pacemaker programmer were present in the operation room throughout the procedure. </li></ul>
  68. 73. <ul><li>American Association of Physicist in Medicine Task Group has recommended in their guidelines for radiation treatment in patients with cardiac pacemakers that pacemaker should not lie in the radiation beam field. </li></ul><ul><li>There should be no episode of hypoxia and hypercapnia throughout the procedure in the present case as pacing threshold may be affected by hypoxia, hypercapnia, metabolic disturbances or electrolyte imbalance. </li></ul>
  69. 74. <ul><li>It has been reported previously that there is minimal cardiac risk in a post cardiac transplant patient with LVEF 15% if CHF is medically optimized by drugs e.g. diuretics, vasodilators and ACE inhibitors </li></ul>
  70. 75. <ul><li>Regional anaesthesia may be an alternative to general anaesthesia in selected patients with DCM. </li></ul><ul><li>Epidural anaesthesia produces changes in the preload and afterload that mimic pharmacological goals in the treatment of this disease. Regional anaesthesia was not used in the present case as extensive sensory level of block required. </li></ul>
  71. 76. <ul><li>Yamaguchi et al reported a case of total prostectomy under continuous epidural anaesthesia and total intravenous venous anaesthesia (TIVA) using ketamine and propofol in a patient of DCM. They demonstrated it a useful combination. </li></ul>
  72. 77. conclusion <ul><li>Patients with DCM with severe LV dysfunction undergoing noncardiac surgery are a challenge to the attending anaesthesiologist. There is further increase in risk if they are on pacemaker. These patients can be very well managed with preoperative optimized medical treatment and well-planned perioperative care </li></ul>
  73. 78. Hypertrophic Cardiomyopathy
  74. 79. Hypertrophic Cardiomyopathy <ul><li>First described by the French and Germans around 1900 </li></ul><ul><li>uncommon with occurrence of 0.02 to 0.2% </li></ul><ul><li>a hypertrophied and non-dilated left ventricle in the absence of another disease </li></ul><ul><li>small LV cavity, asymmetrical septal hypertrophy (ASH), systolic anterior motion of the mitral valve leaflet (SAM) </li></ul>
  75. 80. 65% 35% 10%
  76. 82. Familial HCM <ul><li>First reported by Seidman et al in 1989 </li></ul><ul><li>occurs as autosomal dominant in 50% </li></ul><ul><li>5 different genes on at least 4 chromosome with over 3 dozen mutations </li></ul><ul><ul><li>chromosome 14 (myosin) </li></ul></ul><ul><ul><li>chromosome 1 (troponin T) </li></ul></ul><ul><ul><li>chromosome 15 (tropomyosin) </li></ul></ul><ul><ul><li>chromosome 11 (?) </li></ul></ul>
  77. 83. Pathophysiology <ul><li>Systole </li></ul><ul><ul><li>dynamic outflow tract gradient </li></ul></ul><ul><li>Diastole </li></ul><ul><ul><li>impaired diastolic filling,  filling pressure </li></ul></ul><ul><li>Myocardial ischemia </li></ul><ul><ul><li> muscle mass, filling pressure, O2 demand </li></ul></ul><ul><ul><li> vasodilator reserve, capillary density </li></ul></ul><ul><ul><li>abnormal intramural coronary arteries </li></ul></ul><ul><ul><li>systolic compression of arteries </li></ul></ul>
  78. 84. Clinical Manifestation <ul><li>Asymptomatic, echocardiographic finding </li></ul><ul><li>Symptomatic </li></ul><ul><ul><li>dyspnea in 90% </li></ul></ul><ul><ul><li>angina pectoris in 75% </li></ul></ul><ul><ul><li>fatigue, pre-syncope, syncope  risk of SCD in children and adolescents </li></ul></ul><ul><ul><li>palpitation, PND, CHF, dizziness less frequent </li></ul></ul>
  79. 85. Increase in Gradient and Murmur <ul><li> Contractility Preload Afterload valsalva (strain) ---   standing ---  -- postextrasystole   -- isoproterenol    digitalis   -- amyl nitrite --     nitroglycerine ---   exercise    tachycardia   -- hypovolemia    </li></ul>
  80. 86. Decrease in Gradient and Murmur <ul><li> Contractility Preload Afterload Mueller meneuver ---   valsalva (overshoot) ---   squatting ---   passive leg elevation ---  --phenylephrine --- --  beta-blocker   -- general anesthesia  -- -- isometric grip --- --  </li></ul>
  81. 87. Natural History <ul><li>annual mortality 3% in referral centers probably closer to 1% for all patients </li></ul><ul><li>risk of SCD higher in children may be as high as 6% per year majority have progressive hypertrophy </li></ul><ul><li>clinical deterioration usually is slow </li></ul><ul><li>progression to DCM occurs in 10-15% </li></ul>
  82. 88. Risk Factors for SCD <ul><li>Young age (<30 years) </li></ul><ul><li>“ Malignant” family history of sudden death </li></ul><ul><li>Gene mutations prone to SCD (ex. Arg403Gln) </li></ul><ul><li>Aborted sudden cardiac death </li></ul><ul><li>Sustained VT or SVT </li></ul><ul><li>Recurrent syncope in the young </li></ul><ul><li>Nonsustained VT (Holter Monitoring) </li></ul><ul><li>Brady arrhythmias (occult conduction disease) </li></ul>Br Heart J 1994; 72:S13
  83. 89. Recommendations for Athletic Activity <ul><li>Avoid most competitive sports (whether or not symptoms and/or outflow gradient are present) </li></ul><ul><li>Low-risk older patients (>30 yrs) may participate in athletic activity if all of the following are absent </li></ul>
  84. 90. Recommendations for Athletic Activity <ul><li>Low-risk older patients (>30 yrs) may participate in athletic activity if all of the following are absent </li></ul><ul><ul><li>ventricular tachycardia on Holter monitoring </li></ul></ul><ul><ul><li>family history of sudden death due to HCM </li></ul></ul><ul><ul><li>history of syncope or episode of impaired consciousness </li></ul></ul><ul><ul><li>severe hemdynamic abnormalities, gradient  50 mmHg </li></ul></ul><ul><ul><li>exercise induced hypotension </li></ul></ul><ul><ul><li>moderate or sever mitral regurgitation </li></ul></ul><ul><ul><li>enlarged left atrium (  50 mm) </li></ul></ul><ul><ul><li>paroxysmal atrial fibrillation </li></ul></ul><ul><ul><li>abnormal myocardial perfusion </li></ul></ul>
  85. 91. Management <ul><li>beta-adrenergic blockers </li></ul><ul><li>calcium antagonist </li></ul><ul><li>disopyramide </li></ul><ul><li>amiodarone, sotolol </li></ul><ul><li>DDD pacing </li></ul><ul><li>myotomy-myectomy </li></ul><ul><li>plication of the anterior mitral leaflet </li></ul>
  86. 92. HCM vs Aortic Stenosis <ul><li> HCM Fixed Obstruction carotid pulse spike and dome parvus et tardus </li></ul><ul><li>murmur radiate to carotids  valsalva, standing  squatting, handgrip  passive leg elevation </li></ul><ul><li>systolic thrill 4th left interspace 2nd right interspace systolic click absent present </li></ul>
  87. 93. Other Causes of Hypertrophy <ul><li>Clinical mimics </li></ul><ul><ul><li>glycogen storage, infants of diabetic mothers, amyloid </li></ul></ul><ul><li>Genetic </li></ul><ul><ul><li>Noonan’s, Friedreich’s ataxia, Familial restrictive cardiomyopathy with disarray </li></ul></ul><ul><li>Exaggerated physiologic response </li></ul><ul><ul><li>Afro-Caribbean hypertension, old age hypertrophy, athlete’s heart </li></ul></ul>
  88. 94. HCM vs Athlete’s Heart <ul><li>HCM Athlete </li></ul><ul><li>+ Unusual pattern of LVH - + LV cavity <45 mm - - LV cavity >55 mm + + LA enlargement - + Bizarre ECG paterns - + Abnormal LV filling - + Female gender - -  thickness with deconditioning + + Family history of HCM - </li></ul>Circulation 1995; 91:1596
  89. 95. Hypertensive HCM of the Elderly <ul><li>Characteristics </li></ul><ul><ul><li>modest concentric LV hypertrophy (<22 mm) </li></ul></ul><ul><ul><li>small LV cavity size </li></ul></ul><ul><ul><li>associated hypertension </li></ul></ul><ul><ul><li>ventricular morphology greatly distorted with reduced outflow tract </li></ul></ul><ul><ul><li>sigmoid septum and “grandma SAM” </li></ul></ul>
  90. 96. Anaesthetic management <ul><li>Management of anaesthesia in pt with HOCM is directed towards minimizing LVOT obstruction </li></ul><ul><li>GOAL is to </li></ul><ul><li>Decrese myocardial contractility </li></ul><ul><li>Incresing preload </li></ul><ul><li>Decresing preload </li></ul>
  91. 97. <ul><li>Avoidence of </li></ul><ul><li>Sympathetic stimulation </li></ul><ul><li>Hypovolemia </li></ul><ul><li>Vasodilatation </li></ul><ul><li>Intraoperative problems are </li></ul><ul><li>Severe hypotension </li></ul><ul><li>Myocardial ischemia </li></ul><ul><li>Supraventricular or ventricular tachydysarrythmias </li></ul>
  92. 98. Preoperative evaluation <ul><li>Prior cardiac evaluation is necessary by </li></ul><ul><li>12 lead ECG </li></ul><ul><li>Echocardiogaraphy </li></ul><ul><li>Pt taking b blocker or calcium channel blocker to be continued throughout the perioperative period </li></ul><ul><li>Pt with ICD should have the unit turned off and have an external defibrillitor to be kept ready </li></ul>
  93. 99. Intraoperative management <ul><li>Intravenous anaesthesia induction </li></ul><ul><li>B blocker or volatile anaesthetic to reduce sympathetic activation during intubation </li></ul><ul><li>Smaller tidal volume and higher respiratory rate shuld be used </li></ul><ul><li>Peep to be avoided </li></ul><ul><li>During abdominal insufflation </li></ul><ul><li>Pressure should be below 15 mm Hg </li></ul>
  94. 100. <ul><li>NDMR that have minimal effect on systemic circulation should be used </li></ul><ul><li>Maintainance with drug causing mild depression of cardiac contractility and minimal effect on preload and afterload </li></ul><ul><li>Invasive monitering useful for measurement of BP </li></ul><ul><li>TEE </li></ul><ul><li>Hypotension during intraop treated by using phenylephrine </li></ul><ul><li>Maintaince of normal sinus rhythm </li></ul><ul><li>Intraop tachyarrythmia treated by drugs or electrical cardioversion </li></ul>
  95. 101. Restrictive Cardiomyopathy
  96. 102. Restrictive Cardiomyopathies <ul><li>Hallmark: abnormal diastolic function </li></ul><ul><li>rigid ventricular wall with impaired ventricular filling </li></ul><ul><li>bear some functional resemblance to constrictive pericarditis </li></ul><ul><li>importance lies in its differentiation from operable constrictive pericarditis </li></ul>
  97. 103. Exclusion “Guidelines” <ul><li>LV end-diastolic dimensions  7 cm </li></ul><ul><li>Myocardial wall thickness  1.7 cm </li></ul><ul><li>LV end-diastolic volume  150 mL/m2 </li></ul><ul><li>LV ejection fraction < 20% </li></ul>
  98. 104. Classification <ul><li>Idiopathic </li></ul><ul><li>Myocardial </li></ul><ul><li>1. Noninfiltrative </li></ul><ul><ul><li>Idiopathic </li></ul></ul><ul><ul><li>Scleroderma </li></ul></ul><ul><li>2. Infiltrative </li></ul><ul><ul><li>Amyloid </li></ul></ul><ul><ul><li>Sarcoid </li></ul></ul><ul><ul><li>Gaucher disease </li></ul></ul><ul><ul><li>Hurler disease </li></ul></ul><ul><li>3. Storage Disease </li></ul><ul><ul><li>Hemochromatosis </li></ul></ul><ul><ul><li>Fabry disease </li></ul></ul><ul><ul><li>Glycogen storage </li></ul></ul><ul><li>Endomyocardial </li></ul><ul><ul><li>endomyocardial fibrosis </li></ul></ul><ul><ul><li>Hyperesinophilic synd </li></ul></ul><ul><ul><li>Carcinoid </li></ul></ul><ul><ul><li>metastatic malignancies </li></ul></ul><ul><ul><li>radiation, anthracycline </li></ul></ul>
  99. 105. Clinical Manifestations <ul><li>Symptoms of right and left heart failure </li></ul><ul><li>Jugular Venous Pulse </li></ul><ul><ul><li>prominent x and y descents </li></ul></ul><ul><li>Echo-Doppler </li></ul><ul><ul><li>abnormal mitral inflow pattern </li></ul></ul><ul><ul><li>prominent E wave (rapid diastolic filling) </li></ul></ul><ul><ul><li>reduced deceleration time (  LA pressure) </li></ul></ul>
  100. 106. Constrictive - Restrictive Pattern “ Square-Root Sign” or “Dip-and-Plateau”
  101. 108. Restriction vs Constriction <ul><li>History provide can important clues </li></ul><ul><li>Constrictive pericarditis </li></ul><ul><ul><li>history of TB, trauma, pericarditis, sollagen vascular disorders </li></ul></ul><ul><li>Restrictive cardiomyopathy </li></ul><ul><ul><li>amyloidosis, hemochromatosis </li></ul></ul><ul><li>Mixed </li></ul><ul><ul><li>mediastinal radiation, cardiac surgery </li></ul></ul>
  102. 109. Treatment <ul><li>No satisfactory medical therapy </li></ul><ul><li>Drug therapy must be used with caution </li></ul><ul><ul><li>diuretics for extremely high filling prssures </li></ul></ul><ul><ul><li>vasodilators may decrease filling pressure </li></ul></ul><ul><ul><li>? Calcium channel blockers to improve diastolic compliance </li></ul></ul><ul><ul><li>digitalis and other inotropic agents are not indicated </li></ul></ul>
  103. 110. Anaesthetic management <ul><li>Due to fixed stroke volume ,maintaince of normal sinus rhythm and avoidence of any significant heart rate is necessary </li></ul><ul><li>Maintaince of venous return and intravascular volume is necessary to maintain an acceptable cardiac output </li></ul><ul><li>Anticoagulation is necessary which can negetivly influence the descision to select the regional anaesthesia </li></ul>
  104. 111. conclusion <ul><li>Cardiomyopathies are more common than is widely appreciated. Whilst their impact upon the conduct of anaesthesia can often remain low, it is essential that clinical anaesthetists understand the ‘ideal’ perioperative management aims, so that individualized directed care may be delivered </li></ul><ul><li>  </li></ul>
  105. 112. Discussion