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Case Presentation

Case Presentation. Presented by Assistant lecturer / Rafik E. Doss. The Case. A 71-year-old female was scheduled to undergo an elective total hip arthroplasty .

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Case Presentation

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  1. Case Presentation Presented by Assistant lecturer / RafikE. Doss

  2. The Case • A 71-year-old female was scheduled to undergo an elective total hip arthroplasty. • Her activitylevel is minimal due to arthritic changes of her hips. She has a history of hypertension and hypothyroidism, both under good control with medications. • Prior to her surgery, a systolic murmur was appreciated prompting a full cardiac workup.

  3. The Case • A transthoracic echocardiogram revealed aortic stenosiswith a peak gradient across the aortic valve of 48 mm Hgand a left ventricular EF of 35% with concentric hypertrophy. • No evidence of stress-induced ischemiawas appreciated on a dobutamine stress test.

  4. Objectives: • What is the etiology and pathophysiology of aortic stenosis? • How should preload, afterload, heart rate, and contractility be managed in a patient with aortic stenosis? • How would you optimizethis patient’s condition preoperatively? • What intraoperative monitoring would be appropriate? • How would you anesthetize this patient?

  5. Etiology of Aortic Stenosis Aortic stenosis is usually an idiopathic disease In patients older than 70 years, the most common cause of aortic stenosis is degenerative calcification of the valve (Mönckeberg senile calcific aortic stenosis).

  6. Etiology of Aortic Stenosis • Calcific aortic stenosis also occurs in older patients with congenital or acquired bicuspid valves, but this is usually presented earlier in life (30 – 40 yrs). • Other causes include rheumatic fever–induced aortic stenosis.

  7. Pathophysiology • The normal valve surface area is 2.6–3.5 cm2. A valve area of 1 cm2 or less is likely to cause clinically significant AS. • AVA of < 0.8 cm2 with peak gradient > 50 mmHg is classified as critical AS [capable of causing sudden death]. • Presenting symptoms include angina, syncope, dyspnea and congestive heart failure. Stenotic aortic valve (macroscopic appearance)

  8. Hemodynamic Goals • This patient is classified as having severe AS according to her transvalvular peak gradient (48 mmHg). However, being asymptomatic, she is still compensated due to increased LV mass. • Our goal for preload is high filling pressures, adequate volume administration, and avoidance of factors that decrease venous return.

  9. Hemodynamic Goals • Heart ratemust be maintained at low normal levels [60 – 70 bpm] to allow for adequate ventricular filling and ejection. • Tachycardia should be avoided as  loss of timed atrial stroke   CO  time for coronary filling  angina. Bradycardia as well   CO as a consequence of limited SV.

  10. Hemodynamic Goals • Maintaining sinus rhythm is optimally essential as atrial fibrillation [AF] or junctional rhythm  marked  ventricular filling. • Systemic vascular resistance (Afterload)should be maintained, or even augmented to provide adequate coronary flow. Furthermore, angina may require administration of an α-agonist like phenylepherine rather than nitroglycerin to increase coronary perfusion pressure.

  11. Hemodynamic Goals • Inotropic support is not needed as long as myocardial contractility is maintained by the compensatory LVH.

  12. Preoperative assessment • History and clinical examination: • Careful history and examination • AS: • Drug therapy (β-blockers, diuretics, CCBs or ACEIs). • Other concomitant diseases: Hypertension and Hypothyroidism that may cause difficult airway management.

  13. Preoperative assessment • Oxygen-dependent exercise tolerance testing (METs); couldn’t be assessed in this patients due to her joint disease and was replaced by drug-induced stress testing, revealing no ischemic changes. • Signs of congestive heart failure (dyspnea, orthopnea, congested neck veins, LL edema, gallop, fine basal crepitation) were not observed in this case. • Vital data (HR, BP, RR, UOP, temp).

  14. Investigations: • CBC: Hb, Hct. • Coagulation profile: INR, PT and PTT. • Renal and liver function tests. • CXR: Cardiomegaly, pulmonary congestion, chest infection. • ECG :Rate , dysrhythmias, ischemic changes or chamber enlargement. • Cardiac catheterization and coronary angiography will not be important in this case, as echocardiographic results were conclusive enough.

  15. According to new guidelines of ACC/AHA for preoperative cardiac risk assessment: • Step 1: Evaluate urgency of noncardiac surgery • Emergency requires surgery regardless of risk. • Manage Cardiac Risk Factors postoperatively. • Step 2: Noninvasive cardiac testing not required • No acute cardiovascular disease and able to perform 4 METS without symptoms: • Able to climb one flight of stairs holding a bag of groceries • Able to walk on level ground at 4 miles per hour (1 mile in 15 minutes) • Coronary revascularization in past 5 years: • Must be stable and no recurrent symptoms or signs. • Coronary evaluation in last 2 years: • Evaluation must have been favorable and adequate. • No new symptoms or signs since evaluation. Risk Assessment

  16. Step 3: Indications for noninvasive cardiac testing • Evaluation based on patient risk factors • See Eagle's Cardiac Risk Assessment (typically used for ACC-AHA Guideline) • See Detsky's Modified Cardiac Risk Index • Consider in patients with functional capacity < 4 METS or unknown capacity • Major patient risk: • Indication: Three or more risk factors and cardiovascular surgery. • Cardiac evaluation needed in all cases. • Intermediate Risk: Indications for cardiac evaluation • See High Risk Surgery. • Indication: Vascular Surgery or Intermediate Risk Surgeryand at least 1 risk factor. • Minor risk: Indications for no cardiac evaluation • Evaluate on individual basis. • No symptoms at functional capacity >4 METS activity requires no evaluation.

  17. Our Patient’s assessment: Evaluation of Patient factors: • This patient lies within class II (6 – 12 points) according to modified Goldmancardiac risk index, with complications incidence of 1 – 10%. • While according to Eagle’s risk index, She will be at the major cardiovascular risk category owing to her severe AS. • According to Detsky’s cardiac risk index, this patient is class 1 (0-15 points) which carries the lowest risk.

  18. Evaluation of her functional Capacity: [METs] Evaluation of this patient was non-conclusive due to her limited physical activity attributed to her hip problems. Anaerobic threshold (AT) can be used instead to estimate for her cardiopulmonary exercise tolerance. Considering Surgery-Specific risk: This patient is having elective orthopedic surgery which is considered an intermediate risk surgery with cardiac risk 1 – 5%.

  19. Preoperative Optimization • A. Optimize Medical Therapy • Regarding this patient's hypothyroidism which is adequately controlled by medications, it will be optimal to keep her in the euthyroid (normal thyroid function tests especially TSH) or even mild hypothyroid states to maintain good coronary perfusion. • ACEIs or angiotensin-receptor blockers should beused as the LV EF is less than40%. She should also be taking ß-blockers for tight control of her hypertension. Care must be taken to avoid hypotension and coronary hypoperfusion.

  20. Preoperative Optimization • A. Optimize Medical Therapy • Medications for treatment of AS-induced CHF and consequent pulmonary congestion should be adequately adjusted, these include: Digitalis and diuretics. • All preoperative medications must be tailored to minimize the likelihood of decreases in systemic vascular resistance.

  21. B. Surgical therapy • Indeed, the only effective treatment is relief of the mechanical obstruction to left ventricular ejection by surgical replacement of the diseased aortic valve. • This patient showed no evidence of stress-induced ischemia on dobutamine test. So, in this controversially asymptomatic patient with severe aortic stenosis(48 mmHg pressure gradient), it appears to be relatively safe to delay valve replacement surgery until symptoms develop (i.e. no need to postpone her elective hip arthroplasty).

  22. B. Surgical therapy • Mortality approaches 75% within 3 years after aortic stenosis becomes symptomatic unless the valve is surgically replaced. • The prognosis with surgery even in this age group is acceptable. • She would benefit from balloon aortic valvotomy only if decompensating symptoms occurred just before her elective hip surgery.

  23. C. Antibiotic prophylaxis • NYHA recently updated its guidelines regarding which patients should take a precautionary antibiotic to prevent infective endocarditis (IE). • They show that taking preventive antibiotics is not necessary for most people and, in fact could cause allergic reactions and dangerous antibiotic resistance. • According to these, our patient in is not endangered from IE. • So, antibiotic prophylaxis will be omitted.

  24. D. Premedications • Sedatives are cautiously administered or even totally omitted to avoid respiratory or vasomotor center depression. Besides, this patient will be calm owing to her hypothyroid and age factors. • Anticholinergics are given with care to avoid tachycardia; glycopyrrolate is preferred to atropine.

  25. O’Keefe has suggested that aggressive intraoperative monitoring and prompt recognition of haemodynamic abnormalities can allow for safe anaesthesia in patients with severe, symptomatic AS undergoing non-cardiac surgery.

  26. This patient should be monitored intraoperati--vely by

  27. Defibrillator

  28. Anesthetic Management Management of anesthesia for this patient with severe aortic stenosis includes avoidance of events that may further decrease the cardiac output. There is no evidence that elective orthopedic surgery is associated with increased morbidity and mortality in this patient. General anesthesia is often prefered to epidural or spinal anesthesia because peripheral sympathetic nervous system blockade produced by regional anesthesia can lead to undesirable decreases in systemic vascular resistance.

  29. 1) Anesthetic considerations • Maintain normal sinus rhythm. • Avoid bradycardia. • Avoid sudden increases or decreases in systemic vascular resistance. • Optimize intravascular fluid volume to maintain venous return and left ventricular filling. • Arrhythmias should be treated promptly by cardioversion in the event of haemodynamic compromise.

  30. 2) Induction of Anesthesia • Induction of anesthesia can be achieved by intravenousetomidate (of choice), thiopentone in a small dose can be used but ketamine is avoided. • Tracheal intubation is facilitated by administration of muscle relaxants [vecuronium or atracurium are of choice] with avoidance of stress response by combination of i.v. lidocaine + alfentanyl + deep plane of anesthesia. • Pancuronium is avoided as it produces tachycardia. • The reverse is better with glycopyrrolate (than atropine).

  31. Bradycardia that may be associated with the administration of succinylcholine is undesirable. • Interventions to prevent this rare response (increased heart rate is the more common response) may be considered, including prior administration of anticholinergics.

  32. 3) Maintenance of Anesthesia • Maintenance of anesthesia in this patient with poor LV function (EF = 35 %) is best accomplished with nitrous oxide (cautiously as it increases PVR leading to pulmonary hypertension) plus opioids. • Opioids can be used alone in high doses; fentanyl 50 to 100 μg/kg IV or equivalent doses of other potent opioids except pethidine.

  33. That's to avoid the disadvantage of volatile agents (especially halothane), which depress SAN automaticity junctional rhythm and loss of properly timed atrial contractions. • Furthermore, it is useful to avoid any additional depression of myocardial contractility with volatile anesthetics.

  34. Decreased systemic vascular resistance produced by high concentrations of isoflurane, desflurane, or sevoflurane would be undesirable; in contrast, clinical experience has shown that low concentrations of these drugs are unlikely to be associated with undesirable responses. • Non-depolarizing neuromuscular blocking drugs (mentioned in induction) with minimal effects on the circulation are useful. • Intravascular fluid volume is maintained by prompt replacement of blood loss and liberal administration (5 ml/kg/hr) of intravenous fluids.

  35. 4) Regional Anesthesia • Spinal or epidural anesthesia and the associated sympathetic nervous system blockade have been con­sidered undesirable in patients with aortic stenosis. • Owing to the concentric LVH this patient’s myocardium is susceptible to ischemia even in absence of coronary artery disease. • Large drop in systemic vascular resistance could initiate a cycle of hypotension-induced myocardial ischemia, subsequent ventricular dysfunction, and worsening hypotension.

  36. Ifa regional anesthetic is selected in this patient, it may be useful to consider continuous spinal anesthesia. • Increasingly combined nerve blocks are invading the regional anesthetic field, particularly for prolonging the postoperative analgesic period. • Combined lumbar plexus and sciatic nerve blocks will be very adequate for this elderly patient with severe aortic stenosis undergoing hip replacement surgery. Due to its great hemodynamic and cardiovascular stability.

  37. 5) Intraoperative complications • The onset of junctional rhythm or bradycardia requires prompt treatment with intravenous atropine. • Persistent tachycardia can be treated with opioids, i.v. digitalis (if with AF) 0.25 - 0.5 mg over 10 min, or βB such as esmolol, keeping in mind that this patient may be dependent on endogenous β-adrenergic activity to maintain LV stroke volume especially in the presence of increased SVR that occurs in response to surgical stimulation. • SVT should be promptly terminated with electrical cardioversion.

  38. Lidocaine is kept available, as this patient have a propensity to develop ventricular dysrhythmias. • Hypotension is treated by phenylephrine (pure α agonist) better than ephedrine or dopamine (α and β agonist) as both have β action so; they affect heart contractility & increase HR. • P++ & RVF treated by inotropic support e.g. dopamine, pulmonary VD e.g. nitroprusside. • Hypertension istreated by potent vasodilators with full hemodynarnic monitoring.

  39. 6) Postoperative Risks There is increased risk of pulmonary edema and RVF due to sympathetic overactivity caused by pain, hypoventilation (with subsequent respiratory acidosis) and hypoxemia pulmonary VC. Careful monitoring, O2 supplementation and adequate postoperative analgesia would be essential.

  40. Thank You

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