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Mitral stenosis and Anesthesia

The document discusses the case of a 26-year-old female patient who is 36 weeks pregnant with mitral stenosis. She presents with palpitations, breathlessness, and fatigue. Her history and examination are consistent with mild mitral stenosis of rheumatic origin, as confirmed by echocardiogram findings of a mitral valve area of 2.0 cm2 and transvalvular pressure of 8 mm Hg. The discussion centers on the pathophysiology, diagnosis, and management of mitral stenosis, including the plan for regional anesthesia for her elective caesarean section.

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Case Discussion Anaesthetic Management of a case of mitral stenosis G 2P 1L 1 A 0 with 36 weeks gestation with mitral stenosis for elective caesarean section Speaker: Dr Bhagirath.S.N Panelists: Dr Akkamahadevi.P Dr Srinivas.H.T
Case Patient details Name: Mrs. Savitha Age: 26 years Sex: female I.P.No.: 236455 Chief Complaints G2P1L1A0 with 36 weeks gestation with Palpitations since 6 weeks Breathlessness since 4 weeks Fatigue since 2 weeks
Case………………contd. History of Presenting Illness Palpitation Breathlessness Fatigue Intermittent Associated with exertion Relieved on rest 6 weeks duration Gradual in onset Progressive in nature (NYHA II) Aggravated on lying down Relieved on sitting up 4 weeks duration Feeling of weakness 2 weeks duration There was no history of haemoptysis or recurrent respiratory infections.
Case………………contd. Past History No history of similar complaints in previous pregnancy. History of Rheumatic Heart Disease since 12 years of age. Took treatment in the form of Penicillin injections every 21 days for 8 years till age 20 and then discontinued. No history of cyanotic spells. No history of hypertension, Diabetes Mellitus, Tuberculosis, Bronchial Asthma or Epilepsy.
Case………………contd. No history of similar complaints in the family was noted. Personal History Diet: Vegetarian Appetite: reduced. Bowel & Bladder: Normal. Sleep: disturbed. Habits: None Family History
Case………………contd. A young pregnant female patient, moderately built and nourished No pallor, icterus, cyanosis, oedema, clubbing Pulse rate – 90/min; Weight – 58 Kgs Blood pressure – 110/70 mm of Hg; Height – 155 cms Respiratory rate – 16/min; Respiratory System: Normal Vesicular Breath Sounds heard, No added sounds. Central Nervous System: Normal. No neurological deficits. General Physical Examination
Case………………contd. Per abdominal examination: Distended. Consistent with pregnancy. No free fluid. No dilated veins. Cardiovascular System: Inspection: No deformity, Engorged superficial veins, Scars or sinuses. No visible pulsations Palpation: Apex beat felt in 5th intercostal space medial to left midclavicular line, absence of left parasternal heave Auscultation: S1 S2 Heard. Opening Snap heard near the apex. (after S2) Low pitched mid-diastolic murmur at apex. (no radiation)
Case………………contd. G2P1L1A0 with 36 weeks gestation with Mitral Stenosis of Rheumatic Origin without evidence of congestive cardiac failure. Impression
Case………………contd. Hb: 12.0 gm% Differential count: Neutrophils – 71 Lymphocytes – 24 Monocytes – 02 Eosinophils – 03 Total count – 9, 800 Platelets: 2.73 lakhs/ mm3 PT INR: 1.0 BT: 3’ 00” CT: 4’ 00” Investigations
Case………………contd. RBS: 99 mg/dl Urea: 30 mg/dl Creatinine: 1.1 mg/dl Na+: 135mEq/l K+: 4.8mEq/l Cl-: 104mEq/l HIV 1 & 2: Not detected HBsAg: Not detected Investigations
Case………………contd. ECG: Sinus rhythm. Within normal limits. Heart rate: 80/min. Right axis deviation. 2D ECHOCARDIOGRAPHY: Normal Left Ventricular systolic function No Regional Wall Motion abnormalities Ejection fraction: 56 % Mitral Valve Area – 2.0 cms2 Transvalvular Pressure – 8 mm of Hg. Chest X – Ray: Cardiomegaly. Prominent bronchovascular markings. Management plan Regional anaesthesia for elective caesarean section Investigations
Discussion Causes: - Palpitations Tachyarrhythmias, Atrial fibrillation, Atrial kick Endocrine–Pheochromocytoma, Thyrotoxicosis, Hypogylcemia High Output states – Anemia, Pyrexia, Aortic Regurgitation, Patent Ductus Arteriosus. Drugs – Atropine, Adrenaline, Aminophylline, Thyroxine, Caffeine, Tannin, Alcohol Psychogenic – Prolonged anxiety Idiopathic Atrial kick - Palpitations
Discussion Cardiac causes Atrial kick - Palpitations Respiratory causes Hematological Left heart failure Congenital heart disease Acquired valvular disease Bronchial Asthma Severe Anaemia Acquired valvular disease - Dyspnea Coronary heart disease Breathlessness hypertensive heart disease Cardiomyopathy Chronic obstructive lung disease Chronic restrictive lung disease Pneumonia Pulmonary neoplasm/ embolism Laryngeal/ Tracheal obstruction
Discussion Past History Atrial kick - Palpitations Family History Personal History Rheumatic Heart Disease (RHD) RHD – Most common cause 40% More common in females, typically detected in childhood. Family history of Rheumatic Heart Disease, Congenital Valvular defects may be relevant Disturbed sleep in Paroxysmal Nocturnal Dyspnoea Acquired valvular disease - Dyspnea Recurrent respiratory tract infection indicates pulmonary congestion RHD, Female patient, Childhood history, disturbed sleep
Discussion Oedema Atrial kick - Palpitations Hepatomegaly Mitral Facies Severe Mitral stenosis ultimately leads to right heart failure. Seen in right ventricular failure and pulmonary hypertension. Low Cardiac Output in Mitral Stenosis causes peripheral vasoconstriction producing pinkish purple patches on cheeks. Mitral Flush due to vasodilatation (vascular stasis) is seen Seen in fair skinned individuals Acquired valvular disease - Dyspnea RHD, Female patient, Childhood history, disturbed sleep General Physical Examination Absent here Absent here Edema & Hepatomegaly absent – mild disease
Discussion Inspection Atrial kick - Palpitations No deformity of precordium. – Precordial bulge indicates early onset and longer duration of cardiac disease. Acquired valvular disease - Dyspnea RHD, Female patient, Childhood history, disturbed sleep Cardiovascular Examination Scar marks reveal previous surgeries Engorged Neck Veins indicate high right heart pressures Edema & Hepatomegaly absent – mild disease
Discussion Palpation Atrial kick - Palpitations Tapping character of the apex beat (palpable S1) is typical. Acquired valvular disease - Dyspnea RHD, Female patient, Childhood history, disturbed sleep Cardiovascular Examination Palpable diastolic thrill in mitral area best felt in left lateral position in full expiration. Parasternal heave. (absent here) If one finds engorged superficial veins look for direction of flow. Absent Parasternal heave – mild disease Edema & Hepatomegaly absent – mild disease
Discussion Auscultation Atrial kick - Palpitations S1 is sharp, short, accentuated Acquired valvular disease - Dyspnea RHD, Female patient, Childhood history, disturbed sleep Cardiovascular Examination Opening Snap after S2 Low pitched mid-diastolic rumbling murmur with presystolic accentuation of Grade IV intensity in mitral area without any radiation Murmur best heard at cardiac apex with bell of stethoscope in left lateral position at height of expiration Absent Parasternal heave – mild disease Edema & Hepatomegaly absent – mild disease Absence of click, split, rub or murmur over other areas Opening snap +murmur at apex
Substantiation Atrial kick - Palpitations Acquired valvular disease - Dyspnea RHD, Female patient, Childhood history, disturbed sleep Absent Parasternal heave – mild disease Edema & Hepatomegaly absent – mild disease Opening snap +murmur at apex Childhood history Female Patient Rheumatic Heart Disease Edema & hepatomegaly absent Palpitations Dyspnea Absent parasternal heave – mild disease Opening Snap + low pitched mid diastolic murmur 2D – Echo – Mitral Valve 2.0 cms2,, Transvalvular pressure 8 mm of Hg Mitral Stenosis of Rheumatic Origin without evidence of congestive cardiac failure.
Mitral stenosis at a glance
Anatomy
Anatomy Normal Orifice: 4 – 6 Cms2 4-6 cms2 < 2.5 cms2 1.5- 2.5 cms2 1.0 – 1.5 cms2 < 1.0 cms2 Mild MS – 1.5 – 2.5 Cms2 (Dyspnea on severe exertion) Moderate MS – 1.0 – 1.5 Cms2 (PND ± pulmonary oedema) Severe/ Critical- < 1.0 Cms2 (Orthopnea – Class IV) Symptoms start < 2.5 Cms2
Anatomy Mitral Valve area is calculated using Gorlin’s Equation: Area = Cardiac Output/ (DFP or SEP) (HR) 44.3 C √ΔP DFP = Diastolic Filling Pressure C = Empirical Constant SEP = Systolic Ejection Period ΔP = Pressure Gradient HR = Heart Rate
Pathophysiology Decreased LV filling Increased left atrial pressure and volume Pulmonary vein pressure Transudation of fluid into pulmonary interstitial space Pulmonary compliance Work of breathing Progressive Dyspnea Adaptation Atrial Kick Adaptation Lymphatic drainage and thickening of basement membrane Pulmonary hypertension Palpitations Breathlessness Haemoptysis
Pathophysiology Almost all chambers are shown here , except… Left Ventricle So, are we to assume that Left Ventricle remains unaffected..?
Pathophysiology The answer is NO. Left Ventricle is affected Decreased filling ultimately manifests as 1. muscle atrophy 2. Inflammatory myocardial fibrosis 3. Scarring of sub valvular apparatus 4. Abnormal pattern of left ventricle contraction 5. Decreased left ventricular compliance with diastolic dysfunction 6. Right to left shift due to pulmonary hypertension
Aetiology 1. Rheumatic Heart Disease 2. Congenital – Parachute Mitral Valve 3. Hunter’s Syndrome 4. Hurler’s Syndrome 5. Drugs – Methysergide 6. Carcinoid syndrome 7. Amyloidosis 8. Mitral annular Calcification 9. Rheumatoid Arthritis 10. Systemic Lupus Erythematosis 11. Infective endocarditis with large vegetations. 12. Lutembacher’s Syndrome: Atrial Septal Defect (ASD) + Mitral Stenosis (MS) rheumatic origin
Pathology 1. Diffuse thickening of mitral leaflets and subvalvular apparatus. 2. Commissural fusion 3. Calcification of annulus and leaflets 4. Contracture of Chordae and papillary heads 5. Usually develops over 2-3 decades. Pathological types of Mitral Stenosis 1. Button Hole 2. Fish Mouth 3. Funnel Type
Common symptoms 1. Dyspnoea 2. Orthopnea 3. Paroxysmal Nocturnal Dyspnea 4. Palpitation 5. Fatiguability 6. Haemoptysis 7. Recurrent Bronchitis 8. Cough 9. Chest pain 10. Right hypochondrial Pain (hepatomegaly)
Conditions simulating mitral stenosis 1. Left Atrial Myxoma 2. Cortriatriatum 3. Ball valve thrombus of left atrium 4. Diastolic flow murmurs across normal mitral valve as in VSD, PDA, severe MR 5. Carey-Coomb’s murmur of mitral valvulitis 6. Tricuspid stenosis 7. Austin-Flint murmur
Complications 1. Acute left heart failure and acute pulmonary edema 2. Pulmonary hypertension 3. Right Ventricular failure 4. Atrial Fibrillation 5. Atrial Flutter 6. Ventricular or atrial premature beats 7. Embolic manifestations 8. Haemoptysis 9. Infective Endocarditis 10. Recurrent Broncho-pulmonary infections 11. Complications arising from enlarged left atrium: Hoarseness of voice – left recurrent laryngeal nerve due to enlarged left atrium (Ortner’s Syndrome) Dysphagia – Oesophageal compression 12. Jaundice, Cardiac cirrhosis.
Diagnosis One needs to assess anatomy of Mitral Valve Leaflet in terms of 1. Thickening 2. Calcification 3. Mobility 4. Extent of involvement and subvalvular apparatus One also needs to assess extent of stenosis 1. Mitral Valve area 2. Transvalvular pressure gradient Also to be assessed are 1. Cardiac chamber dimension 2. Pulmonary hypertension 3. Ventricular function 4. Associated valvular disease 5. Examination of Left Atrial Thrombus
Diagnosis Assess extent of calcification 1. Disappearance of Opening snap especially if calcification is more. Assessment of X-Ray (P-A View) 1. Left Atrial Enlargement – Mitralisation of heart 2. Straightening of Left Heart Border 3. Elevation of Left mainstem Bronchus 4. Evidence of Mitral Calcification, Evidence of Pulmonary edema, Pulmonary Vascular Congestion. 5. Kerley’s B lines Assessment of X-Ray (RAO view) 1. Oesophagus is pushed or curved backward by enlarged left atrium.
Diagnosis Assessment of ECG 1. Broad notched “P” Waves signifying atrial enlargement. 2. Atrial Fibrillation (f- waves replacing p-waves) 3. Right Ventricular Enlargement 2D – Echocardiography Doppler study 1. Chamber Enlargement 1. To know the speed and direction of blood flow. 2. Valve pathology 3. Valve movement 4. Mitral Orifice Blood Examination 1. TC and DC 2. ESR 3. ASO Titre
Treatment 1. Mild Mitral stenosis – Diuretics Restriction of physical activity Salt-restricted diet 2. When in Atrial Fibrillation – Digoxin (0.25 mg tablet) β- Blockers Calcium Channel Blockers Control of heart rate is paramount, because tachycardia impairs left ventricular filling and further increases left atrial pressure. 3. Anticoagulation – Warfarin to normalise INR
Treatment 4. Surgery if Pulmonary hypertension develops Percutaneous balloon valvotomy Surgical commisurotomy Valve reconstruction 5. Valve replacement Starr-Edwards ball valve Bjork-Shiley disc valve Porcine bio-prosthesis 6. Prophylaxis against recurrence of rheumatic fever Inj. Benzathine Penicillin 1.2 million units.
Anaesthetic Management
Hemodynamic Parameters Change in normal pregnancy Change during Labour & delivery Change during postpartum Blood volume Increased by 40 % - 50% Increased Decreased (auto diuresis) Heart rate Increased by 10 – 15 beats/ min Increased Decreased Cardiac Output Increased by 30% - 50 % Additional 50 % Decreased Blood Pressure Decreased by 10 mm of Hg Increased Decreased Stroke Volume Increased in first and second trimester Increased (300 – 500 ml/contraction) Decreased Systemic Vascular Resistance Decreased Increased Decreased
Maternal mortality associated with heart disease in pregnancy Group 1: Mortality < 1% Atrial septal defect Ventricular septal defect; PDA Pulmonary/tricuspid disease Tetralogy of Fallot, corrected; Bioprosthetic valve Mitral stenosis, NYHA class I and II Group 2: Mortality 5–15% 2A Mitral stenosis NYHA class III–IV; Aortic stenosis Coarctation of aorta, without valvular involvement Uncorrected Tetralogy of Fallot Previous myocardial infarction Marfan syndrome with normal aorta 2B Mitral stenosis with atrial fibrillation Artificial valve Group 3: Mortality 25–50% Primary pulmonary hypertension or Eisenmenger syndrome Coarctation of aorta, with valvular involvement Marfan syndrome with aortic involvement
Mortality: 0 point-5%,1 point-27%,>1 point-75% CARPREG Score
Anaesthetic Management Principle involved: Cardiac Output Decrease in cardiac output Hypotension Tachycardia Reduced ventricular filling Vicious cycle Increased ventricular filling Trendelenburg' s position, Autotransfusio n due to uterine contraction Precipitation of CHF 1 2 3
Anaesthetic Management Principle involved: 1. Prevent decrease in cardiac output, as hypotension because of this causes reflex tachycardia, which in turn reduces ventricular filling further compromising cardiac output. 2. Avoid hypotension for the same reason listed above. If hypotension ensues, treat with Ephedrine or Phenylephrine. 3. Avoid precipitating Congestive Heart Failure due to factors such as Trendelenburg’s position Autotransfusion due to uterine contraction leading to increased central blood volume. 4. Avoid precipitation of Right Ventricular Failure Hypercarbia Hypoxemia Lung Hyperinflation Increase in lung water If Right Ventricular Failure exists, treat with inotropes and pulmonary vasodilators.
Anaesthetic Management Preoperative Medication 1. Decrease anxiety (decreases tachycardia) 2. Drugs used to control heart rate to be continued till day of surgery 3. Hypokalemia if present secondary to diuretic therapy to be addressed 4. If intended surgery is a minor surgery, continue anticoagulant therapy 5. If intended surgery is a major surgery, discontinue anticoagulant therapy. Induction of Anaesthesia 1. Avoid Ketamine – Increases heart rate, blood pressure 2. Avoid Atracurium – Increased histamine release causes hypotension which manifests as tachycardia.
Anaesthetic Management Maintenance of Anaesthesia 1. Drugs should have minimal effects on hemodynamic pattern 2. Balanced anaesthesia with N2O/ Narcotic/ Volatile anaesthetic 3. N2O causes insignificant pulmonary vasoconstriction. It is significant only if pulmonary hypertension exists. So, one needs to treat pulmonary hypertension preoperatively. 4. Cardiac stable muscle relaxants are to be used. (preferably avoid Pancuronium) 5. Avoid lighter planes of anaesthesia (To avoid tachycardia) 6. Fluid Management: Avoid Hypervolemia - -> Worsens pulmonary edema Avoid Hypovolemia - -> Sacrifices already decreased left ventricular filling, which further decreases Cardiac output. Hypovolemia secondary to blood loss and vasodilatory effects of anaesthesia ought to be avoided.
Anaesthetic Management Monitoring 1. Transesophageal Echocardiography 2. Intra-arterial pressure 3. Pulmonary artery pressure to be monitored 4. Left atrial pressure Principle: 1. Ensure adequacy of cardiac function intravascular fluid volume ventilation oxygenation A word of caution regarding Pulmonary artery pressure monitoring: - When measured too frequently, the risk of pulmonary artery rupture is far too high.
Anaesthetic Management Post Operative 1. Assess postoperative risk of pulmonary oedema and right heart failure and manage accordingly. 2. Avoid pain as pain begets hypoventilation which leads to respiratory acidosis, hypoxemia which manifests as raised heart rate and pulmonary vascular resistance. 3. After Major thoracic or abdominal surgery, the decreased pulmonary compliance and increased work of breathing requires mechanical ventilation.
Anaesthetic Management Category 1 - Immediate threat to life of woman or fetus(baby needs to be removed in 30 min. of making the decision to do LSCS Category 2 - Maternal or fetal compromise, not immediately life threatening(some time can be spent for resuscitation) Category 3 - Needing early delivery but no maternal or fetal compromise Category 4- At a time to suit the woman and maternity team
Anaesthetic Management Anesthetic techniques available are 1. Regional anaesthesia (Sub Arachnoid Block, Epidural, Combined Spinal Epidural) 2. General Anaesthesia Sub Arachnoid Block: subarachnoid causes rapid onset of extensive sympathetic blockade with intense vasodilatation sudden hypotension and severe tachycardia. Epidural Block: epidural anaesthesia might not be an ideal technique as it requires slow induction, delay in the onset of action which may not be possible in an emergency situation. Moreover large volume of local anesthetic is needed for adequate blockade. Combined Spinal Epidural: Combined spinal and epidural will be the technique of choice.CSE offers rapid onset and improved analgesia It offers ability to use low dose spinal with room for post operative analgesia
Anaesthetic Management Why our choice is right..? 1. Rapid onset of spinal block 2. Ability to modify / top-up / prolong anaesthesia with epidural component 3. Spread of spinal anaesthetic can be altered with injection of saline into the epidural space (compression effect of dural sac) 4. Option for post-operative analgesia 5. Reduces need for conversion to general anaesthetic in event of spinal failure 6. Able to use lower dose spinal and modify if required, potentially reducing spinal induced hypotension 7. Advantageous in cardiac conditions 8. Arguably advantageous in pre-eclampsia
Anaesthetic Management Why our choice is right..? 9. Can produce a denser block than either technique in isolation 10. Airway pressures are not altered and avoids hyperventilation 11. Minimal autonomic blockade , hence no sudden decrease in Systemic Vascular resistance 12. Better maintenance of uterine blood flow improving the fetal outcome 13. Auto transfused blood during the third stage of labor is well accommodated 14. Improved microvascular blood flow prevents DVT 15. Allows early ambulation and return of bowel movements
Anaesthetic Management Procedure per se Preparation: 1. All resuscitation equipments and drugs , anaesthesia machine, O2 delivery system, Equipments for G.A. , Suction apparatus are kept ready 2. Patient is given aspiration prophylaxis in the form of 0.3ml SODIUM CITRATE 30ml orally, H2 receptor blocker and antiemetic given 3. Record baseline vitals 4. Secure two wide bore cannulae and infuse 60-75ml/hr of crystalloid 5. Administer infective endocarditis prophylaxis 6. Monitors- SpO2, ECG, NIBP, and urine output 7. Reassure the patient 8. Informed consent is obtained explaining the maternal and fetal risk 9. Adequate Compatible blood
Anaesthetic Management Procedure per se CSE is performed in lateral decubitus position under strict aseptic precautions Epidural space is identified with 18 G Tuohy needle using LOR with saline. Spinal needle is introduced through the Tuohy needle and subarachnoid block is performed.20-30 μg of Fentanyl along with 2.5 -5mg of 0.5% Bupivacaine is given. This is followed by insertion of epidural catheter through which 3 ml of 2% Xylocaine with epinephrine is given. Post operative analgesia is maintained as shown in the table below Drug Initial Injection Continuous Infusion Bupivacaine 10-15 mL of a 0.25%-0.125% solution 0.0625%-0.125% solution at 8-15 mL/hr Ropivacaine 10-15 mL of a 0.1%-0.2% solution 0.5%-0.2% solution at 8-15 mL/hr Fentanyl 50-100 µg in a 10-mL volume 1-4 µg/mL
Anaesthetic Management 1. If Hypotension occurs- vasopressors are used. 2. After the baby is delivered Oxytocin in minimal dose as slow infusion is given 3. Arrhythmias should be treated appropriately. 4. Blood loss should be assessed and replaced accordingly. 5. Immediate post partum period mandates meticulous care as mortality is very high in these patients with Pulmonary artery hypertension. 6. Post operative pain management reduces Cardiovascular-stress response and prevents Deep Vein Thrombosis.
Anaesthetic Management Myths and Worries about Regional anaesthesia 1. Preloading is mandatory and hazardous--CVP guided fluid management negates overloading and maintains adequate cardiac output 2. Regional Anaesthesia is associated with sudden fall in BP. Local anaesthetic with Opioid combination intrathecally followed by epidural to titrate the desired level of block does not produce rapid fall in BP. 3. Delay in performing the actual procedure: this doesnt happen with expert hands 4. The complications of CSE-like total spinal, LA toxicity, epidural hematoma and abscess are negligible with senior anesthesiologists
Anaesthetic Management Controversies about CSE: Risk of epidural catheter through the dural hole Perceived increase in neurotrauma Contraindications to Regional Anaesthesia • Active heavy bleeding • Uncorrected coagulopathy (e.g. HELLP syndrome (Hemolysis, Elevated Liver Enzymes, Low Platelets) associated with pre-eclampsia) • Thrombocytopenia • Systemic sepsis • Local sepsis at site of insertion • Patient refusal
Anaesthetic Management Guidelines for general anaesthesia General anesthesia has the advantages of speed of induction, control of the airway, and superior hemodynamics. Anaesthetic Goals: 1. Maintain the heart rate around 80-100 b/min . 2. Maintain Left Atrial Pressure high enough to take advantage of the increased preload reserve. 3. Avoid pulmonary artery hypertension by treating hypercarbia, hypoxemia, and acidemia. 4. Aggressively treat pulmonary artery hypertension with vasodilator therapy to avoid RV failure. If RV failure does occur, inotropic support of the RV and pulmonary vasodilation may be necessary. The presence of PAH is the major factor that increase the mortality.
Anaesthetic Management Guidelines for general anaesthesia 5. Avoid factors which depress the myocardium:(inhalation agents and drugs) 6. Maintain awareness of potential for LV rupture. 7. Aggressive treatment of arrhythmias if they occur 8. Avoid profound changes in SVR 9. Attenuate pressor response(intubation, extubation, light plane of anesthesia) 10. Adequate analgesia and adequate muscle relaxation guided by Neuro muscular monitoring 11. Aspiration prophylaxis 12. Blood loss assessment and prompt replacement
Anaesthetic Management Guidelines for general anaesthesia
Anaesthetic Management Guidelines for general anaesthesia Other advantages are 1. Rapidly established 2. Better hemodynamic stability 3. Prevention of aspiration as the airway is isolated 4. High FiO2 -which will reduce PVR 5. Ventilation controlled to avoid hypercarbia-which will increase PVR 6. FRC is increased by controlled ventilation 7. Ventilation of atelectatic areas –better V/Q 8. Sinus rhythm can be maintained. In case of SVT and Ventricular arrhythmias promptly reverted by cardioversion
Anaesthetic Management Guidelines for general anaesthesia Other advantages are 9. Peak airway pressure can be kept <20 cms H2O 10. Elective post operative ventilation to tide over the CCF that may be possible after parturition 11. Effective management of Pulmonary oedema - IPPV with PEEP, liberal use of high dose morphine
Anaesthetic Management Guidelines for general anaesthesia The possible complications that can be anticipated 1. failed intubation 2. Aspiration( more common in unprepared case) 3. Hypoxia and hypocarbia -effect on fetus 4. Hypertensive crisis 5. Arrhythmia-hypoxia, hypercarbia, inhalational agents, Drugs 6. Use of poly pharmacy and anaphylaxis 7. Awareness 8. Uterine atony with inhalation agents
Anaesthetic Management Guidelines for general anaesthesia The possible complications that can be anticipated 9. Need for adequate post op. Analgesia 10. Neonatal depression 11. Delayed recovery 12. Anesthetic drug interaction with cerebrovascular drugs(Ca channel blockers and Magnesium) 13. Increased incidence of PONV 14. Prolonged stay ICU
Outlines of Management 1. Pre-conceptual counseling- NYHA III and IV are advised corrective cardiac before pregnancy. It is advisable for certain cardiac diseases where pregnancy is to be avoided They have to be registered, interviewed regarding functional difficulties, regular follow ups starting from early pregnancy. It is advisable to manage them in higher centers where multidisciplinary support is available(Multidisciplinary approach: management by a team of specialists apart from obstetricians that includes the cardiologist(failure prevention, arrhythmia management), CT surgeon(emergent cardiac surgery), neonatologist(preterm baby) anesthesiologist(pain relief-epidural, mechanical Ventilation if necessary) 2. Correct factors which will burden the cardiac lesion like anemia, obesity, Hypertension, arrhythmia 3. Prevention of Infection
Outlines of Management 4. Optimization of Heart rate with pharmacological agents 5. Pregnancy is a hypercoagulable state, which increases the risk of thromboembolic events, especially in the cardiac patient with a prosthetic heart valve, valvular heart disease, or heart failure. Anticoagulant therapy should be considered in these high-risk patients to prevent thromboembolism or thrombus formation. 6. IE prophylaxis -(as per the ACOG guidelines- some of the drugs recommended by ACC/AHA are not recommended for pregnant patients) 7. Monitors- other than the ASA standards recommendation- Advanced monitors like invasive arterial pressure, CVP -, PCWP and TEE are recommended. They should be continued in the post partum period upto 72 hrs at least
Outlines of Management 8. Planning the mode of delivery-vaginal delivery is better tolerated(less blood loss, less catecholamine), Pain relief during Labor - recommended, shortening the second stage- outlet forceps, episiotomy. 9. Large boluses of Oxytocics should be avoided as they cause profound hypotension. Ergometrine better avoided. PGF2 alpha and mesoprostol are used cautiously. 10. If planned for Cesarean section choice of anesthetic should be directed to keep the haemodynamic stable (as near normal Systemic vascular resistance, Preload, Afterload as possible)Adequate replacement of blood loss. 11. All patients with cardiac disease should be kept in High dependency unit and monitored after the delivery for a minimum period of 72hrs 12. Plan and Advise cardiac surgery in the second trimester if is warranted in the interest of the mother's well being
When to give Infective Endocarditis Prophylaxis..?
How to give Infective Endocarditis Prophylaxis..?
References Miller’s Anaesthesia , 7th Edition, Vol 1 Clinical Anesthesia by Paul.G.Barash Morgan’s Clinical Anaesthesiology Kaplan’s Cardiac Anesthesia
References Harrison’s Internal Medicine 17th Edn A Practice of Anesthesiology by Churchill Wylie Stoelting’s Anesthesia & co-existing disease CMDT 2010
References Bedside Clinics in medicine - Kundu A Manual of Practical Medicine by Alagappan Circulation Journal
References Indian Journal of Anaesthesiology

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Mitral stenosis and Anesthesia

  • 1.
    Case Discussion Anaesthetic Managementof a case of mitral stenosis G 2P 1L 1 A 0 with 36 weeks gestation with mitral stenosis for elective caesarean section Speaker: Dr Bhagirath.S.N Panelists: Dr Akkamahadevi.P Dr Srinivas.H.T
  • 2.
    Case Patient details Name: Mrs.Savitha Age: 26 years Sex: female I.P.No.: 236455 Chief Complaints G2P1L1A0 with 36 weeks gestation with Palpitations since 6 weeks Breathlessness since 4 weeks Fatigue since 2 weeks
  • 3.
    Case………………contd. History ofPresenting Illness Palpitation Breathlessness Fatigue Intermittent Associated with exertion Relieved on rest 6 weeks duration Gradual in onset Progressive in nature (NYHA II) Aggravated on lying down Relieved on sitting up 4 weeks duration Feeling of weakness 2 weeks duration There was no history of haemoptysis or recurrent respiratory infections.
  • 4.
    Case………………contd. Past History Nohistory of similar complaints in previous pregnancy. History of Rheumatic Heart Disease since 12 years of age. Took treatment in the form of Penicillin injections every 21 days for 8 years till age 20 and then discontinued. No history of cyanotic spells. No history of hypertension, Diabetes Mellitus, Tuberculosis, Bronchial Asthma or Epilepsy.
  • 5.
    Case………………contd. No history ofsimilar complaints in the family was noted. Personal History Diet: Vegetarian Appetite: reduced. Bowel & Bladder: Normal. Sleep: disturbed. Habits: None Family History
  • 6.
    Case………………contd. A young pregnantfemale patient, moderately built and nourished No pallor, icterus, cyanosis, oedema, clubbing Pulse rate – 90/min; Weight – 58 Kgs Blood pressure – 110/70 mm of Hg; Height – 155 cms Respiratory rate – 16/min; Respiratory System: Normal Vesicular Breath Sounds heard, No added sounds. Central Nervous System: Normal. No neurological deficits. General Physical Examination
  • 7.
    Case………………contd. Per abdominal examination:Distended. Consistent with pregnancy. No free fluid. No dilated veins. Cardiovascular System: Inspection: No deformity, Engorged superficial veins, Scars or sinuses. No visible pulsations Palpation: Apex beat felt in 5th intercostal space medial to left midclavicular line, absence of left parasternal heave Auscultation: S1 S2 Heard. Opening Snap heard near the apex. (after S2) Low pitched mid-diastolic murmur at apex. (no radiation)
  • 8.
    Case………………contd. G2P1L1A0 with 36weeks gestation with Mitral Stenosis of Rheumatic Origin without evidence of congestive cardiac failure. Impression
  • 9.
    Case………………contd. Hb: 12.0 gm% Differentialcount: Neutrophils – 71 Lymphocytes – 24 Monocytes – 02 Eosinophils – 03 Total count – 9, 800 Platelets: 2.73 lakhs/ mm3 PT INR: 1.0 BT: 3’ 00” CT: 4’ 00” Investigations
  • 10.
    Case………………contd. RBS: 99 mg/dl Urea:30 mg/dl Creatinine: 1.1 mg/dl Na+: 135mEq/l K+: 4.8mEq/l Cl-: 104mEq/l HIV 1 & 2: Not detected HBsAg: Not detected Investigations
  • 11.
    Case………………contd. ECG: Sinus rhythm.Within normal limits. Heart rate: 80/min. Right axis deviation. 2D ECHOCARDIOGRAPHY: Normal Left Ventricular systolic function No Regional Wall Motion abnormalities Ejection fraction: 56 % Mitral Valve Area – 2.0 cms2 Transvalvular Pressure – 8 mm of Hg. Chest X – Ray: Cardiomegaly. Prominent bronchovascular markings. Management plan Regional anaesthesia for elective caesarean section Investigations
  • 12.
    Discussion Causes: - Palpitations Tachyarrhythmias, Atrialfibrillation, Atrial kick Endocrine–Pheochromocytoma, Thyrotoxicosis, Hypogylcemia High Output states – Anemia, Pyrexia, Aortic Regurgitation, Patent Ductus Arteriosus. Drugs – Atropine, Adrenaline, Aminophylline, Thyroxine, Caffeine, Tannin, Alcohol Psychogenic – Prolonged anxiety Idiopathic Atrial kick - Palpitations
  • 13.
    Discussion Cardiac causes Atrial kick- Palpitations Respiratory causes Hematological Left heart failure Congenital heart disease Acquired valvular disease Bronchial Asthma Severe Anaemia Acquired valvular disease - Dyspnea Coronary heart disease Breathlessness hypertensive heart disease Cardiomyopathy Chronic obstructive lung disease Chronic restrictive lung disease Pneumonia Pulmonary neoplasm/ embolism Laryngeal/ Tracheal obstruction
  • 14.
    Discussion Past History Atrial kick- Palpitations Family History Personal History Rheumatic Heart Disease (RHD) RHD – Most common cause 40% More common in females, typically detected in childhood. Family history of Rheumatic Heart Disease, Congenital Valvular defects may be relevant Disturbed sleep in Paroxysmal Nocturnal Dyspnoea Acquired valvular disease - Dyspnea Recurrent respiratory tract infection indicates pulmonary congestion RHD, Female patient, Childhood history, disturbed sleep
  • 15.
    Discussion Oedema Atrial kick - Palpitations HepatomegalyMitral Facies Severe Mitral stenosis ultimately leads to right heart failure. Seen in right ventricular failure and pulmonary hypertension. Low Cardiac Output in Mitral Stenosis causes peripheral vasoconstriction producing pinkish purple patches on cheeks. Mitral Flush due to vasodilatation (vascular stasis) is seen Seen in fair skinned individuals Acquired valvular disease - Dyspnea RHD, Female patient, Childhood history, disturbed sleep General Physical Examination Absent here Absent here Edema & Hepatomegaly absent – mild disease
  • 16.
    Discussion Inspection Atrial kick - Palpitations Nodeformity of precordium. – Precordial bulge indicates early onset and longer duration of cardiac disease. Acquired valvular disease - Dyspnea RHD, Female patient, Childhood history, disturbed sleep Cardiovascular Examination Scar marks reveal previous surgeries Engorged Neck Veins indicate high right heart pressures Edema & Hepatomegaly absent – mild disease
  • 17.
    Discussion Palpation Atrial kick - Palpitations Tappingcharacter of the apex beat (palpable S1) is typical. Acquired valvular disease - Dyspnea RHD, Female patient, Childhood history, disturbed sleep Cardiovascular Examination Palpable diastolic thrill in mitral area best felt in left lateral position in full expiration. Parasternal heave. (absent here) If one finds engorged superficial veins look for direction of flow. Absent Parasternal heave – mild disease Edema & Hepatomegaly absent – mild disease
  • 18.
    Discussion Auscultation Atrial kick - Palpitations S1is sharp, short, accentuated Acquired valvular disease - Dyspnea RHD, Female patient, Childhood history, disturbed sleep Cardiovascular Examination Opening Snap after S2 Low pitched mid-diastolic rumbling murmur with presystolic accentuation of Grade IV intensity in mitral area without any radiation Murmur best heard at cardiac apex with bell of stethoscope in left lateral position at height of expiration Absent Parasternal heave – mild disease Edema & Hepatomegaly absent – mild disease Absence of click, split, rub or murmur over other areas Opening snap +murmur at apex
  • 19.
    Substantiation Atrial kick- Palpitations Acquired valvular disease - Dyspnea RHD, Female patient, Childhood history, disturbed sleep Absent Parasternal heave – mild disease Edema & Hepatomegaly absent – mild disease Opening snap +murmur at apex Childhood history Female Patient Rheumatic Heart Disease Edema & hepatomegaly absent Palpitations Dyspnea Absent parasternal heave – mild disease Opening Snap + low pitched mid diastolic murmur 2D – Echo – Mitral Valve 2.0 cms2,, Transvalvular pressure 8 mm of Hg Mitral Stenosis of Rheumatic Origin without evidence of congestive cardiac failure.
  • 20.
  • 21.
  • 22.
    Anatomy Normal Orifice: 4– 6 Cms2 4-6 cms2 < 2.5 cms2 1.5- 2.5 cms2 1.0 – 1.5 cms2 < 1.0 cms2 Mild MS – 1.5 – 2.5 Cms2 (Dyspnea on severe exertion) Moderate MS – 1.0 – 1.5 Cms2 (PND ± pulmonary oedema) Severe/ Critical- < 1.0 Cms2 (Orthopnea – Class IV) Symptoms start < 2.5 Cms2
  • 23.
    Anatomy Mitral Valve areais calculated using Gorlin’s Equation: Area = Cardiac Output/ (DFP or SEP) (HR) 44.3 C √ΔP DFP = Diastolic Filling Pressure C = Empirical Constant SEP = Systolic Ejection Period ΔP = Pressure Gradient HR = Heart Rate
  • 24.
    Pathophysiology Decreased LV filling Increasedleft atrial pressure and volume Pulmonary vein pressure Transudation of fluid into pulmonary interstitial space Pulmonary compliance Work of breathing Progressive Dyspnea Adaptation Atrial Kick Adaptation Lymphatic drainage and thickening of basement membrane Pulmonary hypertension Palpitations Breathlessness Haemoptysis
  • 25.
    Pathophysiology Almost all chambersare shown here , except… Left Ventricle So, are we to assume that Left Ventricle remains unaffected..?
  • 26.
    Pathophysiology The answer isNO. Left Ventricle is affected Decreased filling ultimately manifests as 1. muscle atrophy 2. Inflammatory myocardial fibrosis 3. Scarring of sub valvular apparatus 4. Abnormal pattern of left ventricle contraction 5. Decreased left ventricular compliance with diastolic dysfunction 6. Right to left shift due to pulmonary hypertension
  • 27.
    Aetiology 1. Rheumatic HeartDisease 2. Congenital – Parachute Mitral Valve 3. Hunter’s Syndrome 4. Hurler’s Syndrome 5. Drugs – Methysergide 6. Carcinoid syndrome 7. Amyloidosis 8. Mitral annular Calcification 9. Rheumatoid Arthritis 10. Systemic Lupus Erythematosis 11. Infective endocarditis with large vegetations. 12. Lutembacher’s Syndrome: Atrial Septal Defect (ASD) + Mitral Stenosis (MS) rheumatic origin
  • 28.
    Pathology 1. Diffuse thickeningof mitral leaflets and subvalvular apparatus. 2. Commissural fusion 3. Calcification of annulus and leaflets 4. Contracture of Chordae and papillary heads 5. Usually develops over 2-3 decades. Pathological types of Mitral Stenosis 1. Button Hole 2. Fish Mouth 3. Funnel Type
  • 29.
    Common symptoms 1. Dyspnoea 2.Orthopnea 3. Paroxysmal Nocturnal Dyspnea 4. Palpitation 5. Fatiguability 6. Haemoptysis 7. Recurrent Bronchitis 8. Cough 9. Chest pain 10. Right hypochondrial Pain (hepatomegaly)
  • 30.
    Conditions simulating mitralstenosis 1. Left Atrial Myxoma 2. Cortriatriatum 3. Ball valve thrombus of left atrium 4. Diastolic flow murmurs across normal mitral valve as in VSD, PDA, severe MR 5. Carey-Coomb’s murmur of mitral valvulitis 6. Tricuspid stenosis 7. Austin-Flint murmur
  • 31.
    Complications 1. Acute leftheart failure and acute pulmonary edema 2. Pulmonary hypertension 3. Right Ventricular failure 4. Atrial Fibrillation 5. Atrial Flutter 6. Ventricular or atrial premature beats 7. Embolic manifestations 8. Haemoptysis 9. Infective Endocarditis 10. Recurrent Broncho-pulmonary infections 11. Complications arising from enlarged left atrium: Hoarseness of voice – left recurrent laryngeal nerve due to enlarged left atrium (Ortner’s Syndrome) Dysphagia – Oesophageal compression 12. Jaundice, Cardiac cirrhosis.
  • 32.
    Diagnosis One needs toassess anatomy of Mitral Valve Leaflet in terms of 1. Thickening 2. Calcification 3. Mobility 4. Extent of involvement and subvalvular apparatus One also needs to assess extent of stenosis 1. Mitral Valve area 2. Transvalvular pressure gradient Also to be assessed are 1. Cardiac chamber dimension 2. Pulmonary hypertension 3. Ventricular function 4. Associated valvular disease 5. Examination of Left Atrial Thrombus
  • 33.
    Diagnosis Assess extent ofcalcification 1. Disappearance of Opening snap especially if calcification is more. Assessment of X-Ray (P-A View) 1. Left Atrial Enlargement – Mitralisation of heart 2. Straightening of Left Heart Border 3. Elevation of Left mainstem Bronchus 4. Evidence of Mitral Calcification, Evidence of Pulmonary edema, Pulmonary Vascular Congestion. 5. Kerley’s B lines Assessment of X-Ray (RAO view) 1. Oesophagus is pushed or curved backward by enlarged left atrium.
  • 34.
    Diagnosis Assessment of ECG 1.Broad notched “P” Waves signifying atrial enlargement. 2. Atrial Fibrillation (f- waves replacing p-waves) 3. Right Ventricular Enlargement 2D – Echocardiography Doppler study 1. Chamber Enlargement 1. To know the speed and direction of blood flow. 2. Valve pathology 3. Valve movement 4. Mitral Orifice Blood Examination 1. TC and DC 2. ESR 3. ASO Titre
  • 35.
    Treatment 1. Mild Mitralstenosis – Diuretics Restriction of physical activity Salt-restricted diet 2. When in Atrial Fibrillation – Digoxin (0.25 mg tablet) β- Blockers Calcium Channel Blockers Control of heart rate is paramount, because tachycardia impairs left ventricular filling and further increases left atrial pressure. 3. Anticoagulation – Warfarin to normalise INR
  • 36.
    Treatment 4. Surgery ifPulmonary hypertension develops Percutaneous balloon valvotomy Surgical commisurotomy Valve reconstruction 5. Valve replacement Starr-Edwards ball valve Bjork-Shiley disc valve Porcine bio-prosthesis 6. Prophylaxis against recurrence of rheumatic fever Inj. Benzathine Penicillin 1.2 million units.
  • 37.
  • 38.
    Hemodynamic Parameters Change in normal pregnancy Changeduring Labour & delivery Change during postpartum Blood volume Increased by 40 % - 50% Increased Decreased (auto diuresis) Heart rate Increased by 10 – 15 beats/ min Increased Decreased Cardiac Output Increased by 30% - 50 % Additional 50 % Decreased Blood Pressure Decreased by 10 mm of Hg Increased Decreased Stroke Volume Increased in first and second trimester Increased (300 – 500 ml/contraction) Decreased Systemic Vascular Resistance Decreased Increased Decreased
  • 39.
    Maternal mortality associatedwith heart disease in pregnancy Group 1: Mortality < 1% Atrial septal defect Ventricular septal defect; PDA Pulmonary/tricuspid disease Tetralogy of Fallot, corrected; Bioprosthetic valve Mitral stenosis, NYHA class I and II Group 2: Mortality 5–15% 2A Mitral stenosis NYHA class III–IV; Aortic stenosis Coarctation of aorta, without valvular involvement Uncorrected Tetralogy of Fallot Previous myocardial infarction Marfan syndrome with normal aorta 2B Mitral stenosis with atrial fibrillation Artificial valve Group 3: Mortality 25–50% Primary pulmonary hypertension or Eisenmenger syndrome Coarctation of aorta, with valvular involvement Marfan syndrome with aortic involvement
  • 40.
    Mortality: 0 point-5%,1point-27%,>1 point-75% CARPREG Score
  • 41.
    Anaesthetic Management Principle involved: CardiacOutput Decrease in cardiac output Hypotension Tachycardia Reduced ventricular filling Vicious cycle Increased ventricular filling Trendelenburg' s position, Autotransfusio n due to uterine contraction Precipitation of CHF 1 2 3
  • 42.
    Anaesthetic Management Principle involved: 1.Prevent decrease in cardiac output, as hypotension because of this causes reflex tachycardia, which in turn reduces ventricular filling further compromising cardiac output. 2. Avoid hypotension for the same reason listed above. If hypotension ensues, treat with Ephedrine or Phenylephrine. 3. Avoid precipitating Congestive Heart Failure due to factors such as Trendelenburg’s position Autotransfusion due to uterine contraction leading to increased central blood volume. 4. Avoid precipitation of Right Ventricular Failure Hypercarbia Hypoxemia Lung Hyperinflation Increase in lung water If Right Ventricular Failure exists, treat with inotropes and pulmonary vasodilators.
  • 43.
    Anaesthetic Management Preoperative Medication 1.Decrease anxiety (decreases tachycardia) 2. Drugs used to control heart rate to be continued till day of surgery 3. Hypokalemia if present secondary to diuretic therapy to be addressed 4. If intended surgery is a minor surgery, continue anticoagulant therapy 5. If intended surgery is a major surgery, discontinue anticoagulant therapy. Induction of Anaesthesia 1. Avoid Ketamine – Increases heart rate, blood pressure 2. Avoid Atracurium – Increased histamine release causes hypotension which manifests as tachycardia.
  • 44.
    Anaesthetic Management Maintenance ofAnaesthesia 1. Drugs should have minimal effects on hemodynamic pattern 2. Balanced anaesthesia with N2O/ Narcotic/ Volatile anaesthetic 3. N2O causes insignificant pulmonary vasoconstriction. It is significant only if pulmonary hypertension exists. So, one needs to treat pulmonary hypertension preoperatively. 4. Cardiac stable muscle relaxants are to be used. (preferably avoid Pancuronium) 5. Avoid lighter planes of anaesthesia (To avoid tachycardia) 6. Fluid Management: Avoid Hypervolemia - -> Worsens pulmonary edema Avoid Hypovolemia - -> Sacrifices already decreased left ventricular filling, which further decreases Cardiac output. Hypovolemia secondary to blood loss and vasodilatory effects of anaesthesia ought to be avoided.
  • 45.
    Anaesthetic Management Monitoring 1. TransesophagealEchocardiography 2. Intra-arterial pressure 3. Pulmonary artery pressure to be monitored 4. Left atrial pressure Principle: 1. Ensure adequacy of cardiac function intravascular fluid volume ventilation oxygenation A word of caution regarding Pulmonary artery pressure monitoring: - When measured too frequently, the risk of pulmonary artery rupture is far too high.
  • 46.
    Anaesthetic Management Post Operative 1.Assess postoperative risk of pulmonary oedema and right heart failure and manage accordingly. 2. Avoid pain as pain begets hypoventilation which leads to respiratory acidosis, hypoxemia which manifests as raised heart rate and pulmonary vascular resistance. 3. After Major thoracic or abdominal surgery, the decreased pulmonary compliance and increased work of breathing requires mechanical ventilation.
  • 47.
    Anaesthetic Management Category 1- Immediate threat to life of woman or fetus(baby needs to be removed in 30 min. of making the decision to do LSCS Category 2 - Maternal or fetal compromise, not immediately life threatening(some time can be spent for resuscitation) Category 3 - Needing early delivery but no maternal or fetal compromise Category 4- At a time to suit the woman and maternity team
  • 48.
    Anaesthetic Management Anesthetic techniquesavailable are 1. Regional anaesthesia (Sub Arachnoid Block, Epidural, Combined Spinal Epidural) 2. General Anaesthesia Sub Arachnoid Block: subarachnoid causes rapid onset of extensive sympathetic blockade with intense vasodilatation sudden hypotension and severe tachycardia. Epidural Block: epidural anaesthesia might not be an ideal technique as it requires slow induction, delay in the onset of action which may not be possible in an emergency situation. Moreover large volume of local anesthetic is needed for adequate blockade. Combined Spinal Epidural: Combined spinal and epidural will be the technique of choice.CSE offers rapid onset and improved analgesia It offers ability to use low dose spinal with room for post operative analgesia
  • 49.
    Anaesthetic Management Why ourchoice is right..? 1. Rapid onset of spinal block 2. Ability to modify / top-up / prolong anaesthesia with epidural component 3. Spread of spinal anaesthetic can be altered with injection of saline into the epidural space (compression effect of dural sac) 4. Option for post-operative analgesia 5. Reduces need for conversion to general anaesthetic in event of spinal failure 6. Able to use lower dose spinal and modify if required, potentially reducing spinal induced hypotension 7. Advantageous in cardiac conditions 8. Arguably advantageous in pre-eclampsia
  • 50.
    Anaesthetic Management Why ourchoice is right..? 9. Can produce a denser block than either technique in isolation 10. Airway pressures are not altered and avoids hyperventilation 11. Minimal autonomic blockade , hence no sudden decrease in Systemic Vascular resistance 12. Better maintenance of uterine blood flow improving the fetal outcome 13. Auto transfused blood during the third stage of labor is well accommodated 14. Improved microvascular blood flow prevents DVT 15. Allows early ambulation and return of bowel movements
  • 51.
    Anaesthetic Management Procedure perse Preparation: 1. All resuscitation equipments and drugs , anaesthesia machine, O2 delivery system, Equipments for G.A. , Suction apparatus are kept ready 2. Patient is given aspiration prophylaxis in the form of 0.3ml SODIUM CITRATE 30ml orally, H2 receptor blocker and antiemetic given 3. Record baseline vitals 4. Secure two wide bore cannulae and infuse 60-75ml/hr of crystalloid 5. Administer infective endocarditis prophylaxis 6. Monitors- SpO2, ECG, NIBP, and urine output 7. Reassure the patient 8. Informed consent is obtained explaining the maternal and fetal risk 9. Adequate Compatible blood
  • 52.
    Anaesthetic Management Procedure perse CSE is performed in lateral decubitus position under strict aseptic precautions Epidural space is identified with 18 G Tuohy needle using LOR with saline. Spinal needle is introduced through the Tuohy needle and subarachnoid block is performed.20-30 μg of Fentanyl along with 2.5 -5mg of 0.5% Bupivacaine is given. This is followed by insertion of epidural catheter through which 3 ml of 2% Xylocaine with epinephrine is given. Post operative analgesia is maintained as shown in the table below Drug Initial Injection Continuous Infusion Bupivacaine 10-15 mL of a 0.25%-0.125% solution 0.0625%-0.125% solution at 8-15 mL/hr Ropivacaine 10-15 mL of a 0.1%-0.2% solution 0.5%-0.2% solution at 8-15 mL/hr Fentanyl 50-100 µg in a 10-mL volume 1-4 µg/mL
  • 53.
    Anaesthetic Management 1. IfHypotension occurs- vasopressors are used. 2. After the baby is delivered Oxytocin in minimal dose as slow infusion is given 3. Arrhythmias should be treated appropriately. 4. Blood loss should be assessed and replaced accordingly. 5. Immediate post partum period mandates meticulous care as mortality is very high in these patients with Pulmonary artery hypertension. 6. Post operative pain management reduces Cardiovascular-stress response and prevents Deep Vein Thrombosis.
  • 54.
    Anaesthetic Management Myths andWorries about Regional anaesthesia 1. Preloading is mandatory and hazardous--CVP guided fluid management negates overloading and maintains adequate cardiac output 2. Regional Anaesthesia is associated with sudden fall in BP. Local anaesthetic with Opioid combination intrathecally followed by epidural to titrate the desired level of block does not produce rapid fall in BP. 3. Delay in performing the actual procedure: this doesnt happen with expert hands 4. The complications of CSE-like total spinal, LA toxicity, epidural hematoma and abscess are negligible with senior anesthesiologists
  • 55.
    Anaesthetic Management Controversies aboutCSE: Risk of epidural catheter through the dural hole Perceived increase in neurotrauma Contraindications to Regional Anaesthesia • Active heavy bleeding • Uncorrected coagulopathy (e.g. HELLP syndrome (Hemolysis, Elevated Liver Enzymes, Low Platelets) associated with pre-eclampsia) • Thrombocytopenia • Systemic sepsis • Local sepsis at site of insertion • Patient refusal
  • 56.
    Anaesthetic Management Guidelines forgeneral anaesthesia General anesthesia has the advantages of speed of induction, control of the airway, and superior hemodynamics. Anaesthetic Goals: 1. Maintain the heart rate around 80-100 b/min . 2. Maintain Left Atrial Pressure high enough to take advantage of the increased preload reserve. 3. Avoid pulmonary artery hypertension by treating hypercarbia, hypoxemia, and acidemia. 4. Aggressively treat pulmonary artery hypertension with vasodilator therapy to avoid RV failure. If RV failure does occur, inotropic support of the RV and pulmonary vasodilation may be necessary. The presence of PAH is the major factor that increase the mortality.
  • 57.
    Anaesthetic Management Guidelines forgeneral anaesthesia 5. Avoid factors which depress the myocardium:(inhalation agents and drugs) 6. Maintain awareness of potential for LV rupture. 7. Aggressive treatment of arrhythmias if they occur 8. Avoid profound changes in SVR 9. Attenuate pressor response(intubation, extubation, light plane of anesthesia) 10. Adequate analgesia and adequate muscle relaxation guided by Neuro muscular monitoring 11. Aspiration prophylaxis 12. Blood loss assessment and prompt replacement
  • 58.
  • 59.
    Anaesthetic Management Guidelines forgeneral anaesthesia Other advantages are 1. Rapidly established 2. Better hemodynamic stability 3. Prevention of aspiration as the airway is isolated 4. High FiO2 -which will reduce PVR 5. Ventilation controlled to avoid hypercarbia-which will increase PVR 6. FRC is increased by controlled ventilation 7. Ventilation of atelectatic areas –better V/Q 8. Sinus rhythm can be maintained. In case of SVT and Ventricular arrhythmias promptly reverted by cardioversion
  • 60.
    Anaesthetic Management Guidelines forgeneral anaesthesia Other advantages are 9. Peak airway pressure can be kept <20 cms H2O 10. Elective post operative ventilation to tide over the CCF that may be possible after parturition 11. Effective management of Pulmonary oedema - IPPV with PEEP, liberal use of high dose morphine
  • 61.
    Anaesthetic Management Guidelines forgeneral anaesthesia The possible complications that can be anticipated 1. failed intubation 2. Aspiration( more common in unprepared case) 3. Hypoxia and hypocarbia -effect on fetus 4. Hypertensive crisis 5. Arrhythmia-hypoxia, hypercarbia, inhalational agents, Drugs 6. Use of poly pharmacy and anaphylaxis 7. Awareness 8. Uterine atony with inhalation agents
  • 62.
    Anaesthetic Management Guidelines forgeneral anaesthesia The possible complications that can be anticipated 9. Need for adequate post op. Analgesia 10. Neonatal depression 11. Delayed recovery 12. Anesthetic drug interaction with cerebrovascular drugs(Ca channel blockers and Magnesium) 13. Increased incidence of PONV 14. Prolonged stay ICU
  • 63.
    Outlines of Management 1.Pre-conceptual counseling- NYHA III and IV are advised corrective cardiac before pregnancy. It is advisable for certain cardiac diseases where pregnancy is to be avoided They have to be registered, interviewed regarding functional difficulties, regular follow ups starting from early pregnancy. It is advisable to manage them in higher centers where multidisciplinary support is available(Multidisciplinary approach: management by a team of specialists apart from obstetricians that includes the cardiologist(failure prevention, arrhythmia management), CT surgeon(emergent cardiac surgery), neonatologist(preterm baby) anesthesiologist(pain relief-epidural, mechanical Ventilation if necessary) 2. Correct factors which will burden the cardiac lesion like anemia, obesity, Hypertension, arrhythmia 3. Prevention of Infection
  • 64.
    Outlines of Management 4.Optimization of Heart rate with pharmacological agents 5. Pregnancy is a hypercoagulable state, which increases the risk of thromboembolic events, especially in the cardiac patient with a prosthetic heart valve, valvular heart disease, or heart failure. Anticoagulant therapy should be considered in these high-risk patients to prevent thromboembolism or thrombus formation. 6. IE prophylaxis -(as per the ACOG guidelines- some of the drugs recommended by ACC/AHA are not recommended for pregnant patients) 7. Monitors- other than the ASA standards recommendation- Advanced monitors like invasive arterial pressure, CVP -, PCWP and TEE are recommended. They should be continued in the post partum period upto 72 hrs at least
  • 65.
    Outlines of Management 8.Planning the mode of delivery-vaginal delivery is better tolerated(less blood loss, less catecholamine), Pain relief during Labor - recommended, shortening the second stage- outlet forceps, episiotomy. 9. Large boluses of Oxytocics should be avoided as they cause profound hypotension. Ergometrine better avoided. PGF2 alpha and mesoprostol are used cautiously. 10. If planned for Cesarean section choice of anesthetic should be directed to keep the haemodynamic stable (as near normal Systemic vascular resistance, Preload, Afterload as possible)Adequate replacement of blood loss. 11. All patients with cardiac disease should be kept in High dependency unit and monitored after the delivery for a minimum period of 72hrs 12. Plan and Advise cardiac surgery in the second trimester if is warranted in the interest of the mother's well being
  • 66.
    When to giveInfective Endocarditis Prophylaxis..?
  • 67.
    How to giveInfective Endocarditis Prophylaxis..?
  • 68.
    References Miller’s Anaesthesia , 7thEdition, Vol 1 Clinical Anesthesia by Paul.G.Barash Morgan’s Clinical Anaesthesiology Kaplan’s Cardiac Anesthesia
  • 69.
    References Harrison’s Internal Medicine 17thEdn A Practice of Anesthesiology by Churchill Wylie Stoelting’s Anesthesia & co-existing disease CMDT 2010
  • 70.
    References Bedside Clinics in medicine- Kundu A Manual of Practical Medicine by Alagappan Circulation Journal
  • 71.