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Mitral stenosis with pregnancy

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Mitral stenosis with pregnancy

  1. 1. MITRAL STENOSIS WITH PREGNANCY - DR. ANKITA PATNI - ANAESTHESIOLOGY
  2. 2. INTRODUCTION • Rheumatic mitral stenosis forms 88% of the heart diseases complicating pregnancy in the tertiary referral centre in India. • Rheumatic mitral stenosis complicating pregnancy is still a frequent cause of maternal death. • A better understanding of the physiological changes in pregnancy and the pathological impact of mitral stenosis over pregnancy and a multidisciplinary approach; where the anaesthesiologist plays a major role, in diagnosis and management, reduce the mortality and morbidity.
  3. 3. CARDIOVASCULAR CHANGES DURING PREGNANCY Parameter Percentage of change Cardiac output 40–50% Increase Stroke volume 30% Increase Heart rate 15–25% Increase Intravascular volume 45% Increase Systemic vascular resistance 20% Decrease Systolic BP Minimal Diastolic BP 20% Decrease at mid-pregnancy Pre-pregnant values at term CVP Unchanged O2 consumption 30–40% Increase
  4. 4. HEMODYNAMICS DURING LABOUR Parameter Stage of labour Percentage of change Cardiac output Latent phase 10% Increase Active phase 25% Increase Expulsive phase 40% Increase Immediate post-partum 75–80% Increase Heart rate All stages Increase CVP All stages Increase
  5. 5. HEMODYNAMICS DURING PUERPERIUM Parameter Post-partum Percentage of Change Cardiac output Within 1 h 30% above pre-labour values 24–48 h Just below pre-labour values 2 weeks 10% above pre-pregnant values 12–24 weeks Baseline pre-pregnancy values Heart rate Immediate Decrease 2 weeks Pre-pregnant values Stroke volume 48 h Remains above pre-labour values 24 weeks 10% above pre-pregnant values
  6. 6. MS PREGNANCY DELIVERY DECREAS E LA emptying DECREAS E LV Filling INCREASE HR DECREASE SV DECREASE CO Fixed CO state; Heart cannot cope up with increased demand. AUTOTRANSFUSION from uterus PULMONARY CONGESTION Long- standin g Irreversible chronic Pulmonary Hypertension LA Dilates LA pressure INCREASES At DIASTOL E Pressure gradient develop s between LA and LVHemodynam ic Hallmark of MS
  7. 7. • MS- impairs left ventricular filling- decrease in EDV (pre- load)- decrease in SV- fall in CO. • Reduced ventricular filling- decrease ventricular wall stress (after-load)- decrease in ESV • Decrease in EDV > Decrease in ESV = Decrease in SV
  8. 8. SEVERITY GRADING OF MS Measuremen t Normal Mild Moderate Severe Mitral valve area (cm2) 4.0–6.0 1.5–2.5 1.0–1.5 <1.0 Mean pressure gradient (mmHg) <2 2–6 6–12 >12 Pulmonary artery mean pressure (mmHg) 10–20 <30 30–50 >50
  9. 9. 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 Normal Orifice: 4 – 6 Cms2
  10. 10. MODIFIED NEW YORK HEART ASSOCIATION FUNCTIONAL CLASSIFICATION (NYHA) Class I No functional limitation of activity Asymptomatic except during severe exertion. Class II Mild limitation of physical activity Symptomatic with moderate activity Class III Marked limitation of physical activity Symptomatic with minimal activity Class IV Severe limitation of physical activity Symptomatic at rest
  11. 11. PREDICTORS OF MORTALITY AND MORBIDITY Severity of MS Severe- 67% Moderate- 38% Mild- 26% NYHA Class Class I and II- <1% Class III and IV- Between 5 and 15% Class III and IV- Perinatal mortality- 20- 30%
  12. 12. CARPREG SCORE • THE CARDIAC DISEASE IN PREGNANCY (CARPREG) RISK SCORE (TABLE I) CAN BE CALCULATED TO ESTIMATE A WOMAN'S CARDIAC RISK DURING PREGNANCY. IT IS IS BASED ON 4 RISK PREDICTORS: Mortality: 0 point-5%, 1 point-27%, >1 point- 75%
  13. 13. AETIOLOGY OF MS 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
  14. 14. SYMPTOMS OF MS 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)
  15. 15. DIAGNOSIS OF MS DIAGNOSTIC TOOLS Clinical Examina tion ECG Chest X- Ray Echocardi ography Doppler examinati on Cardiac Catheteriz ation Echocardiography provides information regarding the area of the mitral valve, size of the left atrium, presence of thrombus and the size and function of the left ventricle and Doppler examination provides information about the severity of the stenosis, the presence of other associated valve lesions and the degree of pulmonary hypertension Diagnostic cardiac catheterization is necessary only when echocardiography is non-diagnostic or results are discordant with clinical findings.
  16. 16. GENERAL PHYSICAL EXAMINATION OEDEMA SEVERE MITRAL STENOSIS ULTIMATELY LEADS TO RIGHT HEART FAILURE. HEPATOMEGALY SEEN IN RIGHT VENTRICULAR FAILURE AND PULMONARY HYPERTENSION. MITRAL FACIES 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
  17. 17. CARDIOVASCULAR EXAMINATION- INSPECTION • PRECORDIAL BULGE INDICATES EARLY ONSET AND LONGER DURATION OF CARDIAC DISEASE. • SCAR MARKS REVEAL PREVIOUS SURGERIES • ENGORGED NECK VEINS INDICATE HIGH RIGHT HEART PRESSURES
  18. 18. CARDIOVASCULAR EXAMINATION- PALPATION • TAPPING CHARACTER OF THE APEX BEAT (PALPABLE S1) IS TYPICAL. • PALPABLE DIASTOLIC THRILL IN MITRAL AREA BEST FELT IN LEFT LATERAL POSITION IN FULL EXPIRATION. • PARASTERNAL HEAVE • IF ONE FINDS ENGORGED SUPERFICIAL VEINS LOOK FOR DIRECTION OF FLOW.
  19. 19. CARDIOVASCULAR EXAMINATION- AUSCULTATION • S1 IS SHARP, SHORT, ACCENTUATED • OPENING SNAP AFTER S2 • LOW PITCHED MID-DIASTOLIC RUMBLING MURMUR WITH PRESYSTOLIC ACCENTUATION IN MITRAL AREA. • MURMUR BEST HEARD AT CARDIAC APEX WITH BELL OF STETHOSCOPE IN LEFT LATERAL POSITION AT HEIGHT OF EXPIRATION
  20. 20. ECG FINDINGS 1. BROAD NOTCHED “P” WAVES SIGNIFYING ATRIAL ENLARGEMENT. 2. ATRIAL FIBRILLATION (F- WAVES REPLACING P-WAVES) 3. RIGHT VENTRICULAR ENLARGEMENT
  21. 21. CXR 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 6. DOUBLE CONTOUR OF THE RIGHT BORDER OF HEART
  22. 22. CHEST X-RAY Kerley b lines
  23. 23. ECHOCARDIOGRAPHY
  24. 24. MANAGEMENT MEDICAL DIURETICS, β- BLOCKERS AF- DIGOXIN, ANTI-COAGULANTS SURGICAL VALVULOPLASTY VALVE REPLACEMENT OBSTETRICAL VAGINAL CAESAREAN SECTION
  25. 25. MEDICAL MANAGEMENT FIRST LINE OF TREATMENT IN SYMPTOMATICS • BED REST • OXYGEN THERAPY • DIURETICS • BETA-ADRENERGIC RECEPTOR BLOCKADE- USEFUL TO PREVENT TACHYCARDIA DURING PREGNANCY. PROPRANOLOL OR ATENOLOL DECREASES THE INCIDENCE OF MATERNAL PULMONARY OEDEMA WITHOUT ADVERSE EFFECTS ON THE FOETUS OR NEONATE. • ANTIBIOTIC PROPHYLAXIS FOR ENDOCARDITIS IS RESERVED ONLY FOR PATIENTS WITH A PREVIOUS HISTORY OF ENDOCARDITIS OR PRESENCE OF ESTABLISHED INFECTION. ASSOCIATED WITH ATRIAL FIBRILLATION • DIGOXIN AND BETA BLOCKERS TO REVERT IT TO SINUS RHYTHM. • ANTICOAGULATION TO PREVENT SYSTEMIC EMBOLIZATION. • CARDIOVERSION SHOULD BE PERFORMED IF PHARMACOLOGIC THERAPY FAILS TO CONTROL THE VENTRICULAR RESPONSE.
  26. 26. ANTICOAGULATION DURING PREGNANCY • SC/IV HEPARIN FOR UP TO 12 WEEKS ANTEPARTUM (APTT 1.5–2.5-TIMES OF NORMAL) • WARFARIN FROM 12 TO 36 WEEKS (MAINTAIN INR 2.5– 3.0) • SC/IV HEPARIN AFTER 36 WEEKS • THERAPY WITH LOW-MOLECULAR WEIGHT HEPARIN (LMWH) INSTEAD OF UNFRACTIONATED HEPARIN IS GAINING POPULARITY. ALTHOUGH AN “ANTI XA” ACTIVITY IS USED TO MONITOR LMWH, NO ANTI-XA ACTIVITY-BASED GUIDELINES HAVE BEEN ISSUED TILL DATE.
  27. 27. SURGICAL MANAGEMENT II Trimester Valvuloplasty PERCUTANEOUS (success rate is nearly 100%. It increases the valve area to >1.5 cm2 without a substantial increase in mitral regurgitation.) OPEN (foetal loss is high in open commissurotomy as compared to percutaneous, at a ratio of 1:8) Valve Replacement Reserved for severe cases with calcified valve and in mural thrombus.
  28. 28. OBSTETRIC MANAGEMENT VAGINAL DELIVERY • Tachycardia, secondary to labour pain, increases flow across the mitral valve, producing sudden rises in left atrial pressure, leading to acute pulmonary oedema. VAGINAL DELIVERY • The second stage of delivery should be cut short by instrumentation. • Maintenance of left uterine displacement for good venous return. • Supplemental oxygen administration with pulse oximetry monitoring to minimize increases in pulmonary vascular resistance, fetal heart rate monitoring should be carried out. • Invasive cardiac monitoring like radial artery cannulation and pulmonary catheter are beneficial in assessing the cardiac output, pulmonary artery pressure and for guiding fluid and drug therapy, especially in NYHA III and IV patients. • Sudden drops in systemic vascular resistance (SVR) in the presence of a fixed cardiac output can be prevented by small bolus doses of phenylephrine, with volume expansion when necessary. Good LABOUR ANALGESIA is must. Epidural CS E
  29. 29. OBSTETRIC MANAGEMENT Caesarean section Epidural/Spinal Combined Spinal Epidural General Anaesthesia Only for obstetric reasons 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. Subarachnoid causes rapid onset of extensive sympathetic blockade with intense vasodilatation, sudden hypotension and severe tachycardia. Technique of choice. CSE offers rapid onset and improved analgesia It offers ability to use low dose spinal with room for post operative analgesia
  30. 30. OBSTETRIC 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 4- At a time to suit the woman and maternity team Category 3 - Needing early delivery but no maternal or fetal compromise
  31. 31. GOALS FOR ANAESTHETIC MANAGEMENT • MAINTENANCE OF AN ACCEPTABLE SLOW HEART RATE • IMMEDIATE TREATMENT OF ACUTE ATRIAL FIBRILLATION AND REVERSION TO SINUS RHYTHM • AVOIDANCE OF AORTOCAVAL COMPRESSION • MAINTENANCE OF ADEQUATE VENOUS RETURN • MAINTENANCE OF ADEQUATE SVR • PREVENTION OF PAIN, HYPOXAEMIA, HYPERCARBIA AND ACIDOSIS, WHICH MAY INCREASE PULMONARY VASCULAR RESISTANCE.
  32. 32. EPIDURAL ANALGESIA • ONE OF THE MAJOR ADVANTAGES OF EPIDURAL ANALGESIA IS THAT IT CAN BE ADMINISTERED IN INCREMENTAL DOSES AND THAT THE TOTAL DOSE COULD BE TITRATED TO THE DESIRED SENSORY LEVEL. • SLOWER ONSET OF ANAESTHESIA • THE SEGMENTAL BLOCKADE SPARES THE LOWER EXTREMITY “MUSCLE PUMP,” AIDING IN VENOUS RETURN, AND ALSO DECREASES THE INCIDENCE OF THROMBOEMBOLIC EVENTS. • INVASIVE HAEMODYNAMIC MONITORING, JUDICIOUS INTRAVENOUS ADMINISTRATION OF CRYSTALLOID AND ADMINISTRATION OF SMALL BOLUS DOSES OF PHENYLEPHRINE MAINTAIN MATERNAL HAEMODYNAMIC STABILITY. • NEURAXIAL BLOCK IN AN ANTICOAGULATED PATIENT HAS THE RISK OF EPIDURAL HAEMATOMA. Allows the maternal cardiovascular system to compensate for the occurrence of sympathetic blockade, resulting in a lower risk of hypotension and decreased uteroplacental perfusion.
  33. 33. COMBINED SPINAL-EPIDURAL 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 MICROGRAM IN A 10-ML VOLUME 1-4
  34. 34. 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.
  35. 35. REGIONAL ANAESTHESIA 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
  36. 36. GUIDELINES FOR GENERAL ANAESTHESIA • 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. GENERAL ANAESTHESIA HAS THE ADVANTAGES OF SPEED OF INDUCTION, CONTROL OF THE AIRWAY, AND SUPERIOR HEMODYNAMICS.
  37. 37. ANAESTHETIC GOALS 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
  38. 38. GENERAL ANAESTHESIA • INDUCTION OF ANAESTHESIA 1. AVOID KETAMINE× – INCREASES HEART RATE, BLOOD PRESSURE 2. AVOID ATRACURIUM× – INCREASED HISTAMINE RELEASE CAUSES HYPOTENSION WHICH MANIFESTS AS TACHYCARDIA. • A BETA-ADRENERGIC RECEPTOR ANTAGONIST AND AN ADEQUATE DOSE OF OPIOID LIKE FENTANYL SHOULD BE ADMINISTERED BEFORE OR DURING THE INDUCTION OF GENERAL ANAESTHESIA. • ESMOLOL HAS A RAPID ONSET AND SHORT DURATION OF ACTION, IT IS A BETTER CHOICE IN CONTROLLING TACHYCARDIA. SINCE FOETAL BRADYCARDIA HAS BEEN REPORTED AFTER ESMOLOL, FOETAL HEART RATE SHOULD BE MONITORED.
  39. 39. GENERAL ANAESTHESIA • 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
  40. 40. GENERAL ANAESTHESIA • AFTER DELIVERY OF THE FOETUS, OXYTOCIN 10–20 U IN 1,000 ML OF CRYSTALLOID SHOULD BE ADMINISTERED AT A RATE OF 40– 80 MU/MIN. AN INFUSION OF OXYTOCIN CAN LOWER THE SVR AS WELL AS ELEVATE THE PULMONARY VASCULAR RESISTANCE, RESULTING IN A DROP IN CARDIAC OUTPUT. CARE MUST BE TAKEN DURING ITS ADMINISTRATION. • METHYLERGOMETRINE, OR 15-METHYLPROSTAGLANDIN F2, PRODUCES SEVERE HYPERTENSION, TACHYCARDIA AND INCREASED PULMONARY VASCULAR RESISTANCE. • POST-OPERATIVELY AVOID PAIN AS PAIN BEGETS HYPOVENTILATION WHICH LEADS TO RESPIRATORY ACIDOSIS, HYPOXEMIA WHICH MANIFESTS AS RAISED HEART RATE AND PULMONARY
  41. 41. ADVANTAGES OF GA 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 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
  42. 42. COMPLICATIONS OF GA 1. FAILED INTUBATION 2. ASPIRATION( MORE COMMON IN UNPREPARED CASE) 3. HYPERTENSIVE CRISIS 4. ARRHYTHMIA-HYPOXIA, HYPERCARBIA, INHALATIONAL AGENTS, DRUGS 5. USE OF POLY PHARMACY AND ANAPHYLAXIS 6. AWARENESS 7. UTERINE ATONY WITH INHALATION AGENTS 8. NEED FOR ADEQUATE POST OP. ANALGESIA 9. NEONATAL DEPRESSION 10. DELAYED RECOVERY 11. ANAESTHETIC DRUG INTERACTIONS 12. INCREASED INCIDENCE OF PONV 13. PROLONGED STAY ICU
  43. 43. 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
  44. 44. 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
  45. 45. 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.
  46. 46. THANK YOU

Notas

  • Although the physiologic changes in the cardiovascular system appear to begin in the first trimester, these changes continue into the second and third trimesters, when the cardiac output increases by approximately 40% of the pre-pregnant values. The cardiac output increases from the fifth week of pregnancy and reaches its maximum levels by 32 weeks. Cardiovascular changes during pregnancy are summarized in Table 1.
  • The risk of maternal death is greatest during labour and during the immediate post-partum period. The sudden increase in the pre-load immediately after delivery, due to autotransfusion from the uterus, may flood the central circulation, resulting in severe pulmonary oedema.
  • In addition, there continues to be autotransfusion of blood for 24–72 h after delivery. Thus, the risk of pulmonary oedema extends for several days after delivery. The greatest risk occurs in the peripartum period, and most deaths occur between the second and ninth days post-partum. The cardiovascular changes of pregnancy resolve by 3–6 months after delivery. It may even take a year for the residual effects of cardiovascular remodeling to subside.
  • When the normal mitral valve orifice area of 4–6 cm2 is progressively reduced to 2 cm2, the classical symptoms of MS starts appearing. MS prevents emptying of the LA and subsequent filling of the LV, resulting in decreased SV and decreased CO. Consequent to the fixed CO state, the heart cannot cope up with situations warranting increased metabolic demand or increased blood volume. When the stenosis progresses, the left atrium dilates and the left atrial pressure increases. A pressure gradient develops during diastole between the left atrium and the left ventricle. This pressure gradient is the haemodynamic hallmark of mitral stenosis. Hence, the back pressure on the pulmonary vessels leads to pulmonary congestion and, in severe cases, pulmonary oedema. Longstanding pulmonary venous congestion causes irreversible changes in the vessel wall, leading to chronic pulmonary hypertension. Women with severe MS often do not tolerate the cardiovascular demands of pregnancy. The increased heart rate of pregnancy limits the time available for left ventricular filling, resulting in increased left atrial and pulmonary pressures and an increased likelihood of pulmonary oedema. When the pulmonary capillary pressure exceeds the blood oncotic pressure, pulmonary oedema develops. The sudden increase in the pre-load immediately after delivery, due to autotransfusion from the uterus, may flood the central circulation, resulting in severe pulmonary oedema.
  • Mitral stenosis (red PV loop in figure) impairs left ventricular filling so that there is a decrease in end-diastolic volume (preload). This leads to a decrease in stroke volume (reduced width of PV loop) by the Frank-Starling mechanism and a fall in cardiac output. Reduced ventricular filling and reduced aortic pressure decrease ventricular wall stress (afterload), which may result in a small decrease in ventricular end-systolic volume; however, this is not sufficient to offset the reduction in end-diastolic volume. Therefore, because end-diastolic volume decreases more than end-systolic volume decreases, the stroke volume (shown as the width of the loop) decreases.
  • The incidence of maternal cardiac complications correlates with the severity of the mitral stenosis (67% for severe, 38% for moderate and 26% for mild disease). Mortality rates for class I and II amount to <1%, whereas they range between 5 and 15% for class III and IV. The peri-natal mortality rate for class III and IV is as high as 20–30%.
  • Management of the pregnant woman requires a multidisciplinary team for optimal maternal and foetal outcomes. Antenatal management is directed towards avoiding cardiac decompensation, with regular assessment for volume overload and pulmonary oedema.
  • Due to the high incidence of embryopathy during the first trimester and bleeding during parturition, warfarin should be used during 12–36 weeks of pregnancy only.
  • If mitral stenosis is diagnosed before pregnancy, mitral commissurotomy is preferred. During pregnancy, the second trimester is the preferred period for any invasive procedure. Percutaneous valvuloplasty using the Inoue balloon technique has become the accepted treatment for patients with severe symptomatic mitral stenosis. The maternal outcome in percutaneous balloon mitral valvuloplasty and open commissurotomy are the same.
  • During the second stage of labour, only the uterine contractile force should be allowed rather than the maternal expulsive effort that is always associated with the valsalva maneuver. Therefore, the second stage of delivery should be cut short by instrumentation. Labour pain can affect multiple systems that determine the uteroplacental perfusion. Supplementary epidural anaesthesia can be maintained throughout the immediate post-partum period and the catheter left in situ could provide anaesthesia for immediate or post-partum tubal sterilization.
  • Most reports have recommended vaginal delivery under epidural anaesthesia, unless obstetrically contraindicated. Caesarean section is indicated for obstetric reasons only.
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