Anaesthetic management of a case of valvular heart disease... final
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Anaesthetic management of Valvular Heart Disease
Presented by :- Dr Ravi shankar sharma Sanjay gandhi memorial hospital,Rewa
Patient details
• Name: Mrs. Savitha ,staff nurse• Age: 42 years • Sex: female
• Chief Complaints :-Large pelvic mass(suspected to be ovarian
cyst),scheduled for excision of mass. -Palpitations since 6 weeks -Breathlessness since 4 weeks -Fatigue since 2 weeks
History of Presenting Illness
• Palpitation –Intermittent, Associated with exertion Relieved on rest 6 weeks duration• Breathlessness- Gradual in onset,she can climb
2 flights of stairs without difficulty but feels breathlessness beyond this point
-Progressive in nature (NYHA II) -4 weeks duration
• Fatigue – - Feeling of weakness - 2 weeks duration h/o rheumatic heart disease since 12 yrs of age,
took T/t in form of penicillin injections every 21 days for 8 years till age 20 and then discontinued
h/o normal previous pregnancy 15 year agoH/o Ballon mitral valvotomy -13 yr ago.No h/o hypertension, Diabetes mellitus,
tuberculosis ,bronchial asthma or epilepsy
• Family history:-no h/o similar complaints in the family was
noted• Personal history:-VegetarianReduced appetiteNormal bladder and bowel movementDisturbed sleepNo addiction
General physical examination• An elderly female patient , moderately built and
nourished• No pallor/icterus/cyanosis/oedema/clubbing• weight-55kgs, • Height-160cm,• Pulse-90/min,• B.P.-110/70 mm of hg • Respiratory rate-16/min• JVP:-not raised
• Respiratory system:-B/L equal air entryNormal vesicular breath soundNo added sounds
• Central nervous system:-Conscious Well oriented to time place and personNo neurological deficits
• Per abdominal examionation:- Distended in the pelvic regionNo free fluidNo dilated veins• Cardiovascular system:-Inspection: No deformity, smallscar mark
present over the precordium, no engorged superficial veins , no visible pulsations
Palpation: Apex beat felt in 5th IC space medial to left mid clavicular line , abesence of parasternal heave
• Auscultation:-S1 S2 heard,(S1 is short,shrp,accentuated)Opening snap heard near the apex(after s-2)Low pitched mid diastolic murmur at apex(no
radiation)
Investigations:-
• Hb-12.4 gm%• TLC-7400 cells/cumm(P-76,L-17,M-4,E-3,B-0)• Platelet-2.3lac.• Blood group-B+ve• BT:-3min.• CT:-4 min.• RBS:-94 mg/dl• Urea:-38 mg/dl• Creatinine:-1.3mg/dl
• Na+:-135 meq/l• K+:-4.5meq/l• Cl-: 104meq/l• HIV 1&2-non reactive• HbsAg-Non reactive• ECG:-sinus Rhytm ,H.R.-75/min, Right axis
deviation• ECHO:-normal left ventricular systolic functionNo regional wall motion abnormalitiesEjection fraction-50%• CXR:-cardiomegaly, prominent Bronchovascular
marking
Substantiation
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,(theory), Transvalvular pressure 8 mm of Hg
Mitral Stenosis of Rheumatic Origin without evidence of congestive cardiac failure.
MITRAL STENOSIS
Narrowing of the mitral valve orifice causing obstruction to blood flow from left atrium to the left ventricle.
Etiology of Mitral Stenosis
1. Rheumatic Heart Disease-M.C. cause2. Congenital – Parachute Mitral Valve3. Hunter’s Syndrome4. Hurler’s Syndrome5. Drugs – Methysergide6. Carcinoid syndrome7. Amyloidosis8. Mitral annular Calcification9. Rheumatoid Arthritis10. Systemic Lupus Erythematosis11. Infective endocarditis with large vegetations. 12. Lutembacher’s Syndrome: Atrial Septal Defect (ASD) + Mitral
Stenosis (MS) rheumatic origin
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
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)
Mitral Stenosis: Physical Examination
S1 S2 OS S1
• First heart sound (S1) is loud and snapping
• Opening snap (OS)
• Low pitch diastolic rumble at the apex
• Pre-systolic accentuation (esp. if in sinus rhythm)
GRADING :-
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
Cormier’s grading of Mitral valve anatomy
Echocardiographic group Mitral valve anatomy
Group 1 Pliable non calcified anterior mitral leaflet and mild subvalvular disease(ie thin chordae>/=10mm long)
Group 2 Pliable non calcified anterior mitral leaflet and severe subvalvular disease(thickened chordae<10mmlong)
Group 3 Calcification of mitral valve of any extent as assesed by fuoroscopy ,whatever the state of subvalvular apparatus
DiagnosisOne 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
5. Mitral Valve area
6. Transvalvular pressure gradient Also to be assessed are
7. 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)
2. Left Atrial Enlargement – Mitralisation of heart
3. Straightening of Left Heart Border
4. Elevation of Left mainstem Bronchus
5. Evidence of Mitral Calcification, Evidence of Pulmonary edema, Pulmonary
Vascular Congestion.
6. Kerley’s B lines
Assessment of X-Ray (RAO view)
1. Oesophagus is pushed or curved backward by enlarged left atrium.
DiagnosisAssessment 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
4. Chamber Enlargement 1. To know the speed and direction of blood
flow.
5. Valve pathology
6. Valve movement
7. Mitral Orifice
Blood Examination
1. TC and DC 2. ESR
3. ASO Titre
Treatment1. 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 2.5 to 3.0
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
Anaesthetic ManagementPrinciple involved:
Cardiac Output
Decrease in cardiac output
Hypotension
Tachycardia
Reduced ventricular filling
Vicious cycle
Increased ventricular filling
Trendelenburg's position, Autotransfusion due to uterine contraction
Precipitation of CHF 1
2
3
Anaesthetic ManagementPrinciple 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 waterIf Right Ventricular Failure exists, treat with inotropes and pulmonary vasodilators.
Anaesthetic ManagementPreoperative Medication
1. Decrease anxiety (decreases tachycardia),also avoide anti- cholinergics.
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
6. Avoid Ketamine – Increases heart rate, Avoide Propofol(fall in blood pressure)
(ETOMIDATE/THIOPENTONE)-Better choice
7. Avoid Atracurium – Increased histamine release causes hypotension which
manifests as tachycardia.(vecuronium-preffered)
Anaesthetic ManagementMaintenance of Anaesthesia
1. Drugs should have minimal effects on hemodynamic pattern
2. Balanced anaesthesia with Narcotic/ N2O /Volatile anaesthetic(avoide
halothane)
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 ManagementMonitoring
1. Transesophageal Echocardiography
2. Intra-arterial pressure
3. Pulmonary artery pressure to be monitored
4. Left atrial pressure Principle:
5. 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 ManagementPost 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.
Role of regional anaesthesia in MS:-
Regional anaesthesia (Sub Arachnoid Block, Epidural, peripheral nerve blocks)
Sub Arachnoid Block:-can be used in mild cases of MS only-sympathetic blockade with intense vasodilatation sudden hypotension and severe tachycardia should be avoided
Epidural Block: compared with spinal anaesthesia epidural anaesthesia allow better control of level of sympathectomy and reduction in blood pressure-can be used as a sole anaesthesia technique in patients with mild to moderate MS
Peripheral nerve blocks : can be used safely-ASRA guidelines on regional anaesthesia in patient receiving anticoagulation or thrombolytic theory should be followed
The New York Heart Association (NYHA) Grading of functional capacity of the heart:
CLASS INo functional limitation of activity
Symptoms with extra ordinary physical work.
CLASS II Mild limitation of physical activity.
Symptoms with ordinary physical work
CLASS IIIMarked limitation of physical activity Symptoms with less than
ordinary physical work
CLASS IV Severe limitation of physical activity Symptoms at rest
Management of pregnancy with MS
Prognosis depends on the functional status
v NYHA classes I and II lesions usually do well during pregnancy and have a favorable prognosis (mortality rate of <1%). v NYHA classes III and IV -mortality rate of 5% to 15%. -These patients should be advised against becoming pregnant.
Why does pregnancy aggravate the symptoms of Mitral stenosis
I. ↑ in blood volume by 30-50%→↑ in pulmonary capillary hydrostatic
pressure→ ↑ risk of pulmonary oedemaII. ↓in systemic vascular resistanceIII. ↑ in HR by 10-20 beats /min→ ↓diastolic filling time of LVIV. C.O. ↑ by 30-50% after 5th month &returns to normal within 3 days
of deliveryV. Because TPG ↑by square of CO,TPG ↑ significantly →LA pressure
→symptomsVI. During labour &delivery →sympathetic stimulation →tachycardia →
↑COVII. ↑in venous return to heart d/t autotransfuson and IVC compression
→decompensationVIII. Enlarged atrial dimension predispose to atrial arrythmias including
atrial fibrillationIX. Also induces changes in haemostasis which contribute to increased
coagulability and thromboembolic stroke
Anaesthetic Options
VAGINAL DELIVERY : Recommended whenever possible if the haemodynamic condition is
stable at the end of pregnancy
• Epidural anaesthesia is recommended
• Tachycardia, secondary to labour pain, increases flow across the mitral valve, producing sudden rises in left atrial pressure, leading to acute pulmonary oedema. This tachycardia is averted by epidural analgesia without significantly altering the patient haemodynamics.
• LA can be used to provide Perineal anaesthesia
• Caesarean section is indicated for OBSTETRIC REASONS ONLY.
When to give Infective Endocarditis Prophylaxis..?
Aortic Stenosis• Aortic stenosis (AS) is narrowing of the aortic
valve resulting in obstruction of blood flow from the left ventricle to the ascending aorta during systole.
-Normal aortic valve area is 2.5 to 3.5 cm²
Etiology
• congenital bicuspid aortic valve (2%).
• Rheumatic heart disease.
• Valve Calcification.
Pathophysiology:-
AS severity
Severity Mean gradient,mm Hg
Aortic valvearea, cm2
Mild <25 >1.5
Moderate 25-40 1.0-1.5
Severe >40 <1.0
Critical >80 <0.7
Normal aortic valve area is 2.5 to 3.5 cm²
Aortic Stenosis: Physical Findings
S1 S2 S1 S2
Mild-Moderate Severe
An early peaking murmur is typical for mild to moderate ASLate peaking murmur is consistent with severe AS. Delayed A2Pulsus Tardus-pulse ie slowly rising to peak and then has a low down slope
Medical Treatment• Antibiotic prophylaxis is NOT recommended in all pts with AS for
prevention of infective endocarditis.
• Caution with diuretics and vasodilators (reduce preload)
• HTN should be treated cautiously with appropriate antihypertensives (preload dependence)
• Statins have been studied to see if they cause regression or delayed progression of leaflet calcification (need more data)
Effective treatments for severe AS:-1.Surgical replacement of the aortic valve 2.Transcatheter aortic valve replacement (TAVR)
Anesthesia concerns:– Maintain normal sinus rhythm – Avoide bradycardia or tachycardia– Watch out for vasodilation(hypotension)Rx-
phenylephrine– Optimize i/vascular fluid volume to maintain venous
return and left ventricular filling– Mild to moderate AS may tolerate spinal or epidural
(epidural preferred)– Spinal and epidural contraindicated in severe AS– High risk of myocardial ischaemia
Pregnancy considerations
Caesarean section: -General anaesthesia with the aid of invasive haemodynamic
monitoring. Aggressive maintenance of systemic blood pressure with vasopressors (e.g. phenylephrine).
- Spinal anaesthesia is generally contraindicated. - vaginal delivery under carefully introduced and limited epidural analgesia in mild cases
Mitral Regurgitation A portion of the LV volume is ejected back into
LA during systole because of an incompetent valve.
EtiologyACUTE– Myocardial ischemia
or infarctions– Infective
Endocarditis– Chest trauma
CHRONIC Rheumatic fever Incompetent valve Destruction of mitral valve
annulus
Chronic MR: PathophysiologyVol load imposed on LA & LV (usually it gradually ↑ over time)
Large total SV (supra normal EF) and normal forward SV
MR begets MR (viscious cycle in which further LV/annular dilatation ↑ MR
↑ Preload, LV hypertrophy, & reduced or normal afterload (low resistance LA provides unloading of LV)
↑ LVEDP &↑ LAP
Compensatory dilatation of LA & LV to accommodate vol load at lower pressure; this helps relieve pul congestion
LV hypertrophy (eccentric) stimulated by LV dilatation (↑ wall stress- Laplace Law)
Chronic MR: Pathophysiology..continue
Reduced forward SV/CO
MR begets MR (viscious cycle in which further LV/annular dilatation ↑ MR
Pul congestion & pHTN
Contractile dysfunction
↓ EF, ↑ end-systolic volume ↑ LVEDP/ vol, ↑ LAP
Regurgitant fraction >0.6 -severe mitral regurgitation.
Symptoms and signs
Acute phaseC/f of decompensated
congestive heart failure (i.e. shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea),
- decreased exercise tolerance -Palpitations.- cardiogenic shock
Chronic phase
• may be asymptomatic, with a normal exercise tolerance and no evidence of heart failure.
• individuals may be sensitive to small shifts in their intravascular volume status, and are prone to develop volume overload (congestive heart failure).
MOHAMMAD ALADAM
The symptoms associated with mitral regurgitation are dependent on which phase of the disease.
MITRAL REGURGITATION
Acute Chronic
ECG Normal P mitrale, AF, Left Ventricular Hypertrophy
Heart size Normal Cardiomegaly, left atrial enlargement
Systolic murmurHeard at the base, radiates to the neck, spine, or top of head
Heard at the apex, radiates to the axilla
Apical thrill May be absent Present
Jugular venous distension Present Absent
Chest X Ray- - Enlarged LA and LV,
-Signs of pulmonary venous hypertension-RVH-Mitral calcification (in co existing MS)
Severity of MR evaluated by:-Color-flow and pulsed-wave Doppler-Pulmonary artery occlusion pressure waveform -Cardiac catheterisation-ECHO-confirms diagnosis ,Also assess mechanism and severity of MR
DIAGNOSIS:-
MILD MODERATE SEVERE
Area of MR jet (cm2) <3 3.0-6.0 >6MR jet area as percentage of left atrial area 20–30 30–40 >40
Regurgitant fraction (%) 20–30 30–50 >55
• TREATMENT
• Drugs- Digoxin, diuretics for CHFVasodilators ( ACE inhibitors, nitrates) in acute symptomatic MRWarfarin for AF/Thromboembolism
• Surgery--Mitral annuloplasty/valvuloplasty-Mitral valve repair> replacement
• Patients with an EF <30% or left ventricular end-systolic dimension more than 55 mm do not improve with mitral valve surgery.
• Prevention and treatment of events that decrease CO.• Improve forward LV Stroke Volume and decrease the regurgitant fraction.
Vasodilatation can improve forward flow- NTG/ nitroprusside infusions. Useful in PAH as well but not once RVF sets in.
• Preload – maintain or slightly increase• Maintain or increase HR- Avoid bradycardia • Decrease in afterload beneficial- Avoid sudden increase in SVR• Minimize drug-induced myocardial depression • Avoid hypoxia, hypercarbia and acidosis (all increase PAH)
Anaesthetic goals
PREMEDICATION + INDUCTION:-
• Light premedication preferred• Large dose narcotics induction or• Opoids + Benzodiazepenes ( Fentanyl + midazolam / sufentanyl+ midazolam)
either continuous or intermittent bolus• Muscle relaxant
Pancuronium preferred as increased HR desirableVecuronium/ Atracurium- depending on basal HR
• MAINTAINENCE• Volatile anesthetics ( Isoflurane ,sevo, des)
Increase in heart rate and minimal negative inotropic effects. Vasodilatation desirable.(afterload reduction)
• Nitrous oxide avoided in severe PAH.• myocardial function is severely compromised--- opioid-based anesthetic potent narcotics → bradycardia, deleterious in severe MR.
MAINTAINENCE cont......• Mechanical ventilation → maintain near-normal acid-base and respiratory
parameters.• The pattern of ventilation must provide sufficient time between breaths for
venous return. • Maintenance of intravascular fluid volume is very important for maintaining left
ventricular volume and cardiac output in these patients.
• Monitoring • Invasive monitoring- ( CVP, PAC)
Useful in severe MR- detecting the adequacy of CO and the hemodynamic response to anesthetic and vasodilator drugs
• facilitating intravenous fluid replacement.
• Pulmonary artery occlusion pressure –-V waveform to assess severity of MR
Aortic regurgitation (AR)Aortic regurgitation (AR) is a diastolic reflux of blood from the aorta into the left ventricle owing to failure of coaptation of the valve leaflets during diastole- d/t aortic valve disease/aortic root dilatation or combination of both
Etiology
Acute AR
• Infective endocarditis
• Prosthetic valve dysfunction
• Aortic dissection
• Trauma
• Systemic hypertension
Chornic AR
• Bicuspid Aortic Valve• Rheumatic and SLE• Degenerative
andHypertension• Anorectic drugs • Aortitis• Giant cell arteritis• Ankylosing spodylitis• Connective tissue disorders
Symptoms:-
Asymptomatic: 10-15 Years
PALPITATION -( early symptom), head pounding - on exertion, exertional dyspnoea , orthopnoea , paroxysmal nocturnal dyspnoea ,excessive diaphoresis , angina ,ccf - late
Corrigan pulse or Water hammer pulse or Collapsing pulse ie Rapid rise and rapid fall ,Bisferiens’s pulse -two peaks in systole
Widened pulse pressure along with dec. diastolic blood pressure
Early diastolic murmur, Austin flint murmur( Soft, low pitched rumbling mid diastolic murmur)
Peripheral Signs of AR• Lighthouse sign ( blanching of forehead)• Landolfi’s sign ( alternate dilatation and contraction of iris)• Becker’s sign (prominent retinal artery pulsations)• De Musset’s Sign (head bobs with heart beat)• Corrigan’s sign ( Dancing carotids )• Muller’s sign (systolic pulsation of uvula)• Corrigan’s pulse (water hammer pulse)• Quninckey’s sign (pulsatile nailbed)• Palfrey’s sign ( pistol shot sounds in radial artery )• Rosenbach’s sign (pulsations in liver)• Gerhart’s sign ( pulsations in spleen )• Traube’s sign (Pistol shot sounds in femoral artery)• Duroziez murmur (murmur heard over femoral artery) systolic on
proximal compression , diastolic on distal compression • Hill sign (popliteal systolic pressure – Brachial 20-40 – mild, 40-60 –
mod > 60 mm Hg severe AR)
• ECG- shows Lt axis deviation• CXR- Cardiomegaly ,Hypertrophy and dilatation of LV• Echo• Doppler examination-to identify the presence and severity • AR quantification by Based on– Color flow Doppler (Jet width and jet area measurement)– Continuity equation &Regurgitant jet velocity assessment
Treatment:-Vasodilators , inotropes(improves LV stroke volume
&↓reguirgitant volume chronic aortic regurgitation (requires surgery) Long term Rx with nifedipine/hydralazine –delays the need
of surgey
Diagnosis:-
Anesthetic considerations
– Maintain normal heart rate (avoide bradycardia)– Keep SVR low– Avoid myocardial depression– GA is usual choice for patient with AR– Spinal/Epidural well tolerated.
Pregnancy considerations-During labour, epidural analgesia improves forward flow, and is therefore the anaesthetic of choice in patient’s requiring an operative delivery.
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