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Aortic Regurgitation
Dr. Harshil Joshi
2nd year Resident
DM Cardiac Anesthesia
UNMICRC
Aortic Regurgitation
 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.
 aortic valve disease, aortic root dilatation or combination of both
 The presentation varies depending on the acuity of onset, severity of
regurgitation, compliance of the ventricle and aorta, and hemodynamic
conditions prevalent at the time.
 Whereas chronic AR is well tolerated for years, acute AR can be debilitating and
life threatening if not treated emergently
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
Sinotubular junction dilatation
Dilatation of the sinotubular junction displaces the commissures outward and prevents
the aortic leaflets from coapting, with resulting central aortic insufficiency
AR - Abnormalities of the Aortic Wall
Primary Valve Disease
• Congenital (bicuspid aortic valve)
• Rheumatic fever
• Infective endocarditis
• Collagen vascular diseases
• Degenerative aortic valve disease
• Myxomatous (prolapse)
• Traumatic
• Certain weight loss medications,
such as fenfluramine and
dexfenfluramine
Primary Root Disease
• Longstanding, uncontrolled hypertension
• Marfan syndrome
• Idiopathic aortic dilation
• Cystic medial necrosis
• Senile aortic ectasia and dilation
• Aortic dissection
• Marfan's syndrome
• Syphilitic aortitis
• Giant cell arteritis
• Takayasu arteritis
• Ankylosing spondylitis
• Whipple disease
• Other spondyloarthropathies
Pathophysiology of chronic AR
• AR leads to increased end diastolic volume of LV
• To accommodate this regurgitant volume LV compliance increases
so there is augmented LVEDV without increase in LVEDP.
• There is increase in total stroke volume resulting in forward stroke
volume within normal range (starling law)
• In addition to increase in compliance, ventricle produces new
sarcomers in sereies leading to eccentric hypertrophy. In AS
concentric LVH occurs as the sarcomeres replicate in parallel
Aortic Regurgitation Pathophysiology
Aortic Regurgitation Pathophysiology
Pathophysiology of chronic AR
LAPLACE law
• Left ventricular wall stress a P( LVEDP) X R
• Thickness
• So in response to chronic stress myocardial hypertrophy develop in such a
manner as to maintain peak systolic wall stress within normal limits
• LV systolic function is maintained through the combination of chamber
dilation and hypertrophy. This leads to eccentric hypertrophy. In compensated
AR, there is sufficient wall thickening so that the ratio of ventricular wall
thickness to cavity radius remains normal.
Pathophysiology of chronic AR
• As a result of maintenance of normal LV systolic function and
normal forward stroke volume despite the increase in LV diastolic
volume, most patients with chronic AR remain asymptomatic for
decades
• As AR progresses, LV enlargement surpasses preload reserve on the
Frank-Starling curve, with the EF falling to normal and then
subnormal levels.
• The LV end-systolic volume rises and is a sensitive indicator of
progressive myocardial dysfunction.
Pathophysiology of chronic AR
• This after load mismatch results in reduction in systolic ejection
performance (reversible phase)
• Impaired myocardial contractility also contribute to LV systolic
dysfunction (irreversible phase)
• At this point in natural history patient goes in decompensated phase
and becomes symptomatic
Pressure Volume Relationships in Chronic AR
CO at rest may approach 25 L/min in severe AI with little increase in EDP
very large EDV (Cor Bovinum)
Pathophysiology of Aortic Regurgitation
Backward flow of blood from aorta into LV (Diastolic)
Increased
LV volume
and pressure
Increased SV
(Frank-Starling Mechanism)
Peak systolic pressure
increased because of
increased SV ejected into aorta
Increased diastolic
wall-tension produces
eccentric hypertrophy
Rapid fall of aortic
pressure during diastole
Increased pulse pressure
Increased
LA pressure
Increased
pulmonary
venous pressure
Pulmonary
edema
Myocardial ischemia
• Increase in wall tension – Increase in 02 demand
• Decrease in diastolic pressure – coronary perfusion pressure is reduced
• So increased O2 demand & decreased O2 supply sets myocardial
ischemia
• Increasing LV end-diastolic pressure may also lower coronary
perfusion gradients, causing subendocardial and myocardial ischemia,
necrosis, and apoptosis
• decrease in diastolic coronary perfusion occurs that is compensated
only partially by increased coronary arterial flow during systole.
Clinical presentation of AR
• Most patients are asymptomatic for decades
• Palpitations (it is awareness of forceful left ventricular contraction)
• Non-specific chest pain
• Angina (less common)
• May be related to CAD
• Or it may occur with normal coronaries (low diastolic pressure leads to
decreased myocardial perfusion in the face of increased myocardial oxygen
demand secondary to LVH)
Clinical presentation of AR
• Symptoms of CHF (most common)
• Exertional dyspnoea
• Orthopnea
• PND
• Right heart failure (pedal oedema, ascitis, hepatomegaly)
• Atrial or ventricular arrhythmias, do occur in patients with aortic
regurgitation, OR late when LVF or RVF has supervened
Pathophysiology – Acute AR
• Acute AR leads to increased blood volume in the LV during diastole.
• The LV does not have sufficient time to dilate in response to the sudden increase in volume.
• LV can not acutely increase it’s total stroke volume sufficiently
• Increase in LVEDP with same cardiac output
• Systolic BP maintained by reflex sympathetic response lead to high SVR and tachycardia
• Rising LVEDP can lead to increasing left atrial and PCWP of sufficient magnitude to produce
pulmonary edema.
• Mitral Annular enlargement and functional MR
• Patients with acute AR and decreased cardiac output often present with chest pain that is a result of
decreased coronary blood flow from changes is diastolic perfusion
• In severe cases, heart failure may develop and potentially deteriorate to cardiogenic shock.
Decreased myocardial perfusion may lead to myocardial ischemia.
• IABP is contraindicated
Hemodynamics of aortic regurgitation. A, Normal
conditions. B, The hemodynamic changes that
occur in severe acute aortic regurgitation.
Although total stroke volume is increased, forward
stroke volume is reduced. Left ventricular end-
diastolic pressure (LVEDP) rises dramatically. C,
Hemodynamic changes occurring in chronic
compensated aortic regurgitation are shown.
Eccentric hypertrophy produces increased end-
diastolic volume (EDV), which permits an increase
in total, as well as forward, stroke volume. The
volume overload is accommodated, and left
ventricular filling pressure is normalized.
Ventricular emptying and end-systolic volume
(ESV) remain normal. D, In chronic
decompensated aortic regurgitation, impaired left
ventricular emptying produces an increase in end-
systolic volume and a fall in ejection fraction (EF),
total stroke volume, and forward stroke volume.
There is further cardiac dilation and reelevation of
left ventricular filling pressure. E, Immediately
following valve replacement, preload estimated
by EDV decreases, as does filling pressure. ESV
also is decreased, but to a lesser extent. The
result is an initial fall in EF. Despite these
changes, elimination of regurgitation leads to an
increase in forward stroke volume, and with
time ejection fraction increases. Aop = aortic
pressure; RF = regurgitant fraction.
(From Carabello BA: Aortic regurgitation:
Hemodynamic determinants of prognosis. In Cohn
LH, DiSesa VJ [eds]: Aortic Regurgitation:
Medical and Surgical Management. New York,
Marcel Dekker, 1986, p 99-101.)
Symptoms
Related to pulmonary congestion
 Dyspnoea
 Orthopnea
 Dry cough or with frothy sputum
Related to reduction in cardiac output
 Exertional fatigue
 Apathy
 Deterioration in intellectual function
Related to etiology
 Sudden onset chest and back pain
 Fever with chills and rigor
 Peripheral embolism
 Trauma
Physical Examination – Acute AR
• Tachycardia
• Peripheral vasoconstriction
• Cyanosis
• Pulmonary edema
• Arterial pulsus alternans; normal LV impulse
• Early mitral valve closure
• Early diastolic murmur (lower pitched and shorter than in chronic AR) may
be present.
• A murmur at the right sternal border is associated more often with
dissection than it is with any other cause of aortic regurgitation.
Physical findings in Chronic AR
• Pulse
• Rate is normal
• Sinus tachycardia in patients with CHF
• Collapsing( Corrigan’s or water hammer pulse)
• Blood pressure
• Low diastolic pressure
• Wide pulse pressure
Physical findings
Inspection and palpation
• Evidence of LVH
• Heaving apex
• Apex displaced to the left and downward
Auscultation
• S1- may be soft due to premature closure of the mitral valve.
• A2 –normal or accentuated when AR is due to aortic root disease.
• S2- absent or single or paradoxical splitting
• S3 GALLOP - due to increased LV end diastolic volume or impaired LV function
• Systolic ejection sound - related to abrupt distention of the aorta by the augmented stroke volume.
Murmur
Early diastolic murmur
• High pitched, blowing decrescendo
• Best heard in the 3rd left intercostal space
-with the patient sitting up and leaning forward
-breath held in forced expiration
• Aortic root disorders- murmur is best heard along right sternal border(Harvey sign)
• Cooving or musical murmur- evertion or perforation of the aortic cusps
• Longer the duration of murmur severer the aortic regurgitation
• Becomes short - cardiac failure
Murmur
Ejection systolic murmur- flow murmur
• best heard at the base of the heat
Austin flint murmur
• Soft, low pitched rumbling mid diastolic murmur.
• Diastolic displacement of the anterior leaflet of the mitral valve by the aortic
regurgitation stream.
• Auscultatory events- intensified by handgrip.
S3 Gallop
• A third heart sound (S3) correlates with an increased LV end-diastolic volume. Its
development may be a sign of impaired LV function
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
Chronic AR may results in left axis deviation
• Tall, upright T waves, Q waves in leads I,V1, and V3 to V6 are indicative of diastolic volume
overload.
• Deep S wave in right precordial leads,
• tall R wave in left leads
• Prominent well marked, narrow q waves
Left ventricular conduction defects usually are associated with left ventricular dysfunction.The QRS
complex amplitude is linearly correlated with left ventricular mass.
Chest X-Ray
Cardiomegaly
Hypertrophy and
dilatation of LV
Cor bovinum
Aorta is dilated but not as seen in aortic stenosis
Echocardiography
ME Lax view Transducer at 130o
• Based on
• Color flow Doppler (Jet width and jet area measurement)
• Continuity equation
• Regurgitant jet velocity assessment
AR quantification
TEE view for jet width measurement
ME Lax view Transducer at 130o
Jet width to LVOT diameter ratio
Jet width-LVOT diameter ratio > 65% indicate severe AR
Color M mode
75/
214
=0.35
TEE views for jet area measurement
ME Sax view Transducer at 40o
Vena Contracta
Vena Contracta width of
> 6 mm indicate Severe AR
Deceleration Slope and Pressure-half time
• The velocity of regurgitant
jet during diastole is directly
related to pressure gradient
between aortic root and LV.
• A large regurgitant defect
will rapidly decrease
pressures gradient and the
velocity of regurgitant jet,
hence slope of AR jet
indicate severity of AR
CWD analysis of AR jet transgastric
or deep transgastric view
Regurgitant jet Slope Decay
Ao
LV pressure
CWD LVOT
Mild AR Severe AR (>3m/sec2)
Ao
LV
Holo-diastolic flow reversal
Severe AR
Angiography
• To estimate the severity of aortic insufficiency if echocardiographic
studies are equivocal or if there is concomitant CAD.
• The amount of regurgitant flow can be determined regurgitant
fraction.
• In general, a regurgitant fraction of less than 20% is GRADE1 aortic
insufficiency. An increase in regurgitant fraction to 60% corresponds
to GRADE 4 insufficiency
MRI Angiography
Diagnosis and Follow-Up
• TTE is indicated in patients with signs or symptoms of AR (stages A to D) for accurate diagnosis of
the cause of regurgitation, regurgitant severity, and LV size and systolic function, and for
determining clinical outcome and timing of valve intervention (34, 76-85). (Level of Evidence: B)
• TTE is indicated in patients with dilated aortic sinuses or ascending aorta or with a bicuspid aortic
valve (stages A and B) to evaluate the presence and severity of AR (86). (Level of Evidence: B)
• CMR is indicated in patients with moderate or severe AR (stages B, C, and D) and suboptimal
echocardiographic images for the assessment of LV systolic function, systolic and diastolic
volumes, and measurement of AR severity (87, 88). (Level of Evidence: B)
Medical Therapy
Class I
• Treatment of hypertension (systolic BP >140 mm Hg) is recommended in patients with chronic AR
(stages B and C), preferably with dihydropyridine calcium channel blockers or
angiotensinconverting enzyme (ACE) inhibitors/angiotensin-receptor blockers (ARBs) (84, 89).
(Level of Evidence: B)
Class IIa
• Medical therapy with ACE inhibitors/ARBs and beta blockers is reasonable in patients with severe
AR who have symptoms and/or LV dysfunction (stages C2 and D) when surgery is not performed
because of comorbidities (90, 91). (Level of Evidence: B)
2014 AHA/ACC Guideline for the Management of Patients
With Valvular
Heart Disease: Executive Summary
2014 AHA/ACC Guideline for the Management of Patients
With Valvular
Heart Disease: Executive Summary
Indication for Surgery
Class I
• AVR is indicated for symptomatic patients with severe AR regardless of LV systolic function (stage D).
(Level of Evidence: B)
• AVR is indicated for asymptomatic patients with chronic severe AR and LV systolic dysfunction (LVEF
<50%) at rest (stage C2) if no other cause for systolic dysfunction is identified. (Level of Evidence: B)
• AVR is indicated for patients with severe AR (stage C or D) while undergoing cardiac surgery for other
indications. (Level of Evidence: C)
Class IIa
• AVR is reasonable for asymptomatic patients with severe AR with normal LV systolic function (LVEF 50%)
but with severe LV dilation (LV end-systolic dimension [LVESD] >50 mm or indexed LVESD >25 mm/m2)
(stage C2). (Level of Evidence: B)
• AVR is reasonable in patients with moderate AR (stage B) while undergoing surgery on the ascending aorta,
coronary artery bypass graft (CABG), or mitral valve surgery. (Level of Evidence: C)
Class IIb
• AVR may be considered for asymptomatic patients with severe AR and normal LV systolic function at rest
(LVEF 50%, stage C1) but with progressive severe LV dilatation (LV enddiastolic dimension >65 mm) if
surgical risk is low. (Level of Evidence: C)
Anesthesia Management in Aortic Regurgitation
Pre-operative Optimization of patient
Sinus rhythm/control of Hypertension
1. ACE Inhibitor
2. CCB (verapamil/diltiazem: 0.075-0.15mg/kg IV)
3. NTG- decrease SVR
4. Inotropic agents
Norepinephrine
Dopamine
Dobutamine
5. Inodilators
Amrinone
Milrinone
6. Plenty of fluids
HEMODYNAMIC GOALS
Preload Increased
Because of increased LV volumes, need increased
preload to maintain forward flow. Avoid hypovolemia.
Heart Rate Increased
Increased HR reduces diastolic time and reduces
regurgitant fraction. Also raises diastolic BP and
decreases LVEDP. 90 beats/min seems to be optimal,
improving cardiac output and improvement in
subendocardial blood flow
Contractility Maintain
Must be maintained. use of pure β-agents or
phosphodiesterase inhibitors can increase stroke
volume through a combination of peripheral dilation
and increased contractility
SVR Decreased
Afterload reduction is helpful in improving forward
flow.
PVR Maintain
PA pressures remain relatively normal except in
patients with end-stage disease.
• ANAESTHETIC MANAGEMENT
• Premedication
• Light premedication is given.
Morphine 0.1-0.2mg/kg
Fentanyle 5-8 ug/kg
Benzodiazepenes can be given ( reduce dose of
morphine)
• Anticholinergics- May be given. As it will do
tachycardia.
• Monitoring
• ECG-lateral precordial lead, IBP, Spo2, capnography,
temperature
• Invasive monitoring-
-Direct arterial pressure
-CVP- measure loading conditions and means of transfusing
inotropes/dilators
-Pulmonary artery catheter-
• A PAC allows determination of basal filling Pressures(PCWP)
and cardiac output-useful in AR
• To accurately monitor ventricular preload and CO response to
pharmacologic interventions
• Other requirement for a PAC is to allow for pacing when it is
anticipated
• ANAESTHETIC MANAGEMENT
• Induction
• Etomidate best for hemodynamic stabilty .
• Any intravenous induction drug except ketamine( H.R.)
• Midazolam,Narcotic( morphine 0.5mg/kg or Fentanyl 5-
10 ug/kg)
• Avoid Propofol- direct and indirect effects on ventricular
preload
• Avoid tracheal stress response since a sudden rise in
arterial blood pressure may cause a dramatic increase in
regurgitant fraction leading to acute LV failure
• Muscle relaxants
Vecuronium + Narcotics- dangerous bradycardia.
Hence pancuronium preferred unless basal heart rate is
high
Rocuronium- vagolytic. Hence slightly decrease HR
and PAP↓
• Avoid atracurium- histamine release
• Benzodiazepenes (midazolam) – use cautiously as
can cause profound vasodilatation with narcotics.
• Maintainence
• A balanced anesthesia that includes low
concentrations of a volatile anesthetic is desirable.
Avoid halothane- arrythmogenic
• Isoflurane(tachy cardia),Sevoflurane(ideal).
• Intraoperative fluid replacement must be done
adequately to maintain preload.
Going on CPB
Before cross-clamp placement
• The ventricle is at risk for distention with AR during CPB
• The intraventricular pressures equilibrate with the aortic root pressures.
Under these conditions, there is no coronary perfusion, and the ventricle
may dilate rapidly and become profoundly ischemic.
• In patients with unknown or uncorrected AR, removal of the cross-clamp
causes the same ventricular dilation and ischemia if a rhythm and ejection
are not rapidly established.
Giving Cardioplegia
Either by Coronary Sinus or through the Coronary artery under direct
visualisation
WEANING FROM CPB
• Complicated by LV dysfunction secondary to sub- optimal myocardial
protection and coronary air embolism.
• Mild trans- prosthetic valve gradient with LV dysfunction---decreases
CO so Inotropes required.
• avoid further LV dilation and dysfunction
• Preload augmentation must be continued to maintain filling of the
dilated LV
Post operative management
• Immediately following aortic valve replacement, the LVEDP and LVEDV decrease But EF
will also decrease.
• a decline in LV function may necessitate inotropic or intra-aortic balloon pump support
• Inotropic support and vasodilator therapy should be
continued for prolonge period.
• Maintain Mean BP below 75 mmHg.
• a mean left atrial pressure of 10 to 12 mmHg, considered appropriate
• When heart rate exceeds 100 beats/min ,a β-blocker should be administered to reduce the rate.
• May require a period of mechanical ventilation:
- avoid Pain and hypoventilation
• Relief of postoperative pain with opioid useful
Post-operative
Complication
• Thrombo-embolism
• Heart failure
• Arrhythmia
Guideline for INR
• INR of 2.5- normal LA size and LV function
• INR of 3.0 -left atrium is enlarged or LV function impaired.
• INR of 3.5 to 4.0 -Severe left atrial enlargement, greatly impaired LV
function, or echocardiographic evidence of stasis in the left atrium
Some evidence indicates that adding aspirin (81 mg daily) further
reduces risk of thromboembolism.
References
• Kaplan’s Cardiac Anesthesia; 5th edition
• Miller’s Anesthesia; 7th edition
• Kirklin cardiac surgery
• Henseley martin cardiac anesthesia
THANK YOU

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Anesthesia Management in Aortic Regurgitation

  • 1. Aortic Regurgitation Dr. Harshil Joshi 2nd year Resident DM Cardiac Anesthesia UNMICRC
  • 2. Aortic Regurgitation  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.  aortic valve disease, aortic root dilatation or combination of both  The presentation varies depending on the acuity of onset, severity of regurgitation, compliance of the ventricle and aorta, and hemodynamic conditions prevalent at the time.  Whereas chronic AR is well tolerated for years, acute AR can be debilitating and life threatening if not treated emergently
  • 3. 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
  • 4. Sinotubular junction dilatation Dilatation of the sinotubular junction displaces the commissures outward and prevents the aortic leaflets from coapting, with resulting central aortic insufficiency AR - Abnormalities of the Aortic Wall
  • 5. Primary Valve Disease • Congenital (bicuspid aortic valve) • Rheumatic fever • Infective endocarditis • Collagen vascular diseases • Degenerative aortic valve disease • Myxomatous (prolapse) • Traumatic • Certain weight loss medications, such as fenfluramine and dexfenfluramine Primary Root Disease • Longstanding, uncontrolled hypertension • Marfan syndrome • Idiopathic aortic dilation • Cystic medial necrosis • Senile aortic ectasia and dilation • Aortic dissection • Marfan's syndrome • Syphilitic aortitis • Giant cell arteritis • Takayasu arteritis • Ankylosing spondylitis • Whipple disease • Other spondyloarthropathies
  • 6. Pathophysiology of chronic AR • AR leads to increased end diastolic volume of LV • To accommodate this regurgitant volume LV compliance increases so there is augmented LVEDV without increase in LVEDP. • There is increase in total stroke volume resulting in forward stroke volume within normal range (starling law) • In addition to increase in compliance, ventricle produces new sarcomers in sereies leading to eccentric hypertrophy. In AS concentric LVH occurs as the sarcomeres replicate in parallel
  • 9. Pathophysiology of chronic AR LAPLACE law • Left ventricular wall stress a P( LVEDP) X R • Thickness • So in response to chronic stress myocardial hypertrophy develop in such a manner as to maintain peak systolic wall stress within normal limits • LV systolic function is maintained through the combination of chamber dilation and hypertrophy. This leads to eccentric hypertrophy. In compensated AR, there is sufficient wall thickening so that the ratio of ventricular wall thickness to cavity radius remains normal.
  • 10. Pathophysiology of chronic AR • As a result of maintenance of normal LV systolic function and normal forward stroke volume despite the increase in LV diastolic volume, most patients with chronic AR remain asymptomatic for decades • As AR progresses, LV enlargement surpasses preload reserve on the Frank-Starling curve, with the EF falling to normal and then subnormal levels. • The LV end-systolic volume rises and is a sensitive indicator of progressive myocardial dysfunction.
  • 11. Pathophysiology of chronic AR • This after load mismatch results in reduction in systolic ejection performance (reversible phase) • Impaired myocardial contractility also contribute to LV systolic dysfunction (irreversible phase) • At this point in natural history patient goes in decompensated phase and becomes symptomatic
  • 12. Pressure Volume Relationships in Chronic AR CO at rest may approach 25 L/min in severe AI with little increase in EDP very large EDV (Cor Bovinum)
  • 13. Pathophysiology of Aortic Regurgitation Backward flow of blood from aorta into LV (Diastolic) Increased LV volume and pressure Increased SV (Frank-Starling Mechanism) Peak systolic pressure increased because of increased SV ejected into aorta Increased diastolic wall-tension produces eccentric hypertrophy Rapid fall of aortic pressure during diastole Increased pulse pressure Increased LA pressure Increased pulmonary venous pressure Pulmonary edema
  • 14. Myocardial ischemia • Increase in wall tension – Increase in 02 demand • Decrease in diastolic pressure – coronary perfusion pressure is reduced • So increased O2 demand & decreased O2 supply sets myocardial ischemia • Increasing LV end-diastolic pressure may also lower coronary perfusion gradients, causing subendocardial and myocardial ischemia, necrosis, and apoptosis • decrease in diastolic coronary perfusion occurs that is compensated only partially by increased coronary arterial flow during systole.
  • 15. Clinical presentation of AR • Most patients are asymptomatic for decades • Palpitations (it is awareness of forceful left ventricular contraction) • Non-specific chest pain • Angina (less common) • May be related to CAD • Or it may occur with normal coronaries (low diastolic pressure leads to decreased myocardial perfusion in the face of increased myocardial oxygen demand secondary to LVH)
  • 16. Clinical presentation of AR • Symptoms of CHF (most common) • Exertional dyspnoea • Orthopnea • PND • Right heart failure (pedal oedema, ascitis, hepatomegaly) • Atrial or ventricular arrhythmias, do occur in patients with aortic regurgitation, OR late when LVF or RVF has supervened
  • 17. Pathophysiology – Acute AR • Acute AR leads to increased blood volume in the LV during diastole. • The LV does not have sufficient time to dilate in response to the sudden increase in volume. • LV can not acutely increase it’s total stroke volume sufficiently • Increase in LVEDP with same cardiac output • Systolic BP maintained by reflex sympathetic response lead to high SVR and tachycardia • Rising LVEDP can lead to increasing left atrial and PCWP of sufficient magnitude to produce pulmonary edema. • Mitral Annular enlargement and functional MR • Patients with acute AR and decreased cardiac output often present with chest pain that is a result of decreased coronary blood flow from changes is diastolic perfusion • In severe cases, heart failure may develop and potentially deteriorate to cardiogenic shock. Decreased myocardial perfusion may lead to myocardial ischemia. • IABP is contraindicated
  • 18. Hemodynamics of aortic regurgitation. A, Normal conditions. B, The hemodynamic changes that occur in severe acute aortic regurgitation. Although total stroke volume is increased, forward stroke volume is reduced. Left ventricular end- diastolic pressure (LVEDP) rises dramatically. C, Hemodynamic changes occurring in chronic compensated aortic regurgitation are shown. Eccentric hypertrophy produces increased end- diastolic volume (EDV), which permits an increase in total, as well as forward, stroke volume. The volume overload is accommodated, and left ventricular filling pressure is normalized. Ventricular emptying and end-systolic volume (ESV) remain normal. D, In chronic decompensated aortic regurgitation, impaired left ventricular emptying produces an increase in end- systolic volume and a fall in ejection fraction (EF), total stroke volume, and forward stroke volume. There is further cardiac dilation and reelevation of left ventricular filling pressure. E, Immediately following valve replacement, preload estimated by EDV decreases, as does filling pressure. ESV also is decreased, but to a lesser extent. The result is an initial fall in EF. Despite these changes, elimination of regurgitation leads to an increase in forward stroke volume, and with time ejection fraction increases. Aop = aortic pressure; RF = regurgitant fraction. (From Carabello BA: Aortic regurgitation: Hemodynamic determinants of prognosis. In Cohn LH, DiSesa VJ [eds]: Aortic Regurgitation: Medical and Surgical Management. New York, Marcel Dekker, 1986, p 99-101.)
  • 19. Symptoms Related to pulmonary congestion  Dyspnoea  Orthopnea  Dry cough or with frothy sputum Related to reduction in cardiac output  Exertional fatigue  Apathy  Deterioration in intellectual function Related to etiology  Sudden onset chest and back pain  Fever with chills and rigor  Peripheral embolism  Trauma
  • 20. Physical Examination – Acute AR • Tachycardia • Peripheral vasoconstriction • Cyanosis • Pulmonary edema • Arterial pulsus alternans; normal LV impulse • Early mitral valve closure • Early diastolic murmur (lower pitched and shorter than in chronic AR) may be present. • A murmur at the right sternal border is associated more often with dissection than it is with any other cause of aortic regurgitation.
  • 21. Physical findings in Chronic AR • Pulse • Rate is normal • Sinus tachycardia in patients with CHF • Collapsing( Corrigan’s or water hammer pulse) • Blood pressure • Low diastolic pressure • Wide pulse pressure
  • 22. Physical findings Inspection and palpation • Evidence of LVH • Heaving apex • Apex displaced to the left and downward Auscultation • S1- may be soft due to premature closure of the mitral valve. • A2 –normal or accentuated when AR is due to aortic root disease. • S2- absent or single or paradoxical splitting • S3 GALLOP - due to increased LV end diastolic volume or impaired LV function • Systolic ejection sound - related to abrupt distention of the aorta by the augmented stroke volume.
  • 23. Murmur Early diastolic murmur • High pitched, blowing decrescendo • Best heard in the 3rd left intercostal space -with the patient sitting up and leaning forward -breath held in forced expiration • Aortic root disorders- murmur is best heard along right sternal border(Harvey sign) • Cooving or musical murmur- evertion or perforation of the aortic cusps • Longer the duration of murmur severer the aortic regurgitation • Becomes short - cardiac failure
  • 24. Murmur Ejection systolic murmur- flow murmur • best heard at the base of the heat Austin flint murmur • Soft, low pitched rumbling mid diastolic murmur. • Diastolic displacement of the anterior leaflet of the mitral valve by the aortic regurgitation stream. • Auscultatory events- intensified by handgrip. S3 Gallop • A third heart sound (S3) correlates with an increased LV end-diastolic volume. Its development may be a sign of impaired LV function
  • 25. 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)
  • 26. ECG Chronic AR may results in left axis deviation • Tall, upright T waves, Q waves in leads I,V1, and V3 to V6 are indicative of diastolic volume overload. • Deep S wave in right precordial leads, • tall R wave in left leads • Prominent well marked, narrow q waves Left ventricular conduction defects usually are associated with left ventricular dysfunction.The QRS complex amplitude is linearly correlated with left ventricular mass.
  • 27. Chest X-Ray Cardiomegaly Hypertrophy and dilatation of LV Cor bovinum Aorta is dilated but not as seen in aortic stenosis
  • 28. Echocardiography ME Lax view Transducer at 130o
  • 29. • Based on • Color flow Doppler (Jet width and jet area measurement) • Continuity equation • Regurgitant jet velocity assessment AR quantification
  • 30. TEE view for jet width measurement ME Lax view Transducer at 130o
  • 31. Jet width to LVOT diameter ratio Jet width-LVOT diameter ratio > 65% indicate severe AR
  • 33. TEE views for jet area measurement ME Sax view Transducer at 40o
  • 34. Vena Contracta Vena Contracta width of > 6 mm indicate Severe AR
  • 35. Deceleration Slope and Pressure-half time • The velocity of regurgitant jet during diastole is directly related to pressure gradient between aortic root and LV. • A large regurgitant defect will rapidly decrease pressures gradient and the velocity of regurgitant jet, hence slope of AR jet indicate severity of AR CWD analysis of AR jet transgastric or deep transgastric view
  • 36. Regurgitant jet Slope Decay Ao LV pressure CWD LVOT Mild AR Severe AR (>3m/sec2) Ao LV
  • 38. Angiography • To estimate the severity of aortic insufficiency if echocardiographic studies are equivocal or if there is concomitant CAD. • The amount of regurgitant flow can be determined regurgitant fraction. • In general, a regurgitant fraction of less than 20% is GRADE1 aortic insufficiency. An increase in regurgitant fraction to 60% corresponds to GRADE 4 insufficiency
  • 40. Diagnosis and Follow-Up • TTE is indicated in patients with signs or symptoms of AR (stages A to D) for accurate diagnosis of the cause of regurgitation, regurgitant severity, and LV size and systolic function, and for determining clinical outcome and timing of valve intervention (34, 76-85). (Level of Evidence: B) • TTE is indicated in patients with dilated aortic sinuses or ascending aorta or with a bicuspid aortic valve (stages A and B) to evaluate the presence and severity of AR (86). (Level of Evidence: B) • CMR is indicated in patients with moderate or severe AR (stages B, C, and D) and suboptimal echocardiographic images for the assessment of LV systolic function, systolic and diastolic volumes, and measurement of AR severity (87, 88). (Level of Evidence: B)
  • 41. Medical Therapy Class I • Treatment of hypertension (systolic BP >140 mm Hg) is recommended in patients with chronic AR (stages B and C), preferably with dihydropyridine calcium channel blockers or angiotensinconverting enzyme (ACE) inhibitors/angiotensin-receptor blockers (ARBs) (84, 89). (Level of Evidence: B) Class IIa • Medical therapy with ACE inhibitors/ARBs and beta blockers is reasonable in patients with severe AR who have symptoms and/or LV dysfunction (stages C2 and D) when surgery is not performed because of comorbidities (90, 91). (Level of Evidence: B)
  • 42. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary
  • 43. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary
  • 44. Indication for Surgery Class I • AVR is indicated for symptomatic patients with severe AR regardless of LV systolic function (stage D). (Level of Evidence: B) • AVR is indicated for asymptomatic patients with chronic severe AR and LV systolic dysfunction (LVEF <50%) at rest (stage C2) if no other cause for systolic dysfunction is identified. (Level of Evidence: B) • AVR is indicated for patients with severe AR (stage C or D) while undergoing cardiac surgery for other indications. (Level of Evidence: C) Class IIa • AVR is reasonable for asymptomatic patients with severe AR with normal LV systolic function (LVEF 50%) but with severe LV dilation (LV end-systolic dimension [LVESD] >50 mm or indexed LVESD >25 mm/m2) (stage C2). (Level of Evidence: B) • AVR is reasonable in patients with moderate AR (stage B) while undergoing surgery on the ascending aorta, coronary artery bypass graft (CABG), or mitral valve surgery. (Level of Evidence: C) Class IIb • AVR may be considered for asymptomatic patients with severe AR and normal LV systolic function at rest (LVEF 50%, stage C1) but with progressive severe LV dilatation (LV enddiastolic dimension >65 mm) if surgical risk is low. (Level of Evidence: C)
  • 46. Pre-operative Optimization of patient Sinus rhythm/control of Hypertension 1. ACE Inhibitor 2. CCB (verapamil/diltiazem: 0.075-0.15mg/kg IV) 3. NTG- decrease SVR 4. Inotropic agents Norepinephrine Dopamine Dobutamine 5. Inodilators Amrinone Milrinone 6. Plenty of fluids
  • 47. HEMODYNAMIC GOALS Preload Increased Because of increased LV volumes, need increased preload to maintain forward flow. Avoid hypovolemia. Heart Rate Increased Increased HR reduces diastolic time and reduces regurgitant fraction. Also raises diastolic BP and decreases LVEDP. 90 beats/min seems to be optimal, improving cardiac output and improvement in subendocardial blood flow Contractility Maintain Must be maintained. use of pure β-agents or phosphodiesterase inhibitors can increase stroke volume through a combination of peripheral dilation and increased contractility SVR Decreased Afterload reduction is helpful in improving forward flow. PVR Maintain PA pressures remain relatively normal except in patients with end-stage disease.
  • 48. • ANAESTHETIC MANAGEMENT • Premedication • Light premedication is given. Morphine 0.1-0.2mg/kg Fentanyle 5-8 ug/kg Benzodiazepenes can be given ( reduce dose of morphine) • Anticholinergics- May be given. As it will do tachycardia.
  • 49. • Monitoring • ECG-lateral precordial lead, IBP, Spo2, capnography, temperature • Invasive monitoring- -Direct arterial pressure -CVP- measure loading conditions and means of transfusing inotropes/dilators -Pulmonary artery catheter- • A PAC allows determination of basal filling Pressures(PCWP) and cardiac output-useful in AR • To accurately monitor ventricular preload and CO response to pharmacologic interventions • Other requirement for a PAC is to allow for pacing when it is anticipated
  • 50. • ANAESTHETIC MANAGEMENT • Induction • Etomidate best for hemodynamic stabilty . • Any intravenous induction drug except ketamine( H.R.) • Midazolam,Narcotic( morphine 0.5mg/kg or Fentanyl 5- 10 ug/kg) • Avoid Propofol- direct and indirect effects on ventricular preload • Avoid tracheal stress response since a sudden rise in arterial blood pressure may cause a dramatic increase in regurgitant fraction leading to acute LV failure
  • 51. • Muscle relaxants Vecuronium + Narcotics- dangerous bradycardia. Hence pancuronium preferred unless basal heart rate is high Rocuronium- vagolytic. Hence slightly decrease HR and PAP↓ • Avoid atracurium- histamine release • Benzodiazepenes (midazolam) – use cautiously as can cause profound vasodilatation with narcotics.
  • 52. • Maintainence • A balanced anesthesia that includes low concentrations of a volatile anesthetic is desirable. Avoid halothane- arrythmogenic • Isoflurane(tachy cardia),Sevoflurane(ideal). • Intraoperative fluid replacement must be done adequately to maintain preload.
  • 53. Going on CPB Before cross-clamp placement • The ventricle is at risk for distention with AR during CPB • The intraventricular pressures equilibrate with the aortic root pressures. Under these conditions, there is no coronary perfusion, and the ventricle may dilate rapidly and become profoundly ischemic. • In patients with unknown or uncorrected AR, removal of the cross-clamp causes the same ventricular dilation and ischemia if a rhythm and ejection are not rapidly established. Giving Cardioplegia Either by Coronary Sinus or through the Coronary artery under direct visualisation
  • 54. WEANING FROM CPB • Complicated by LV dysfunction secondary to sub- optimal myocardial protection and coronary air embolism. • Mild trans- prosthetic valve gradient with LV dysfunction---decreases CO so Inotropes required. • avoid further LV dilation and dysfunction • Preload augmentation must be continued to maintain filling of the dilated LV
  • 55. Post operative management • Immediately following aortic valve replacement, the LVEDP and LVEDV decrease But EF will also decrease. • a decline in LV function may necessitate inotropic or intra-aortic balloon pump support • Inotropic support and vasodilator therapy should be continued for prolonge period. • Maintain Mean BP below 75 mmHg. • a mean left atrial pressure of 10 to 12 mmHg, considered appropriate • When heart rate exceeds 100 beats/min ,a β-blocker should be administered to reduce the rate. • May require a period of mechanical ventilation: - avoid Pain and hypoventilation • Relief of postoperative pain with opioid useful
  • 57. Guideline for INR • INR of 2.5- normal LA size and LV function • INR of 3.0 -left atrium is enlarged or LV function impaired. • INR of 3.5 to 4.0 -Severe left atrial enlargement, greatly impaired LV function, or echocardiographic evidence of stasis in the left atrium Some evidence indicates that adding aspirin (81 mg daily) further reduces risk of thromboembolism.
  • 58. References • Kaplan’s Cardiac Anesthesia; 5th edition • Miller’s Anesthesia; 7th edition • Kirklin cardiac surgery • Henseley martin cardiac anesthesia