Aortic RegurgitationDr. 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 increasesso there is augmented LVEDV without increase in LVEDP.

• There is increase in total stroke volume resulting in forward strokevolume within normal range (starling law)

• In addition to increase in compliance, ventricle produces newsarcomers in sereies leading to eccentric hypertrophy. In ASconcentric 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 amanner as to maintain peak systolic wall stress within normal limits

• LV systolic function is maintained through the combination of chamberdilation and hypertrophy. This leads to eccentric hypertrophy. In compensatedAR, there is sufficient wall thickening so that the ratio of ventricular wallthickness to cavity radius remains normal.

Pathophysiology of chronic AR

• As a result of maintenance of normal LV systolic function andnormal forward stroke volume despite the increase in LV diastolicvolume, most patients with chronic AR remain asymptomatic fordecades

• 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 ejectionperformance (reversible phase)

• Impaired myocardial contractility also contribute to LV systolicdysfunction (irreversible phase)

• At this point in natural history patient goes in decompensated phaseand becomes symptomatic

Pressure Volume Relationships in Chronic AR

CO at rest may approach 25 L/min in severe AI with little increase in EDPvery 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 aorticregurgitation, 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.)

SymptomsRelated 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.

MurmurEarly 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 regurgitantjet 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 transgastricor 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 regurgitantfraction.

• 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 ValvularHeart Disease: Executive Summary

2014 AHA/ACC Guideline for the Management of Patients With ValvularHeart Disease: Executive Summary

Indication for SurgeryClass 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)

Pre-operative Optimization of patient

Sinus rhythm/control of Hypertension1. ACE Inhibitor2. CCB (verapamil/diltiazem: 0.075-0.15mg/kg IV)3. NTG- decrease SVR4. Inotropic agents

NorepinephrineDopamineDobutamine

5. InodilatorsAmrinoneMilrinone

6. Plenty of fluids

HEMODYNAMIC GOALS

Preload IncreasedBecause 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 DecreasedAfterload reduction is helpful in improving forward

flow.

PVR MaintainPA 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/kgBenzodiazepenes 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 relaxantsVecuronium + Narcotics- dangerous bradycardia. Hence pancuronium preferred unless basal heart rate is highRocuronium- 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