Anaesthesia for closed heart procedures pda & coa

ANAESTHESIA FOR

CLOSED HEART

PROCEDURE

CLOSED HEART PROCEDURES

•LESIONS CORRECTED WITH CLOSED PROCEDURES

•CLOSED PALLIATIVE PROCEDURES

LESIONS CORRECTED WITH CLOSED PROCEDURES

Patent ductus arteriousus Co-arctation of aorta

CLOSED PALLIATIVE PROCEDURES

o PA Banding o Blalock - Taussig shunto Balloon atrial septostomies (Rashkind

Procedures)

PATENT DUCTUS ARTERIOUSUS

1 in 2500live , full term births 10 % of all congenital heart defects Girls are affected twice than boys Prenatal exposure to rubella virus during first

trimester of pregnancy

ANATOMY PDA extends from the post. Descending aorta

near the origin of left sub clavian artery to the anterior surface of the main pulmonary artery

It is the remnant of sixth branchial arch A bilateral PDA is possible

STRUCTURAL DIFFERENCE BETWEEN PDA& AORTA + PULMONARY ARTERY Aorta & pulmonary artery`s internal media is

composed of elastic fibers Internal media of PDA is composed of smooth

muscle in both longitudinal & circumferential arrangementsThe muscle constrict when exposed to increased Pao2 This response becomes more dramatic as the fetus

matures

PATHOPHYSIOLOGY In the fetus blood flow from the RV is diverted

from the high resistance pulmonary bed via the ductus to the descending aorta

Hemodynamics of a PDA is similar to VSD- left to right shunt flow is determind by the capacity of the ductus to impede flow from the aorta to the PA

If the ductus is large,stunted blood flow is determined by the pulm. Vasculature resistance to systemic vascular resistance

NATURAL COURSE o Functional closure of ductus is due to vas o

Constriction after term

o Anatomic closure is due to intimal proliferation

and fibrosis which is complete at one month

CATEGORIZATION OF PDA

Done on the degree of left to right shunt,which is determined by both the size and the length of the duct and the diff. bet. the SVR and PVR

SILENT: tiny PDA detected by echocardiographySMALL: continuous murmer common;Qp/Qs of

1.5to2.2:1MODERATE: continous murmer

present;Qp/Qs>2.2:1EISSNMENGER:continous murmer

absent;substantial pulm.HT,differential hypoxemia;and differential cyanosis(pink fingers,blue toes)

DIAGNOSIS Signs

tachypneadiaphoresisdecreased exercise tolerance failure to thrive recurrent respiratory infection lobar emphysema / collapsecardiac failurecardiac enlargementbacterial endocarditis irreversible pulmonary vascular disease

PHYSICAL EXAMINATION continuous machine murmur which gets louder through

out systole with a peak at the 2nd heart sound & gets softer through out diastole

Murmur is loudest at 1st or 2nd inter costal space at left sternal border

Pulse pressure- wide- prominent or bounding pulse Pulse biferiens-two distinct peaks seprated by a deep

cleft, noted on the intra-arterial wave form is a specific & sensitive indicator of PDA with Left to right shunting in the neonate

ECG- usually normalwith large L-R flow- LVH or Lt arterial enlargement

o RVH- if PDA has caused pulmonary occlusive diseaseo Chest x-rayo small PDA – normal X-rayo as flow increases- prominent pulmonary

-prominent aortic knobo further increase in flow

- left heart enlargement

- increase in pulmonary vascular marking

( indicative of failure)

o Echocardiographyo main diagnostic procedure for PDAo 2D Echo- can identify the aortic end of the ductuso Continuous wave Doppler – can detect abnormal flow in PAo Color flow Doppler- can visualize the jet of abnormal flow &

determine more information about the size and shape of the ductus

INDICATION FOR INTERVENTION

Unnecessary in an asymptomatic infant with a small left to right shunt

Necessary for those who have signs of a significant ductal left –to- right shunt during the course of the respiratory distress syndrome

Surgical ligation is required in the infants who are unresponsive to Indomethacin

C.I TO DUCTAL CLOSURE Irreversible pulmonary HT Active endarteritis

PREOPERATIVE PREPARATION Prophylactic antibiotics Vit. K (preterm infants)

INTRA-OPERATIVE MONITERING ECG B .P – invasive Capnography Pulse oximeter (two) – Rt hand & one on

lower extrimity Temperature monitering Esophageal stethoscope – to listen to murmur

PREMEDICATION

Usually not recquired ORAL PREMEDICANT COMBINATIONS Mepridine – 1.5 mg/kg(max. 100mg) Atropine -0.02mg/kg(max.0.4mg) Diazepam 0.15mg/kg(10mg)

or Mepridine – 2- 3mg/kg(max.100 mg) Diazepam -0.1 mg/kg(max.10mg) Fentanyl(oral/transmucosal) – 15 – 20 micro gram/kg

or Midazolam -0.5 – 0.75 mg/kg(max.5mg) INTRAMUSCULAR PREMIDICANT COMBINATIONS Morphine 0.2 mg /kg(max.10mg)

oro Midazolam -0.08mg/kg(max5mg)

(recommended for children over 1 year of age)

INDUCTION Fentanyl – 2microg/kg body wt. Sleep dose of thiopentone Succinyl choline – 1mg/kg Ventilation Larynx sprayed with 2% ligocaine Maintenance with N2O & O2 mixture( 60:40) Halothane and non depolarising agents Other supplemental drugs used are

ketamine,isoflurane and midazolam

MAINTENANCE N2O +O2+ Halothane + non depolarising agents Sodium Nitropruside – 1 vial in 5% of 500 ml of

dextrose in micro drip set started when the ductus is dissected out and the systolic pressure is brought down to 60 mm Hg

Once the ligation is complete the SNP is stopped and continued if the pressure rises post -operatively

FOLL. LIGATION OF PDA Diastolic pressure rises in the typical PDA pt. In selected pt`s – PA pressure monitoring m/b

carried out In typical PDA pt`s with no change in PA

pressure after occlusion If PA pressure falls in pt`s with pulmonary HT,

then the degree of increased resistance is minimal & the ductus m/b ligated safely

If PA pressure increases with severe pulmonary HT – then ligation carries a high mortality

ON THE CLOSURE OF DUCTUS The diastolic component of the murmur will

disappear Systolic component persist but without

significance

SERIOUS COMPLICATION A serious complication is increased PVR with

severe Pulmonary hypertension- reversal of flow –RHF

• If ligation of the ductus is performed at this stage death may occur promptly owing to the closure of the escape route of the pulmonary circuit

o Damage to the laryngeal nerve

INTERVENTIONAL TECHNIQUES

TRANSCATHTER TREATMENT -for ducts smaller than 8mm have been establised

SURGICAL TREATMENT -either by ligation or by putting clips

-greater morbidity and mortality

-immediate closure in more than 95%of patients

-surgical mortality in adults is 1%to 3.5% and is due to pulmonary art. Hypertension and difficult ductal morphology

-reserved for those in whom PDA is too large for device closure

VIDEO ASSISTED THORACOSCOPIC SURGERY

-costly

-experience is required

CO –ARCTATION OF AORTA Etiology and risk of occurrence -1 in 2000 live births Sixth most common congenital heart disease Narrowing of aortic lumen from protrusion from within

posterior and lateral aortic media Mortality is associated with - cardiac failure (25%)

-Aortic rupture(21%)

-Endocarditis (18%)

-Cerebrovascular hemorrhage(11.5%)

-Others –HT

-CAD

ANATOMY Classification of co-arctation is based on the

relationship with the ductus arteriosus Preductal – proximal to the ductus , infantile

type Postductal – distal to the fibrosed ductus,adult

type

SEGMENTS OF THE AORTA

SEGMENTS OF THE AORTA Ascending aorta to innominate to artery proximal arch from innominate to left carotid Distal arch from left carotid to left subclavian

artery Isthmus from left subclavian to co –arctation Aorta at the level of the diaphragm

PRE – DUCTAL CO ARC TATION Morphology -Localised shellf in the postero lateral aortic wall

opposite the ductus More assoc. with neonates CLINICAL FEATURES More in males Associated with –gonadal dysgenesis (Turner syndrome

-Biscuspid aortic valve

-VSD

-MS/MR

NEONATES Left ventricular failure –

increase in left ventricular wall stress after closure of arterial duct

Systemic hypo perfusionLeft to right shunting across patent foramen ovale

(PFO) and pulmonary venous hyper tension secondary to heart failure cause pulmonary arterial hypertension

Peripheral pulse are weak If L.V function is improved with medical

management, a significant pressure difference then develops between the arms & the legs, allowing detection of a pulse discrepancy

LAB INVESTIGATION ECG –RAD &RVH Chest x- ray

Cardiomeagalypulmonary arterial & venous engorgementEchocardiographyDemonstrates the posterior shelf & the degree of

associated isthmic or transverse arch hyopoplasia Doppler echo cardiography -is helpful if ductus is closed

- it demonstrates a high velocity jet during systole & diastole

MANAGEMENT Prostaglandin therapy

PGE1 infusion to dilate the ductus arteriosus, the pressure difference may be obliterated across the site of co-arctation because the fetal flow pattern is re-established

This also improves the renal perfusion, which in turn reverses the associated metabolic acidosis

INTERVENTIONSurgical- excision of the area of co-arctation and

extended end to end repair or end to side anastomosis with absorbable

sutures to allow remodeling of the aorta with time

Subclavian flap aortoplasty- Less popular now days

Balloon dialation – does not have in management in this age group

Early surgery – lower incidence of long term hypertension

INFANTS & CHILDRENPRESENTATION Reduced femoral pulses Hypertension Heart failure is uncommon because, the L.V has

a chance to become hypertrophied Complaints of headache, cold extremities and

claudication with exercise is noted in older child & adolescent age group

Midsystolic murmur over the anterior chest, back is most frequent

Lab investigation ECG

-LVH with co-existing RVHo CHEST-X RAY

pre –stenotic & post stenotic dilatation of the proximal descending thoracic aorta

Rib notching – unilateral or bilateral in 50% of caseECHO cardiography

- Demonstrates a post. Shelf

-A well expanded isthmus and trasverse aortic arch

-High velocity continuous jet through the co-arctation site

INTERVENTION Balloon dilation Surgery reserved for arch hypoplasia

Extended end to end anastomosis is the currently favored surgical approach with patch augmentation

COMPLICATIONS Paradoxical HT in immediate post. Op ( not seen

with balloon dilation ) Becoz of HT – cerebral aneurysm & hemorrage

Hypertensive encephalopathyRupture of aortaL V F Infective endocarditis

ADULT PRESENTATION Presents with simple co-arctation Associated anomalies –

bicuspid aortic valve(80 %)Intracranial aneurysms (2-10%)

CLINICAL FEATURES Asymptomatic Epistaxis Headache Leg weakness on exertion C H F Angina Aortic stenosis Aortic dissection Un explained intracerebral hemorrhage Leg claudication ( pain)

CLINICAL EXAMINATION Upper limb HT Differential systolic blood pressure of atleast

10mm Hg(brachial>popliteal) Radial-femoral pulse delay Auscultation- interscapular systolic murmur Fundoscopic examination-corkscrew tortuosity

of retinal arterioles

INTERVENTION Surgical Balloon dilatation

ANAESTHETIC MANAGEMENT PRE-OP PREPARATION

Prophylatic antibioticsControl of BPBETA-blockerso Intra Operative Monitoring

Invasive arterial pressure monitoring in right radial artery and femoral artery

o CVP Monitoringo Capnographyo Pulse Oximitryo Spinal Cord Monitoring -

ANAESTHETIC INDUCTION G.A with controlled ventilation is the

technique of choice Epidural anaesthesia avoided as it may mask

paraplegia Total IV Anaesthesia with opiates is useful in

neonates with cardiac failure or cardiovascular instabilty

Avoid ketamine Isoflurane preffered becoz of its effect on

afterload

MAINTENANCE

Monitor lower body pressure closely-pressure should not fall 45mmHg

Provide analgesia for intra&postop Epidural analgesia technique+/-; Intercostal nerve blocks not recommended

becoz of collaterals Volatile agents make blood pressure control

easy Start antihypertensive control early after

cross clamp has been removed,using beta –blockade,then nitroprusside

THANK YOU