Cardiac Surgical issues

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Cardiac Surgical Issues:

Cardiac Surgical Issues

Slide2:

Dr Isha Deshmukh Pediatrics Department GMC Mumbai

Points to discuss…:

Points to discuss… To outline the optimal timing of interventions in common CHD’s To formulate evidence based guidelines for assessment of operability in left  right shunt lesions. No single rule & decision is individualized.

Advantage of Neonatal Repair:

Advantage of Neonatal Repair Early elimination of cyanosis Early elimination of CCF Optimal circulation for growth & development Reduced anatomic distortion from palliative procedures Reduced hospital admissions while awaiting repair Reduced parental anxiety for awaiting repair

Newborn considerations:

Newborn considerations Rapid response to stress – changes in pH , lactic acid, blood glucose & temperature Diminished fat & carbohydrate reserve Higher metabolic rate & O2 consumption  rapid onset Hypoxemia Immature liver & kidney function Increased Total Body water  Capillary leak Less compliant neonatal myocardium, less responsive to increase in preload / less tolerant to increase in afterload Prone for hypothermic ischemia  CPB

Pre- operative Examination & Lab. Data:

Pre- operative Examination & Lab. Data Extent of cardio-pulmonary impairment Airway abnormalities Intercurrant pulmonary infections Presence , duration & degree of hypoxemia  PCV Chest X –Ray , ECG Severe Hypochloremic Metabolic Alkalosis To discontinue digoxin pre –operatively To avoid hyperventilation Administration of calcium during induction of anesthesia To prevent Post op Fibrillation.

Echo & Doppler Assessment :

Echo & Doppler Assessment Accurate anatomic diagnosis Color flow mapping techniques  ASD/ VSD 3 D echo  Define mechanism of valve regurgitation, visualization of complex anatomy Doppler measurements  measure pressure gradients across valves Used modality to diagnose  VSD, Complete AVC defect, TOF, IAA, HLHS, CoA,

Cardiac Catheterization…:

Cardiac Catheterization … Older children with complex anatomy(single ventricle Description of direction, magnitude & approximate location of intracardiac shunts Intracardiac & intravascular pressures are measured to determine the presence of obstruction & whether shunt orifices are restrictive / non-restrictive SVC  best indicates true mixed venous O2 sat. Levels  RA – ASD RV – VSD PA – PDA Magnitude of L R shunt ( Qp:Qs)  Fick’s Equation

Assessment of Patient status & Predominant Pathophysiology:

Assessment of Patient status & Predominant Pathophysiology How does the SVR reach the systemic arterial circulation to maintain CO? What is level of intracardiac mixing/ shunting? Association of outflow tract obstruction? Increased / decreased PBF? Is there Volume / Pressure overload? Is the circulation in series / parallel? Are the defects amenable to 2 ventricle / 1 ventricle repair?

10 Intensive Care Strategies to Diagnose & Support Low CO States:

10 Intensive Care Strategies to Diagnose & Support Low CO States 1.Know in detail the cardiac anatomy and its physiologic consequences 2. Understand the specialized considerations of the newborn & implications of reparative rather than palliative surgery 3. Diversify personnel to include experts in neonatal 4. Monitor, measure, and image the heart to rule out residual disease as a cause of postoperative hemodynamic instability or low cardiac output 5. Maintain aortic perfusion & improve the contractile state 6. Optimize preload (including atrial shunting) 7. Reduce afterload 8. Control heart rate, rhythm, and synchrony 9. Optimize heart lung interactions 10. Provide mechanical support when needed

Signs of Heart Failure / Low CO States:

Signs of Heart Failure / Low CO States S igns Cool extremities/poor perfusion Oliguria and other end-organ failure Tachycardia Hypotension Acidosis Cardiomegaly Pleural effusions

Cont…:

Cont… M onitor and M easure Heart rate, blood pressure, intracardiac pressure Extremity temperature, central temperature Urine output Mixed venous oxygen saturation Arterial blood gas - pH and lactate Laboratory measures of end-organ function Echocardiography

Common Causes of Elevated Left Atrial Pressure after Cardiopulmonary Bypass:

Common Causes of Elevated Left Atrial Pressure after Cardiopulmonary Bypass 1.Decreased ventricular systolic/diastolic function Myocardial Ischemia Dilated cardiomyopathy Systemic ventricular hypertrophy 2. Left atrioventricular valve disease 3. Large left-to-right intracardiac shunt 4. Chamber hypoplasia 5. Intravascular or ventricular volume overload 6. Cardiac tamponade 7. Arrhythmia Tachyarrhythmia, junctional rhythm Complete heart block

Critical Care Strategies for Postoperative Treatment of Pulmonary Hypertension:

Critical Care Strategies for Postoperative Treatment of Pulmonary Hypertension 1.Anatomic investigation 2. Opportunities for right-to- left shunt as “popoff” 3. Sedation/anesthesia 4. Moderate hyperventilation 5. Moderate alkalosis 6. Adequate inspired oxygen 7. Normal lung volumes 8. Optimal hematocrit 9. Inotropic support 10. Vasodilators

To avoid post –op…:

To avoid post –op… 1.Residual anatomic disease 2. Intact atrial septum in right heart failure 3. Agitation/pain 4. Respiratory acidosis 5. Metabolic acidosis 6. Alveolar hypoxia 7. Atelectasis or overdistention 8. Excessive hematocrit 9. Low output and coronary perfusion 10. Vasoconstrictors/increased afterload

Factors Contributing to a Lower Than Anticipated Oxygen Saturation in Patients with Common Mixing Lesions:

Factors Contributing to a Lower Than Anticipated Oxygen Saturation in Patients with Common Mixing Lesions Low FIO2 Low delivered oxygen concentration Failure of oxygen delivery device Pulmonary vein desaturation Ventilation perfusion defects Alveolar process, e.g., edema/infectious/atelectasis Restrictive process, e.g, effusion/bronchospasm 2. Intrapulmonary shunt Severe RDS Pulmonary AVM PA-to-PV collateral vessel(s)

Slide17:

↓ Pulmonary blood flow Anatomic RV outflow obstruction Anatomic pulmonary artery stenosis Increased PVR Atrial level right-to-left shunt Ventricular level right-to-left shunt ↓ Oxygen content Low mixed venous oxygen level Increased O 2 extraction: hypermetabolic state Decreased O 2 delivery: low cardiac output state 2. Anemia

Goals of surgery…:

Goals of surgery… Total correction - This results in the heart being anatomically normal in the sequence of blood flow. Partial correction Palliative surgery – which does not correct the problem, but rather minimizes the problems that result from any given disorder.

Slide19:

Timing of Intervention Predicted Natural History Predicted Procedural Outcome Exact anatomy Immediate & long term Hemodynamic effects results of the procedure Clinical variables in a given patient Natural history information

Precise Anatomic Diagnosis:

Precise Anatomic Diagnosis Small & apparently trivial variations are common Sub-aortic VSD requires closure to prevent aortic valve prolapse Small muscular VSD – spontaneous closure

Hemodynamic assessment:

Hemodynamic assessment Shunt quantification Determination of PVR in L-> R shunts Assessment of severity of obstructive lesions (valve stenosis / outflow obstruction) Assessment of severity of regurgitation Evaluation of ventricular function In VSD – Echo – defect size, flow direction across defect, predicted PA pressure, LV & LA enlargement, Qp/ Qs estimation

Clinical evaluation:

Clinical evaluation Nutrition Prematurity Respiratory infections Associated conditions involving other organ systems Chromosomal & genetic associations e.g. lethal aberrations. (trisomy 13, 18)

Common Adverse Consequences of CHD:

Common Adverse Consequences of CHD Duct dependent systemic blood flow in newborns: HLHS Systemic hypo perfusion Critical CoA & death with defect Interrupted Aortic Arch closure Critical AS Duct dependent pulmonary blood flow in newborns: PA + IVS Fetal hypoxia & death PA with closure of Critical PS ductus. Severe Ebstein’s anomaly

Slide24:

Conditions with PBF L  R shunts CHF TGA + PTA/ VSD/ DORV Freq . LRTI Single ventricle Growth retardation TA without obstruction PVOD Aortic R – VSD Mitral R – ASD Conditions with PBF & R->L shunts TOF cyanotic spells, cerebral VSD + PS abscess, polycythemia

Slide25:

Obstructive lesions AS CHF PS Sudden Death Supra- valvar AS Dysrhythmias Infundibular Stenosis CoA PPS

Spontaneous Closure of Defects :

Spontaneous Closure of Defects 1. Age at evaluation PDA – 2-4 wks VSD / ASD – 3 yrs 2. Size of defects ASD > 8 mm – unlikely to close Large NR VSD 3. Location of defect Fossa ovalis ASD – tendency to close Sub pulmonic VSD – AR as outcome

Atrial Septal Defect :

Atrial Septal Defect Spontaneous closure  Rare if defect > 8 mm at birth. ASD primum – deficit in inferior portion of the atrial septum ( endocardial cushion) ; with cleft in ant. Leaflet of MV. ASD secundum- most common , deficit in septum primum Sinus venosus defects – near junction of RA & SVC / IVC; freq. association with PAPVR. L->R shunt occurs at atrial level  Low pressure volume load to RV  PBF. ( late )

Slide28:

Later , LV  less compliant & LA pressures increase  L-R shunt and volume load increases  symptoms of CHF Rarely , long standing PBF  PVOD. Associated lesions – PAPVC, LVIO, AP window Treatment: Defect closure directly with sutures / synthetic patch. Associated with RV volume overload. Device closure – central ASD. 4. Timing of surgery : Asymptomatic – 2-4 Yr. Sinus venosus defect – 4-5 Yrs. Symtomatic – (8-10%) – CHF or Severe PAH  Early closure.

Atrial Septal Defect Repair:

Atrial Septal Defect Repair

ASD and PAPVR:

ASD and PAPVR A hole of variable size in the atrial septum and is most common cardiac malformation with various location of defect, fossa ovalis, posterior, ostium, primum, coronary sinus, subcaval (sinus venosus) Uncomplicated ASD or of PAPVC with RV volume overload (Qp/Qs>1.5 or 2.0) : an indication Scimitar syndrome Isolated PAPVC Optimal age : under 5 years but recently 1-2 years to avoid RV volume overload

Cont…:

Cont… If late presentation, timing of Surgery depends on RV volume load & PVR  Elective closure. Associated PAPVR  more extensive patch. MR  ASD primum repair Near normal CV function & reserve post surgery Arrhythmias are rare. If persistent symptoms of CHF  Residual PAPVC  L-R shunt.

VSD:

VSD Magnitude of PBF – size of VSD & PVR Non restrictive defect – High LV flows & pressures – transmitted to PA  Surgery in < 2 yrs life Progressive PVR rise  Established PVOD > Surgery in late cases If PVR > SVR R- L shunt through VSD  progressive hypoxemia (Eisenmenger syndrome)  Closing VSD – Acute RHF & increase in PVR. Size of defect : Large - Diameter of defect = Aortic orifice Systemic RV systolic pressures Degree of shunt depends on PVR

Slide33:

2. Moderate – d of defect < AO RVP is ½ to 2/3 systemic Left – Rt shunt > 2:1 3. Small – D of defect < 1/3 of AO RVP – N L -> R shunt < 2:1 Location – Type l – Sub Arterial Type ll – Perimembranous Type lll – Inlet Type lV - Muscular

Timing Of Closure…:

Timing Of Closure… Large VSD + CHF  As early as possible Large VSD + Severe PAH  3 -6 Mths Moderate VSD + PASP 50-66% Systemic Pressure  Bet. 1-2 yrs, Early if LRTI / FTT Small VSD + N PAP + L R shunt 1.5:1  Elective closure at 2-4 yrs Small outlet VSD (< 3mm) without AV prolapse  Yearly follow up for AV prolapse Small outlet VSD with AVP without AR  2-3 yrs

Slide35:

Small outlet VSD with AVP with any degree of AR  surgery when AR detected Small membranous VSD with AVP with mild degree of AR  1-2 yr follow up to detect increase in AR Small peri-membranous VSD with aortic cusp prolapse with >mild degree of AR  surgery when AR detected Small VSD with 1/ >1 e/o IE  Early closure

Surgical Approach & Post. Op. complications:

Surgical Approach & Post. Op. complications Membranous defect – Rt atriotomy & TV Lesions in inferior apical muscular septum / those high in ventricular outflow tract  left / rt. Ventriculotomy. Post op. ventricular function is impaired. Post op. excess TLW + CHF  Prolonged MV Limited tolerance for Anaesthesia / maneuvers that increase PBF. If rise in PVR pre-op., increase in RV afterload caused by closure of VSD  poorly tolerated. Inotropic support + measures to reduce PVR.

Slide37:

Septal patch device closure – LVOT obst. AR – prolapse of one of aortic valve cusps  sub- aortic / sub – pulmonic VSD Heart block  > Patch closure Late closure – Vent dysfunction & PHTN

Patent Ductus Arteriosus (PDA):

Patent Ductus Arteriosus (PDA) Size of PDA – Large PDA – Lt sided volume overload, CHF, Severe PAH. Moderate – lesser degree of Vol. overload, no/mild CHF, mod. PAH. Continuous murmur + Small PDA – no CHF/ PAH. Systolic murmur + Silent PDA – no murmur, No PAH. Diagnosed on 2 D echo.

Slide39:

Spontaneous closure – Small PDA – upto 3 mths Timing of closure : Large PDA + CHF + PAH  3 – 6 Mths Mod. PDA , no CHF  6 mth – 1 yr If CHF +, early closure considered Small PDA – 12 – 18 months Mode of closure – Individualized Surgical ligation - < 6 months Device closure / occlusion coil / ligation - > 6 mths Indomethacin not used – IVH, Renal dysfunction , hyperbilirubinemia, term infants. Transcatheter closure of small defects has become standard therapy

Ductus Dependent lesions:

Ductus Dependent lesions Pulmonary artery hypoplasia Pulmonary atresia Tricuspid atresia Transposition of the great arteries Aortic valve atresia Mitral valve atresia with hypoplastic left ventricle Severe coarctation of the aorta

AV canal defects:

AV canal defects Defect in Atrial + Ventricular septa + AV valvular tissue defect All 4 chambers communicate and share a single common AV valve PVR governs the degree of PBF NR VSD + LV  RA shunt  total left  right shunting

Normal Anatomy:

Normal Anatomy

Surgery for AVSD:

Surgery for AVSD Division of common AV valve & closure of ASD, VSD with a single patch Mitral /Tricuspid valve – suture approximation Post op – prolonged MV, MR, increased PVR  PH, residual VSD  CHF. Timing of Intervention : Complete AVSD + uncontrolled CCF  Early Sx Complete AVSD + controlled CCF  3 – 6 mo Partial AVSD , stable pt  2- 3 yrs of age

Coarctation of Aorta:

Coarctation of Aorta Timing of Intervention: CoA + LV dysfunction + CCF / HTN in UL  Immediate Intervention CoA + N LVF + no CCF + mild HTN  Intervention beyond 3 – 6 months CoA  1 – 2 yrs of age Intervention not required  if Doppler gradient across coarcted segment < 20 mm Hg with N LVF. Balloon dilatation  > 6 months age Surgery repair  < 6 months of age Balloon dilatation + Stent deployment  > 10 yrs

Repair of CoA :

Repair of CoA

Complications with repair of CoA:

Complications with repair of CoA Post Coarctectomy syndrome abdominal pain / distension  Mesenteric ischemia from reflex vasoconstriction after restoration of pulsatile aortic flow. RLN / Phrenic Nerve trauma  Vocal cord paralysis & hemidiaphragm paralysis Chylous effusion  disruption of lymphatic vessels or thoracic duct trauma Cather directed Balloon Angioplasty  native & residual CoA / recurrent CoA

Aortic Stenosis:

Aortic Stenosis For infants & older children Left vent dysfunction : Immediate intervention by Balloon dilatation irrespective of gradient Normal LVF – Balloon dilatation if Peak Gradient > 80 mm Hg Mean Gradient > 50 mm Hg ST – T wave changes in ECG Symptoms due to AS if Mean Gr < 5O mm Hg For Neonates : Balloon Dilatation if symptoms / LVD / left vent. Hypoplasia or Doppler Peak > 75 mm Hg

Pulmonary Stenosis:

Pulmonary Stenosis A form of RV outflow obstruction in which stenosis is usually valvar or both valvar & infundibular or only infundibular Critical PS in neonate : Percutaneous balloon valvotomy Valvotomy with CPB Transannular RVOT patch widening Valvotomy with inflow occlusion technique PS in infants and children : indicated with Sx & Pr gradient over 50mmHg Surgical treatment is not indicated with mild stenosis

PA with Intact Ventricular septum:

PA with Intact Ventricular septum A cardiac anomaly in which the pulmonary valve is atretic, coexisting with variable degree of right ventricle and tricuspid valve hypoplasia Indication of operation Size of the TV : Z-value of the tricuspid valve < -4 --- Systemic-pulmonary artery shunt -2~-4 --- RVOT patch + shunt > -2 --- RVOT patch Evaluation after 6-12 mo after initial procedure : Two ventricle repair One and half ventricle repair Fontan procedure

Minimal Invasive Surgery (“Touch-Free” Surgery for Congenital Heart Defects :

Minimal Invasive Surgery ( “Touch-Free” Surgery for Congenital Heart Defects Robotic and videoscopic techniques are complementing refined surgical procedures, enabling surgeons to repair CHD using a minimally invasive approach. At California Pacific, the term minimally invasive congenital heart surgery describes a surgical philosophy in which the heart is repaired through limited surgical incisions and robotics. With small incisions - only allow room for sterilized instrumentation, the surgeon’s hands& fingers rarely touch one’s tissue. As a result, patients have a reduced incidence of infection, a shorter hospital stay & better cosmetic results.

Neonatal Diseases for Repair (MIS) :

Neonatal Diseases for Repair (MIS) Tetralogy of Fallot Atrioventricular septal defects Arterial switch procedure Neonatal Ross procedure Single ventricle palliation including the Modified Norwood procedure

MINIMALLY INVASIVE SURGERY :

MINIMALLY INVASIVE SURGERY

A Comparison:

A Comparison

Key points…….:

Key points……. The post-operative length of stay using robotic applications in pediatric cardiac surgery is 2 days for the majority of patients. 4 – 6 hour procedure Providing better visualization in the surgical field Significantly lowering infection rates.

Cardiopulmonary Bypass ( CPB):

Cardiopulmonary Bypass ( CPB) Cardiopulmonary bypass is generally used to describe the techniques by which some of the functions of the heart and lungs are temporarily replaced with a mechanical system in order to support the remaining organ systems of the patient during surgical interventions on the cardiovascular and/or pulmonary subsystems. Consists of – Pump device to deliver blood Oxygenator A heat exchanger

CPB:

CPB

Principles and Mechanics of CPB:

Principles and Mechanics of CPB The primary function of cardiopulmonary bypass is to circulate blood of appropriate composition to the body to maintain viability of the patient. O2 & CO2 content, pH, temperature, hematocrit, oncotic pressure, electrolyte and glucose composition, and the pharmacologic milieu. Circulation  Venous system – RA / VC  siphoning of blood from pt. to Reservoir – larger cannula used to prevent air entrainment in circuit  Oxygenator  Systemic arterial system (AA). Deep hypothermic circulatory arrest is used to achieve ideal operating conditions for complex intracardiac repairs, especially in infants.

Diagrammatic representation CPB:

Diagrammatic representation CPB

Cont….:

Cont…. Cardiopulmonary bypass usually is accompanied by hypothermia, which reduces metabolic rate by about 50% for every 10°C below 37°C. At 20°C oxygen consumption is approximately 20% of its value at 37°C. The ability to deliver pulsatile flow is particularly limited in neonates/infants because only small arterial cannula (10-12F) can be placed into the ascending aorta, and in general these cannula considerably dampen any pulsatile waveform. Safe circulatory arrest time may be as short as 35 to 40 minutes

Respiration:

Respiration The introduction of oxygen & the removal of carbon dioxide occurs in the oxygenator portion of the CPB apparatus. This gas exchange must occur across an interface between the gas(es) introduced into the oxygenator & the plasma and erythrocytes that are in the oxygenator at that moment. pH stat and alpha stat  to maintain optimum pH, PaO2 & Pa CO2

Slide61:

Alpha stat  With the alpha-stat strategy, P co 2 is reduced, and consequently pH rises during hypothermia. pH-stat approach  P co 2 and pH are maintained such that the values are 40 torr and 7.40, respectively, at the given temperature. These values are the “corrected” values that account for the patient's temperature. The important effect of CO 2 on cerebral blood flow and thus on cerebral protection is a particularly important consideration in the choice of pH management strategy.

Temperature:

Temperature Hypothermia has protective effects other than the reduction in metabolic rate. If the central nervous system has a safe ischemic period of 5 minutes at normothermia, then a five fold reduction in metabolic demand would only be expected to increase the “safe” interval of ischemia to 25 minutes. Clinically, it seems that total circulatory arrest times of up to 45 to 60 minutes are well tolerated neurologically in pts. ( Protective effects) Cooling on bypass is carried out for at least 15 minutes, & the tympanic and rectal temperatures are brought to < 20°C. Ice is placed around the head, and the cooling blanket remains cold during the period of circulatory arrest.

Hematocrit & oncotic pressure:

Hematocrit & oncotic pressure Hypothermia  the viscosity of blood increases, which contributes to a rise in the resistance to blood flow, particularly in the microcirculation. When this factor is added to the nonpulsatile nature of bypass flow, significant underperfusion of the microcirculation  tissue ischemia . A second advantage to hemodilution is the reduction in usage of blood products to “prime” the cardiopulmonary bypass circuit with its attendant reduction in transfusion risk .

Electrolyte & glucose concentrations:

Electrolyte & glucose concentrations Glucose concentrations during bypass have frequently been raised using glucose-containing priming solutions with the goal of inducing an osmotic diuresis during bypass thereby To minimize the risk of renal failure in the postbypass period Evidence -- elevated glucose levels may have a deleterious effect on CNS tissue due to ischemia. A calcium-free crystalloid priming solution, not supplemented with calcium. Ionized calcium concentrations are generally about 0.3 mM/L during the preischemic phase & are not raised to normocalcemic levels until midway through the postischemic rewarming period near the end of bypass .

Pharmacology:

Pharmacology Bypass elicits an inflammatory response from the contact of the blood and plasma with the nonendothelial surfaces of the pump oxygenator, which involves the kallikrein-bradykinin system & complement activation. C3a is released in the early phases of bypass and is continually produced throughout the duration of bypass The multiple antiinflammatory effects of corticosteroids, including the reduction of complement activation during bypass, rational justification for the use of steroids prior to bypass. Mannitol, which originally was used to induce an osmotic diuresis, has now been shown to be a free radical scavenger and therefore may have significant benefit in reducing free radical injury that occurs during reperfusion after a period of ischemia

Myocardial Protection:

Myocardial Protection The basic components of cardioplegic solutions seem to be potassium (to achieve diastolic arrest) and cold temperatures to reduce the metabolic demands of the heart during ischemia . Substrate modification, particularly by the addition of amino acids such as aspartate & glutamate. To maintain the perfusion pressures in the range from 20 to 30 mmHg during the early phases of reperfusion.

Thank You…………:

Thank You…………

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