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Published byAlfred Cross Modified over 9 years ago
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Peri-operative Management of Pulmonary Hypertension
DR SP MACHAWIRA University of Wits
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Introduction Pulmonary hypertension complicates 2% of patients undergoing congenital cardiac surgery(Adatia I et al 2009) In India 60% of post operative deaths due to PHT crises(Choudhary SK et al Ann Thorac Surg 1999) The functional and structural status of the pulmonary bed important Immediate post-operative period the most vulnerable time Pulmonary endothelium dysfunction the most important factor but pathophysiology incompletely understood
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Introduction The outcome of patients has improved due to better understanding of peri-operative management PHT is an independent risk factor in morbidity and mortality in patients undergoing congenital cardiac surgery Pulmonary hypertensive crisis is the extreme end and a feared complication associated with increased morbidity and mortality
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Hypertensive Pulmonary Crisis
Complicates 0.75% of congenital cardiac surgery and has a mortality of 20% Pathophysiology incompletely understood and complex Increased post operative vasoreactivity to sympathetic stimuli Vasospastic stimuli result in sudden increase of pulmonary artery pressure and resistance Right heart failure with TR Systemic hypotension and MI Increased airway resistance
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Management Complex and unpredictable Prevention is the best
Identifying patients at risk Pre-operative care Intra-operative care Post-operative care
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General Early surgery prevents the development of pulmonary vascular obstructive disease Sedation with fentanyl and paralysis first 24 hours Prevent acidosis: pH and not pCO2 increases pulmonary vascular resistance Correct hypothermia Maintain adequate oxygenation but avoid baro and volutrauma Correct polycythaemia to reduce PVR
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Patients At Risk Difficult to predict influenced by age, lesion & pre-existing endothelial cell dysfuction Usually affects patients with reactive pulmonary vascular beds Patients with pulmonary venous hypertension(TAPVC) have extremely reactive beds Extra-cardiac syndromes eg Trisomy 21, omphalocele
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Patients at risk PA arising from the aorta, Truncus arteriosus, AP window Single ventricle physiology with unrestricted pulmonary blood flow mPAP >25mmHg or 50-60% of systemic on coming off bypass with signs of low cardiac output Patients with residual lesions
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Pre-operative Care Severe CCF needs significant resuscitation
Intubation and ventilation may be necessary to correct metabolic derangements Control and treat sepsis Avoid hypotension at induction may cause cardiac ischaemia Need to maintain Qp:Qs at 1:1 to ensure adequate organ perfusion as pulmonary overcirculation implies systemic hypoperfusion Hypercapnia and low FiO2 increase PVR to ensure adequate systemic blood flow Research on pre-op iNO, sildenafil and endothelin inhibitors
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Intra-operative Strategies
Smaller tidal volumes once sternum open Cardiopulmonary bypass, hypothermia and circulatory arrest enhances pulmonary vaso-reactivity Complete repair where possible PFO may be a life saving procedure allowing for pop-off valve Use of PAP lines debatable increased risk of bleeding, overreacting to changes, considered mandatory in research on new drugs
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Effect of Bypass on Haemodynamicc
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Post-operative ICU care plays a critical role in the patient outcome
Anticipate and treat PHT crises aggressively Sedation with Fentanyl and paralysis in the first 24 hours especially when suctioning to avoid pain and anxiety Adequate oxygenation without barotrauma or hyperoxygenation Avoid hypercapnia however pH control more important pH> 7.4 or pH>7.5 when patient has had a crisis: HCO3 and hyperventilation may be necessary
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III. INOTROPIC SUPPORT IN THE PERI-OP PERIOD
Effect of pH and CO2 on PVR
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Post-operative Strategies
Use of inodilators eg milrinone, dobutamine, low dose adrenaline with nitroglycerin Specific pulmonary vasodilators iNO, prostacyclin, sildenafil Investigate surgical accuracy ie residual lesions ECMO RVAD
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Inhaled Nitric Oxide Nitric oxide produced by endothelial cell final pathway to vasodilation Accepted mode of treatment for post-operative pulmonary hypertension Easy to administer, minimal side effects and specific for pulmonary vascular bed Dose 2-80ppm, however no clinical benefits of doses>10-20ppm Rebound PHT wean slowly from 5ppm at 0.5ppm/2hours- prolongs ventilation Side effect methaemoglobinaemia(>5%) negligible
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iNO vs Placebo on PVRI
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Sildenafil Type 5 phosphodiesterase inhibitor
Can be used to assist with weaning off iNO hence earlier extubation At doses of mg/kg/6hourly can be used to prevent rebound PHT on weaning iNO Can be used in conjuction with iNO, and inhaled Illoprost in patients who are in refractory PHT May be useful in transition to chronic therapy
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Illoprost Prostacyclin analogue, inhibits thrombocyte aggregation and brings about vasodilation Can be inhaled or intravenous Inhaled has half life 30 minutes No toxic effects Effect comparable to iNO Can be used in PHT resistant iNO Can be used intermittently thus allows for weaning off from ventilation
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Other Strategies ECMO used much less often due to general improvement in peri-operative care RVAD Prophylactic therapy citrulline, sildenafil and endothelin receptor inhibitors Combination therapy in refractory cases
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