dr sp machawira university of wits. pulmonary hypertension complicates 2% of patients undergoing...
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DR SP MACHAWIRAUniversity of Wits
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
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
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
Complex and unpredictable Prevention is the best Identifying patients at risk Pre-operative care Intra-operative care Post-operative care
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
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
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
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
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
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
Effect of pH and CO2 on PVR
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
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
Type 5 phosphodiesterase inhibitor Can be used to assist with weaning off iNO
hence earlier extubation At doses of 0.3-0.5mg/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
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
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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