Pulmonary Hypertension ICU Therapies
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With increasing survival comes morbidity. Pulmonary hypertension in the critical care population represents a secondary disease of myriad pathologies for children and adults. Whilst often cardiac failure or respiratory disease complicated by pulmonary hypertension, the exact aetiology of secondary pulmonary hypertension can be a diagnostic challenge. Yet an understanding of the pathophysiological basis for pulmonary hypertension may allow for patient guided therapy and predictions of reversibility. With pulmonary vasodilators of various mechanistic and non-specific sites of action backed by limited disease specific clinical evidence, are we in the jungle treating secondary pulmonary hypertension or can one management regime encompass all critical care patients?
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Pulmonary Hypertension ICU Therapies
- 1. Bennett Sheridan Paediatric Cardiac Intensivist Pulmonary hypertension and ICU therapies
- 3. Pulmonary arterial hypertension PAPm > 25mmHg at rest PVR > 3 WU LVEDP < 15mmHg
- 4. Gold standard PVR = PAPm - PCW CO
- 5. Non invasive assessment TR PR Mean Diast 2* TR Aduen JF, et al. J Am Soc Echocardiogr. 2009: 22; 814-819 RVSP = TR peak gradient + RAP Mean PA pressure = PR peak gradient + RAP = Mean systolic RV-RA gradient + RAP
- 6. WHO Classification of PH
- 7. Children: Not just small adults
- 12. Management principals N Engl J Med 2004; 351:1425-1436
- 19. Effects of sildenafil on prognosis in patients with pulmonary hypertension after lef Heart Lung Circ. 2014 Jul;23(7):680-5. Specific insights
Hinweis der Redaktion
- I would like to thank the meeting organisers for the invitation to speak about paediatric Ventricular Assist Devices, a therapy for end stage heart failure which has become one of my passions as a cardiac intensivist. Pulmonary hypertension and ICU therapies
- My only disclosure is that I am a paediatric intensivist No conflict of interest Jean Louis spoke yesterday about the challenge of speaking after Prof Pinsky…. let’s just say I know how you feel
- Intensivists know about pulmonary hypertension. But I would like to start with my basic assumptions: Diagnosis of PH is simply defined by a PAPm >25 mm Hg at rest. Specific diagnosis of PAH requires LVEDP < 15 mm Hg. Some guidelines include PVR >3 WU in the haemodynamic definition BUT Notable that specific PH populations can have elevated PAP yet normal PVR - examples from the paediatric population include patients with elevated LVEDP or high pulmonary blood flow lesions LVEDP > 15 mm Hg used to define pre-capillary PH, although patients HF-PEF remain a diagnostic challenge in this group
- Gold standard for diagnosis is invasive haemodynamics including pressure in RA / RV / PA / Wedge + CO and MVO2 - PVR can be inferred from TPG / CO ECHO and Angiography is required to exclude anatomic lesions of the right and left heart Bedside haemodynamics including all gold standard variables are available using a Swann Ganz catheter: KEY - although the Swann of death is infrequently used in paediatric units
- Many ECHO methods to estimate mPAP - be really careful to understand what you Cardiologist is telling you What we really need is mean PAP when assessing PH All measurement require the addition of RAP - which we usually have for intensive care patients RVSP is usually quoted - but this is a reflection of PA systolic pressure and RV hypertension does not equal abnormal PVR especially if there is any level of pulmonary obstruction Mean PAP is traditionally estimated by PI envelope derived from Peak gradient A method I have recently adopted is Mean systolic RV-RA gradient (Stroke Distance), which seems an accurate estimation
- Classification as defined by WHO at the World symposium of PH Major categories include PAH and PH secondary to lung disease, which is logically considered pre capillary (LVED normal) PH secondary to left heart disease usually occurs with an elevated LVEDP and normal PVR - although some patients in the left heart obstruction group develop a mixed picture with elevated PVR Interestingly…. CHD may be categorised in either group 1 and group 2 depending upon aetiology
- Whilst most intensive care patients with pulmonary hypertension have disease secondary to heart or lung pathology There are some important differences between adults and children Children with PH are more likely to be responsive on acute vasodilator testing and perhaps due to this increased vascular reactivity Children are prone to severe pulmonary hypertensive crises in response to triggering events such as hypoxia
- There are many diagnostic algorithms available for pulmonary hypertension, mostly unnecessarily complicated. In essence: ECHO is the best screening test and if PH is severe enough to cause symptoms, the ECHO will be abnormal Evidence of PH on ECHO = look hard for any cardiac and respiratory cause and treat underlying disease - I understand in adult population it is common to have 3 co-morbidities which may be contributory VQ or CT scan is essential to excluded chronic pulmonary embolism Invasive haemodynamics and angiography are required to establish a diagnosis of PAH, although we generally rely on non-invasive assessment in children due to the inherent anaesthetic risk with diagnostic catheterisation
- Management of PH can be considered in terms of acute and ongoing therapies. Acute management includes modification of factors which may act to raise PVR and the use of pulmonary vasodilators, usually inhaled therapy. - oxygen is a widely available pulmonary vasodilator…. although arterial oxygen tension is the main determinate of PVR - Intensivists who work with single ventricle patients understand the potency of inspired oxygen as a pulmonary vasodilator, we have been know to do outrageous things like adding nitrogen to the inspired gas mix to achieve an Fi02 of 18%
- Nitric oxide is an inhaled therapy which will acutely reduce PVR, albeit offering no survival benefit in patients with ARDS. The potential benefits of nitric oxide include mild bronchodilatation, improved VQ matching, decreased intrapulmonary shunt and decreased RV after load - all of which generally result in increased cardiac output and improved oxygenation
- Pulmonary hypertensive crises are provoked by hypoxemia, anxiety, hypercapnia, acidemia, hypothermia, vasoconstriction and elevated sympathetic tone. When I manage these patients in cardiac ICU - pay careful attention to the basics…. normal acid base / normal pCO2 / well oxygenated with just enough PEEP to prevent collapse / normal temperature / adequate analgesia and sedation and I extubate them relatively deep then manage the airway The role of paralysis in patients with ARDS was discussed in a previous session, I wish to highlight the importance of avoiding histamine releasing muscle relaxants such as atracurium in PH patients and that Ketamine does increase PVR in those who are not catecholamine depleted.
- Pharmocological therapies for PH fall into 3 mechanistic groups - and it is postulated that combination therapies using agents from each pathway are additive therapies. ERA’s, PDEi type 3 and 5 and prostacyclin derivatives all act by causing smooth muscle relaxation - or vasodilation along with the potentially disease modifying action with blockade of smooth muscle proliferation.
- For PAH - CCB first for those responsive to pulmonary vasodilator challenge - there is often not a sustain response but I know a few patients well managed for years on CCB as a single agent High risk patients are those with evidence of RV failure and rapid progression of symptoms to a high degree of functional impairment - these patients require an intravenous prostacyclin derivative although an oral prostacyclin agent is now in phase 3 trials. Lower risk patients are usually managed with an ERA or PDE5 inhibitor, often used in combination. Pulmonary vasoreactivity testing for identification of calcium channel blocker “responders” is recommended only for patients with IPAH. In all other forms of PH, pulmonary vasoreactivity testing is not recommended because “responders” are exceedingly rare among these patients
- Therapies for PAH do not translate directly to patients with PH secondary to cardiac and respiratory disease. Expert opinion sees patients managed with oxygen and diuretics when there is RHF. CCB have moderate evidence in those who are responders ERA and PDE inhibitors have good evidence in patients with PH secondary to cardiac and respiratory disease. In practice - the severe patients receive a combination of 3 therapies. IV Prostacycline / ERA / PDE inhibitor But there are some exceptions….
- Combination therapy in PH is controversial because there is much conflicting data from RCT’s As with most things in medicine…. you can find a trial to back your own opinion. I make note of the guanylate cyclase stimulators acting on the nitric oxide pathway, an agent I have no experience with in children, which has positive trial data in combination with both ERA’s and Prostacycline but not with PDE inhibitors.
- One thing that is clear for group 2 patients with end stage heart failure - if you can successfully treat the heart failure then PH will resolve. And the ultimate therapy for end stage heart failure is LVAD. PH resolved within 6 months of LVAD initiation, with ongoing PH therapy. And these patients become much lower risk transplant recipients once the PH has resolved.
- Others will speak about MCS for the right heart. My favourite topic. RVAD in an ECMO configuration for 6 weeks in an infant with lung disease and severe PH. Successful bridge to recovery.
- I would like to offer some specific insights. Rebound pulmonary hypertension is common once inhaled nitric oxide is ceased. In a small study published from my unit…. we demonstrated that premeditation with oral Sildenafil dramatically reduced pulmonary artery pressure as nitric oxide was weaned resulting in a reduced duration of mechanical ventilation In my practice I always premeditate with a single dose of enteral sildenafil prior to the cessation of inhaled nitric oxide
- Great caution is required if you are to use pulmonary vasodilators in patients with left heart obstructive lesions In a small blinded RCT - Sildenafil was demonstrated to be safe in patients with PH following left sided valve surgery. Duration of mechanical ventilation and ICU stay were actually reduced. On the other hand - a placebo controlled trial of Sildenafil in patients more than 1 year following successful left heart valve surgery with ongoing PH demonstrated no clinical benefit Confusion in PH therapy is common…. the best we can offer is patient specific therapy where each agent is introduced with careful non invasive assessment of treatment effect