Pulmonary hypertension cao huyết áp

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SOURCES

<small>ESC 2015 PH </small>

<small>Simonneau G, Montani D, Celermajer DS, et al. Haemodynamic </small>

<small>definitions and updated clinical classification of pulmonary hypertension. Eur Respir J 2019; 53: 1801913. </small>

<small>Pulmonary Arterial Hypertension in 2019: From death sentence to chronic disease Trushil Shah, M.D. </small>

<small>Galiè N, McLaughlin VV, Rubin LJ, et al. An overview of the 6th World Symposium on Pulmonary Hypertension. Eur Respir J 2018. </small>

<small>2019 up to date Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults. </small>

<small>2019 up to date Treatment of pulmonary hypertension in adults. </small>

<small>2019 up to date Prognosis of pulmonary hypertension in adults </small>

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BỆNH ÁN

<small>Tiền căn: thông liên nhĩ 1 năm nay, đang điều trị với Bosentan, và Ditilazem. Bệnh sử: cách nhập viện Chợ Rẫy 1 ngày, bệnh nhân nhập viện sản Từ Dũ với chẩn đoán : con so, thai 29 tuần 2 ngày, thai chậm tăng trưởng, thiểu ối – Thông liên nhĩ, shunt 2 chiều, tăng áp động mạch phổi nặng được chỉ định mổ lấy thai ở bệnh viện Từ Dũ. </small>

<small>Sau mổ gây tê ngoài màng cứng, bệnh nhân cảm giác mệt và khó thở. Huyết áp 120/80mmHg, mạch: 114 lần/phút, nhịp thở: 30 lần/phút, SpO2: 62%, nhịp tim đều, phổi trong, bụng mềm, vết thương mổ khô, tử cung gò khá. Điều trị: Augbidil 1,2g – 3 lọ/ngày → bệnh viện Chợ Rẫy điều trị tiếp. </small>

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BỆNH ÁN

<small>TTPT MỔ LẤY THAI (12h20 ngày 28 tháng 5 năm 2019) </small>

<small>Phương pháp phẫu thuật: phẫu thuật ngang đoạn dưới tử cung lấy thai lần đầu Phương pháp vô cảm: gây tê màng cứng </small>

<small>Rạch da, bóc tách phúc mạc đoạn dưới tử cung, rạch mổ ngang đoạn dưới tử </small>

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<small>Đường huyết mao mạch: 41mg/dl </small>

<small>Xử trí: thở mask 10l/p, NaCl 0.9% 1 chai giữ vein, Glucose 20% 250 1 chai TTM XX g/p </small>

<small> chuyển Nội Tim Mạch điều trị </small>

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BỆNH ÁN

<small></small> Bệnh nhân tỉnh, tiếp xúc được

SpO2 : 65%

<small></small> Than mệt, khó thở, không ho, không sốt

<small></small> Chi ấm, niêm hồng, mạch rõ, tím đầu chi, ngón tay dùi trống

<small></small> Tim đều rõ, phổi trong, bụng mềm, phù nhẹ 2 chi dưới.

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BỆNH ÁN

<small></small> Siêu âm Doppler tim:

<small>Dãn buồng tim phải. TAPSE = 12mm. </small>

<small>Chức năng co bóp trong giới hạn bình thường EF = 74% (pp Teicholz). </small>

<small>Thơng liên nhĩ lỗ thứ phát d = 23mm, shunt phải trái. </small>

<small>Tăng áp động mạch phổi nặng PAPs = 116mmHg. </small>

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BỆNH ÁN

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BỆNH ÁN

<small>12:26 BUN : 30 mg/dL, creatinine: 1.58 mg/dL. eGFR: 43.76 mL/phút/1.73 m2 da. Na: 133 mmol/L, K 7.0 </small>

<small>mmol/L, Cl 104 mmol/L. </small>

<small>17:03 BUN : 29 mg/dL, creatinine: 1.55 mg/dL. eGFR: 44.78 mL/phút/1.73 m2 da. Na: 133 mmol/L, K 5.3 </small>

<small>mmol/L, Cl 105 mmol/L. </small>

<small>AST/ALT: 59/27 U/L. Troponin I: 0.697 ng/mL </small>

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BỆNH ÁN

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<small>Chẩn đốn tại 7b3: Thơng liên nhĩ shunt P – T (đã đảo shunt) – Suy thất Phải – Tăng áp động mạch phổi – Suy thận cấp – Hậu phẫu mổ bắt con so ngày 2 </small>

<small>Điều trị: </small>

<small>Thở oxy mask 10l /p </small>

<small>Herbesser 60mg 1/2 v (uống) Bosentan 125mg 1 v (uống) </small>

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<small>Theo dõi sát sinh hiệu Đặt sonde tiểu lưu </small>

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DEFINE

Hypertension (WSPH) (mPAP) ≥ 25 mm Hg.

<small></small> 2009, Kovacs et. al. performed a systematic review on right heart catheterization (RHC) data on 1187 individuals: normal mPAP 14 ― 3.3 mm Hg → mPAP rarely > 20 mm Hg (97.5^th %).

<small>PH - mPAP > 20 mm Hg. </small>

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Vascular Pressure in Systemic and

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PH: The Importance of Hemodynamics

<b><small> Pulmonary venous hypertension </small></b>

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HAEMODYNAMIC DEFINITIONS

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HAEMODYNAMIC DEFINITIONS

<b><small>SOURCES HAEMODYNAMIC DEFINITIONS</small></b>

<b><small>Pulmonary Arterial Hypertension (PAH) </small></b>

<small>(PCWP) ≤ 15 mm Hg and </small>

<small>Pulmonary vascular resistance > 3 </small>

<b><small>Pulmonary hypertension due to left heart disease </small></b>

<small>(PCWP) > 15 mm Hg </small>

<b><small>Pulmonary hypertension due to lung disease and/or hypoxia </small></b>

<small>(PCWP) ≤ 15 mm Hg and </small>

<small>concomitant lung disease and/or hypoxia </small>

<b><small>Pulmonary hypertension due to pulmonary artery obstructions </small></b>

<small>(PCWP) ≤ 15 mm Hg and </small>

<small>an entity causing pulmonary artery obstruction </small>

<b><small>Pulmonary hypertension with unclear and/or multifactorial mechanisms </small></b>

<small>multifactorial mechanisms or </small>

<small>unclear underlying pathophysiological mechanisms </small>

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Cause of death

<small></small> right heart failure with circulatory collapse and superimposed respiratory failure.

<small>6% survived > 90 days. </small>

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Acute decompensated pulmonary hypertension

<small></small> Sudden worsening of clinical signs of right heart failure with subsequent systemic circulatory

insufficiency and multisystem organ failure. <small></small> In-hospital mortality: 14% to 100%.

<i><small>1. Haddad F, Peterson T, Fuh E , et al. Characteristics and outcome after hospitalization for acute right heart failure in patients with pulmonary arterial </small></i>

<i><small>hypertension. Circ Heart Fail 2011; 4: 692–699. </small></i>

<i><small>2. Jiang R, Ai Z-S, Jiang X, et al. Intravenous fasudil improves in-hospital mortality of patients with right heart failure in severe pulmonary </small></i>

<i><small>hypertension. Hypertens Res 2015; 38: 539–544. </small></i>

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Gradual evolution towards end-stage pulmonary

hypertension.

<b><small>Laurent Savale et al. Eur Respir Rev 2017;26:170092 </small></b>

<small>©2017 by European Respiratory Society </small>

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CLINICAL PRESENTATION

20% patients severe-serious symptoms : 2 years. <small></small> Dyspnea and fatigue.

<small></small> Symptoms of right ventricular (RV) : •Exertional chest pain.

•Exertional syncope.

•Weight gain from edema.

•Anorexia and/or abdominal pain and swelling

<small>Brown LM, Chen H, Halpern S, et al. Delay in recognition of pulmonary arterial hypertension: factors identified from the REVEAL Registry. Chest 2011; 140:19.</small>

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<b><small>New York Heart Association functional classification </small></b>

<b><small>Class 1 </small></b> <small>No symptoms with ordinary physical activity. </small>

<b><small>Class 2 </small></b> <small>Symptoms with ordinary activity. Slight limitation of activity. </small>

<b><small>Class 3 </small></b> <small>Symptoms with less than ordinary activity. Marked limitation of activity. </small>

<b><small>Class 4 </small></b> <small>Symptoms with any activity or even at rest. </small>

<b><small>World Health Organization functional assessment classification </small></b>

<b><small>Class I </small></b> <small>Patients with PH but without resulting limitation of physical activity. Ordinary </small>

<small>physical activity does not cause undue dyspnea or fatigue, chest pain, or near syncope. </small>

<b><small>Class II </small></b> <small>Patients with PH resulting in slight limitation of physical activity. They are </small>

<small>comfortable at rest. Ordinary physical activity causes undue dyspnea or fatigue, chest pain, or near syncope. </small>

<b><small>Class III </small></b> <small>Patients with PH resulting in marked limitation of physical activity. They are </small>

<small>comfortable at rest. Less than ordinary activity causes undue dyspnea or fatigue, chest pain, or near syncope. </small>

<b><small>Class IV </small></b> <small>Patients with PH with inability to carry out any physical activity without symptoms. These patients manifest signs of right-heart failure. Dyspnea and/or fatigue may even be present at rest. Discomfort is increased by any physical activity. </small>

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Signs on examination

<small></small> _{Jugular venous pressure (JVP) abnormalities.} <small>Right-sided auscultatory: </small>

<small>-A right-sided third or fourth heart sound (ie, a gallop) in association with a left parasternal heave or a downward </small>

<small>subxiphoid thrust. </small>

<small>-Wide splitting of the second heart sound. </small>

<small>-A holosystolic murmur of tricuspid regurgitation, </small>

<small>diastolic pulmonic systolic ejection murmur, diastolic pulmonic regurgitation murmur. </small>

<small>Hepatomegaly, a pulsatile or tender liver, peripheral edema, ascites, and pleural effusion, splenomegaly </small>

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Imaging

Chest x-ray:

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Imaging

Chest CT scan:

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Imaging

Chest CT scan:

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Imaging

ECG

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Imaging

<b><small>Echocardiographic probability of pulmonary hypertension in symptomatic patients with a suspicion of pulmonary hypertension </small></b>

<small>≤2.8 or not measurable No Low ≤2.8 or not measurable Yes </small>

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Imaging

<b><small>Echocardiographic signs suggesting pulmonary hypertension used to assess the probability of pulmonary hypertension in addition to tricuspid regurgitation velocity measurement in Table A </small></b>

<b><small>A: The ventricles¶B: Pulmonary artery¶C: Inferior vena cava and right atrium¶</small></b>

<small>Right ventricle/left ventricle basal diameter ratio >1.0 </small>

<small>Right ventricular outflow </small>

<small>Doppler acceleration time <105 msec and/or midsystolic </small>

<small>notching </small>

<small>Inferior cava diameter >21 mm with decreased inspiratory collapse (<50% with a sniff or <20% with quiet inspiration) </small>

<small>Flattening of the interventricular septum (left ventricular </small>

<small>eccentricity index >1.1 in systole </small>

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Imaging

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Imaging video

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Risk assessment

pulmonary arterial hypertension

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Diagnostic algorithm

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DIAGNOSIS PH

Conclusions: DE estimates of PASP are inaccurate in patients with PH and should not be relied on to make the

diagnosis of PH or to follow the efficacy of therapy. CHEST 2011; 139(5):988–993

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DIAGNOSIS PH

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Classification 5 groups PH

<b><small>1 </small></b> <small>PAP </small>

<b><small>2 </small></b> <small>PH due to left heart disease </small>

<b><small>3 </small></b> <small>PH due to chronic lung disease and/or hypoxemia </small>

<b><small>4 </small></b> <small>PH due to pulmonary artery obstructions </small>

<b><small>5 </small></b> <small>PH due to multifactorial mechanisms </small>

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Risk assessment

pulmonary arterial hypertension

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<small></small> The use of angiotensin-converting enzyme inhibitors, angiotensin-2 receptor antagonists, beta-blockers and ivabradine <b>is not recommended </b>in patients with PAH.

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Oxygen

<small></small> 1-4 l/min.

<small></small> SpO2 > 90%.

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Anticoagulation

<small></small> MECHANISM: intrapulmonary vascular

thrombosis and venous thromboembolism and early studies that suggested a mortality benefit.

<small></small> INDICATIONS: group 1 PAH

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Digoxin

<small></small> COPD and biventricular failure. <small></small> Control AF.

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<small>oral contraceptive). </small>

<small></small> <b><small>Avoid pregnant.</small></b><small> Surgical (patient or partner) methods. </small>

<small>Travel: WHO-FC III and IV and those with arterial blood O2 < 60mmHg with supplemental O2. </small>

<small>In elective surgery: epidural rather than general anaesthesia. </small>

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Management

acute decompensated PH.

<b><small>Laurent Savale et al. Eur Respir Rev 2017;26:170092 </small></b>

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PH SPECIFIC THERAPY

cause of the PH.

IV despite treatment of the underlying cause → PH-specific therapy centers.

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PH1 SPECIFIC THERAPY

<small>Nifedipine LA Oral </small>

<small>30 mg per day. Increase to the maximum tolerated dose over days to weeks. </small>

<small>Diltiazem </small>

<small>extended-release </small>

<small>Oral </small>

<small>120 mg per day. Increase to the maximum tolerated dose over days to weeks. </small>

<small>Amlodipine Oral </small>

<small>2.5 mg per day. Increase to the maximum tolerated dose over days to weeks. </small>

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Vasoreactivity test

<small>inhaled iloprost : </small>

<small>systemic effects and is therefore better tolerated than the intravenous agents listed below. </small>

<small>●Epoprostenol 1 to 2 ng/kg per min and increased by 2 ng/kg per min every 5 to 10 minutes until a clinically significant fall in blood pressure, an increase in heart rate, or adverse symptoms (eg, nausea, vomiting, headache). </small>

<small>●Adenosine 50 mcg/kg per min and increased every two minutes until uncomfortable symptoms develop or a maximal dose of 200 to 350 mcg/kg per min is reached. </small>

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Mechanism of PH1 target therapy

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PH (group 1) therapy WHO functional class

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Initial drug combination

PH (group 1) WHO functional class

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THE LAST THERAPY

<small>atrial septostomy and placement of a Potts shunt via a transcatheter. </small>

<small>Severely high pulmonary vascular resistance (from obstructive </small>

<small>shock)→ reduction in left ventricular preload, systemic pressure→ elevating systemic blood flow and maintaining tissue perfusion, albeit with less oxygenated blood. </small>

<small> cardiac output and  systemic oxygen: 27%. </small>

<small>refractory severe PAH and right heart failure, despite aggressive advanced therapy and maximal diuretic therapy. </small>

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THE LAST THERAPY

<small></small> Bilateral lung or heart-lung transplantation <small></small> 3 year survival patients: 50%

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Correction

congenital heart disease with shunts

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Treatment

congenital heart disease with shunts

<small>Eisenmenger syndrome. </small>

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PREGNENCY

<b>FDA category X</b>.

complications.

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BỆNH ÁN

<small>Nữ 28 tuổi </small>

<small>Tiền căn: thông liên nhĩ shunt P→T-tăng áp phổi nặng-hậu phẩu mổ lấy thai N2 đang điều trị Bosentan, Diltiazem. </small>

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BỆNH ÁN

<small>Nữ 28 tuổi </small>

<small>Tiền căn: thông liên nhĩ shunt P→T-tăng áp phổi nặng-hậu phẩu mổ lấy thai N2 đang điều </small>

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<b>CẢM ƠN </b>

<b>SỰ LẮNG NGHE QUÝ ĐỒNG NGHIỆP </b>

</div>