Pulmonary hypertension cao huyết áp

HAEMODYNAMIC DEFINITIONS SOURCES HAEMODYNAMIC DEFINITIONSPulmonary Arterial Hypertension PAH PCWP ≤ 15 mm Hg and Pulmonary vascular resistance > 3 Pulmonary hypertension due to left hear

PULMONARY HYPERTENSION

DR DANG QUY DUC ARRHYTHMIA DEPARTMENT CARDIOLOGY DEPARTMENT

CHORAY HOSPITAL

SOURCES

 ESC 2015 PH

 Simonneau G, Montani D, Celermajer DS, et al Haemodynamic

definitions and updated clinical classification of pulmonary hypertension Eur Respir J 2019; 53: 1801913

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

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

 2019 up to date Clinical features and diagnosis of pulmonary hypertension

of unclear etiology in adults

 2019 up to date Treatment of pulmonary hypertension in adults

 2019 up to date Prognosis of pulmonary hypertension in adults

BỆNH ÁN

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

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

BỆNH ÁN

TTPT MỔ LẤY THAI (12h20 ngày 28 tháng 5 năm 2019)

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

Rạch da, bóc tách phúc mạc đoạn dưới tử cung, rạch mổ ngang đoạn dưới tử cung

Bắt ra bằng đầu 1 bé TRAI, Apgar 6

Sổ nhau tự nhiên

Khâu tử cung, cầm máu Không dẫn lưu Đóng bụng Máu mất 200mL

 Đường huyết mao mạch: 41mg/dl

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

  chuyển Nội Tim Mạch điều trị

BỆNH ÁN

 Bệnh nhân tỉnh, tiếp xúc được

SpO2 : 65%

 Than mệt, khó thở, không ho, không sốt

 Chi ấm, niêm hồng, mạch rõ, tím đầu chi, ngón tay dùi trống

 Tim đều rõ, phổi trong, bụng mềm, phù nhẹ 2 chi dưới

BỆNH ÁN

 Siêu âm Doppler tim:

 Dãn buồng tim phải TAPSE = 12mm

 Chức năng co bóp trong giới hạn bình thường EF = 74% (pp Teicholz)

 Thông liên nhĩ lỗ thứ phát d = 23mm, shunt phải trái

 Tăng áp động mạch phổi nặng PAPs = 116mmHg

BỆNH ÁN

BỆNH ÁN

 Chẩn đoán tại 7b3: Thông 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

 Điều trị:

 Thở oxy mask 10l /p

 Herbesser 60mg 1/2 v (uống)

 Bosentan 125mg 1 v (uống)

M: 0 Monitor: nhịp rời rạc ĐHMM: 190 mg/dL

Tiến hành đặt Nội khí quản

Ấn tim ngoài lồng ngực Adrenalin 1mg 2A ™ Thở máy A/C FiO2 100%, f = 16, PS : 12, Vt 400mL PEEP : 5cmH20

HA: 0/0 M: 0 Monitor nhịp rời rạc

Adrenalin 1mg 2A x2 ™ Natri bicarbonate 4.2% 250mL 1 chai (TTM) XXX g/p

Mạch: 106 l/p HA: khó đo SpO2: 45%

Monitor: nhịp nhanh xoang

Noradrenalin 4mg 2A BTTĐ : 5 mL/h

M: 0 Monitor: nhịp rời rạc

Ấn tim ngoài lồng ngực Adrenalin 1%

2A x 15 ™ Natribicarbornate 4.2% 250mL 1 chai (TTM)

XX g/p

HA: 137/89mmHg M: 113l/p

Theo dõi sát sinh hiệu Đặt sonde tiểu lưu

Mạch: 0 HA: 0/0 Monitor: nhịp rời rạc ĐH: 102 mg/dL

Ấn tim ngoài lồng ngực Adrenalin 1mg 2Ax 10™

Natribicarbonate 4.2% 250mL 1 chai (TTM)

XX g/p Calcichlorua 0.5g 1 A (TMC))

Monitor: nhịp rời rạc

Adrenalin 1% 2A x15 ™ Adrenalin 10A + NaCl 0.9% TTM XX g/p

DEFINE

Hypertension (WSPH) (mPAP) ≥ 25 mm Hg

 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 (97.5th %)

 PH - mPAP > 20 mm Hg

Vascular Pressure in Systemic and

Pulmonary Circulations (mm Hg)

Pulmonary Circulation

Right Atrium Mean >6

Right Ventricle 25/2-5

Left Ventricle 120/5-10

Lung Body

PVR= 1.8

PH: The Importance of Hemodynamics

Pulmonary venous hypertension

PCWP ≤15 mm Hg PVR ≤3 Wood units

HAEMODYNAMIC DEFINITIONS

HAEMODYNAMIC DEFINITIONS

SOURCES HAEMODYNAMIC DEFINITIONS

Pulmonary Arterial Hypertension

(PAH)

(PCWP) ≤ 15 mm Hg and Pulmonary vascular resistance > 3

Pulmonary hypertension due to left

heart disease

(PCWP) > 15 mm Hg

Pulmonary hypertension due to lung

disease and/or hypoxia

(PCWP) ≤ 15 mm Hg and concomitant lung disease and/or hypoxia

Pulmonary hypertension due to

pulmonary artery obstructions

(PCWP) ≤ 15 mm Hg and

an entity causing pulmonary artery obstruction

Pulmonary hypertension with unclear

and/or multifactorial mechanisms

multifactorial mechanisms or unclear underlying pathophysiological mechanisms

HAEMODYNAMIC DEFINITIONS

Characteristics Clinical group Pre-capillary PH mPAP > 20mmHg

PAWP ≤ 15mmHg PVR ≥ 3WU

1-3-4-5

Isolated post-capillary

PH

mPAP > 20mmHg PAWP > 15mmHg PVR < 3WU

2-5

Combined pre- and

post-capillyry PH

mPAP > 20mmHg PAWP > 15mmHg PVR ≥ 3WU

2-5

Acute decompensated pulmonary hypertension

 Sudden worsening of clinical signs of right heart failure with subsequent systemic circulatory

insufficiency and multisystem organ failure

 In-hospital mortality: 14% to 100%

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

hypertension Circ Heart Fail 2011; 4: 692–699

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

hypertension Hypertens Res 2015; 38: 539–544

Gradual evolution towards

end-stage pulmonary

hypertension

Laurent Savale et al Eur Respir Rev 2017;26:170092

©2017 by European Respiratory Society

CLINICAL PRESENTATION

20% patients severe-serious symptoms : 2 years

 Dyspnea and fatigue

 Symptoms of right ventricular (RV) :

•Exertional chest pain

•Exertional syncope

•Weight gain from edema

•Anorexia and/or abdominal pain and swelling

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.

New York Heart Association functional classification

Class 1 No symptoms with ordinary physical activity

Class 2 Symptoms with ordinary activity Slight limitation of activity

Class 3 Symptoms with less than ordinary activity Marked limitation of activity

Class 4 Symptoms with any activity or even at rest

World Health Organization functional assessment classification

Class I Patients with PH but without resulting limitation of physical activity Ordinary

physical activity does not cause undue dyspnea or fatigue, chest pain, or near syncope

Class II Patients with PH resulting in slight limitation of physical activity They are

comfortable at rest Ordinary physical activity causes undue dyspnea or fatigue, chest pain, or near syncope

Class III Patients with PH resulting in marked limitation of physical activity They are

comfortable at rest Less than ordinary activity causes undue dyspnea or fatigue, chest pain, or near syncope

Class IV 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

-Wide splitting of the second heart sound

-A holosystolic murmur of tricuspid regurgitation, diastolic pulmonic systolic ejection murmur, diastolic pulmonic regurgitation murmur

 Hepatomegaly, a pulsatile or tender liver, peripheral edema, ascites, and pleural effusion, splenomegaly

Imaging

Chest x-ray:

Imaging

Chest CT scan:

Imaging

Chest CT scan:

Imaging

ECG

Imaging

Echocardiographic probability of pulmonary hypertension in symptomatic

patients with a suspicion of pulmonary hypertension

≤2.8 or not measurable No Low

≤2.8 or not measurable Yes

Intermediate 2.9 to 3.4 No

2.9 to 3.4 Yes

High

>3.4 Not required

Right ventricle/left ventricle

basal diameter ratio >1.0

Right ventricular outflow Doppler acceleration time <105 msec and/or midsystolic

notching

Inferior cava diameter >21 mm with decreased inspiratory collapse (<50% with a sniff or

<20% with quiet inspiration)

Flattening of the interventricular

septum (left ventricular

eccentricity index >1.1 in systole

and/or diastole)

Early diastolic pulmonary regurgitation velocity >2.2 m/sec

Right atrial area (end-systole)

>18 cm2

PA diameter >25 mm

Imaging

Imaging video

Risk assessment

pulmonary arterial hypertension

Diagnostic algorithm

Patients With Pulmonary Hypertension ???

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

DIAGNOSIS PH

Classification 5 groups PH

1 PAP

2 PH due to left heart disease

3 PH due to chronic lung disease and/or hypoxemia

4 PH due to pulmonary artery obstructions

5 PH due to multifactorial mechanisms

Risk assessment

pulmonary arterial hypertension

Oxygen

 1-4 l/min

 SpO2 > 90%

Anticoagulation

 MECHANISM: intrapulmonary vascular

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

 INDICATIONS: group 1 PAH

Digoxin

 COPD and biventricular failure

 Control AF

 Physiotherapist

 Psychologist

 Stable in 2 months/medical therapy

oral contraceptive )

 Avoid pregnant. Surgical (patient or partner) methods

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

 In elective surgery: epidural rather than general anaesthesia

Management acute decompensated PH

Laurent Savale et al Eur Respir Rev 2017;26:170092

PH SPECIFIC THERAPY

cause of the PH

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

Vasoreactivity test

inhaled iloprost :

systemic effects and is therefore better tolerated than the intravenous agents listed below

● 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)

● 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

Mechanism of PH1 target therapy

PH (group 1) therapy WHO functional class

Initial drug combination

PH (group 1) WHO functional class

THE LAST THERAPY

 atrial septostomy and placement of a Potts shunt via a transcatheter

 Severely high pulmonary vascular resistance (from obstructive

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

  cardiac output and  systemic oxygen: 27%

 refractory severe PAH and right heart failure, despite aggressive advanced therapy and maximal diuretic therapy

THE LAST THERAPY

 Bilateral lung or heart-lung transplantation

 3 year survival patients: 50%

Correction

congenital heart disease with shunts

Treatment

congenital heart disease with shunts

Eisenmenger syndrome

PREGNENCY

FDA category X

complications

BỆNH ÁN

 Nữ 28 tuổi

 Tiền căn: thông liên nhĩ shunt P→T-tăng

áp phổi nặng-hậu phẩu mổ lấy thai N2

đang điều trị Bosentan, Diltiazem

BỆNH ÁN

 Nữ 28 tuổi

 Tiền căn: thông liên nhĩ shunt

P→T-tăng áp phổi nặng-hậu

phẩu mổ lấy thai N2 đang điều

(non-→ HFrEF

CẢM ƠN

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