7 cor pulmonale

Cor Pulmonale(Pulmonary Heart Disease)

Guo Yubiao, M.D & Ph.D

Pulmonary & Critical Care Medicine The first Affiliated Hospital of Sun-Yat Set University

Presentation Outline

Definition Epidemiology/Classification Clinical manifestations

Symptoms Signs

Diagnostic workup & Differential Diagnosis Diagnosis Differential Diagnosis

Treatment & Prevention Summary

Classification

Acute Cor Pulmonale Massive pulmonary embolism

Chronic Cor Pulmonale

Epidemiology

High prevalence(1992, 4.42‰) District difference Smoking Acute exacerbation

Definition of Chronic Cor Pulmonale

Hypertrophy and dilatation of the right ventricle Secondary to the pulmonary hypertension Caused by disease of the pulmonary parenchym

a, and/or chest wall, and/or pulmonary vascular system

With or without right heart failure Exclusion the causes of congenital heart

disease and left heart disease

Etiology

Pulmonary parenchyma disease COPD80%~90%,asthma,bronchiectasis,severe tuberculosis, idiopathic interstitial pneumonia,

sarcoidosis, eosinophilic granuloma,silicosis, etc.

Disorders of the neuromuscular apparatus and chest wall Poliomyelitis ,Guillain-Barré syndrome,

Kyphoscoliosis

Etiology

Pulmonary vascular disorders chronic pulmonary thromboembolism,

pulmonary arteriolitis, allergic granulomatosis, primary pulmonary hypertension

Others primary alveolar hypoventilation,

sleep apnea syndromes

Pathophysiology

The formation of pulmonary hypertension Functional factors of increase of vascular

resistance Anatomical factors of increase of vascular

resistance Increased blood volume and hyperviscosity

Cardiac disorders and heart failure Damage to other vital organs

Functional factors of increase of vascular resistance

Hypoxia is the most important factor for pulmonary hypertention.

Hypoxic pulmonary vasoconstriction Determined mostly by the ratio of vasoconstrictive

substances to vasodilative substances Leukotriene, 5-HT, Ang II, PAF,EDCF/ NO, PGI2 ,EDRF

Direct effect of hypoxia on the increase of the smooth muscular cell membrane permeability to Ca2+

Acidosis increases the sensitivity of vasoconstriction to hypoxia

Anatomical factors of increase of vascular resistance

Vasculitis Emphysema, increased intra-alveolar

pressure, compressed pulmonary capillaries

Reduction in pulmonary capillary bed Pulmonary vascular remodeling Multiple pulmonary micro-arteriole

thrombosis

Increased blood volume and hyperviscosity

Secondary polycythemia and hyperviscosity Water and sodium retention

Aldosterone Renal arteriole constriction

Cardiac disorders and heart failure

Right ventricular hypertrophy secondary to pulmonary hypertension.

Sustained pulmonary hypertension exceeds the compensation of right ventricle, and causes the increase of right ventricular end diastolic pressure, and dilation and failure of right ventricle.

A few may develop left heart failure.

Damages to other vital organs

Hypoxia and acidosis can also do damages to other vital organs, e.g. brain,liver,kidney,gastrointestine,

endocrine system.

Pulmonary diseases

Hypoxia, hypercapnia/acidosis

Pulmonary Destruction of capillary bed Blood volume ↑

vasoconstrition Blood viscosity ↑

Pulmonary hypertension

Right heart workload↑ Right ventricular hypertrophy

Right heart failure

Impaired Toxic effect from bacteria

Cardiac

myocardial function on myocardium arrythmia

Myocardial hypoxia Recurrent Electrolytic and

Accumulation of lactate pneumonia acid-base disturbance

Clinical manifestations Compensatory stage of the respiratory

and cardiac function De-compensatory stage of the

respiratory and cardiac function

Compensatory stage of the respiratory and cardiac function

Symptoms: cough, sputum, short of breath, dyspnea and palpitation on exertion, fatigue and decrease of exercise tolerance

more severe in acute exacerbation. A few with chest pain or hemoptysis.

Compensatory stage of the respiratory and cardiac function

Signs: cyanosis, signs of emphysema, moist rales and/or rhonchi,

distal heart sound, systolic murmur of tricuspid area, P2>A2 , subxiphoid visible/palpable cardiac impulse, distended jugular venous pulsation

De-compensatory stage of the respiratory and cardiac function

Respiratory failure Symtoms: severe dyspnea,especially at

night, headache, insomnia,inappetence,

somnolence, dizziness,confusion, even delirium.

Signs: congunctiva congestion and edema, retinal vasodilatation, optic papillary edema. weakness or disappear of deep reflexes, pathological reflexes, redness, sweaty

Right heart failure

Symptoms: predominant short of breath,palpitation, inappetence,nausea

Signs: cyanosis,tachycardia,arrhythmia,subxiphoid systolic murmur or even diastolic murmur. Tender hepatomegaly,Hepatojugular reflux, lower extremity edema, ascites

signs

Chest radiography Signs of pulmonary hypertension: Enlarged right descending pulmonary artery with

diameter ≥15mm The ratio of the diameter of right descending

pulmonary artery to trachea≥1.07 Bulge of pulmonary artery/with the height≥3mm dilation of the main pulmonary artery and its

branches with concurrent underperfusion of the peripheral branches

Signs of right ventricular enlargement Signs of underlying diseases and infection

Electrocardiography Right-axis deviation with a frontal plane axis

greater than +90° Marked clockwise rotation of the electrical axis Rv1+Sv5≥1.05mv P-pulmonale pattern Incomplete or rarely complete right bundle

branch block Low voltage QRS Occasional large Q wave or QS in V1,V2, even

V3,suggesting healed myocardial infarction

Electrocardiography of Chronic Cor Pulmonale

Echocardiography The right ventricular outflow ≥ 30 m m The right ventricular internal dimension ≥20mm Anterior RV wall thickness Ratio of left to right ventricular internal dimension <2 Increased right pulmonary artery or pulmonary artery

dimension (Peak systolic pulmonary artery pressure) Increased right atrium dimension

Arterial blood gas analysis

Hypoxemia and/or hypercapnia Respiratory failure: PaO2<60mmHg PaCO2>50mmHg

Serum assessment

Increased RBC count and Hemoglobin Increased blood and plasma viscosity Increased WBC count and neutrophilic

ratio when infection occurs Change of renal or hepatic function Electrolyte imbalance

Others

Pulmonary function test For early stage or non-exacerbation

stage patients Sputum culture

For guidance of antibiotics selection in patients with acute exacerbation stage

Diagnosis

History of COPD and pulmonary parenchymal or chest wall or pulmonary vascular disease,

Symptoms and signs of pulmonary hypertension and right heart dilation or failure,

combined with the signs of right heart hypertrophy and dilation by ECG, X-ray,UCG.

Differential Diagnosis Coronary atherosclerotic heart diseases

History of left heart failure, hypertension, hyperlipoidemia ； Symtoms of angina pectoris, myocardial infarction Left ventricular hypertrophy in P.E. and X-ray, myocardial isc

hemia in ECG Rheumatic heart diseases

History of rheumatic arthritis and myocarditis Usu. involving other cardiac valves Special signs in X-ray, ECG and UCG

Primary cardiomyopathy No history of chronic pulmonary diseases Enlargement of entire heart No signs of pulmonary hypertension in X-ray

Therapy

Stage of Acute exacerbation Control of infection Oxygen therapy Control of heart failure Control of cardiac arrythmia Anticoagulatory therapy Patient care

Control of infection

Antibiotics based on sputum culture Before the culture, based on infection

acquired location and sputum smear gram stain

CAP: G positive; HAP:G negative Penicillins,

aminoglycerides,quinolones and cephalosporins

Secondary fungal infection

Oxygen therapy

Clearance of respiratory tract Correction of hypoxia and

hypercapnia

Control of heart failure Different to heart failure caused by

other cardiac disease May be improved after control of

infection and normality of blood gas Diuretics Vasodilators Positive inotropic agents-digitalis

Diuretics Reduction of blood volume and right

heart load,elimination of edema Small dosage and short period Moderate

degree:HCT .antisterone;Severe cases: furosemide

Adverse effect: alkalosis with low K+&CL-

thickened sputum blood condensation

Vasodilators

Reduction of cardiac pre- and after- load and oxygen consumption, improve the myocardial contractibility.

Adverse effect: low blood pressure, tachycardia and hypoxemia and hypercapnia

Positive inotropic agents-digitalis

Low tolerance to digitalis due to chronic hypoxia and infection: arrhythmia

Correction of hypoxia and hypokalemia before use Low dosage, fast action and fast metabolite agents:

lanatoside C(cedilanid),strophanthin K Indications:

refractory edema after improvement of infection and respiratory function and no effect on diuretics

right heart failure without obvious infection acute left heart failure

Control of arrhythmia:usually self-limited

Anticoagulatory therapy:heparin or low molecular weight heparin

Intensive patient care:monitoring, airway secretion aspiration

Stage of non-exacerbation

Combined with Chinese medicine Long-term home oxygen therapy Pulmonary Rehabilitation Regulation of immune system Nutrition

Complications

Pulmonary encephalopathy Acid-base and electrolyte

disturbance Cardiac arrhythmia:af,aF,at Shock Gastrointestional haemorrhage Disseminated intravascular

coagulation

Prognosis

Recurrent acute exacerbation, progressing with gradually impairment of pulmonary function

Motality of 10%-15% Prolong lifespan and improve

quality of life

Prevention

Smoking cessation Treatment of the predisposing

factors respiratory tract infection, inhalation

of noxious gases, occupational protection, etc

Education

Thank You!