USCOM For Assessing Patients With COPD
USCOM For Assessing Patients With COPD
Objective

 The Ultrasonic Cardiac Output Monitor (USCOM) is a non-invasive, quantitative method for
 measuring and monitoring cardiovascular haemodynamic parameters in patients. The aims of this
 study are:

 1. To investigate whether there is any correlation between haemodynamic parameters and COPD
 severity.

 2. To investigate whether USCOM-derived haemodynamic variables may be used as prognostic
 indicators of 6-month, 1-year, 3-year and 5-year readmission.

 3. To investigate whether USCOM-derived haemodynamic variables may be used as prognostic
 indicators of 6-month, 1-year, 3-year and 5-year all-cause mortality.

 Design, Setting and Subjects This prospective observational study will be conducted in the
 Prince of Wales Hospital in Hong Kong.

 Interventions Haemodynamic measurements made using the USCOM, and spirometry, will be
 performed as appropriate on subjects in respiratory clinic, the emergency department, medical
 wards and on ICU. In order to assess inter-observer variability, a second, blinded operator
 will repeated 15% of scans.
Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the
 world, a lung disorder which is characterized by a partially reversible airflow limitation,
 which is usually progressive, and associated with an abnormal inflammatory response to
 noxious particles or gases. In 2005, among elderly Hong Kong Chinese (age ≥60 years) in Hong
 Kong with COPD defined as an FEV1/FVC <70%, 19.6% males and 11.9% females suffered from
 moderate levels of severity.

 From an initial stable condition, an acute exacerbation of COPD (AECOPD) is characterized by
 a sudden onset of breathlessness, purulent sputum, and increases in sputum volume. Other
 symptoms include increasing cough, wheeze, chest tightness or fatigue. The major cause of
 AECOPD is infection, although other stimulating factors include air pollution, withdrawal of
 medication, and low temperature. After the first admission of an exacerbation, the
 readmission rate for patients with AECOPD is high. The mean number of annual readmissions is
 2.2 episodes, with a one-year mortality rate of 14%.

 Spirometry can help to diagnose COPD patients, and a post-bronchodilator FEV1/FVC<0.7
 confirms the presence of airflow limitation. The classification of severity of airflow
 limitation in COPD is based on GOLD category. The lower the post-bronchodilator FEV1, the
 higher is the severity. This method is useful for assessing patients with stable COPD only.
 For those with AECOPD, this method may not be easy to conduct and assess patients immediately
 due to patients' difficulty in breathing.

 A common dilemma facing clinicians is whether patients presenting with breathlessness, cough
 and wheeze have an acute exacerbation of COPD, an acute exacerbation of left ventricular
 failure (LVF), or some degree of both. Making an accurate diagnosis is important as the
 treatment in each case is different, and a quick recovery depends upon appropriate and timely
 intervention and treatment.

 Unlike acute exacerbations of asthma, there are no objective guidelines on how to assess the
 severity and prognosis of patients presenting to hospital with acute exacerbations of COPD.
 However, the CURB65, originally intended for assessing patients with pneumonia, has been
 evaluated in this context. High CURB65 scores in patients presenting with acute exacerbations
 of COPD do predict increasing risk of hospital and one month mortality from 2 to 21% but do
 not predict patients with very high risk.

 In healthy subjects, the presence or absence of carbon dioxide retention influences the
 body's haemodynamic response. Hypercapnia has been shown to increase mean pulmonary artery
 pressure (PAP), pulmonary vascular resistance (PVR), heart rate (HR), stroke volume (SV),
 cardiac output (CO), and mean arterial BP (MAP). However, hypercapnia does not appear to
 affect indices of systolic function, such as peak aortic velocity and aortic mean and peak
 acceleration, or plasma renin, angiotensin II, and aldosterone activity.

 In stable patients with compensated COPD, elevations in CO2 trigger central and peripheral
 chemoreceptors resulting in an increased depth and rate of respiration, bradycardia (via
 vagal stimulation), and systemic vasoconstriction (via sympathetic stimulation). Therefore,
 cardiovascular parameters may be either normal or, if there is a degree of carbon dioxide
 retention resulting in catecholamine release and autonomic stimulation, then moderately
 hyperdynamic. Patients with COPD should have a cardiac Index (CI), which is elevated either
 towards the upper half or above the normal range, and may be as high as 5L/min/m2, an
 elevated SI, an elevated SVR and elevated DO2.

 The Smith-Madigan Index II (SMII) is a novel measure of inotropy, which in stable COPD
 patients should either be normal or, if there are adrenergic effects, then may be elevated to
 as much as 1.6. The effects of hypercapnia in patients with COPD on potential to kinetic
 energy ratio (PE/KE, PKR), flow time (FT), peak velocity (Vpk) and mean pressure gradient
 (Pmn) are unknown.

 These changes contrast with patients with acute LVF, where CI is low and the SMII is usually
 less than 1.0, and commonly around 0.7 - 0.8. PE/KE and SVR are generally much higher, and FT
 (as a function of SV) is longer. Vpk and Pmn are also lower in LVF.

 We have conducted a preliminary study to evaluate the correlation between severity of COPD
 and haemodynamic parameters. 86 stable COPD patients, 43 AECOPD patients and 36 healthy, age
 and gender matched subjects were recruited. It was found that the severity of COPD correlated
 positively with mean heart rate, cardiac index (CI), ejection time percentage (ET%) oxygen
 delivery index (DO2I) and inotropy. When compared with healthy controls, stable GOLD IV
 patients had a significantly higher CI (3.98 vs 3.15 l/min/m2, p<0.005), inotropy (2.14 vs
 1.72 W/m2, p<0.01) and DO2I (679.8 vs 530.7 ml/min/m2, p<0.01), and a significantly lower
 potential to kinetic energy ratio (PKR) (43.0 vs 56.6, p<0.05). Moreover, the 30-day
 readmission rate was the highest in GOPD IV patients. Based on the existing findings, it
 would be interesting to study the long-term prognostic effect of haemodynamic parameters in
 COPD patients.

 Aim

 The aims of the present study for patients visited respiratory clinic or admitted to the
 Emergency Department (ED), including those admitted to resuscitation room or emergency high
 dependency unit, are:

 1. To investigate whether there is any correlation between haemodynamic parameters and COPD
 severity.

 2. To investigate whether USCOM-derived haemodynamic variables may be used as prognostic
 indicators of 6-month, 1-year, 3-year and 5-year readmission.

 3. To investigate whether USCOM-derived haemodynamic variables may be used as prognostic
 indicators of 6-month, 1-year, 3-year and 5-year all-cause mortality.

 Measurements

 -  Haemodynamic measurements using an Ultrasonic Cardiac Output Monitor (USCOM®; USCOM Pty
 Ltd, NSW, Australia)

 -  Lung function assessment using Spirometry (MICROLAB 3300 spirometer; Micro Medical,
 Kent, UK)

 -  6-minute walk test

 -  Borg dyspnoea scale

 -  Blood pressure

 -  End-tidal CO2

 Definition of haemodynamic parameters:

 -  Velocity time integral (vti) is the integral of the flow profile, i.e. the distance the
 blood travels in one beat. The unit of vti is m/s.

 -  Cardiac output (CO) is the volume of blood pumped by the heart in one minute: CO = SV x
 HR. The unit is l/min.

 -  Cardiac index (CI) is equal to CO divided by BSA. The unit is l/min/m2.

 -  Stroke volume (SV) is the volume of blood ejected from the heart during one systolic
 stroke. SV = vti x πr2,where πr2 = flow cross sectional area. The unit of SV is ml.

 -  Stroke volume index (SVI) is SV divided by BSA and the unit is ml/m2.

 -  Stroke volume variation (SVV) is the percentage change in SV between a group of beats.
 SVV = (SVmax - SVmin x 100) / [(SVmax + SVmin)/2].

 -  Systemic vascular resistance (SVR) is the pressure against which the heart pumps. SVR =
 MAP/CO. The unit is d.s.cm-5.

 -  Systemic vascular resistance index (SVRI) SVRI = SVR x BSA d.s.cm-5m2.

 -  Oxygen delivery (DO2) is calculated by the equation: DO2 = 1.34 x Hb x SpO2/100 x CO,
 where Hb = hemoglobin in grams of hemoglobin per litre of blood (g/l); SpO2 = the
 peripheral oxygen saturation as a percentage (%). The unit of DO2 is ml/min.

 -  Oxygen delivery index (DO2I) is equal to DO2 divided by BSA. The unit of DO2I is
 ml/min/m2.

 -  Inotropy index refers to (Potential energy + Kinetic energy) divided by body surface
 area. The unit of inotropy is W/m2.

 -  Potential to kinetic energy ratio (PKR) is the energy used to produce blood pressure
 divided by the energy used to produce blood flow.
Inclusion Criteria:

 -  Age >40 years;

 -  Clinically diagnosed as COPD by physicians;

 -  Obtain any one of exacerbating symptoms (increased dyspnoea, sputum production, sputum
 volume, wheeze, cough or exertional dyspnoea);

 Exclusion Criteria:

 -  Known or suspected pregnancy, lactating patients, active malignancies, severe mobility
 problems (e.g. significant painful arthritis), and confusion or dementia .