Non-Smokers Are More Prone to Pulmonary Oedema Than Smokers
Non-Smokers Are More Prone to Pulmonary Oedema Than Smokers
Objectives: Acute coronary syndrome (ACS) patients are prone to develop pulmonary oedema with varied degree of hypoxaemia. The aim was to compare the risk for pulmonary oedema and related complications during ACS amongst non-smokers vs. smokers.
Methods: Prospective, observational study was performed in consecutive 68 patients presenting with ACS. They were divided into two groups; group 1 (n = 33) non-smokers and group 2 (n = 35) chronic smokers. Standard conservative treatment was given to maintain mean arterial pressure ≥ 60 mmHg, oxygen saturation > 95%. The bedside chest x-ray was graded for Battler grading (0-4) for pulmonary oedema. All patients were evaluated for troponin, serial creatinine kinase, echocardiography, arterial blood gas, renal function and correlated with inotropes requirement, active respiratory support, coronary care unit (CCU) stay and hospital outcome.
Results: Patients in both the groups had similar cardiac involvement for cardiothoracic ratio, troponin, ejection fraction and creatinine kinase muscle and brain (CK-MB). The bedside chest x-ray revealed significant (p < 0.05) lung oedema grades (3 and 4) in 60% non-smokers (group 1) vs. smokers (11%). These patients (group 1) also presented with significant (p < 0.001) hypoxaemia (lower PaO2/FiO2-201 ± 44), metabolic acidosis (higher lactate; 2.1 ± 0.72 mmol/l, base deficit; -5.1 ± 4.8) and hypocarbia (28 ± 2.9 mmHg) than smokers (group 2). The risk estimates for active respiratory support (OR =1.716) and inotrope use (OR = 1.836) was three times higher in non-smokers than smokers.
Conclusions: The higher degree of pulmonary oedema and hypoxemia probably contributed to poor short-term outcome in non-smokers than smokers. It would be important to recognise and treat hypoxaemia in non-smokers during ACS.
What's known: The patients during acute coronary syndrome are vulnerable to develop backpressure changes on pulmonary bed presenting as the pulmonary oedema, and the associated ventilation perfusion mismatch. Short-term better outcome of active smokers 'smokers paradox' during ACS has been reported. Based on data of national registry the paradox was correlated with younger age, more men smokers and with fewer cardiovascular risk factors such as hypertension or diabetes. However, the phenomenon was not fully explained by the measured covariates.
What's new: Chronic smoking induced lung fibrosis altered shape in alveoli and related pulmonary hypertension probably countered development of pulmonary oedema during ACS in smokers more than in non-smokers. This factor reported by us makes non-smokers more prone for poor short-term outcome during ACS being perceived as 'smoker's paradox'. Thus, an early suspicion for pulmonary oedema and treatment is warranted in non-smokers during ACS.
Patients of acute coronary syndrome (ACS) often get admitted in the coronary care unit (CCU) with varied degree of left ventricle dysfunction, low cardiac output, low tissue perfusion and cardiogenic shock. These patients are thus vulnerable to develop backpressure changes on pulmonary bed presenting as the pulmonary oedema and the associated ventilation perfusion mismatch. These changes predispose patients to varied degree of hypoxaemia, metabolic acidosis and the compensatory respiratory alkalosis. These factors together are likely to cast changes in the arterial blood gas (ABG) depending upon the extent of cardiac insult and the compensatory response. As smoking is a predisposing factor to coronary artery disease, a significant number of ACS patients might be chronic smokers as well. Short-term better outcome of active smokers 'smokers paradox' during ACS has been reported. Based on the data of national registry, the paradox was correlated with younger age, more men smokers and with fewer cardiovascular risk factors such as hypertension or diabetes. However, the phenomenon was not fully explained by the measured covariates. Chronic smoking is associated with airway-alveolar changes in smokers than in the non-smoker. We hypothesise that the smoking related lung changes might show different clinical presentation during ACS than that of non-smoker. As we have not come across any such report after extensive literature search, we prospectively compared clinical presentation of ACS patients in terms of being chronic smoker or the non-smokers.
Abstract
Objectives: Acute coronary syndrome (ACS) patients are prone to develop pulmonary oedema with varied degree of hypoxaemia. The aim was to compare the risk for pulmonary oedema and related complications during ACS amongst non-smokers vs. smokers.
Methods: Prospective, observational study was performed in consecutive 68 patients presenting with ACS. They were divided into two groups; group 1 (n = 33) non-smokers and group 2 (n = 35) chronic smokers. Standard conservative treatment was given to maintain mean arterial pressure ≥ 60 mmHg, oxygen saturation > 95%. The bedside chest x-ray was graded for Battler grading (0-4) for pulmonary oedema. All patients were evaluated for troponin, serial creatinine kinase, echocardiography, arterial blood gas, renal function and correlated with inotropes requirement, active respiratory support, coronary care unit (CCU) stay and hospital outcome.
Results: Patients in both the groups had similar cardiac involvement for cardiothoracic ratio, troponin, ejection fraction and creatinine kinase muscle and brain (CK-MB). The bedside chest x-ray revealed significant (p < 0.05) lung oedema grades (3 and 4) in 60% non-smokers (group 1) vs. smokers (11%). These patients (group 1) also presented with significant (p < 0.001) hypoxaemia (lower PaO2/FiO2-201 ± 44), metabolic acidosis (higher lactate; 2.1 ± 0.72 mmol/l, base deficit; -5.1 ± 4.8) and hypocarbia (28 ± 2.9 mmHg) than smokers (group 2). The risk estimates for active respiratory support (OR =1.716) and inotrope use (OR = 1.836) was three times higher in non-smokers than smokers.
Conclusions: The higher degree of pulmonary oedema and hypoxemia probably contributed to poor short-term outcome in non-smokers than smokers. It would be important to recognise and treat hypoxaemia in non-smokers during ACS.
What's known: The patients during acute coronary syndrome are vulnerable to develop backpressure changes on pulmonary bed presenting as the pulmonary oedema, and the associated ventilation perfusion mismatch. Short-term better outcome of active smokers 'smokers paradox' during ACS has been reported. Based on data of national registry the paradox was correlated with younger age, more men smokers and with fewer cardiovascular risk factors such as hypertension or diabetes. However, the phenomenon was not fully explained by the measured covariates.
What's new: Chronic smoking induced lung fibrosis altered shape in alveoli and related pulmonary hypertension probably countered development of pulmonary oedema during ACS in smokers more than in non-smokers. This factor reported by us makes non-smokers more prone for poor short-term outcome during ACS being perceived as 'smoker's paradox'. Thus, an early suspicion for pulmonary oedema and treatment is warranted in non-smokers during ACS.
Introduction
Patients of acute coronary syndrome (ACS) often get admitted in the coronary care unit (CCU) with varied degree of left ventricle dysfunction, low cardiac output, low tissue perfusion and cardiogenic shock. These patients are thus vulnerable to develop backpressure changes on pulmonary bed presenting as the pulmonary oedema and the associated ventilation perfusion mismatch. These changes predispose patients to varied degree of hypoxaemia, metabolic acidosis and the compensatory respiratory alkalosis. These factors together are likely to cast changes in the arterial blood gas (ABG) depending upon the extent of cardiac insult and the compensatory response. As smoking is a predisposing factor to coronary artery disease, a significant number of ACS patients might be chronic smokers as well. Short-term better outcome of active smokers 'smokers paradox' during ACS has been reported. Based on the data of national registry, the paradox was correlated with younger age, more men smokers and with fewer cardiovascular risk factors such as hypertension or diabetes. However, the phenomenon was not fully explained by the measured covariates. Chronic smoking is associated with airway-alveolar changes in smokers than in the non-smoker. We hypothesise that the smoking related lung changes might show different clinical presentation during ACS than that of non-smoker. As we have not come across any such report after extensive literature search, we prospectively compared clinical presentation of ACS patients in terms of being chronic smoker or the non-smokers.