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Coincidence of COPD and heart failure (HF) is challenging as both diseases interact on multiple levels with each other, and thus impact significantly on diagnosis, disease severity classification, and choice of medical therapy. The current overview aims to educate caregivers involved in the daily management of patients with HF and (possibly) concurrent COPD in how to deal with clinically relevant issues such as interpreting spirometry, the potential role of extensive pulmonary function testing, and finally, the potential beneficial, but also detrimental effects of medication used for HF and COPD on either disease., (© 2014 The Authors. European Journal of Heart Failure © 2014 European Society of Cardiology.)

The prevalence and mortality of heart failure (HF) increase with age. As a result, the early diagnosis of HF in this population is useful to reduce cardiovascular morbidity and probably mortality. However, the diagnosis of HF in the elderly is a challenge. These challenges arise from the under-representation of elderly patients in diagnostic studies and clinical trials, the increasing prevalence of HF with relatively normal ejection fraction, the difficulty in accurate diagnosis, the underuse of diagnostic tests, and the presence of co-morbidities. Particularly in the elderly, symptoms and signs of HF may be atypical and can be simulated or disguised by co-morbidities such as respiratory disease, obesity, and venous insufficiency. This review aims to provide a practical clinical approach for the diagnosis of older patients with HF based on the scarce available evidence and our clinical experience. Therefore, it should be interpreted in many aspects as an opinion paper with practical implications. The most useful clinical symptoms are orthopnoea and paroxysmal nocturnal dyspnoea. However, confirmation of the diagnosis always requires further tests. Although natriuretic peptides accurately exclude cardiac dysfunction as a cause of symptoms, the optimal cut-off level for ruling out HF in elderly patients with other co-morbidities is still not clear. In our opinion, echocardiography should be performed in all elderly patients to confirm the diagnosis of HF, except in those cases with low clinical probability and a concentration of brain natriuretic peptide (BNP) or N-terminal proBNP (NT-proBNP) lower than 100 or 400 pg/mL, respectively.

The authors describe a case of platypnoea orthodeoxia syndrome in an 83-year-old man with a fenestrated atrial septal defect and severe coronary artery disease. The patient had been admitted to hospital six times in the previous year with acute breathlessness, attributed to paroxysmal atrial fibrillation. The patient's symptoms resolved completely following surgical repair of the defect and coronary artery bypass grafting.

Diaphragmatic palsy after acute stroke is a novel clinical entity and may result in a high incidence of respiratory dysfunction and pneumonia, which especially cause greater morbidity and mortality. Generally, internal capsule and complete middle cerebral artery (MCA) infarctions are major risk-factors for developing diaphragmatic palsy. Herein, we present a case with contralateral diaphragmatic palsy after a subcortical MCA infarction without capsular involvement. Dyspnea occurred after stroke, while a chest X-ray and CT study disclosed an elevated right hemidiaphragm without significant infiltration or patch of pneumonia. A phrenic nerve conduction study showed bilateral mild prolonged onset-latency without any significant right-left difference. This suggested a lesion causing diaphragmatic palsy was not in the phrenic nerve itself, but could possibly originate from an above central location (subcortical MCA infarction). We also discussed the role of transcranial magnetic stimulation study in the survey of central pathway and demonstrated diaphragmatic palsy-related orthopnea.

We describe a case of a 56 year old man with no previous medical history who presented with sudden onset dyspnoea, expressive dysphasia, and right arm sensory loss and paresis. A diagnosis of bilateral pulmonary embolism and transient cerebral ischaemic attack was confirmed by CT pulmonary angiogram and MRI. Paradoxical embolism through an occult patent foramen ovale (PFO) was subsequently proven by contrast echocardiography. This case highlights a number of short and long-term management conundrums, that to date are incompletely addressed by clinical trials. These include timing of anticoagulation in patients with both venous thromboembolism and cerebral infarction, and the risk:benefit ratio of surgical closure of patent foramen ovale.

This study assessed the convergent validity of 2 dyspnea measures, the transition measure and the change measure, by comparing them with each other in patients admitted to the hospital with acute decompensated heart failure. Static measures of dyspnea were obtained at baseline (pre-static measure) and at time 1 hour and 4 hour (post-static measures). The change measure was calculated as the difference between the pre-static and post-static measures. Transition measures were obtained at time 1 hour and 4 hour. Visual analog scales and Likert scales were used. Both physicians and patients measured the dyspnea independently. A total of 112 patients had complete data sets at time 0 and 1 hour and 86 patients had complete data sets at all 3 time points. Correlations were calculated between the transition measures and static measures (pre-static, post-static, and change measure). Bland-Altman plots were generated and the mean difference and limits of agreement between the transition measures and the change measures were calculated. In general, short-term dyspnea assessment using transition measures and serial static measures can not be used to validate each other in this population of patients being admitted with acute decompensated heart failure., (© 2010 Wiley Periodicals, Inc.)

Dyspnea is a common presenting complaint in the emergency department (ED). Rapid identification of heart failure as the etiology leads to early implementation of targeted therapies. Although having only intermediate sensitivity, the S3 is a highly specific finding among older adults with heart failure. Identification of an S3 by routine auscultation can be problematic given the chaotic and noisy ED environment, patient comorbid conditions, and intolerance of ideal positioning for auscultation. Technologies using computerized analysis of digitally recorded heart tones have recently been developed to aid the clinician with bedside detection of abnormal heart sounds. Data using these technologies and their applications in the ED are reviewed as well as implications for future use and research.

Single-chamber ventricular pacing remains a frequent pacing method for symptomatic bradyarrhythmias. VVI pacing is effective in maintaining an acceptable ventricular rate, preventing severe bradycardia. However it may cause many important symptoms as a consequence of loss atrio-ventricular synchrony. Pacemaker syndrome (i.e. symptoms and signs caused by inadequate timing of atrial and ventricular contractions) may range in severity from vague pacing awareness to congestive heart failure. This event may be related more to retrograde ventricular-atrial conduction than to the absence of atrio-ventricular synchrony. We report 2 cases of VVI pacing complicated by nocturnal dyspnea (sign of congestive heart failure) as severe manifestation of pacemaker syndrome. By implantation of dual-chamber pacemaker, atrio-ventricular synchrony was restored, nocturnal dyspnea disappeared and has not recurred during clinical follow-up (12 and 4 months respectively for the first and second case.

A 42-year-old patient with acute left-ventricular failure is described in whom pheochromocytoma was diagnosed only after prolonged and fruitless efforts. Pheochromocytoma may present without the typical features of paroxysmal or sustained hypertension, headache, increased sweating, and palpitations. Therefore, in cases of acute left-sided cardiac failure of primarily undetermined origin, pheochromocytoma should be considered in differential diagnosis.

Bronchial responsiveness has been evaluated in patients with chronic lung congestion secondary to mitral valve disease. Methacholine bronchial challenge was performed by intermittent aerosol generation in 31 patients with mitral valve disease, 18 in New York Heart Association (NYHA) Class II and 13 in NYHA Class III, non-atopic and with baseline forced expiratory volume in one second/vital capacity (FEV1/VC) greater than 85% of predicted and in 30 normal controls. Haemodynamic data were available in 17 patients. The methacholine bronchial provocation dose causing a 35% fall of airway conductance (PD35sGaw) was significantly lower in patients (507 +/- C.I. 205 micrograms) than in normals (2779 +/- C.I. 358 micrograms), (p less than 0.001). In patients log PD35sGaw was significantly correlated with mean pulmonary artery pressure (r = 0.53, p less than 0.05), mean pulmonary capillary wedge pressure (r = 0.67, p less than 0.01), but not with any spirometric parameters. Bronchial hyperresponsiveness seems to be common in patients with mitral valve disease and evidence of lung congestion.

Epinephrine is a potent bronchodilator currently used to treat severe asthma, although there is no proven advantage of this drug over beta 2 adrenergic agonists. By contrast, as demonstrated here, the use of such a potent vasoconstrictor can worsen hemodynamic status when left ventricular dysfunction is associated with asthma or is the cause for dyspnea. We describe the case of a 60-year-old man with an history of chronic asthmatic bronchitis admitted for status asthmaticus. Bronchodilator therapy, including high dosages of intravenous epinephrine, failed to improve the patient and he was intubated and mechanically ventilated. Several hours later, a right heart catheterization revealed severe unexpected left heart dysfunction with a capillary wedge pressure of 45 mmHg and a cardiac index of 1.7 l/min/m2. Epinephrine was gradually stopped which resulted in a decrease in mean arterial blood pressure and an improvement of hemodynamic status. He was discharged on home mechanical ventilation. In this patient, ischemic left heart failure was revealed by a clinical picture mimicking status asthmaticus. Epinephrine, given as bronchodilator therapy on an empiric basis precipitated the patient into cardiogenic shock. Therefore this drug should not be recommended in face of the possibility of cardiac asthma or associated cardiac dysfunction.

The authors report a case of double aortic arc revealed by respiratory problems of obstructive type in a teenager. The diagnosis suggested by routine radiological check up as confirmed by aortography. After surgical disruption of the vascular ring, the respiratory troubles disappeared.

Bronchospasm due to cardiac disease results from increased pulmonary capillary pressure and impaired lymphatic drainage. Bronchospasm can usually be attributed to cardiac disease if physical and roentgenographic examination support the diagnosis of cardiac failure. The latter is especially helpful in revealing interstitial edema and redistribution of blood flow to the upper lobes. Therapy is directed at decreasing lung water, improving gas exchange and searching for the underlying mechanism of cardiac failure.

Thirty-seven patients with dyspnea, clinical chronic obstructive pulmonary disease and abnormal pulmonary function tests demonstrating an obstructive airways pattern underwent six-foot posteroanterior chest radiography, radionuclide ventriculography and sphygmomanometer-monitored arterial pressure response during a bedside Valsalva maneuver. Patients could be separated into three groups (square wave, absent overshoot, sinusoidal) on the basis of their Valsalva response which corresponded to left ventricular ejection fractions on radionuclide ventriculography of 0.19 +/- 0.05, 0.42 +/- 0.20, 0.64 +/- 0.13 (p less than 0.005 for differences between all group means). Pulmonary function test results and a detailed patient history could not accurately separate patients with primary pulmonary dyspnea from those with concomitant left ventricular dysfunction (ejection fraction less than 0.50). In this population of patients, however, both the sensitivity (88 percent) and predictive value (88 percent) for the presence of left ventricular dysfunction of an abnormal (square wave or absent overshoot) systolic arterial pressure response during Valsalva maneuver were high. Thus, in dyspneic subjects with clinical evidence of chronic obstructive airways disease, concomitant left ventricular dysfunction can be accurately diagnosed using the simple Valsalva maneuver without sophisticated equipment or highly trained personnel.

Cough and wheezing are common findings in left heart failure. However, it is still questionable whether nonallergic bronchial hyperresponsiveness, the hallmark of asthma, is also associated with this condition. In 12 subjects with acute decompensation of chronic postischemic LV failure, we assessed the PC20 methacholine during an episode of acute LV failure and after five to 15 days of intensive diuretic therapy. Weight, arterial blood gases, plethysmographic lung volumes, and expiratory flows were also measured on both visits. Extravascular lung water was estimated indirectly with a radiologic score. During acute decompensation, six subjects had significant airway obstruction and eight had a PC20 less than or equal to 16 mg/ml (significant bronchial hyperresponsiveness). After diuretic therapy, subjects improved significantly, losing an average of 2.2 kg, but they still had chronic LV failure and evidence of an obstructive breathing defect. Although mean PC20 was unchanged, three subjects had significantly improved PC20 after treatment. We conclude that: (1) left ventricular failure is often associated with mild bronchial hyperresponsiveness, although it is not excluded that smoking and the resulting possibility of bronchial obstruction can also play some role; and (2) acute treatment does not generally alter bronchial responsiveness to methacholine, suggesting that chronic LV failure can cause chronic changes to the airways.

The relation of dyspnea of presumed cardiac origin to regional and global left ventricular (LV) function was evaluated among 67-year old men sampled from the general population of Gothenburg, Sweden. From a screened cohort of 644 men, 42 men with cardiac dyspnea and without obstructive pulmonary disease, and 45 controls were sampled. Dyspnea was measured and graded according to the World Health Organization standard. Two-dimensional and M-mode echocardiography, carotid pulse tracing, apexcardiography and phonocardiography were used to evaluate regional wall motion, systolic time intervals, LV ejection indices, wall stress, diastolic time intervals, direct and indirect indices of LV filling properties, and indices of pulmonary hypertension. The plasma concentrations of immunoreactive atrial natriuretic peptide (IrANP) and catecholamines were also assessed. The dyspneic men had more regional wall motion abnormalities than the controls. Systolic, as well as diastolic LV impairment, and increased LV mass were more abundant. Dyspnea grade was significantly related to either of these abnormalities in univariate analyses, and also in multivariate analyses when clinical information, such as chest X-ray, electrocardiogram, and clinical history were taken into account. Multivariate analyses of all the studied indices of cardiac function, together with clinical information, showed dyspnea grade to be significantly and independently related to mitral valve E-point to septal separation (EPSS), presence of akinetic segments, a history of angina pectoris, exercise capacity, and left atrial dimension. Taken together these variables explained 74% of dyspnea grade variance. There was also a relation between dyspnea grade and IrANP, which was independent of clinical findings, but only appeared under conditions of severe dyspnea. It is concluded that the degree of dyspnea is associated with a fairly similar progressive impairment of diastolic, regional and systolic function. In mild heart failure LV hypertrophy and diastolic abnormalities are more prevalent than systolic dysfunction. In severe dyspnea a mixture of regional, systolic, and diastolic abnormalities are present. A decrease of fractional shortening and increased levels of IrANP are late phenomena. EPSS may be a useful indicator of LV dysfunction in population studies.

Cardiac asthma has been used as a synonym for episodes of cough, dyspnea, and wheezing caused by left ventricular dysfunction. The similarity of the terms bronchial asthma and cardiac asthma, and the observed symptoms of each disease implies a common pathophysiology. Bronchial asthma is characterized pathologically by airway narrowing, inflammation, edema, and obstruction by mucus. Bronchial asthma is defined as increased responsiveness of the tracheobronchial tree, which is manifested clinically as reversible expiratory airflow obstruction. The classic symptoms of bronchial asthma are cough, dyspnea, and wheezing. Cardiac asthma produces the same symptoms, but the pathophysiology producing these symptoms is not well described. We describe two patients with cardiac asthma who failed to demonstrate airway hyperresponsiveness to nonspecific bronchoprovocation testing and we postulate that these patients' symptoms were produced exclusively by left ventricular failure.

Compare the chest film with previous films, if possible. Changes in heart size and interstitial and vascular markings can thus be seen more readily, as can air trapping; this also aids in differentiation of acute from chronic changes. A Holter monitor study should be obtained if dyspnea occurs irregularly, has acute onset and termination, or is associated with dizziness or syncope; or if the resting ECG shows frequent premature atrial contractions, premature ventricular contractions, bradycardia, or periods of advanced heart block.

A poor therapeutic response may be explained by incomplete or erroneous diagnostic assessment, by failure to employ optimal drug doses and combinations, or by inadequate attention to the non-pharmacologic aspects of management. Poor compliance and counterproductive patient attitudes may need to be addressed. These problems and the approach to asthma concomitant with other diseases are discussed.