Contralateral diaphragmatic palsy after subcortical middle cerebral artery infarction without capsular involvement.

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.

Dyspnoeic dysphasia: a series of unfortunate events.

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.

Unique presentation of cricoid cartilage fracture causing intermittent dyspnea without preceding trauma.

Cricoid cartilage fracture is generally caused by significant neck trauma and causes continuous dyspnea, neck pain, or hoarseness developing immediately after the traumatic episode. A 69-year-old woman without any history of trauma was admitted to our hospital with intermittent dyspnea. Six months before admission she had started to complain of dyspnea occurring several times a month without warning, improving spontaneously within a few hours without treatment. Her primary care doctor diagnosed asthma and she was treated with inhaled short-acting beta agonists and glucocorticoids, without improvement. On initial evaluation at our hospital, the cause of dyspnea was unclear. Laryngoscopy was performed, which excluded vocal cord dysfunction. A further attack of dyspnea occurred on the fourth admission day. Stridor was evident during the attack, and bronchoscopy revealed subglottic narrowing of the trachea on both inspiration and expiration with no mass or foreign objects. Computed tomography (CT) of the neck revealed cricoid cartilage fracture causing airway narrowing and dyspnea. She was orally intubated, and tracheostomy was performed 2 weeks later to maintain her airway, which resolved her dyspnea. This patient's presentation was unique in two aspects. First, there was no history of trauma that may cause her cricoid cartilage fracture. Second, her symptoms of dyspnea were intermittent rather than continuous. These aspects led to suspicions of other diseases such as asthma or vocal cord dysfunction, thus delaying the diagnosis. Cricoid cartilage fracture should be considered in patients with dyspnea of unknown cause, irrespective of continuous or intermittent symptoms and preceding traumatic episodes.

Dyspnea: the heart or the lungs? Differentiation at bedside by use of the simple Valsalva maneuver.

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.

Bronchial hyperresponsiveness to inhaled methacholine in subjects with chronic left heart failure at a time of exacerbation and after increasing diuretic therapy.

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.

Cardiac asthma presenting as status asthmaticus: deleterious effect of epinephrine therapy.

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 difficult asthmatic.

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.

Dyspnea in the elderly: cardiac or pulmonary?

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.

[Paroxysmal nocturnal dyspnea as a severe expression of the pacemaker syndrome]. / Dispnea notturna paradossa come severa espressione di sindrome da pacemaker.

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.

Chronic obstructive pulmonary disease in heart failure: accurate diagnosis and treatment.

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.

Diagnosis of elderly patients with heart failure.

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.

If at first you do not succeed, think again!

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.

Assessing validity by comparing transition and static measures of dyspnea in patients with acute decompensated heart failure.

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.